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elderlyhematomassyndrome
Does Lysis Improve Quality of Life - Timeline | (SAM) Pulmonary embolism intervention - Self-assessment module (SAM) session
Does Lysis Improve Quality of Life - Timeline | (SAM) Pulmonary embolism intervention - Self-assessment module (SAM) session
2016Angiodynamicsapneachapterchroniccomorbiditiesconcludedcopddiastolicdysfunctiondyspneaembolismendpointexerciseexertionalfull videoheparinHypertensionhypotensiveintolerancelysedpatientspercentpersistentpressureprogressivepulmonaryqualitysbvSIRsyndromesystolicthromboembolicventricularzone
DEBATE: Ultrasound-Enhanced Thrombolysis Yields No Benefit Over Thrombolysis Alone
DEBATE: Ultrasound-Enhanced Thrombolysis Yields No Benefit Over Thrombolysis Alone
2014acousticacuteadjunctiveAngiodynamicsarisesassistedbleedingcatheterembolicendpointextrinsicfiberhistoryhoursidenticaliliacimplementingisispatencypatientpatientspercentprimaryrandomizationrandomizedrateremovalresidualroutinesbvsecondarystandingstatisticallystenosesstenosisstentingsubacutesyndrometherapytroubleultrasonicultrasoundversus
Post-thrombotic Syndrome | Patient Selection for CDT
Post-thrombotic Syndrome | Patient Selection for CDT
2016AngiodynamicschapterconditiondiagnosisDVTdysfunctionfull videohyperpigmentationiliofemoralpatientspoplitealproximalsbvSIRswellingsyndrome
SVC Syndrome | Balloon Angioplasty and Tamponade | 29 | Male
SVC Syndrome | Balloon Angioplasty and Tamponade | 29 | Male
2016acuteangiogramangioplastyantegradeballoonballoonscardiochronicdilateddraininflatedintimalocclusionocclusionspericardialprogressedrenalSIRsyndrome
Audience Response Question: CDT in Acute DVT | Patient Selection for CDT
Audience Response Question: CDT in Acute DVT | Patient Selection for CDT
2016AngiodynamicsbleedingchapterDVTdysfunctionfull videoiliofemoralischaemiamoderatepatientpreventrisksbvSIRsyndrometherapythrombosisthrombus
Evidence for Catheter-directed Thrombolysis | Patient Selection for CDT
Evidence for Catheter-directed Thrombolysis | Patient Selection for CDT
2016Angiodynamicsanticoagulationcathetercatheter directedchapterclotcompressiondirectedfull videoiliofemoralmechanicalmulticenterpatencypatientspharmacolpreventproximalrandomizedremoverisksbvSIRstentsstockingsstudysyndrometherapythrombolysistrial
Thrombolysis For DVT: Predictors Of Success
Thrombolysis For DVT: Predictors Of Success
2015accpachieveanatomiccavalchronicclinicalDVTfailureguidelineshypercoagulableiliaciliofemoralincompletelysislyticmalepatencypatientpatientspharmacomechanicalphlegmasiapredictorsprothromboticrecurredrecurrenceregressionsurgerysyndromethrombolysisthromboticthrombustreatedultrasoundvenousvillalta
Audience Response Question: Evidence for Use of DCT | Patient Selection for CDT
Audience Response Question: Evidence for Use of DCT | Patient Selection for CDT
2016AngiodynamicschapterDVTfull videoiliofemoralrandomizedreducerisksbvSIRsyndromethrombus
Outcome by Treatment Mode and Primary Safety Endpoint
Outcome by Treatment Mode and Primary Safety Endpoint
2016adjuvantAngiodynamicsangioplastyarterialhematomasinterventionmechanicalpatientsPenumbrapercentpercutaneousperfusionsbvSIRstentthrombectomytpa
Management - Post Thrombotic Syndrome | (SAM) Management of chronic venous disease - Self-assessment module (SAM) session
Management - Post Thrombotic Syndrome | (SAM) Management of chronic venous disease - Self-assessment module (SAM) session
2016ambulationAngiodynamicschaptercoagulationdevelopdiseaseDVTfull videopatientspercentprevalenceproximalsbvSIRsyndromeulceration
Physics of MRI 5: Relaxation and Image Contrast - Part 2a
Physics of MRI 5: Relaxation and Image Contrast - Part 2a
2012acquireacquiredacquisitionadjacentangleassumecenterchaptercompletecontrastcorrespondsechoevolveexamineflipfull videogenerategeneratedgeneratesgradientimageinitialintensityiterationsliesmagneticmechanismsMRImyocardiumparametersplotportionpulserecoverrecoveryrepeatsequencesequencesshortersignalsimplyspinstartingsteadytimetippedtissuetransverseUHN
Upper Limb DVT | Medical Management of DVT
Upper Limb DVT | Medical Management of DVT
2016AngiodynamicsanticoagulationcathetercentralchapterdurationDVTextremityfull videoisispatientsproximalsbvSIRsuggestedsurgerysyndromethrombolyticundergovenous
Audience Response Question: Prevention of Post Phlebitis Syndrome | (SAM) Management of chronic venous disease - Self-assessment module (SAM) session
Audience Response Question: Prevention of Post Phlebitis Syndrome | (SAM) Management of chronic venous disease - Self-assessment module (SAM) session
2016ablationAngiodynamicschaptercompressionelasticfull videooccludedrandomizedsaphenoussbvSIRstentingsyndromeveins
Physics of MRI 3: K-Space and Gradients - Part 1
Physics of MRI 3: K-Space and Gradients - Part 1
2012acquireapplybandwidthcomponentscompositeconceptconceptscyclecyclesdatadeterminedistributionequalessentiallyevolvesevolvingfieldfrequencyfunctiongenerategradientgradientsimageimaginginitiallecturelocalizelowestmagneticmiddleMRIoccurrencepositionprescribeproduceproducingproportionalregionrelativerepresentationresolutionreviewrotatingsamplingsignalsignalssimplyspacingstrengthtimestransformtransformingUHNultimateunderlyingvaluesvariablevarieswater
ATTRACT Study Of rt-PA For Acute DVT: Almost 7 Years And Almost 700 Patients, Almost Done: What Will We Find
ATTRACT Study Of rt-PA For Acute DVT: Almost 7 Years And Almost 700 Patients, Almost Done: What Will We Find
2015accpacuteadjunctiveattractcathetercomparabledeepDVTendovascularenrollevaluatingfemoraliliaciliofemorallimbpatientspercutaneouspostproximalrandomizationrecommendedriskroutineseveritysteeringstratifiedsureshsyndromethrombolysisthrombosisthromboticthrombusvedanthamvenousvillalta
Severe Illiac Obstructive PTS - Strategy  | Evidence Gaps in the Treatment of Chronic Venous Insufficiency
Severe Illiac Obstructive PTS - Strategy | Evidence Gaps in the Treatment of Chronic Venous Insufficiency
2016ablatingchapterfull videoHypertensioniliacimprovedrefluxsaphenoussbvSIRsyndromethrombosisveinvenous
Does Lysis Improve Quality of Life - Timeline
Does Lysis Improve Quality of Life - Timeline
2016AngiodynamicsapneachroniccomorbiditiesconcludedcopddiastolicdysfunctiondyspneaembolismendpointexerciseexertionalheparinHypertensionhypotensiveintolerancelysedpatientspercentpersistentpressureprogressivepulmonaryqualitysbvSIRsyndromesystolicthromboembolicventricularzone
Severe Illiac Obstructive PTS - Strategy
Severe Illiac Obstructive PTS - Strategy
2016ablatingchapterHypertensioniliacimprovedrefluxsaphenoussbvSIRsyndromethrombosisveinvenous
Audience Response Question: Prevention of Post Phlebitis Syndrome
Audience Response Question: Prevention of Post Phlebitis Syndrome
2016ablationAngiodynamicscompressionelasticoccludedrandomizedsaphenoussbvSIRstentingsyndromeveins
SVC Syndrome | Balloon Angioplasty and Tamponade | 29 | Male | Treating chronic venous occlusive disease - Case-based workshop
SVC Syndrome | Balloon Angioplasty and Tamponade | 29 | Male | Treating chronic venous occlusive disease - Case-based workshop
2016acuteangiogramangioplastyantegradeballoonballoonscardiochapterchronicdilateddrainfull videoinflatedintimalocclusionocclusionspericardialprogressedrenalSIRsyndrome
Major and Minor Complication Rates
Major and Minor Complication Rates
2016AngiodynamicsbleedingclinicallycompartmentdilationembolisationembolizegrowinghematomahematomasoccurredpatientsperforationsretroperitonealsbvSIRsyndromethrombolysisthromboses
Physics of MRI 5: Relaxation and Image Contrast - Part 2b
Physics of MRI 5: Relaxation and Image Contrast - Part 2b
2012acquirecartilagecausedcentercontrastcorrespondsdefineddegreeechoessentiallyfastfastergenerategradientinitialintensitylobemagneticmetersmovesoccursparameterplaypulserelativerotatingsignalspacespintimetipsUHN
Major and Minor Complication Rates | Thrombolysis: Arterial and Venous - Scientific session
Major and Minor Complication Rates | Thrombolysis: Arterial and Venous - Scientific session
2016Angiodynamicsbleedingchapterclinicallycompartmentdilationembolisationembolizefull videogrowinghematomahematomasoccurredpatientsperforationsretroperitonealsbvSIRsyndromethrombolysisthromboses
Who to Choose? | Patient Selection for CDT
Who to Choose? | Patient Selection for CDT
2016anatomicAngiodynamicsanticoagulationbleedingcandidateschaptercontraindicatedDVTfull videohemorrhagicintracranialpatientpatientspostpartumpreventprocedurerisksbvSIRsyndrometherapythrombolytic
Physics of MRI 6: Magnetic Resonance Imaging Options
Physics of MRI 6: Magnetic Resonance Imaging Options
acquireacquiredacquiringacquisitionadjustaffectanglebandwidthchaptercomponentdatadecreasedecreaseddecreasesdirectlydiscussequalessentiallyfactorfieldflipfull videoimageimagesimagingincreaseinitiallargerlongitudinalmagneticmagnitudematrixMRInoiseoptionsparameterspixelplaneproportionalpulseratiorecallresolutionrootsamplingscansignalsimplysizeslicespatialsquarethicknesstimetransformtransverseviewwedge
Physics of MRI 5: Relaxation and Image Contrast - Part 2a
Physics of MRI 5: Relaxation and Image Contrast - Part 2a
2012acquireacquiredacquisitionadjacentangleassumecenterchaptercompletecontrastcorrespondsechoevolveexamineflipfull videogenerategeneratedgeneratesgradientimageinitialintensityiterationsliesmagneticmechanismsMRImyocardiumparametersplotportionpulserecoverrecoveryrepeatsequencesequencesshortersignalsimplyspinstartingsteadytimetippedtissuetransverseUHN
Outcome by Treatment Mode and Primary Safety Endpoint | Thrombolysis: Arterial and Venous - Scientific session
Outcome by Treatment Mode and Primary Safety Endpoint | Thrombolysis: Arterial and Venous - Scientific session
2016adjuvantAngiodynamicsangioplastyarterialchapterfull videohematomasinterventionmechanicalpatientsPenumbrapercentpercutaneousperfusionsbvSIRstentthrombectomytpa
Management - Post Thrombotic Syndrome
Management - Post Thrombotic Syndrome
2016ambulationAngiodynamicscoagulationdevelopdiseaseDVTpatientspercentprevalenceproximalsbvSIRsyndromeulceration
Transcript

Good morning, my name is Professor Kieran Murphy, I am going to discuss with you this morning work that I've done with my colleagues, Dr Sheila Waa, Amanda Chan and Agnes Sauter in the area of trying to identify typical radiological findings in the elderly who've been physically abused. This is an area that hasn't previously been investigated and yet there is significant evidence that this is a growing problem in our society. This investigation or work

began for me about 16 years ago when I was on call in New York and I was bothered by the large number of elderly people that we were seeing with subdural hematomas and periorbital trauma, and I began to suspect that there might be a syndrome there that was akin to the shaken baby syndrome or Caffe syndrome that we know occur in children. So to investigate this, we

reviewed reports in the medical literature on the distribution of physical injuries due to elder abuse. To see if we could characterize a pattern that would be useful for the diagnosis of this problem in the clinical setting or in a social context. In terms of background, abuse of older people by family members or are those known to them in their homes are in long term care institutions. Is it growing

thing i want to talk about is quality of life and when we're talking about quality life and pulmonary embolism the primary determinant of that the best of

my knowledge is residual or persistent or progressive pulmonary hypertension which Rex exercise tolerance and cause shortness of breath first described about 90 years ago by young dal then toyed with by dale and Albert who

concluded that a chronic corporal manali the word used back then before CTF was even known is an extraordinarily unlikely complication of PE the late great can moser fault that maybe as many as four hundred fifty patients had this

syndrome of what he started calling chronic thromboembolic pulmonary hypertension but then rivière ok mout and showed that up to forty percent of patients post PE end up with high pressures that are persistent

progressive over the next five years pingo concluded that about three percent of patients went on to develop the full C tough syndrome and at the time this new england journal paper came out that number was about 10-fold most experts

thought now we're thinking more in terms of a transition where there's a larger number of patients maybe 25 to 40 percent that have a partial seat s syndrome not the full concrete in the lungs syndrome that causes the need for

the operation but progressive pulmonary hypertension that's not explained by smoking or sleep apnea or elevated left ventricular end diastolic pressure it's not just comorbidities this is work that I did where we took a hundred and

twenty-seven patients that had no previous comorbidities except we did not exclude obesity and smoking and we found forty-one percent of them either had a bad-looking echo or dyspnea at rest or exercise intolerance six months later

clock found the quality of life was not good after PE with numbers that looked similar to like COPD with over half of patients reporting exertional dyspnea and seventy percent having new or worsening dyspnea after their PE lots of

evidence that PE messes up quality of life including some in 2014 from our friends in Australia from challenge at all child at all that found a 25-percent had all of these things impaired exercise capacity heart rate recovery

pulmonary hypertension and raised PVR and right ventricular dysfunction is important point that he had is the corollary is they were apparently normal when you talk to them but was only when you provoke them did you find these

abnormalities we studied a cohort of patients of 200 patients that had some massive PE they were normotensive if they became hypotensive they got lice that's these patients this is the right ventricular pressure on the x-axis the

y-axis at diagnosis and six months later all the patients that got lysed had reductions in their systolic pressures on the right side of the heart these are patients that just got heparin alone the red lines are those that

increase the pressure that was one-third of all the patients that just got heparin alone plus a higher rate of exercise intolerance and dyspnea at rest and the topcoat study we looked at a composite of endpoints including bad

stuff on the front end and bad stuff on the back in what we considered a patient-centered endpoint and you were three times more likely to hit the bad end point with placebo compared to connect a place here it is shown another

way with bar charts that are just so horizontally patients want to be in the white zone they are more likely to be in the white zone if they were treated with connected place

determine ladies and gentlemen were a lot about this ecosystem ultrasonic assisted trouble is the question do we need that at all in our patients that I don't have any disclosures to make here we heard about the coven I think this is just a door reopen off for CDT that the

disadvantages that trials that the durational trouble arises was at a mean of 2.4 days keeping the patient on intermediate care and going along with the major playing rate of nine percent and another drawback of that study is

that the PTA standing right in coven was down to seventeen percent knowing that we have at least sixty percent on the lying stenoses of the iliac veins creating probably or being the reason for the trombones in these patients so

implementing that we routinely stint are that the residual Venus cells is either well this is true Moses or extrinsic stenosis it doesn't matter we do a routine standing and we are implementing ultrasonic assisted character director

criminalizes and fix those fixed timing of 20 milligrams per 15 hours in our Center since 2010 when you see we have a standing rate of eighty percent of the from the first series of 87 / patient's we heard about the arm ultrasound system

the mechanism is we have fiber in separation and acoustic drug delivery we have active drug delivery by acoustic steaming to intensifying the effect of CDT that's our meaning and that's our wish arm we separated a little bit how

good is trouble izes according to the history if we have a real acute few days history have a 89% slices up to 15 hours of more than fifty percent if you see if we go to acute on chronic or more subacute history in these patient goes

down to sixty percent if we have that what I said the routine standing we anyway have a primary patency rate of eighty-seven percent secondary Peyton cre8 at 12 month of eight ninety six percent and the process traumatic

syndrome development at 12 month into patients that makes six percent so the question now is it the standing horses ultrasound assisted trouble arises that gave the much better results regarding pay to see in our patients so

we started a randomized controlled trial that is completely independent of the industry is funded by the Swiss research research research foundation is the burn ultrasound assist Rumble Isis for healio femoral deep vein thrombosis versus

standard CDT trial so as you see here patients were enrolled according the acute DV te ephemeral randomization was either to echo system fixed dozing of 20 milligrams over 15 hours versus CDT alone so all patient got the echoes

catheter inserted but in half of the patient where it was switched on and the other half it was not switched on the primary endpoint was assessed by a blinded correlate that was there was the flipper feet after 15 hours duration of

the license so it was a percentage of rumbles load reduction from baseline to 15 hours of capitalizes pretty fair done randomization these patients secondary endpoints adjunctive trembles removal spending rate bleeding rate and a

3-month follow-up in these patients and this is the primary endpoint i leave you with that for a second so percentage reduction and promised load by the length adjusted trembles score done by core lap was completely identical if we

go to the secondary outcomes adjunctive therapy objective capital rumbles removal therapy was slightly higher in the CDT only group but there were statistically not significant a small number is twenty-four hours twenty-four

patients adjunctive stenting number of implanted stands completely identical in both groups and safety major bleeding in one of our patients 4.2 percent in the echoes arm vs 0 in the CTR that is not statistically significant and probably

by chance minor bleeding in one in two patients in each arm so secondary outcome at three months primary patency hundred percent 96 secondary patency hundred percent mean alot to score three points

your pres- three-point miners 1.9 class minnows 1.9 at statistically not significant so in conclusion ladies and gentlemen catheter directed traumatizes will fix those regimen followed by routine stenting of residual veena

stenosis is safe and associated with a high pregnancy rate and low risk of post-traumatic syndrome the addition of intravascular ultrasound seems not to facilitate Trump's resolution this is done in a industry independent

randomized small size truck tire the results of the beautiful try may not necessarily apply to other echoes indications including PE or trauma embolic arterial disease thank you for your attention

point where people normally show the nastiest picture they have of patients with post-traumatic syndrome

it is important to know that while ulcers you know are something that is part of the syndrome it is by no means the most common presentation of post-traumatic syndrome more commonly patients are just presenting with daily

leg pain swelling this heaviness and that combination of symptoms significantly in Paris quality of life you can also get some skin changes hyperpigmentation and fibrosis and for the Trude diagnosis of post-traumatic

syndrome you should wait till at least three months out from their initial diagnosis of their their dvt to not confuse some delayed effects with residual swelling from their acute episode and make sure that it's truly a

chronic condition because of some underlying a Venus damage involve dysfunction it is a lifelong condition that patients deal with the severity of course and impacts our overall quality of life

so who's developing post-traumatic syndrome not every patient who gets a DVT developed post-traumatic syndrome but several studies have shown that approximately fifty percent of patients with the proximal dbt that's you know

more proximal to the popliteal vein will develop a post-traumatic syndrome or patients with dvt specifically in the iliofemoral region that increases the risk to about sixty percent of patients so if you have a clock there and its

So the final case is I think the worst complication that I caused, it's I feel awful about it and hopefully it will be a learning lesson for yourself it certainly was for me. This was a 29 year old who had a terrible SVC syndrome with advanced with spiritry/g compromised as well as chemosis and almost not quite

comatose but really in quite a bad way from his SVC syndrome. His background history was that he had chronic renal failure since infancy and had had two failed renal transplants and innumerable lines in his upper extremities in both his eye IJs. He was HIV and Hepatitis C positive from transfusion related issues. He was on aspirin at the time for cardio protection,

and he had two needs, one of which was an access for haemodialisis and then the second was treatment of this SVC syndrome, but he certainly needed access immediately. This was a CT that we did at the time, you can see the seclusion

here in his SVC. Very dilated azygos vein. We do quite a bit of SVC recanalization for access, for dialysis access, short gut syndrome, TPN, that sort of thing.

One of the things I will say to you is that when you're looking at the CTs, the level of the occlusion is really crucial. That the lower it is the more dangerous it is. And this is the illustrative case of that, that if the occlusion is higher up, it's outside of the potential for pericardial involvement to

can be a little bit more aggressive. When it's lowered down like this, this is where you can run into trouble. So we did what we usually do which is an antegrade access from a recanalized external jugular vein, brought a sheath down and you

can see the run here is showed really just enormous [UNKNOWN] stylation system feeding back with no evidence of an SVC at all. It actually wasn't that hard to recanalize, didn't require sharp recantalization again, most of these we do require sharp recanalization, but here a wire and catheter and a few sheaths managed to get us through.

And you can see the position of the wire in the SVC going down through the atriam/g to the IVC with the position of the [UNKNOWN] behind us. I then proceeded to ciliary dilate and started off with six and eight very tight ways to tuck her off, but it gradually began to

open with some high pressure balloons and I did intimate non geography to see how I was doing despite opening it to I think this is after a ten balloons zero antegrade flow through the system still all going down through the [UNKNOWN] Proceeded up with some further larger balloons, and at this point

I did another angiogram after this it was a 14 millimeter balloon and there was a finding that I missed at that time that is very important, and I'll give you a second just have a look at the angiogram yourself to see if you're better than me. And this is what it is. So this, what I believe was an intimal tear in the acute thrombotic

formation on an intimal tear of the SVC was on this one. I did not appreciate it at the time and proceeded with further balloon angioplasty because again there was no antegrade flow leading down into his SVC and into his right atrium at that point. Proceeded with further balloon angioplasty this is with an 18 balloon and got it up to full and then as I took it down he began to complain

of a strange sensation in his chest that rapidly progressed to him being [INAUDIBLE] that rapidly progressed to him collapsing cardio dynamically and then I performed this angiogram and you can see here as we go through the run this large rent/g here and free extravazation from the SVC

into the pericardial space and [INAUDIBLE] there. So this was complicated by an acute [UNKNOWN] immediately I would say within 30 seconds, he began to change [INAUDIBLE] with the chance of respiration within a minute he had arrested and was requiring

quite a bit of chest [UNKNOWN] followed by as you can see we put in a pericardial drain immediately I inflated the balloon to expand it and he ended up being shocked several times. The options were discussed with the arrest team, we felt that given his age given that he was 29 and this was an acute issue, we would to do our best

to preserve everything in it's place [INAUDIBLE] while that was being set up I kept the balloon inflated and there was a thought that perhaps his balloon tapered out enough release. This showed that no it wasn't, this is after 45 minutes of balloon tamponad/g you can see there is still this large hole,

this is not gonna be repaired by simply tamponading/g the hole, and I ended up placing a viabahn stent across the area. Unfotunately we didn't have atrian/g in this particular lab at that time.

So this sealed the hole and we were able to stabilize him at this stage the bright red blood that was pumping out of his tamponade/g drain that was pericardial drain ceased immediately, and he became [INAUDIBLE] stable again and we were able to move him upstairs. Unfortunately, he had a drastic postoperative course with a global hypoxic injury and actually passed away three days later.

So the take home from this case for us, for me in particular was to be very wary of dilating chronic SVC occlusions particularly those that are low down the super cardinal recess of the pericardium extends to the level of the [UNKNOWN] when you're chronic occlusions at that level to be very very particularly if the major clinical question is accessed,

they do not need to be dilated to 18 like I did, but in the access, settle in there, and you can always come back and treat the SVC syndrome at a different time, perhaps in a different way. But certainly it was a very [INAUDIBLE] point for myself. >>

which of the following is not an appropriate scenario and rationale to

consider catheter directed therapy for acute deep vein thrombosis a iliofemoral thrombosis associated with limb-threatening Venus ischaemia to prevent limb loss and death be extensive cable pharmacist to prevent organ

dysfunction see fanpop dvt in a patient with moderate bleeding hers to prevent the post-traumatic syndrome d iliofemoral thrombus and a patient and patient with low bleeding risk to prevent post-traumatic syndrome or none

of the above these are in the answer is the so patients with them pop with a moderate bleeding risk with the modern bleeding risk on top of the location they would not be great patience for this sort of

therapy next question the use of

another thing I cared about and I wanted to work on

since residency in Albany was the radiology appearance of Elder Abuse where are used to shaken baby syndrome I was sure in the elderly that there was a similar appearance that they would get characteristic fractures the trouble is

differentiating it from slip-and-fall fractures so we put about three years of work into this and we identified a pattern of combined sociological conditions and Radiological fractures and so this now is a poster that's on

the wall in Weill Cornell in New York and in University of Rochester University Toronto and this awareness is beginning to spread that there are typical fractures that happen the elderly who've been assaulted by a

caregiver and and in a certain social context so this is the kind of stuff I like to do and I've got about eight and a half years left before I get my aortic valve replaced again and I want to get as much work

done as possible so I have a countdown clock on my computer each day it tells me how much time I've got left and so I work harder and harder to do something useful and this is you know this is

leading to post-traumatic syndrome then if you remove the clot that should in theory decrease your risk of developing post-traumatic syndrome and that has been proved as a proof of concept with many studies when patients are put on

anticoagulation so if patients you know are decreasing their risk just with anticoagulation then if you remove the clot potentially earlier with the development and the implementation of catheter directed

thrombolysis and preserving the overall integrity of the vein is that really going to speed symptom relief is it going to spare the valve function is it good going to preserve the maintenance patency and is it going to really

ultimately prevent post-traumatic syndrome the very first randomized trial and to date the only randomized trial was a Scandinavian study out of Norway where they looked at patients specifically with high proximal dbt so

the iliofemoral dbt and they randomized them to standard therapy which was anticoagulation and compression stockings versus standard treatment with additional catheter directed therapy and they demonstrated an absolute risk

reduction of fourteen percent so41 per se forty-one percent of patients still developed post-traumatic syndrome when they got the additional catheter directed therapy but with some

significant reduced from those patients who just received the anticoagulation alone then of note there was a small increase bleeding risk associated with that therapy this therapy of our this study although it is good data doesn't

necessarily reflect the current practice of what we do today more commonly what we're doing is pharmacol mechanical from back to me or catheter directed from back to me so using you know different devices and

tools and stents to help improve the primary patency of the van once we re-establish flow that isn't really reflected in what this study was designed to do therefore the track trial which we all

know was really designed to address the form of mechanical components of catheter directed from therapy and really does that prevent post-traumatic syndrome against a multicenter study the control group was

the same as the region study with anticoagulation and compression stockings the treatment group was that in addition to the pharmacol mechanical therapy there followed for two years and overall it was a more robust study with

powered to test for a third reduction they have closed registration they had just under 700 patients registered and now we're just waiting for the follow-up in the data to come out on that in

Thank you very much for the introduction. I have nothing to disclose. So in the way of a background, and you've heard about all this, catheter-directed techniques and pharmacomechanical thrombolysis are increasingly used to treat ilofemoral DVT because of the multiple reported advantages, as Tony has mentioned earlier. The clinical benefit continues to be debated, however, in terms of

what the guidelines tell us there is some conflict between the ACCP guidelines and other guidelines in terms of how aggressive we should be. Immediate failure has been clearly reported to occur in up to 20% of patients depending on which series you read. In our own institution, 13% of patients may experience immediate

failure. In addition to that, the two-year patency rate varies, there's a big range, 65 to 90%, that has been reported, and at our own institution the patency of the treated venous segment is 83% at about four years. This is why we decided to look at the predictors of immediate and

long term failure of thrombolysis for iliofemoral DVT, not only to guide patient selection to achieve the perfect outcomes, but also to set patient and physician expectations. This was recently published in JVS Venous. So this was a retrospective study looking at consecutive patients treated over a period of five years or so.

We looked at demographics as well as records, and the endpoints that we were mainly interested in were immediate failure as defined as 30 day recurrence or less than 50% lysis. Anatomic failure was determined by ultrasound, and this is how we looked at long term ultrasound patency, and the post-thrombotic syndrome was defined as a Villalta score of more than five.

118 limbs were treated in 93 patients. The mean age was about 49, almost equally distributed between men and women. 55% on the left side, and almost half of the patient had caval involvement.

Most patients were treated with a combination of catheter and pharmacomechanical techniques, and 56% required iliac vein stenting. Ultrasound follow up, which determined anatomic failure, was available at 16 months, and clinical follow-up to determine the post thrombotic syndrome was available at 21. Immediate failure was seen in 11 patients or 12%, and the causes

were as follows, seven patients had recent surgery and had to have a short lytic intervention because of bleeding complications, three patients had acute on chronic lesions and recurred because of their chronic DVT lesions, and one patient potentially had a hypercoagulable state.

In the logistics regression model, if you look at the predictors of immediate failure, and this included recent surgery as well as phlegmasia as an indication for treatment, there was a trend for male gender and age, but these were not significant. If you look at anatomic failure and DVT recurrence, so 72% were

patent at up to three years, and in a multivariate regression model incomplete lysis, and malignancy, and recent surgery were predictive of immediate or of anatomic failure at forty-eighth month. Similarly, if you look at the prothrombotic syndrome, this occurred in 28% of patients at 36 months. And in a logistic regression model the predictors of the occurrence of the prothrombotic

syndrome included incomplete lysis, male gender, phlegmasia as an indication, advanced age, and iliocaval involvement. When this was broken down however, by whether a patient had an immediate failure or not, you can clearly tell that the instance of a prothrombotic syndrome was significantly lower in those patients who were able to achieve successful lysis following treatment.

So in conclusion, thrombolysis can achieve high rates of immediate thrombus clearance and PTS morbidity reduction, yet a significant number of patients will experience immediate or late failure find as anatomic or clinical failure. And those are the patients who had recent surgeries, male gender, perhaps, phlegmasia as an indication

for treatment, and patients with a malignancy. And as we know from this series and others, lysis needs to be complete with at least more than 50% lysis in order to achieve the lowest rate of DVT recurrence and PTS. Thrombolysis for symptomatic iliofemoral DVT can be successful, and if the case is in the short and long term run.

And as Tony has mentioned earlier, we hope that the results of the ATTRACT file will clarify which patient will derive the most benefit from lytic therapy. Thank you very much for your attention. >> [APPLAUSE]

catheter directed therapy in which of the following acute dvt scenarios is supported by randomized trial data a flag measure like measures really don't to prevent loss bidc thrombus see

iliofemoral dbt to reduce the risk of the post-traumatic syndrome d fanpop dvt to reduce the risk of the post-traumatic syndrome re none of the above the answer is C the iliofemoral dvt to

reduce the risk of post-traumatic syndrome that was our Comment study the

you look again about fifty percent of those patients that were treated with a penumbra integral frontline only to me

two or three posted to go number into your treatment of from over eighty-one percent after intervention over ninety-five percent TPA and then use the number indigo again even slightly better results no significant change after

intervention with angioplasty and stent placement also as far as mechanical come back to me prior to remember again about the same with hundred percent perfusion post both usable for adjuvant TPM account therapies obviously these are

patients that we started out with those patients that we couldn't get lice we couldn't use a get other mechanical thrombectomy devices to use went to the number is the last ditch effort and obviously a hundred percent of patients

then we establish flow safety there was procedurally SI es in about seven percent of patients obviously none of those were device-related this is obviously a percutaneous arterial intervention vast majority of those four

hematomas at the site mostly in patients that are already previously had from political or other mechanical thrombectomy thermolysis so really none device related complications at all

management of of dvt can be broken and very simply into ambulation blood thinners compression stocking pretty

good evidence that each at each level on the recommendation but we know that there is a need for more because we're seeing these patients with post-traumatic syndrome patients who have chronic disease and so what are we

looking at well its patients who have leg swelling and pain people who come in with the heavy leg syndrome and these are the sort of images that we know will see fairly regularly and these the ones that are usually association with

proximal disease in the video cable segments it's extremely common if you run the numbers somewhere between twenty and fifty percent of all patients who develop whoever dbt will develop some form of pts despite being on the best

our ad coagulation and obviously people who can't be out Greg later a higher risk and all those people somewhere about ten percent will develop a severe form of PTSD can go onto ulceration so that the probability of

one of us getting a DVT and that going onto ulceration is somewhere up to five percent so huge number when you think about the the prevalence of this disease and this has a as big societal costs so

Hi, my name is Marshall Sussman. I'm an MRI physicist at University Health Network, in University of Toronto. This lecture is gonna be the second part of my Relaxation and Image Contrast in MRI talk. So in first part of this lecture we briefly reviewed what image contrast is, and then we discussed a number of different MR mechanisms that can be used to generate contrast. So in this lecture what I'm gonna do is, I'm going to show how those contrast

mechanisms can be used within various different MR pulse sequences to create contrast. So the pulse sequences that I'm gonna be talking about are gradient echo and spin echo. So image contrast in image depends on a number of factors. So first is the tissue parameters. So this is proton density, T2, T2*, T1, which we've obviously mentioned, pulse sequence, and the pulse sequence parameters. So all three

of these things will affect the ultimate contrast we see in an image. Now often, when I interact with people who aren't necessarily really familiar with some of the details in MR physics, often, various different mnemonic devices are used. So people say if I have a short tear in my pulse sequence that gives me a T1-weighted contrast image. If I have a long TE

that gives me a T2-weighted contrast in my image. And that's true for many pulse sequence types, but it's not true in all cases. There are certain pulse sequences where these sets of parameters could give you different types of contrast. And really, in order to fully understand the contrast you're gonna generate in an image you really have to examine the pulse sequence, the parameters, and the underlying

contrast mechanisms. And it's really only from that complete understanding that you can really get a good comprehension of what types of contrast you're going to be generating. So with that in mind, let's move on to the first pulse sequence that we're gonna look at, Which is gradient echo. So this is one that we've looked at, a number of different times in the previous lectures, but I'm just gonna

briefly review it here. So basic pulse sequence timing diagram, you can see here, it starts with an RF pulse, which we know tips down the magnetization away from the external magnetic field. And we then turn on our gradients which is what move us through k-space to acquire our data. So initially, after we do our RF pulse, we always start at the center of k-space. We then turn on our Y gradient, and that

moves us up into a particular position in the vertical direction. We turn on our negative polarity X gradient which moves us out to the left hand side of k-space, and then that's followed by our positive polarity gradient, which sweeps out a complete line of k-space. And that's when we acquire our data. We then increase the strength of the Y gradient, and that moves us up to another

line in k-space, and repeat that same procedure. So we just simply step through this, repeat this procedure as many times as necessary in order to cover off all lines of k-space. Now within this basic gradient echo pulse sequence, there's three different adjustable parameters that we can manipulate. The first is the Flip angle or theta so that's really the RF pulse, and it's just simple

the angle that the magnetization makes with the external magnetic field. So this is something that we can control. The second parameter is the TR or the repetition time. And this is simply the time between the acquisition of adjacent k-space line. So essentially the time that it takes us to repeat this cycle. Third is the TE or the echo time, and this is defined at the time between when we first tip

our magnetization down, so we first put out our RF pulse and the time with which when we acquire the central portion of k-space. So in this case it's the center point of this gradient loop, cause that corresponds to when we go through the center of k-space. So in the next few slides I'm gonna show how these parameters can be used to modulate the contrast we see in an MR image. So first of

all, is the echo time or TE. So as we saw from the first part of the lecture, after we play at our RF pulse, the signal intensity decays away over time with T2* decay. So here we have, let's say this tissue here has a T2* value of T2A, T2A*. So the signal decays away like you see here. [BLANK_AUDIO] Now at this point in time here, when we go through the center of k-space which corresponds to this echo

time, the signal has therefore decayed away up till this point here. If we now have a second tissue with a different T2* value, so indicated by the red line, T2B*, then at the echo time, which again is the time we go through the center of k-space here, you can see that the signal will have decayed away, a different amount than the first one, again because it has a T2* value.

Now the contrast we're gonna get in our image, is simply gonna be the difference in signal intensity, at this point, at this echo time. So it's just gonna be e to the -t over T2A*, minus e to the -TE, over T2B*. So by setting up this echo time, we generate a T2*-weighted contrast in our image. Now what if we move the echo time to an earlier time point? So we've

now shortened the echo time TE to this point here. So again, the contrast we're gonna get in our image, is again just simply the difference in signal intensity between these two lines here. But in this case, because our echo time is shorter you can see that we haven't generated as much contrast, so there's less contrast in this case. So in general, when we shorten the TE we reduce the

T2*-weighted contrast in the case of gradient echo pulse sequence. Now I've been mentioning here that, the echo time, the TE in code contrast, which corresponds to the time we go through the center of k-space. But why is it the center of k-space is important, what's special about it? Well here we have a slide that I showed in my earlier talks on k-space. Here we have the

complete image and the corresponding k-space data that generates that image, again recall via Fourier transform. Now if instead of generating the image from the complete k-space data set, I just generate an image from the central portion of k-space, resulting image you see looks like this here. So in this case you can see, importantly, that we encode the contrast in this image.

So the center of k-space still generates the contrast that we see in this image. The outer portion, so if we reconstruct the image just from the outer portion of k-space, you can see that we see the edge information, but there's really no contrast in the image. The image is essentially a uniform color. So that's the reason why the center of k-space is important, because that really encodes

the contrast in our image. So that's why we care about when we go through the center of k-space, and that's what we set our echo time to be. So just to summarize what we've got to date. The echo time, TE, corresponds to the time of acquisition of the center of k-space. The center of k-space, as we know, determines the image contrast, so therefore as a rule of thumb, the longer the TE, the heavier

the T2* weighting. So the more difference in T2* weighting we're gonna have between tissues with different T2* values. So here I just have an example of, this is an image of the heart, one acquired with an echo time of 2 ms, and one acquired with an echo time of 16 ms on a gradient echo scan. So if we compare say the myocardium and the blood in these two cases, you can

see in the one with a 16 millisecond echo time, there's a much larger contrast between the myocardium and the blood. Again because the myocardium has a much shorter T2* value. So it decayed away, much ore dramatically, in the 16 millisecond case, than it had in the 2 millisecond case. The next pulse sequence parameter we're gonna talk about is the

repetition time or TR. So recall the TR it's just simply the time between we acquired adjacent k-space line, so basically the time that we repeat this cycle. So let's look at what's going on with the magnetization. So initially we started out with our magnetization at its full, complete value. So let's say, as a value, for purposes of this discussion as one. So we then play out our pulse, and in this case let's assume

we have a 90 degree pulse, so that tips down the magnetization completely into this transverse plane here. Following that we have T2* decay. So the signal is then going to decay away completely. So following the magnetization decay, the magnetization will then regrow back towards its initial value due to T1 recovery. So here we have again this formula here, 1 - e to the -TR

over T1. Now if we set our TR to be long enough, then that magnetization will regrow back to its initial value. So in other words, the magnetization will regrow back to its initial state. But what happens if I set my TR to a shorter period of time, the magnetization doesn't regrow back to its initial value. Then instead of recovering completely, it will only recover partially. So let's say in this case, it only

recovers to a value of 0.8. So when we then foot the magnetization down, it now, instead of having a value of 1, it only has a value of 0.8. So when we then have our T2* decay on the next iteration, the signal intensity starts from a value of 0.8, and then decays away completely. It then regrows back to a value, again, of 0.8. It's decayed away completely, and we have the same TR value, so it goes back

to a value of 0.8. Now this is called, essentially, the steady state of the magnetization because the magnetization lies in a steady state on every single iteration. So it lies in exactly the same position on each iteration we do. So we tip the magnetization down, it decays, it then regrows back to a value of 0.8. We tip it down again, it decays away completely,

regrows back to a value of 0.8. So a steady state just simply means the magnetization is the same from one TR to the next. And in general, we almost always we'd acquire images when the magnetization is in a steady state. So now, let's examine the contrast it's generated as a result of a particular choice of repetition TR. So as we mentioned in the previous slide, this magnetization in

the red lies in the steady state. So we're constantly going between these two situations. We tip the magnetization down, it has a value of 0.8, it decays away to 0, then recovers to a value of 0.8, and the process is repeated. So it's the same each time. Now, this value of 0.8, the reason it recovered to this point, obviously, depends on the TR value. So if we change

the TR value to some other value, then the magnetization will recover to a different point. But the value that it recovers to also depends on the T1 value of the tissue. So for example, if I had tissue with a different T1 value as indicated by this green line here, so let's say I had a longer T1 value, then it would recover at a time TR to a different point. So in this case let's say it recovers only to

a value of 0.5. And important thing to note is that this magnetization also lies in its own steady state. So it's gonna continuously oscillate between, it's gonna decay away to, it's gonna be tipped down, and it's gonna decay away, and recover back to a value of 0.5. It's gonna be tipped down, decay away to 0, recover to a value of 0.5. If we look at this plot down on the right here, you can see that the red magnetization

is in a steady state where it has a value of 0.8, the green magnetization has a steady state value of 0.5. So in other words, we generate a contrast between these two signals, a T1-weighted contrast, which we capture when we tip the magnetization down. So in this case, the red magnetization would have a stronger signal intensity than the green one would.

And this is a contrast that depends on a T1 value. Now, if I change my TR, that's gonna change the relative amount of recovery between these two magnetization. So the relative T1-weighted contrast is gonna change if I adjust my TR. Now, as a general rule of thumb, the shorter the TR, the greater the T1 weighting because that means that the shorter one's gonna recover more quickly than tissues

with a longer T1 value. So TR affects the T1 weighting. Generally speaking, the shorter the TR value, the greater the T1 weighting. Now, there are some exceptions to this, of course, that if you have a very, very long TRs then the contrast basically disappears. And similarly if we had very, very short TRs then there really isn't much time

for a contrast to evolve so there overall won't be very much difference in signal intensity. [BLANK_AUDIO] Couple of additional comments on this contrast generated by TR. First of all, in this case, we always assume that the magnetization decays way to 0 each time. So that was sort of our steady state condition.

We tip the magnetization down, decays away to zero, then recovers back to it's steady state value. Typically, if that's not the case, we often tip away/g with something called spoiling. So that's just simply a gradient which dephases the demagnetization to get rid of any of the residual magnetization that's lying in the transverse plane. There's also RF spoiling, which is another way of

accomplishing the same thing. Another thing to consider is that I've assumed that when we tip the magnetization down we're capturing that T1-weighted contrast exactly as it's stored along the z axis here. But as we know, that if we have a TE that's not equal to zero, we're gonna start to have some T2*-weighted contrast evolve in our image. So if our TE is anything other than

zero then we're going to have, not only this T1-weighted contrast, but we're gonna have an additional T2*-weighted contrast that's superimposed on top of it. So we're gonna have sort of a mixture of both T1 and T2* weighting, which would complicate the interpretation of the image, cause it's hard to distinguish which mechanism is dominating. So typically, we wanna choose TE to be as short as possible in these

sort of gradient echo scans where we're trying to highlight T1-weighted contrast. We wanna choose TE as close to zero as we possibly can. Now let's move on to talk about the effects of flip angle on the contrast we have in a gradient echo pulse sequence. And again to examine this one we have to look at, again the magnetization, so in the previous case

we assumed that when we play our RF pulse we're tipping it down with a 90 degree pulse. So, in this case, let's generalize it, to say, we're gonna have an RF pulse with an angle theta. So, in this case, instead of the magnetization being completely tipped down in the transverse plane, it's only tipped down with angle theta. So at that point, instead of the magnetization, initially

had a value of one, but now in the transverse plane, where again we're our signal, it only has a value of 0.7 because we haven't tipped it completely down. So part of this magnetization lies along the z axis and part lies along the transverse plane. Okay, so once we do that, the signal we know decays away with T2* decay, just as before. So we assume that this signal disappears along

the transverse plane, and then once a signal's disappeared we're gonna then experience T1 recovery, and the magnetization is gonna regrow back to its initial value. But remember that unlike the previous case, it's not starting from zero because we didn't tip the magnetization completely down. Rather it's starting from this point of, in this case,

0.7. So the magnetization will then recover with this equation here. It's gonna start at 0.7 and recover back to its initial value. In this case, let's just assume we choose a particular TR, let's say, it's gonna recover back to a value of 0.9. And just to show you that this magnetization essentially recovers, this is basically the latter/g part of the T1 recovery curve. Cause initially, if we started

from zero it would recover like this, but in this case we don't have this portion of the curve cause we're starting at 0.7 already. So that's on the first iteration. We then have to tip the magnetization down again, but it actually gets to be quite complicated, because in general, the magnetization is gonna now start from a value of 0.9, it's gonna be tipped down to some value other than 0.7. And in general,

it's gonna take several iterations until we get into the steady state. So I'm not gonna draw the diagram here cause I 'd probably would have to go through four or five iterations of this until we finally get into the steady state. So generally speaking it's gonna take, if the angle is something other than 90, it's gonna take a longer period of time to get into this steady state of magnetization, but

we typically have to wait until we're in the steady state before we start imaging. Now what happens in terms of the contrast? So let's say we, again, flip our magnetization down with angle theta, it decays away, and then begins to recover. Now if we have two different magnetizations with different T1 values then obviously it will recover to different amounts. So if we plot the recovery on the

plot on the left, the shorter T1 value recovers more rapidly whereas the longer T1 value recovers more slowly. And again recall, they're starting from different points in time here at different values here. This is starting from value 0.5, this is starting from a value of 0.8. So in general, when we have different flip angles this also produces different T1-weighted contrasts. But unfortunately, the relationship

is quite complex between the two, and there really isn't a straightforward relationship between flip angle and T1-weighted contrast. As a rough guide, and this is only a very rough guide, larger flip angles generally produce a heavier T1 weighting, but that's not always the case. Here we just have an example, we have four different images of the brain acquired at different flip angles, 5 degrees,

20 degrees, 40 degrees, 90 degrees. And you can appreciate that the contrast of the brain tissue changes with differences in our flip angle. Okay, so let's just summarize what we've talked about so far with gradient echo. So we showed that there's three different parameters that we can vary in the pulse sequence. There's the flip angle theta, there's the echo time or TE, the time from the RF pulse

to the center of the acquisition of k-space, and there's the TR or the repetition time, which is just the time between the acquisition of adjacent k-space lines. We showed that if we have a longer TE, this is going to produce a heavier T2* weighting. If we have a shorter TR that's gonna produce a heavier T1 weighting. And finally, if we have a larger flip angle,

that's gonna, generally, produce/g a heavier T1 weighting although the relationship is complex, and it's not quite as straightforward. So now we're gonna move on to discussing some of the contrast mechanisms underlying spin echo. So just a brief review of the spin echo pulse sequence.

involving the actual more proximal rains it is suggested so it is not recommended it is suggested to do anticoagulation

rather than trumbull aces and in patients who undergo trumbull Isis they should undergo the same intensity and duration of the anti correlations in patients who do not undergo a humble Isis so if the patient has a central

venous catheter associated different rumbles it is suggested that anticoagulation is done without central venous catheter removal and if the symptoms failed to resolve or period then the CVC mobile can be considered

again it is suggested that the anticoagulation should be continued for at least three months are for the duration in which the central venous catheter is still present whichever is longer and at least three

months of anticoagulation is a property in patients who develop upper extremity DVD associated with pacemaker wire in patients who have drastic outlet syndrome or pages shorter syndrome which is related to approximately duty

thrombolytic therapy followed by surgery has been advocated but an optimal approach is still not clear although most of the people tend to follow doing a traumatic to be who our page sorter syndrome and then followed by surgery

with the scaling ectomy for stripper section in addition to traditional anticoagulation pregnancy-related dvt

are cosmetic next question for you here which of the following has been shown to prevent the progression of the post traumatic syndrome is it thermal ablation of saphenous veins stenting of occluded veins elastic compression and

tax a filing or none of the above who and the answer is that's correct the answer it's been shown at least two large randomized studies but the biggest are the probably the best of which done by prayer and Oni the elastic

compression prevents post-traumatic syndrome but i'm going to throw a big question mark in their reason I'm going

Hi, my name is Marshall Sussman, I'm an MRI physicist at the University Health Network and the University of Toronto, I'm giving a series of lectures on basic MRI physics. This lecture is going to be the third in the series, and this one's called k-space in gradients. Now, in the second lecture, I went through the relationship between k-space and image formation MRI, and I showed how we use gradients to move around in k-space and acquire data in MRI. But what

I didn't tell you is how the gradients actually move you around in case phase. So in this third lecture here that is what we're going to get into a little bit more details. And this lecture is divided into two pieces. To give an outline of what's in this lecture, I'm gonna start of by doing just a brief review of some of the physics that we've talked about so far. So I'm gonna again review fourier

transform theory that we talked about in the k-space lecture previously and I'm also gonna give a brief of you of signal generation which we discussed in the very first lecture. Then we're gonna move on and describe how we use gradients to localize spacial position in one dimension. And then we're gonna talk about how gradients and k-space are related in one dimension.

Then I'm gonna move on to talking about how we can localize spacial position in two dimensions. So, let's begin with the brief review of some of the physics concepts. So first of all, fourier transform theory, again, this will just be a repeat of what we covered in the previous lecture. So we know that we can describe a signal as in a time domain, a signal just oscillating as a function

of time. In this case, this signal oscillates at a rate of one cycle per second. So you can see we have this red lining here, to indicate that we've gone through one complete cycle within one second. So, an equivalent way of representing that signal, is in the histogram domain. So on the left here you can see we have now an occurrence of one cycle per second, a frequency of one cycle per second, occurring

exactly once. Here, we have a second signal oscillating at two cycles per second. Again, you can see the red line indicating we go through two complete cycles in one second, and the histogram representation of that signal again a single occurrence at two cycles per second. We can add various different components of those signals together. So if we add these two signals together, we get a composite signal

that looks like this. And in the histogram domain, we get representation that looks like this. So one occurrence at one cycle per second and the second occurrence at two cycles per second. And we can extend that concept and add various different combinations of different frequency components together. So here we have one combination of one cycle per second and two cycles per second. Counts of the

signal you get looks like what you see here. The signal has a function of time, and representation looks like this on the left. So here we have a single current at one cycle per second and we have two occurrences at two cycles per second. And we showed previously how this two are related by a fourier transform which is just a simple mathematical

operation. So we can get one if we just have the signal in one domain, we can determine what the representation signal, the other domain will be, by applying a fourier transform. Second concept I wanna review is the basic concept underlying signal generation. So from the first lecture we saw that we apply on RF pulse and that causes a magnetization to tip away from the direction o f the magnetic

field. Once we do that, magnetization begins to rotate around the direction of the magnetic field, and in turn the spears and an important concept is that the speed of rotation is proportional to the strength of the magnetic field. So the higher the magnetic field the faster the signal rotates. And as a result of that rotation, we have an electrical signal that's

generated. And this is what we ultimately detect as our signal. So, that just is a very brief review of some of the concepts we went over in our first two lectures. So now, we're gonna move on to talking about how we can localize spacial position in one dimension. So, the way we do that, is through the use of gradient. So, we talked about gradients already briefly in some of our previous lectures.

And we saw that gradients are simply magnetic fields that vary linearly with spacial position. And these are magnetic field gradients that are superimposed on top of the main external magnetic field. So just to give an example here, here we have a person lying in the MR scanner. And as a result of the external magnetic field, the magnetic field is uniform everywhere inside that person's body.

If we turn on our magnetic field gradients, then the magnetic field now varies linearly as a function of spacial position. So, we can see that towards the head, the magnetic field is slightly lower than the initial magnetic field and as we go towards the feet, the magnetic field continuously increases till it's on this side, slightly larger than the initial magnetic field. I'm gonna

look at three particular locations. So here we have at the head magnetic field that's less than B zero which is the main initial magnetic field. It's B zero equals to the initial magnetic field at the center, and equal to slightly greater value at the feet. [SOUND] Now, if you recall from the review I just did a few slides ago, remember that I said speed of rotation, of the magnetization is

proportional to the strength of the magnetic field. So in particular what that means, is that this different spacial positions, magnetization is going to be rotating at a different frequency. So in particular the one towards the head is gonna be rotating at the slowest frequency because it has the lowest magnetic field, whereas the one at the feet, is gonna be rotating the fastest because it experiences

the highest magnetic field. Now, another fact which I need to mention here, is that the frequency of the signal that you emit in MRI, is directly proportional to the rotational frequency. So if we are rotating at say 63 megahertz, we made a signal of 63 megahertz. So if we rotate at 64 megahertz, the signal is emitted at 64 megahertz. So what that means is the

frequency of each one of this signals is going to be slightly different, in particular the one at the head because it sees the lowest magnetic field, is gonna have the lowest frequency. The one at the feet because it sees the highest magnetic field, is gonna have the highest spacial frequency. So up until this point, I've been using this figure of the body to represent the

subject that's being imaged in MRI. But the body is is obviously quite a complicated structure, so to simplify the explanation, instead of dealing with the body, I'm gonna actually just describe my contents based on imaging jugs of water. So here we have in this case one jug of water at this position, three jugs of water in the middle position, and two jugs of water on the opposite side. So if we consider

what's going on with the signal, so again we still have the same concept where magnetic field strength varies linearly in space or position. So just as before the signal is gonna be at the lowest frequency here and the middle frequency in the center position and the highest frequency on the right, which is indicated here but now in this case we have three jugs of water here so there's

gonna be three times as much signal at the middle frequency. And the signal on the right, is going to have twice as much signal as the one on the other end emitted at the highest frequency. So this slide here shows you what the overall signal that we're going to receive, when we do our MR experiment with these three jugs of water. So essentially at this stage we can't distinguish between

the signal coming from any of these individual jugs of water. We're just measuring a net signal. So it's just simply the sum of all the signals coming from these different components here. So particular as before have one signal at this frequency here, three signals at the middle frequency and, two signals at the highest frequency. And that will add up to produce this overall composite signal,

because this is what we're gonna measure in our MR experiment. Now this is essentially what I would like to call the forward solution of MRI. What I mean by that is that if we have a known distribution of water, in this case jugs of water, we can then go through the physics behind what's going on, and predict what the signal we get out at the end of the days. But, obviously in a real experiment

that's actually not what we want, it's the inverse of that, because we actually don't know what the distribution of water is. That's what we're actually trying to measure. So we wanna actually get the reverse solution. We wanna say, given this signal here, we measure this signal here. We wanna be able to go backwards and generate the relative distribution of water that

generates this particular signal here. So in the next slide, I'm gonna show you how we do that. So, just to, again, rewrite this same diagram here, we have these different amounts of water using different amounts of signal at different frequencies and we get a composite signal. Now, if you look at this diagram closely, this is actually exactly similar to this fourier transform theory concept

that I described earlier. In the fourier transform example we had different amounts of signal occurring at different frequencies adding up to produce a composite signal. So, in this case we had one signal oscillating leading at the lowest frequency and two signals oscillating at the higher frequency to produce this composite signal here. In my MRI example, I have one jug here producing this lowest

frequency, three jugs producing the middle frequency and two jugs producing a highest frequency producing this composite signal here. So, in the case of the fourier transform, to determine what is the distribution of water, what is the distribution of signals, I applied a fourier transform, and that gave me the underlying distribution of frequency components. So I can do the exact same thing in my MRI case, if

I just simply apply a fourier transform for that signal, that gives me a histogram that tells me the relative distribution of frequencies. In particular it's gonna tell me I have one unit at the lowest frequency, three units of the middle frequency, and two units of the highest frequency. And I can convert this into an image if I simply map the height of this histogram into a grey

scale image. I can actually generate an image of these three jugs of water here. So the black one has the lowest intensity, so the lowest amount of water, the middle one has the highest amount of water, and the far one in the far right has the intermediate amount of water. So just using these basic signal processing concepts in fourier transform,

I can essentially get the reverse solutions. I have this composite signal generated by my MRI data, when I apply a fourier transform, I can then uncover what the underlying distribution of water that produce that signal was. [BLANK_AUDIO] [SOUND] So that illustrates the concept of spacial localization in one n dimension.

Now we're gonna talk a little bit more detail about how gradients and k-space are related in one dimension. So here I have this same example just to recall what we we're using before and just to put some concreteness to this example, I'm gonna use some specific frequency values on these numbers here. Now, these frequency values aren't real, the real MR frequencies are much higher, but just for

the sake of this illustration, these are the ones I'm using. So let's say that this position here the signal is emitted at one hertz, the middle one is emitted at two hertz, and the far one is emitted at three hertz. Mathematical format of these signals are sine [UNKNOWN] So it's just simply the sine of the frequency times time that describes

each of this signals. So this one is sine of one hertz times time, sine of two hertz times time, because it's a frequency of two hertz but now there's three times the signal because there's three jugs of water so we multiply by three, and similar the high one sine of three hertz times time and there's two jugs of water there. So again the conficite signal is just simply the sum of all those

and mathematically the signal is described by this equation here, it's just simply the sum of three components from I equals one to three, because we have three different locations here. The A here, is the relative amount of each of these signals present so A at this position is 1, a at this position is 3 and a at this position

is 2, times the sine of the frequency, and obviously that also varies at each one of these positions. So the A, is what we're ultimately interested in, because that's really tells us the distribution of water, the relative amount of water at each position. And the frequency, we know that the frequency is proportional to the strength of the magnetic field. And we further know that the strength of

the magnetic field, is equal to the gradient times the spacial position, because that's the linear magnetic field gradient, plus the static magnetic field, which is what which always exist. Now, just to simplify the Math since the static magnetic field of this bizia/g magnetic field is the same at all spacial positions, I'm gonna ignore that, so I'm gonna get rid of that from this term here.

So now let's write down what the signal looks like making the substitutions. So here I have my signal as this, and my frequency is going to be replaced now by, the gradient times the spacial position. So if I do that, my signal now takes on this Mathematical form here. Now, the key to this whole concept of k-space is that we make this substitution here. We define this variable

and we call it K equal to the gradient times the time. [BLANK_AUDIO] With that substitution, the signal B takes on this format on the bottom here. So the signal is the sum of the distribution of water which is the same as before. Now it's a sine of this K variable times X, the special position. So now how can we interpret

the signal? So again here's my initial format, so we have the signal of all means and it's function of time before I place in my k-space variable. So if you look at the signal oscillating is a function of time it just simply appears like this. If we make this case substitution, we can equivalently consider the signal to evolve as a function of the K variable so instead of

the signal evolving as a signal of time, we now have the signal evolving as a function of this K variable from zero to same X value. And this really discourages the whole K concept of why when we turn on the gradients we move through k-space because essentially, if we don't have any gradients on we're essentially starting at zero position. As soon as we turn this gradients on

we're essentially moving through k-space, so this K variable is evolving so this is why the gradients allow you to move through k-space and this is really the the piece that we were missing in the first [UNKNOWN] So K is just directly proportional to the gradients. So as long as there are gradients on, we are moving through k-space. So equivalent that you can think of as we're moving through

the k-space, we're essentially mapping out these grey scale values that you see here. So I've just converted this signal loss in this function of time to simply a grey scale intensity and that's the more familiar form of k-space that we see. [BLANK_AUDIO]

So as the signal evolves the function of time, this is essentially filling up the k-space data matrix. [BLANK_AUDIO] On one hand it seems like sort of a simple almost a trivial substitution. Okay I've just replaced this K with a [UNKNOWN]

gradient times time with this variable K. But as I'm gonna show you in this slide here, it does have some pretty important ramifications, because in particular what it tells us, is that it doesn't really matter what our gradients is doing, as long as we cover the same region of k-space, then the data that we acquire is gonna be exactly the same in both cases. And that's how we can get to different

k-space trajectories. So let's start out with this first example here, we have a gradient that's a constant gradient on as a function of time. So this is what the gradient's doing on the left, and on the right, I'm going to show you what goes on in k-space. So if we turn our gradient as a function of time, our k-space simply evolves from its initial zero position

because remember we always start at zero position k-space out to some maximum k-space value. And the speed that we're going at is just simply proportional to the strength of the gradient. So now let's have a second example here where turn a gradient on for a period of time, turn it off, and then turn it back on. So what's going on in k-space? So in k-space we're simply have the

gradients on, we are acquiring data just like in the first case. But now because we've stopped, we're not doing anything. So we just sit there at that same k-space position. We then resume and we turn the gradient back on and then we resume form that same k-space position. So again these are two very different gradient wave forms, but in fact we still cover exactly the same k-space

region. Again we just have to go back to the substitution here to see what exactly is going on. And as I mentioned in previous lectures, in general infinite numbers of k-space trajectories are possible. So I could, cover this exact same region of k-space by having essentially an infinite number of different ways of doing this. So turn it

on and off 3 times, 4 times you know a 1000 times, it wouldn't matter as long as I'm covering the same ultimate region of k-space, the image I generate will be exactly the same. And to say I just to [INAUDIBLE] that point in, the ultimate image you get doesn't matter how you covered k-space, it just matters what k-space data you've acquired.

[BLANK_AUDIO] Now, let's go a little bit deeper into what's going on with k-space. So the gradient is just simply a linear magnetic field gradient. So if we have this initial gradient we're training on here, we cover k-space in the manner that I just showed you. If I increase the strength of the gradient that means that I'm increasing this

g-value. So I'm increasing the slope of this magnetic field. So the magnetic field changes more rapidly as a functional spacial position. So how does that affect how we go through k-space? Well it just simply speeds up how we go through k-space. If this gradient is larger, that means we're gonna go through K faster. So in particular if I have a gradient that's

twice as large, but only half as long, again going back to this k-space substitution, here you'd see that that just simply means I'm gonna go through k-space twice as first. Again I'm covering the same region of k-space so when I reconstruct the image it's gonna look exactly the same. But I've now gone through k-space, I've acquired my data twice as fast. Similarly, if I invert the

polarity of the gradient, that just simply adds a minus sign onto this G. And again looking at the k-space variable you can probably anticipate what this is gonna do to how we go through k-space it's just simply going to invert the direction that we go through k-space. So instead of going right to left, we're gonna be going left to right. So we just fill up our k-space in exactly the

opposite direction. Now, we're gonna look into some issues related to gradients and image reconstruction. So as we've said many times now the images are reconstructed by fourier transforming the k-space data. So we acquire a series of k-space data and we apply a fourier transform on that and we get in this case the distribution or the relative distribution of order

that's generating that signal. So what's happening mathematically? So we saw that we can consider the signal evolving as a function of K, and that's indicated by this formula here. So if we apply a fourier transform to this signal as a function of K, that's applying a fourier transform to the right hand side of this equation. Now again I'm not gonna go through the Math to derive this, but I'm just gonna

tell you the result that fourier transforming this equation gives you this A variable here. And as we recall the A, is the relative distribution of the water. So this is actually the A of the image that we are ultimately interested. So this image or this distribution of water and the k-space signal data are often referred to as fourier transform pairs. So signal is a function

of K, or image is a function of spacial position, are related to each other via fourier transform, that's why they're called fourier transform pairs. So now we are gonna go into a little bit more detail, on to how the properties of k-space affect the ultimate properties of your image. So the first thing we are gonna talk about is how k-space is related to the ultimate spacial resolution

of your image. So we call again before k-space position is equal to gradient times time. So we turn our gradient on for a period of time, we go through k-space as before. Now, one question is how long do we acquire the data force. So I cut off my data acquisition at this point here but there is nothing special of this particular

point in time. Why couldn't I have expended it further we're going short. Determines how long we acquire the data acquisition for. But it turns out that the special resolution of an image is inversely proportional to the maximum k-space value you acquire. So if

we go out further in k-space, we generate an image of higher and higher spacial resolution. In the previous k-space lecture we saw why that a wide as you go to higher and higher k-space values this gives you more and more fine detail. But mathematically this is what's going on. So the spacial resolution of image, is inversely proportional to how far you go out in k-space. So for example lets say

this first example here where I go up to this particular region of k-space, lets say this provides me with a spacial resolution of one millimeter so the image has a spacial resolution of one millimeter. Finally go out half this far in k-space, another way is I only acquire data for half as long, and what's going to happen to my resolution, is it's going to get worse by a factor of two. So I'll

go only half as far in k-space and my resolution is now courser, instead of one millimeter It's now two millimeters. So again, if you want to determine how far we need to go out in k-space we just simply have to determine what is the spacial resolution you want to get, what is our gradient, and that tells us how long we have to acquire the data for. Another

important property of imaging is the field of view. So that's how big of a region are we going to be imaging with MR. So again here is our initial gradient, it's function of time and is the initial k-space region we cover. Now, the MR signal that we're generating from the body, is generated continuously. So continuously is a function of time. But in practice since we can't store an infinite

amount of data, the signal that we actually measure is only sampled discretely. So we only measure it at the discrete distributional points like you see on the image on the right. So what determines how finely we sample that? Well, it turns out the field of view of our imag,e is inversely proportional to how finely these are sampled, so in other words the larger spacing

in between these k-space points, the smaller our field a view. And in turn we know that K is equal to the gradient times time, so essentially the spacing is determined by how finely or how quickly we sample our data which is this Delta T here. So on most scanners, it's the sampling rate that's controlled explicitly through the bandwidth. So as an example let's say that we specify a bandwidth

of 32 kilohertz, that's 32,000 samples per second. That means that in turn, we have a sample rate of 1 over 32,000 or in other words, 31 microseconds per sample. We're basically sampling our data every 31 microseconds. So as I said on most scanners it's this bandwidth that's controlled explicitly. So we prescribe a particular field of view, we prescribe a particular bandwidth and then

the scanner we're going to calculate what gradient we need, in order to generate the appropriate k-space spacing, to produce the field of view that we've specified. So that's going to end the first part of this lecture, so we've basically done a brief review of the concepts of the fourier transform signal generation, and we talked talked about how we can use gradients to localize

spacial position in one dimension. So in the next lecture I'm gonna move on and talk about how we can extend this concept to localized spacial positioning in two or even more dimensions. [BLANK_AUDIO]

[BLANK_AUDIO] Thank you Dr Wakefield, Dr Garcia. Ladies and gentlemen I'm pleased to represent the steering committee of the ATTRACT trial, and very importantly, pleased to represent Dr Suresh Vedantham who as as a principal investigator, I think, set a new standard for national PIs. These are the disclosures. [BLANK_AUDIO]

The ATTRACT trial is the Acute Venous Thrombosis: Thrombus Removal with Adjunctive Catheter-Directed Thrombolysis, and this is an NIH sponsored trial. We know that in general management of deep venous thrombosis is guided by international guidelines, and arguably the most influential guidelines are those put out by the American College of Chest

Physicians. Now the eight edition, in 2008, were in play when ATTRACT was initiated, but I think it's important to look at what was in play when ATTRACT was designed and when it was funded. And in 2004, the ACCP recommended against the routine use of

catheter-directed thrombolysis. Strong recommendation, a little data to support it, and that catheter-directed thrombolysis should be confined to selective patients requiring limb salvage. It's very rare, exceptionally rare, to have a deep venous thrombolysis causing limb threat,

and they recommended against the routine use of, here we go, and they recommended that in selected patients such as those with massive iliofemoral DVT at risk of limb gangrene, they suggested IV thrombolysis. And we know IV thrombolysis has no effect in patients with extensive deep venous thrombosis.

And that IV delivery is of course minimally affected. So despite therapeutic anti-coagulation we know that post thrombotic syndrome occurs frequently, it's life long, and that patients are at increased risk for recurrence with PTS, and recurrent DVT increases the risk and severity of post thrombotic

syndrome. And we know that iliofemoral DVT is particularly bad. Now the objectives of the study design were to reflect the actual use of percutaneous catheter-directed thrombolysis in the United States, get an accurate answer,

have a good inflexibility in practice, results credible to percutaneous catheter-directed thrombolysis in terms of evaluating the results from the ATTRACT trials. We thought that this was a best fair test of this technique. And there was also a focus on items that affected cost and clinical

decision making. We attempted to enroll a representative cohort of patients and accommodate a diversity of practice in anti-coagulation as well as endovascular therapy, and the structural design of the trial promoted rigor integrity and balance in the evaluations.

And we are rigorously evaluating post thrombotic syndrome, quality of life, the safety of the techniques, and we have the limited ability to look at secondary issues. So patients with symptomatic proximal DVT involving the iliac to the femoral veins were included. They were stratified by thrombus extent, and in actuality 60% of our

patients had iliofemoral DVT. We excluded patients that are high risk of bleeding, with central nervous system lesions, acute limb threat symptom duration of more than two weeks, or post thrombotic syndrome in the same leg. And you can see when patients came in they were stratified to either

illiofemoral deep venous thrombosis or femoral popliteal, and when stratified they were randomized to either anti-coagulation alone, or anti-coagulation plus catheter based thrombus removal. There was operational separation of the PI from the study data. This was to minimize bias. There was comparable use of anti-coagulation,

anti-platelet therapy as well as comparable use of filters. There's equal surveillance of patients in both arms, central randomization protocol, and allocation was concealed for those individuals that were making the assessment of post thrombotic syndrome. Patients are evaluated according to the Villalta score. 692 patients

were randomized, and we will evaluate severity of PTS, quality of life, likelihood of pain relief, safety, and mechanism of post thrombotic syndrome which is badly needed, abstraction versus reflux. We're not looking at biomarkers, and we're not looking at biological

effects of catheter or devices on the vein wall. This is a photograph of the Steering Committee, and we received enormous support from the NIH, from the surgeon general, and from other major organizations. So I do think in early 2017 we will have important answers to these

important questions. Thank you very much. >> [APPLAUSE]

rightly so post-traumatic syndrome i want to mention one thing this is that

the Venus also component of it we know it has a major impact on daily quality of life and on patients just ability to live their lives we know that thrombosis of the iliac are common femoral vein is often present not always but often

present people with the most severe post-traumatic syndrome as you see here and over the years some of us have started to apply basically a strategy of just reducing venous hypertension using standing of chronic me and iliac vein

obstruction reassess the patient and if they have significant saphenous reflux ablating the saphenous reflux to achieve a global reduction in venous hypertension and hopefully he'll also has an improved symptoms and improved

clinical signs of post-traumatic

thing i want to talk about is quality of life and when we're talking about quality life and pulmonary embolism the primary determinant of that the best of

my knowledge is residual or persistent or progressive pulmonary hypertension which Rex exercise tolerance and cause shortness of breath first described about 90 years ago by young dal then toyed with by dale and Albert who

concluded that a chronic corporal manali the word used back then before CTF was even known is an extraordinarily unlikely complication of PE the late great can moser fault that maybe as many as four hundred fifty patients had this

syndrome of what he started calling chronic thromboembolic pulmonary hypertension but then rivière ok mout and showed that up to forty percent of patients post PE end up with high pressures that are persistent

progressive over the next five years pingo concluded that about three percent of patients went on to develop the full C tough syndrome and at the time this new england journal paper came out that number was about 10-fold most experts

thought now we're thinking more in terms of a transition where there's a larger number of patients maybe 25 to 40 percent that have a partial seat s syndrome not the full concrete in the lungs syndrome that causes the need for

the operation but progressive pulmonary hypertension that's not explained by smoking or sleep apnea or elevated left ventricular end diastolic pressure it's not just comorbidities this is work that I did where we took a hundred and

twenty-seven patients that had no previous comorbidities except we did not exclude obesity and smoking and we found forty-one percent of them either had a bad-looking echo or dyspnea at rest or exercise intolerance six months later

clock found the quality of life was not good after PE with numbers that looked similar to like COPD with over half of patients reporting exertional dyspnea and seventy percent having new or worsening dyspnea after their PE lots of

evidence that PE messes up quality of life including some in 2014 from our friends in Australia from challenge at all child at all that found a 25-percent had all of these things impaired exercise capacity heart rate recovery

pulmonary hypertension and raised PVR and right ventricular dysfunction is important point that he had is the corollary is they were apparently normal when you talk to them but was only when you provoke them did you find these

abnormalities we studied a cohort of patients of 200 patients that had some massive PE they were normotensive if they became hypotensive they got lice that's these patients this is the right ventricular pressure on the x-axis the

y-axis at diagnosis and six months later all the patients that got lysed had reductions in their systolic pressures on the right side of the heart these are patients that just got heparin alone the red lines are those that

increase the pressure that was one-third of all the patients that just got heparin alone plus a higher rate of exercise intolerance and dyspnea at rest and the topcoat study we looked at a composite of endpoints including bad

stuff on the front end and bad stuff on the back in what we considered a patient-centered endpoint and you were three times more likely to hit the bad end point with placebo compared to connect a place here it is shown another

way with bar charts that are just so horizontally patients want to be in the white zone they are more likely to be in the white zone if they were treated with connected place

rightly so post-traumatic syndrome i want to mention one thing this is that

the Venus also component of it we know it has a major impact on daily quality of life and on patients just ability to live their lives we know that thrombosis of the iliac are common femoral vein is often present not always but often

present people with the most severe post-traumatic syndrome as you see here and over the years some of us have started to apply basically a strategy of just reducing venous hypertension using standing of chronic me and iliac vein

obstruction reassess the patient and if they have significant saphenous reflux ablating the saphenous reflux to achieve a global reduction in venous hypertension and hopefully he'll also has an improved symptoms and improved

clinical signs of post-traumatic syndrome

are cosmetic next question for you here which of the following has been shown to prevent the progression of the post traumatic syndrome is it thermal ablation of saphenous veins stenting of occluded veins elastic compression and

tax a filing or none of the above who and the answer is that's correct the answer it's been shown at least two large randomized studies but the biggest are the probably the best of which done by prayer and Oni the elastic

compression prevents post-traumatic syndrome but i'm going to throw a big question mark in their reason I'm going

So the final case is I think the worst complication that I caused, it's I feel awful about it and hopefully it will be a learning lesson for yourself it certainly was for me. This was a 29 year old who had a terrible SVC syndrome with advanced with spiritry/g compromised as well as chemosis and almost not quite

comatose but really in quite a bad way from his SVC syndrome. His background history was that he had chronic renal failure since infancy and had had two failed renal transplants and innumerable lines in his upper extremities in both his eye IJs. He was HIV and Hepatitis C positive from transfusion related issues. He was on aspirin at the time for cardio protection,

and he had two needs, one of which was an access for haemodialisis and then the second was treatment of this SVC syndrome, but he certainly needed access immediately. This was a CT that we did at the time, you can see the seclusion

here in his SVC. Very dilated azygos vein. We do quite a bit of SVC recanalization for access, for dialysis access, short gut syndrome, TPN, that sort of thing.

One of the things I will say to you is that when you're looking at the CTs, the level of the occlusion is really crucial. That the lower it is the more dangerous it is. And this is the illustrative case of that, that if the occlusion is higher up, it's outside of the potential for pericardial involvement to

can be a little bit more aggressive. When it's lowered down like this, this is where you can run into trouble. So we did what we usually do which is an antegrade access from a recanalized external jugular vein, brought a sheath down and you

can see the run here is showed really just enormous [UNKNOWN] stylation system feeding back with no evidence of an SVC at all. It actually wasn't that hard to recanalize, didn't require sharp recantalization again, most of these we do require sharp recanalization, but here a wire and catheter and a few sheaths managed to get us through.

And you can see the position of the wire in the SVC going down through the atriam/g to the IVC with the position of the [UNKNOWN] behind us. I then proceeded to ciliary dilate and started off with six and eight very tight ways to tuck her off, but it gradually began to

open with some high pressure balloons and I did intimate non geography to see how I was doing despite opening it to I think this is after a ten balloons zero antegrade flow through the system still all going down through the [UNKNOWN] Proceeded up with some further larger balloons, and at this point

I did another angiogram after this it was a 14 millimeter balloon and there was a finding that I missed at that time that is very important, and I'll give you a second just have a look at the angiogram yourself to see if you're better than me. And this is what it is. So this, what I believe was an intimal tear in the acute thrombotic

formation on an intimal tear of the SVC was on this one. I did not appreciate it at the time and proceeded with further balloon angioplasty because again there was no antegrade flow leading down into his SVC and into his right atrium at that point. Proceeded with further balloon angioplasty this is with an 18 balloon and got it up to full and then as I took it down he began to complain

of a strange sensation in his chest that rapidly progressed to him being [INAUDIBLE] that rapidly progressed to him collapsing cardio dynamically and then I performed this angiogram and you can see here as we go through the run this large rent/g here and free extravazation from the SVC

into the pericardial space and [INAUDIBLE] there. So this was complicated by an acute [UNKNOWN] immediately I would say within 30 seconds, he began to change [INAUDIBLE] with the chance of respiration within a minute he had arrested and was requiring

quite a bit of chest [UNKNOWN] followed by as you can see we put in a pericardial drain immediately I inflated the balloon to expand it and he ended up being shocked several times. The options were discussed with the arrest team, we felt that given his age given that he was 29 and this was an acute issue, we would to do our best

to preserve everything in it's place [INAUDIBLE] while that was being set up I kept the balloon inflated and there was a thought that perhaps his balloon tapered out enough release. This showed that no it wasn't, this is after 45 minutes of balloon tamponad/g you can see there is still this large hole,

this is not gonna be repaired by simply tamponading/g the hole, and I ended up placing a viabahn stent across the area. Unfotunately we didn't have atrian/g in this particular lab at that time.

So this sealed the hole and we were able to stabilize him at this stage the bright red blood that was pumping out of his tamponade/g drain that was pericardial drain ceased immediately, and he became [INAUDIBLE] stable again and we were able to move him upstairs. Unfortunately, he had a drastic postoperative course with a global hypoxic injury and actually passed away three days later.

So the take home from this case for us, for me in particular was to be very wary of dilating chronic SVC occlusions particularly those that are low down the super cardinal recess of the pericardium extends to the level of the [UNKNOWN] when you're chronic occlusions at that level to be very very particularly if the major clinical question is accessed,

they do not need to be dilated to 18 like I did, but in the access, settle in there, and you can always come back and treat the SVC syndrome at a different time, perhaps in a different way. But certainly it was a very [INAUDIBLE] point for myself. >>

11 patients representing 3.5 persons there was one day you to interest arable

bleeding and thrombolysis significant bleeding growing hematomas and retroperitoneal bleeding and compartment syndrome in three patients minor complications occurred in fifty-nine patients most frequently peripheral

embolisation in 40 but fortunately all of those embolize were removed by mechanical means during the procedures they were also six RT perforations related to rotor ex that were treated by long-term balloon dilation or by

implementation of colored stance clinically insignificant growing hematoma thromboses compartment syndrome MERS occurred in 36 patients conclusions

So now we're going tomove on to discussing some of the contrast mechanisms underlying spin echo. So just a brief review of the spin echo pulse sequence, so again it's actually very similar to the gradient echo. So here we have our initial RF pulse, and our gradients to read out the data. So the only two differences are first of all, we almost always use a 90 degree pulse in spin echo scan. And the major adddition is we add this 180 degree refocusing pulse, which

as we saw in previous lectures, purposes to refocus the magnetization. So let's just show what's going on here. So initially we play out our 90 degree RF pulse that tips the magnetization down, and we know that begins the signal. Now, we then do our 180 that tips the magnetization around by 180 degrees, and then we do our turn on our gradients, and that reads out the case based data. So again

we put on a negative X gradient that means it's out to the left hand side of case base then we turn on a positive polarity gradient that allows us to sweep out a line of case base and acquire a line of case base data. So that's the basic mechanism underlying spin echo pulse sequence. So now we are going to show in the next couple of slides how we can generate contrast, what sorts of contrast we can generate

with this pulse sequence. So now let's examine what sort of contrast we can generate with the spin echo pulse sequence. So in this slide I'm going to consider the case again where we have three different water molecules which you see a slightly different magnetic field. So initially we play out RF pulse or initial 90 degree RF pulse that tips the magnetization down into the translation/g plane. So now let's

see what occurs a period of time after we've tipped our magnetization down. So we call again that each of the water molecule sees a slightly different magnetic field, because it sees a slightly different magnetic field we're going torotate at slightly different frequencies and therefore over time they are going to be begin to deface relative to each other. So for example let's say

the white one is going tobe rotating in the counter clockwise relative to the others. The orange one is going tobe stationary relative to the others and the black one is going tobe rotating in the clockwise direction relative to the others. Now we saw from earlier, from the T2* decay that when you have this dephasing that causes a signal loss. And this as I mentioned is the T2* decay because now

the magnetization adds up destructively because now they're incoherent relative to each other. So now the next thing we do, we play out our 180 degree RF pulse. So this seems like a relatively simple thing to do but as you see it has a profound effect so when we do a 180 pulse that rotates the magnetization around by 180 degrees. Now the key to note that occurs here is the white one that's still

rotating at the same speed. We've flipped it around but it's still rotating at the same speed relative to the others. So in particular it's still rotating in the counter clockwise direction, similarly the black one is also rotating at the same speed it's rotating in the clockwise direction. So after a period of time this individual the magnetizaion associated

with these individual water molecules will begin to re-phase relative to each other at this time point here. So the analogy that people often use to explain this concept is runners in a race. Let's say, runners at a race start off in a race, and after a 100 meters, the faster runners will be further ahead than the slower runners. If at a 100 meters they all turn around and run back

to the starting line, and by the time they get back to the starting line they'll all be again in phase with each other. Each other because the faster runners will still be running faster, the slow runners will still be running slower but the faster runners now have further to go. And this concept of turning around after 100 meters is exactly the same as the 180 degree pulse so it essentially

causes the magnetization to reverse what it had previously done. So because the magnetization is now back in phase signal will then re-grow, sort of re-grow and we'll get back the signal. And in fact this is called an echo or a spin echo because it is essentially an echo of the original signal we have, so we re-grow signal. Now one important feature to note about the way I

have drawn this is if you notice the echo is actually the lower intensity than the initial signal intensity. And the reason for that is because well we've been able to correct for the decay caused by inhomogeneities, we are not able to correct for the decay caused by T2 decay. So simultaneous with this, all this 180 degrees rephasing and dephasing that's occurring, we're getting an overall T2 decay

of the tissue. So, this signal is decaying away with T2. So, our echo is never quite the same intensity as our initial value. And, the echo time, the TE, controls when that rephasing occurs. So, the rephasing occurs exactly at the echo time TE. So that's the parameter that we're going to control in a spin echo sequences, the echo time. So, if you're called from, what I mentioned earlier

in my first talk, signal loss caused by inhomogeneities is often described as e^-t/T2*. And the overall signal loss is then going to be the sum of the T2 signal loss and the T2 prime signal loss. And that's reflected in a T2* value, e^-t/T2*. So, the

effect of spin echo, is essentially to remove this T2 prime component. So remove any decay caused by inhomogeneities so the spin echo produces a decay that's purely due to T2. So there's no T2* in this case it's equal to T2 cause there's no T2 prime component. So, here we have an example of a T2 weighted image produced by spin echo. So, these are two images of the knee acquired in an

echo time of 7 milliseconds and an echo time of 33 milliseconds. I'm going to highlight three different tissues here we have muscle with a T2 value of about 50 milliseconds, fluid with a T2 value of about a 1,000 milliseconds and cartilage with a T2 value somewhere between 30 and 70 milliseconds. So in our initial, here we have our initial

echo time of 7 milliseconds and if we compare that to an image a part of the later echo time 33 milliseconds, you can see that the cartilage and the muscle have decayed away substantially relative to the signal from the fluid. Because again the fluid has a much longer T2 value so its signal has not decayed away to a great extent in comparison with the cartilage and the muscle. So I want to make

a final comment on contrast we generate with fast spin echo imaging. Because as I have mentioned in previous lectures fast spin echo has virtually replaced spin echo in routine clinical MR scans. So, here we have the basic fast spin echo pulse sequence which we'll just briefly review here, so we start out with our initial

90 degree RF pulse followed by the 180 degree RF pulse which we now know the purpose is to revoke its magnetization. We then play out our initial Y gradient which again we are starting in the center of case space this moves us down to a particular line in case space and we then play out the negative lobe of our X gradient which moves us to the left hand

side of case space followed by the positive lobe of the X gradient which allows us to read out a line of case space. Now up to this point, this is the same as fast spin echo. So if this is spin echo we would stop here. But in the case of fast spin echo we then repeat that procedure, following another 180. So we play another 180 that again refocuses the magnetization and then we acquire

another line of case space. So we essentially play out another Y gradient that moves up, on the vertical direction, moves to another line of case space and we read out the second line in case space. We can repeat that procedure as many times as we want in some cases, you can do what is called a single shot fast spin echo imaging when you essentially acquire the full extentive case space following the initial 93 RF pulse. So one question that arises

here is what is the echo time in this case? Because in this case we're actually going through multiple lines of case space. It's not just one single line. Well the echo time in this case is defined as the time between the initial RF pulse and the time where we go through the very central portion of case space. So whichever line in here corresponds to when we go through the very central portion

of case space, that is defined as the echo time or the TE value of a fast spin echo pulse sequence. And let's just look what goes on with the signal in a fast spin echo pulse sequence. So here we have our initial spin echo pulse sequence, so again we have our decay and the refocusing so we have the echo here. If we add in another 180 then again we're going to refocus the magnetization a second time

following this 180. And again recall that during this period of time we have consistent T2 decay occurring. So the echo time TE again just corresponds to time at which we acquire the central line of case space and that T2 waiting will correspond to how much decay has occurred during that period time. So let's just summarize the concepts for contrast in spin echo or equivalently fast spin echo. So in this

case we just had really a single parameter that we can vary which is the echo time or the TE and again defined as a time between the RF pulse and a time when we acquire the center of case space, which in case the spin echo follows 180 degree pulse. Generally speaking the longer the TE the heavier the T2 weighting because this allows more time for T2 decay and therefore allows for more signal discrepancy

with tissues with different T2 values. So that's the end of the relaxation and contrast lecture thank you.

11 patients representing 3.5 persons there was one day you to interest arable

bleeding and thrombolysis significant bleeding growing hematomas and retroperitoneal bleeding and compartment syndrome in three patients minor complications occurred in fifty-nine patients most frequently peripheral

embolisation in 40 but fortunately all of those embolize were removed by mechanical means during the procedures they were also six RT perforations related to rotor ex that were treated by long-term balloon dilation or by

implementation of colored stance clinically insignificant growing hematoma thromboses compartment syndrome MERS occurred in 36 patients conclusions

down to really the clinicals very is it an urgent / emergent procedure in a patient with a threatened limb then of course you're going to place a stronger

priority on doing something for that patient is at a first-line treatment in a patient who you're really trying to prevent post-traumatic syndrome or is it a patient who has been on anticoagulation and now they've had

either progression of their clot or have not resolved their symptoms and you're using more of a salvager a second-line treatment to help that patient with their problem anatomic severity really the data shows

that LOL femoral dvt has at least twice the risk of developing post-antibiotic syndrome so those patients really are the ones at risk for the late consequences so they should highly be considered for additional therapy you

have to balance the benefits with the risks they're obviously the risk of increased bleeding using the from ballistic material or medication so many patients with an intracranial or spinal lesion any patient who is actively

bleeding or had a recent GI bleed anybody with Rumble side opinion recent trauma postpartum what I'll have increased risk of bleeding anybody who has uncontrolled hypertension adding the thrombolytic on top of that increases

the risk of hemorrhagic stroke and then anybody who has suspicions for in fact infected promise it's relatively contraindicated to do thrombolytic therapy in your patient selection the whole point is to help we prevent

post-traumatic syndrome and relieve their underlying our current swelling so patients who are bedridden at baseline or you know don't have that long of a life expectancy really are going to see the

long-term benefits of this sort of therapy so they would not be the best candidates patients who you know can't lie prone on the table lay still for an extended period of time or otherwise are going to be able to tolerate the

procedure would also not be good candidates for this procedure and then because there's not great robust data a lot of its going to rely on you know having a front conversation with your patient and what their values are and

where they fall on the spectrum of doing something more aggressive versus something a little bit more conservative so with that we go to the questions so

[MUSIC] Hi, my name is Marshall Sussman. I'm an MRI physicist at the University Health Network and the University of Toronto. I'm giving a series of lectures on basic MRI physics. Topic of today's lecture is, Magnetic Resonance Imaging Options. [SOUND] Here are the screen capture of a console on MR scanner. And you can see in this console, that there's a number of different options that we can vary, and these options alter

the way that we acquire our MR images, and may affect the resulting appearance and quality of the MR images. So today, I'm gonna discuss a number of these imaging options. So, first of all what are imaging options? Why do we have different imaging options? Well, there is a number of different reasons. First of all is because they can affect the resolution of the image, signal to noise ratio,

the contrast in the image, and there's also some additional options that I would classify under special features, which may give some specific properties to a particular type of imaging modality. In today's lecture, what I'm going to talk about is, focused on two aspects of the imaging options. So first of all I'm gonna focus on those imaging options that affect

the resolution. So in particular the ones we want to vary are the field of view, matrix size and the slice thickness. I'm also going to discuss the imaging options of the fact without the signal to noise ratio, specifically the spatial resolution, date acquisition time, bandwidth, knacks which will get to a number of expectations and the flip angle. So let's start off with spatial resolution. So what is spatial

resolution? It's just simply the sharpness of an image. So if you look at the image on the left compared to the image on the right, you can see the one on the left, is much sharper so it has a finer spatial resolution or a better spatial resolution, the one on the right is blurry relative to the one on the left. So what is spatial resolution specifically? Well, if you recall our images are divided up

into a grid and they consist of a series of pixels. So the individual size of one pixel element, is equal to spatial resolution of the image, so the smaller that individual element, the finer that spatial resolution or the better the special resolution will be. So what factors, what imaging options affect the size of the pixel? Well it's just simply the field of view,

so in other words how big our image is, divided by the matrix size so essentially the number of gid elements. So view to those are changed the size of the individual pixel element will change. So just to give an example of that if we change the matrix size so if we let's say double our matrix size, you can see that the individual pixel element gets smaller, so increase in our matrix size will

lead to a finer spatial resolution or a better spatial resolution. Here we just have an example of that. This is an image of the knee and you can see the image on the left was acquired with a matrix size of 128 by 128. The image on the right was acquired with a matrix size of 512 by 512. So larger matrix size. We increased it by a factor of 4.

And when you do that you can rate those two images. You can see the one on the right has a much finer spatial resolution as you can see the image much more sharply. Again that's just simply because we increased the matrix size. So increase in matrix size, finer spatial resolution. [SOUND]

So what about field of view? So here we have our initial image n here and a corresponding initial pixel size. If we decrease our field of view down and maintain the same matrix size, again the effect is the same, you can see that we decrease the size of our pixel element. So if we decrease the field of view, that again leads us to a finer spatial resolution. So here we just have an example

of that, here we have two images the one on the left. These are again images of the knee, the one on the left has a field of view of 28 centimeters, if we now drop that field of view down by a factor of 2 to 14 centimeters, you can see that again, the spatial resolution increases. So just to make that a little bit more packed I'm gonna zoom in a little bit more closely so you can have an easier comparison

of these two images. And again you can see the image with the 14 centimeter field of view, has a finer spatial resolution so the edges are sharper. Now, a final thing we have to talk about spatial resolution, most people appreciate the incline spatial resolution of an image, in the previous examples it was quite obvious when the spatial resolution gets better. Something that people don't

sometimes appreciate, is there's also resolution in the through plane direction as well. And that's just simply equal to the slice thickness so typically in MR where excite a particular slice in the anatomy for doing a 2D acquisition, and the thickness of that slice, corresponds to the spatial resolution in the third dimension on the through plane dimension. So for example, if we decreased

the slice thickness, that would cause an increase or an improvement in the spatial resolution or spatial resolution will get finer, as we decreased the slice thickness. So again through plane resolution is just simply equal to slice thickness and the thinner the slice thickness, the better the through plane resolution. Now, this concept is a little bit harder to demonstrate in practice, but

what I'm gonna show you here is an image of the phantom. The image on the left was acquired with a slice thickness of one millimeter and the image on the right was acquired with a slice thickness of five millimeters. If you look at the in plane resolution, it's the same in both cases. One thing I want you to focus on, is the line at the very center of the phantom. Because this line consists of essentially a wedge that's

angled in the through plane direction, so the thicker our slice, the more of that wedge you're gonna see, because more of it will be included in the image. So if you compare the one millimeter image to the five millimeter image, you can see that in the case of the five millimeter image, the wedge is larger because more of it is going to be included. This give you more of an appreciation of how change in the slice thickness

will change the through plane resolution. [SOUND] So let's go back to our outline. In terms of imaging options, we've so far discussed the resolution. And you can see from this console on the MR scanner, that we have a number of different parameters indicated by the yellow arrows that will change the through plane resolution, so the ones you see here affect

the field of view, matrix size and slice thickness. So now, we're gonna move on and talk about signal to noise ratio. What are the options that affect signal to noise ratio? So again just to recall from our earlier lecture signal to noise ratio is just a measure by definition of the amount of signal in

the image between opting noise. And recall that noise are just simply then fluctuations that are super imposed on top of the image. So in this case, the image on the left has a high signal to noise ratio whereas the image on the right, has a little signal to noise ratio and you can appreciate that by larger relative magnitude of those random fluctuations in the little SNR image. So what are the imaging

options that affect signal to noise ratio? So there's five of them that I've listed here, is the spatial resolution, the data acquisition time, or its often abbreviated as DAT, a bandwidth, the NEX which stands for a number of excitations and and the flip angle. All of these different imaging options are related through this formula that you see here at the bottom, and I'm gonna

refer back to this formula multiple times through the remainder of the talk. You can see that the signal to noise ratio is proportional to the resolution and proportional to the square of the data acquisition time, square of the NEX and inversely proportional to the square of the bandwidth. So as you'll see in the next slides, I'm gonna repeatedly refer back to this formula. So let's start off

with the resolution. So the signal to noise ratio is directly proportional to the resolution, so that means the finer the resolution, the lower the SNR. So what are the imaging options that affect the resolution? Well we just discussed that earlier. So there is this three different lies, the field of view matrix size and slice thickness and all of these, if you adjust this we'll adjust the resolution but you'll

also adjust the signal to noise ratio. So just to give an example of that, here we have this same example that I showed you before the knee, where you had the image on the left was acquired with the matrix size 120 by 128, the image on the right increase the matrix size so it has to 512 by 512, and this gives us a fore fold improvement

in spatial resolution. So earlier, we started highlighting the difference in spatial resolution but what I wanna highlight in this slide, is the difference in signal to noise ratio, if you look at the 512 by 512 image with the finest spatial resolution, you can see that it has a corresponding lower SNR so the magnitude

of the noise is larger in that image compared to the 128 by 128 case. So then signal to noise ratio is directly proportional to resolution. So lets just go back to our slide here we've seen all the imaging options so again signal to noise ratio in terms of the effect in resolution, you know that

field of view matrix size and slice thickness affect the resolution and therefore they affect the signal to noise ratio. Now let's move on to discuss data acquisition time. So first of all what is data acquisition time or what's usually abbreviated as DAT. That's just simply defined as the total time the data is acquired for. So it sounds like a fairly straight forward thing but one

thing I'd like to emphasize that's often not appreciated, is data acquisition time is not the same thing as scan time. So just to illustrate why that is. Here we have our basic gradient-echo pulse sequence. So as we have shown many times now already, the RF pulse tip magnetization down into a transverse plane hitting them at the signal. We turn on the negative polarity X-gradient, that good

sort to the edge of k-space, we turn on the positive polarity X-gradient and that is when we switch to the line of k-space and acquire our data. That essentially acquires one line of k-space. We then repeat that procedure a second time or as many times as necessary to acquire all the other lines of k-space. The time that occurs between the acquisition of adjacent lines of k-space is governed by this repetition

time or the TR parameter which we've discussed in earlier lectures. So what you can appreciate from this, is that during this whole procedure, we're really only acquiring data for a portion of the total amount of time during the scan so its really only when that positive polarity X-gradient is on, that we're actually requiring data. In fact we could adjust our TR essentially

arbitrarily, and the scan time would have basically a wide range of values, but the data acquisition time, would not change so its very important to distinguish those two concepts. Data acquisition time is not like equal to scan time so just because you linked in your scan time doesn't necessarily mean you can improve your SNR from a data acquisition point of view. So if we go back for a formula,

you can see that signal to noise ratio, is proportional to the square root of data acquisition time. So what are the parameters that affect the data acquisition time?So if you recall in MRI we acquire data in the case base domain, so we acquire essentially fourier transform data. So the data we acquire in k-space is divided up into a grid and when we are acquiring data on our MR scanner,

we basically just simply acquiring all the elements of that matrix. We then apply fourier transform to generate the image. So in this case, you can appreciate that the data acquisition time, is just equal to the number of elements in that data matrix. So for example if I double the number of elements, and that's gonna mean I gotta take twice as much time to acquire the data, so the data acquisition

time is just simply directly proportional to the matrix of it. So if I increase the matrix size, I increase the amount of data I have to acquire. So if we look at our above formula, we know that the signal to noise ratio is proportional to the square root of the acquisition time, so that means that the signal to noise ration is therefore going to be proportional to the square root of the

matrix size. However, as we saw previously, we know that the resolution is also proportional to the matrix size. So if we increase the matrix size the spatial resolution increases. And further more we know that signal to noise is proportional to the resolution. So therefore, what that means is that if we affect the matrix size

we're gonna be affecting two thing simultaneously. So on one hand we're going to be affecting the data acquisition time so we're going to be increasing the data acquisition time which is gonna lead to an increase in our signal to noise ratio. However, what we're going to be doing, is we're going to be having a finer spatial resolutions we're going to be essentially improving the spatial

resolutions so that the number is gonna be getting smaller, so those two things essentially work in opposite to each other, increased matrix size we got to finer a spatial resolution which is gonna decrease the SNR, but we have a longer data acquisition time which is going to increase the SNR. So let's just give a concrete example of that concept to illustrate the point. So let's say we have a

case where we are doubling our matrix size, so what's gonna happen to resolution what's gonna happen to our data acquisition time? So data acquisition time is gonna increase by a factor four because we are now doubling the matrix size in both the X and Y dimensions. [SOUND] The resolution, is gonna get finer in both the X and Y dimensions, so the resolution has been improved by a factor of two.

So, if we go back to our formula here, how is that going to affect the SNR? Well in terms of the resolution, the resolution gets finer by a factor of two in both dimensions, so the SNR is gonna drop down by a factor four based on the improvement in resolution. The data acquisition time, again, it increases by a factor of four, but the SNR goes to the square root of data acquisition time. The SNR is

gonna go therefore as the square root of four, based on the data acquisition time. So if we multiply those two factors together, what that means is that overall, the SNR is gonna drop down by a factor of two. So if we double our matrix size, the SNR goes down by factor of two. Just give an example of that, here we have two images. The one on the left was acquired with an matrix size of

512 by 512. One on the right was acquired with a matrix size out of a 1024 over 1024. So again we doubled our matrix size. So in these images I took the measurements of the signal to noise signal. Ratio and the one on the left had a signal to noise ratio of 17, the one on the right had a signal to noise ratio of 7. So you can see that the SNR approximately decreased by a factor of two

when we doubled our matrix size. [SOUND] So going back to our overview slide here, again the imaging options that affect resolution, field of view, matrix size, slice thickness and data acquisition time, its matrix size. So now let's move on and discuss what happens to SNR, as we adjust the bandwidth. So

again we're gonna start off by definition of what is bandwidth. So bandwidth, is just simply the frequency that data is sampled at. So for example 125 kilohertz, means we're sampling data at 125,000 samples per second. Now, the data acquisition time is gonna be inversely proportional to the bandwidth. So why is that? So just imagine, let's say we acquire 100 data points at a rate of 100 points per

second. So that means we're gonna acquire our data in one second. If I then double my bandwidth, so I'm now acquiring the data at 200 samples per second I'm gonna inquire that same 100 data points now only in half a second. So the data position time is inversely proportional to the bandwidth. So if I increase the bandwidth or I increase the sampling rate that decreases the data acquisition time. Now

we know from the earlier slide, the signal is always ratio is directly proportional to the square root of the data acquisition time. So, therefore that implies that the SNR is going to be inversely proportional to the square root of the bandwidth. So if we increase our bandwidth we are going to decrease the signal optimize ratio. I should however point out that changing the bandwidth can also

affect some other parameters in the MR scan. So we all just simply wanna always use the lowest bandwidth possible, because one thing it may affect the minimum echo time we can achieve in minimum TE, and that's important for the contrast that we saw in our earlier talk. It may also affect the sharpness of the image, so in general if we use much very low bandwidths that may blur out the image,

and also importantly, bandwidth is also has, it can have an important effect on the artifacts, especially those related to the magnetic fields in homogeneity. So as a result, that means that although in our scenario point of view using a lower bandwidth is also a good thing, but may be the other fact is that mitigate against using as lowness

in our bandwidth as we can. Here, we just have an example illustrating the relationship between signal to noise ratio and bandwidth. We have two cardiac acquisitions. The one on the left was acquired with a bandwidth of 83 kHz, the one on the right was acquired with a bandwidth of 125 kHz. Now the differences in SNR are a little bit subtle to appreciate in these images because again the SNR only

decreases as the square of the bandwidth and I just increased it by a factor of 1.5 in this case. But if you focus on the myocardium, if you look at it, you can see the acquisition that was acquired with the bandwidth of 124 kilohertz, is just a little bit grainier because the SNR is a bit lower in the 125 kilohertz case. Going back to our outline here, the next thing we're gonna discuss is the NEX.

NEX simply just stands for number of excitations and different vendors will use different acronyms for this. Some call it number of averages, and they all mean essentially the same thing. Essentially what that means, is you repeat the image acquisition equal to the number of excitation times so the number of NEX times. Once you do that you add the image together and when you do that the SNR improves.

In fact the SNR goes as the square root of the number of excitations. Now one thing you might ask, is okay why not just simply always use a really large number of excitations, we can get a really high signal to noise ratio. The problem with that, is that the scan time is directly proportional to the number of excitations readings. So if I say double the number of citations I do, that means my scan time

is gonna increase by a factor of two. And SNR now we'll increase by root two, but my scan time will increase by a factor of two. So this is often penalty that in a routine clinical environment you just can't afford to take. Let's just give an example of signal to noise ratio varying as a function of the number of excitations. So let's say we have an

image of the heart here, and let's say it has initial image of SNR zero. I then acquire a second image of the heart, and I add those two images together, what you expect is the signal to noise ratio is gonna increase by root two. If you look at the graininess of the initial images to the combined image, you can see that in fact that is the case. The SNR is increasing. Just to kind of

drive this point home further, let's say add four images together and I add them together, the SNR is gonna increase by root four or a factor of two and again comparing that composite image to the original one, you can clearly see that signal to noise ratio is improving. One additional point I should just mention on number of excitations, is in fact that's actually really just simply equal to the

data acquisition time, because if I increase my number of excitations by some factor, that essentially means I'm increasing my data acquisition time by that same factor. So the number of excitations data acquisition time really are the same thing. I just distinguish them here just for the sake of illustrative purposes. So the last thing we're gonna talk about is the flip angle. So now let's look into how flip angle

affects the signal to noise ratio. If you recall we put a person in the MR scanner, the magnetization lines up with the direction of the magnetic field. We then turn on an RF pulse, and that tips the magnetization down away from the direction of the external magnetic field by a specified flip angle

which I call theta. So at this stage, the magnetization has two components, has a longitudinal component along the direction of the external magnetic field as well as a transverse component. Now if you recall, it's only the transverse component that gives us any signal. So therefore the magnitude of the transverse component is proportional to the signal to noise ratio. Now based on this

description alone, you would conclude that well we'd always wanna use let's say a 90 degree flip angle because that would put the entire magnetization into the transverse plane and that would give us the maximum signal to noise ratio. n That

would be true, however the call that there is different relaxations that occur once the magnetization tip down. So first of all is there is a T2 decay which causes the transverse magnetization to decay, there is also a T1 recovery which causes the longitudinal magnetization to re-grow, so both of these factors

can affect the length of magnetization as it goes into the transverse plane. If you recall from our earlier talk essentially we have to get the magnetization into a steady state, and that steady state depends on flip angle T1 and T2 value, so it's not quite a straight forward, the 90 degree flip angle will not necessarily always give you larger signal to noise ratio. So here we have an example of

that, here we have images of the brain required at four different flip angles, 5, 20, 40, and 90 degrees. In this case, you can see the maximum signal to noise ratio is achieved at a foot angle of 40 degrees, not for example 90 degrees, and again that's due to relaxation, so in general the relationship SNR flip angle is quite complicated. Now the other thing you can appreciate from this image, is the tissue

contrast, also changes when the flip angle varies. So for example the difference in intensity between the white matter and grey matter or the variation of the scalp, varies as a function of a different flip angles.

So in general while the signal to noise ratio does change with foot angle is not the only thing that changes and furthermore the relationship is quite complex. So you have to be cautious when you are increasing the flip angle as to do the SNR, because in general relationship is not simple. So just

to summarize what we talked about in this lecture, I've shown you that there is a number of different imaging options that we can adjust on the MR scanner and this affect different properties of the MR image. We showed you some of the options that you can affect to you can alter to change spatial resolution in particular a field of view, matrix size, and slice thickness.

I've also showed you some of the imaging options that adjust to affect signal to noise ratio, those related to resolution, date acquisition time, bandwidth, NEX, and flip handle. There is also some special features which I didn't go into in this lecture. These are additional special options that often are related specifically to particular pulse sequence of, things such as fat saturation, or a spatial saturation

which I didn't discuss in this lecture. So thank you for listening and I hope you'll join me for the other lectures in the series. Thank you.

Hi, my name is Marshall Sussman. I'm an MRI physicist at University Health Network, in University of Toronto. This lecture is gonna be the second part of my Relaxation and Image Contrast in MRI talk. So in first part of this lecture we briefly reviewed what image contrast is, and then we discussed a number of different MR mechanisms that can be used to generate contrast. So in this lecture what I'm gonna do is, I'm going to show how those contrast

mechanisms can be used within various different MR pulse sequences to create contrast. So the pulse sequences that I'm gonna be talking about are gradient echo and spin echo. So image contrast in image depends on a number of factors. So first is the tissue parameters. So this is proton density, T2, T2*, T1, which we've obviously mentioned, pulse sequence, and the pulse sequence parameters. So all three

of these things will affect the ultimate contrast we see in an image. Now often, when I interact with people who aren't necessarily really familiar with some of the details in MR physics, often, various different mnemonic devices are used. So people say if I have a short tear in my pulse sequence that gives me a T1-weighted contrast image. If I have a long TE

that gives me a T2-weighted contrast in my image. And that's true for many pulse sequence types, but it's not true in all cases. There are certain pulse sequences where these sets of parameters could give you different types of contrast. And really, in order to fully understand the contrast you're gonna generate in an image you really have to examine the pulse sequence, the parameters, and the underlying

contrast mechanisms. And it's really only from that complete understanding that you can really get a good comprehension of what types of contrast you're going to be generating. So with that in mind, let's move on to the first pulse sequence that we're gonna look at, Which is gradient echo. So this is one that we've looked at, a number of different times in the previous lectures, but I'm just gonna

briefly review it here. So basic pulse sequence timing diagram, you can see here, it starts with an RF pulse, which we know tips down the magnetization away from the external magnetic field. And we then turn on our gradients which is what move us through k-space to acquire our data. So initially, after we do our RF pulse, we always start at the center of k-space. We then turn on our Y gradient, and that

moves us up into a particular position in the vertical direction. We turn on our negative polarity X gradient which moves us out to the left hand side of k-space, and then that's followed by our positive polarity gradient, which sweeps out a complete line of k-space. And that's when we acquire our data. We then increase the strength of the Y gradient, and that moves us up to another

line in k-space, and repeat that same procedure. So we just simply step through this, repeat this procedure as many times as necessary in order to cover off all lines of k-space. Now within this basic gradient echo pulse sequence, there's three different adjustable parameters that we can manipulate. The first is the Flip angle or theta so that's really the RF pulse, and it's just simple

the angle that the magnetization makes with the external magnetic field. So this is something that we can control. The second parameter is the TR or the repetition time. And this is simply the time between the acquisition of adjacent k-space line. So essentially the time that it takes us to repeat this cycle. Third is the TE or the echo time, and this is defined at the time between when we first tip

our magnetization down, so we first put out our RF pulse and the time with which when we acquire the central portion of k-space. So in this case it's the center point of this gradient loop, cause that corresponds to when we go through the center of k-space. So in the next few slides I'm gonna show how these parameters can be used to modulate the contrast we see in an MR image. So first of

all, is the echo time or TE. So as we saw from the first part of the lecture, after we play at our RF pulse, the signal intensity decays away over time with T2* decay. So here we have, let's say this tissue here has a T2* value of T2A, T2A*. So the signal decays away like you see here. [BLANK_AUDIO] Now at this point in time here, when we go through the center of k-space which corresponds to this echo

time, the signal has therefore decayed away up till this point here. If we now have a second tissue with a different T2* value, so indicated by the red line, T2B*, then at the echo time, which again is the time we go through the center of k-space here, you can see that the signal will have decayed away, a different amount than the first one, again because it has a T2* value.

Now the contrast we're gonna get in our image, is simply gonna be the difference in signal intensity, at this point, at this echo time. So it's just gonna be e to the -t over T2A*, minus e to the -TE, over T2B*. So by setting up this echo time, we generate a T2*-weighted contrast in our image. Now what if we move the echo time to an earlier time point? So we've

now shortened the echo time TE to this point here. So again, the contrast we're gonna get in our image, is again just simply the difference in signal intensity between these two lines here. But in this case, because our echo time is shorter you can see that we haven't generated as much contrast, so there's less contrast in this case. So in general, when we shorten the TE we reduce the

T2*-weighted contrast in the case of gradient echo pulse sequence. Now I've been mentioning here that, the echo time, the TE in code contrast, which corresponds to the time we go through the center of k-space. But why is it the center of k-space is important, what's special about it? Well here we have a slide that I showed in my earlier talks on k-space. Here we have the

complete image and the corresponding k-space data that generates that image, again recall via Fourier transform. Now if instead of generating the image from the complete k-space data set, I just generate an image from the central portion of k-space, resulting image you see looks like this here. So in this case you can see, importantly, that we encode the contrast in this image.

So the center of k-space still generates the contrast that we see in this image. The outer portion, so if we reconstruct the image just from the outer portion of k-space, you can see that we see the edge information, but there's really no contrast in the image. The image is essentially a uniform color. So that's the reason why the center of k-space is important, because that really encodes

the contrast in our image. So that's why we care about when we go through the center of k-space, and that's what we set our echo time to be. So just to summarize what we've got to date. The echo time, TE, corresponds to the time of acquisition of the center of k-space. The center of k-space, as we know, determines the image contrast, so therefore as a rule of thumb, the longer the TE, the heavier

the T2* weighting. So the more difference in T2* weighting we're gonna have between tissues with different T2* values. So here I just have an example of, this is an image of the heart, one acquired with an echo time of 2 ms, and one acquired with an echo time of 16 ms on a gradient echo scan. So if we compare say the myocardium and the blood in these two cases, you can

see in the one with a 16 millisecond echo time, there's a much larger contrast between the myocardium and the blood. Again because the myocardium has a much shorter T2* value. So it decayed away, much ore dramatically, in the 16 millisecond case, than it had in the 2 millisecond case. The next pulse sequence parameter we're gonna talk about is the

repetition time or TR. So recall the TR it's just simply the time between we acquired adjacent k-space line, so basically the time that we repeat this cycle. So let's look at what's going on with the magnetization. So initially we started out with our magnetization at its full, complete value. So let's say, as a value, for purposes of this discussion as one. So we then play out our pulse, and in this case let's assume

we have a 90 degree pulse, so that tips down the magnetization completely into this transverse plane here. Following that we have T2* decay. So the signal is then going to decay away completely. So following the magnetization decay, the magnetization will then regrow back towards its initial value due to T1 recovery. So here we have again this formula here, 1 - e to the -TR

over T1. Now if we set our TR to be long enough, then that magnetization will regrow back to its initial value. So in other words, the magnetization will regrow back to its initial state. But what happens if I set my TR to a shorter period of time, the magnetization doesn't regrow back to its initial value. Then instead of recovering completely, it will only recover partially. So let's say in this case, it only

recovers to a value of 0.8. So when we then foot the magnetization down, it now, instead of having a value of 1, it only has a value of 0.8. So when we then have our T2* decay on the next iteration, the signal intensity starts from a value of 0.8, and then decays away completely. It then regrows back to a value, again, of 0.8. It's decayed away completely, and we have the same TR value, so it goes back

to a value of 0.8. Now this is called, essentially, the steady state of the magnetization because the magnetization lies in a steady state on every single iteration. So it lies in exactly the same position on each iteration we do. So we tip the magnetization down, it decays, it then regrows back to a value of 0.8. We tip it down again, it decays away completely,

regrows back to a value of 0.8. So a steady state just simply means the magnetization is the same from one TR to the next. And in general, we almost always we'd acquire images when the magnetization is in a steady state. So now, let's examine the contrast it's generated as a result of a particular choice of repetition TR. So as we mentioned in the previous slide, this magnetization in

the red lies in the steady state. So we're constantly going between these two situations. We tip the magnetization down, it has a value of 0.8, it decays away to 0, then recovers to a value of 0.8, and the process is repeated. So it's the same each time. Now, this value of 0.8, the reason it recovered to this point, obviously, depends on the TR value. So if we change

the TR value to some other value, then the magnetization will recover to a different point. But the value that it recovers to also depends on the T1 value of the tissue. So for example, if I had tissue with a different T1 value as indicated by this green line here, so let's say I had a longer T1 value, then it would recover at a time TR to a different point. So in this case let's say it recovers only to

a value of 0.5. And important thing to note is that this magnetization also lies in its own steady state. So it's gonna continuously oscillate between, it's gonna decay away to, it's gonna be tipped down, and it's gonna decay away, and recover back to a value of 0.5. It's gonna be tipped down, decay away to 0, recover to a value of 0.5. If we look at this plot down on the right here, you can see that the red magnetization

is in a steady state where it has a value of 0.8, the green magnetization has a steady state value of 0.5. So in other words, we generate a contrast between these two signals, a T1-weighted contrast, which we capture when we tip the magnetization down. So in this case, the red magnetization would have a stronger signal intensity than the green one would.

And this is a contrast that depends on a T1 value. Now, if I change my TR, that's gonna change the relative amount of recovery between these two magnetization. So the relative T1-weighted contrast is gonna change if I adjust my TR. Now, as a general rule of thumb, the shorter the TR, the greater the T1 weighting because that means that the shorter one's gonna recover more quickly than tissues

with a longer T1 value. So TR affects the T1 weighting. Generally speaking, the shorter the TR value, the greater the T1 weighting. Now, there are some exceptions to this, of course, that if you have a very, very long TRs then the contrast basically disappears. And similarly if we had very, very short TRs then there really isn't much time

for a contrast to evolve so there overall won't be very much difference in signal intensity. [BLANK_AUDIO] Couple of additional comments on this contrast generated by TR. First of all, in this case, we always assume that the magnetization decays way to 0 each time. So that was sort of our steady state condition.

We tip the magnetization down, decays away to zero, then recovers back to it's steady state value. Typically, if that's not the case, we often tip away/g with something called spoiling. So that's just simply a gradient which dephases the demagnetization to get rid of any of the residual magnetization that's lying in the transverse plane. There's also RF spoiling, which is another way of

accomplishing the same thing. Another thing to consider is that I've assumed that when we tip the magnetization down we're capturing that T1-weighted contrast exactly as it's stored along the z axis here. But as we know, that if we have a TE that's not equal to zero, we're gonna start to have some T2*-weighted contrast evolve in our image. So if our TE is anything other than

zero then we're going to have, not only this T1-weighted contrast, but we're gonna have an additional T2*-weighted contrast that's superimposed on top of it. So we're gonna have sort of a mixture of both T1 and T2* weighting, which would complicate the interpretation of the image, cause it's hard to distinguish which mechanism is dominating. So typically, we wanna choose TE to be as short as possible in these

sort of gradient echo scans where we're trying to highlight T1-weighted contrast. We wanna choose TE as close to zero as we possibly can. Now let's move on to talk about the effects of flip angle on the contrast we have in a gradient echo pulse sequence. And again to examine this one we have to look at, again the magnetization, so in the previous case

we assumed that when we play our RF pulse we're tipping it down with a 90 degree pulse. So, in this case, let's generalize it, to say, we're gonna have an RF pulse with an angle theta. So, in this case, instead of the magnetization being completely tipped down in the transverse plane, it's only tipped down with angle theta. So at that point, instead of the magnetization, initially

had a value of one, but now in the transverse plane, where again we're our signal, it only has a value of 0.7 because we haven't tipped it completely down. So part of this magnetization lies along the z axis and part lies along the transverse plane. Okay, so once we do that, the signal we know decays away with T2* decay, just as before. So we assume that this signal disappears along

the transverse plane, and then once a signal's disappeared we're gonna then experience T1 recovery, and the magnetization is gonna regrow back to its initial value. But remember that unlike the previous case, it's not starting from zero because we didn't tip the magnetization completely down. Rather it's starting from this point of, in this case,

0.7. So the magnetization will then recover with this equation here. It's gonna start at 0.7 and recover back to its initial value. In this case, let's just assume we choose a particular TR, let's say, it's gonna recover back to a value of 0.9. And just to show you that this magnetization essentially recovers, this is basically the latter/g part of the T1 recovery curve. Cause initially, if we started

from zero it would recover like this, but in this case we don't have this portion of the curve cause we're starting at 0.7 already. So that's on the first iteration. We then have to tip the magnetization down again, but it actually gets to be quite complicated, because in general, the magnetization is gonna now start from a value of 0.9, it's gonna be tipped down to some value other than 0.7. And in general,

it's gonna take several iterations until we get into the steady state. So I'm not gonna draw the diagram here cause I 'd probably would have to go through four or five iterations of this until we finally get into the steady state. So generally speaking it's gonna take, if the angle is something other than 90, it's gonna take a longer period of time to get into this steady state of magnetization, but

we typically have to wait until we're in the steady state before we start imaging. Now what happens in terms of the contrast? So let's say we, again, flip our magnetization down with angle theta, it decays away, and then begins to recover. Now if we have two different magnetizations with different T1 values then obviously it will recover to different amounts. So if we plot the recovery on the

plot on the left, the shorter T1 value recovers more rapidly whereas the longer T1 value recovers more slowly. And again recall, they're starting from different points in time here at different values here. This is starting from value 0.5, this is starting from a value of 0.8. So in general, when we have different flip angles this also produces different T1-weighted contrasts. But unfortunately, the relationship

is quite complex between the two, and there really isn't a straightforward relationship between flip angle and T1-weighted contrast. As a rough guide, and this is only a very rough guide, larger flip angles generally produce a heavier T1 weighting, but that's not always the case. Here we just have an example, we have four different images of the brain acquired at different flip angles, 5 degrees,

20 degrees, 40 degrees, 90 degrees. And you can appreciate that the contrast of the brain tissue changes with differences in our flip angle. Okay, so let's just summarize what we've talked about so far with gradient echo. So we showed that there's three different parameters that we can vary in the pulse sequence. There's the flip angle theta, there's the echo time or TE, the time from the RF pulse

to the center of the acquisition of k-space, and there's the TR or the repetition time, which is just the time between the acquisition of adjacent k-space lines. We showed that if we have a longer TE, this is going to produce a heavier T2* weighting. If we have a shorter TR that's gonna produce a heavier T1 weighting. And finally, if we have a larger flip angle,

that's gonna, generally, produce/g a heavier T1 weighting although the relationship is complex, and it's not quite as straightforward. So now we're gonna move on to discussing some of the contrast mechanisms underlying spin echo. So just a brief review of the spin echo pulse sequence.

you look again about fifty percent of those patients that were treated with a penumbra integral frontline only to me

two or three posted to go number into your treatment of from over eighty-one percent after intervention over ninety-five percent TPA and then use the number indigo again even slightly better results no significant change after

intervention with angioplasty and stent placement also as far as mechanical come back to me prior to remember again about the same with hundred percent perfusion post both usable for adjuvant TPM account therapies obviously these are

patients that we started out with those patients that we couldn't get lice we couldn't use a get other mechanical thrombectomy devices to use went to the number is the last ditch effort and obviously a hundred percent of patients

then we establish flow safety there was procedurally SI es in about seven percent of patients obviously none of those were device-related this is obviously a percutaneous arterial intervention vast majority of those four

hematomas at the site mostly in patients that are already previously had from political or other mechanical thrombectomy thermolysis so really none device related complications at all

management of of dvt can be broken and very simply into ambulation blood thinners compression stocking pretty

good evidence that each at each level on the recommendation but we know that there is a need for more because we're seeing these patients with post-traumatic syndrome patients who have chronic disease and so what are we

looking at well its patients who have leg swelling and pain people who come in with the heavy leg syndrome and these are the sort of images that we know will see fairly regularly and these the ones that are usually association with

proximal disease in the video cable segments it's extremely common if you run the numbers somewhere between twenty and fifty percent of all patients who develop whoever dbt will develop some form of pts despite being on the best

our ad coagulation and obviously people who can't be out Greg later a higher risk and all those people somewhere about ten percent will develop a severe form of PTSD can go onto ulceration so that the probability of

one of us getting a DVT and that going onto ulceration is somewhere up to five percent so huge number when you think about the the prevalence of this disease and this has a as big societal costs so

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