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Introduction & Objectives | STEMI wake up!
Introduction & Objectives | STEMI wake up!
2016acuteAVIRcardiologistsembolicinterventionocclusivesbv
STEMI Management | STEMI wake up!
STEMI Management | STEMI wake up!
2016acuteAVIRbenchmarkscoronaryembolismfasterinflammationinterventionallyticsminutesoccurssbvsymptomthrombolyticsthrombustypically
Fibrinolysis for STEMI patients | STEMI wake up!
Fibrinolysis for STEMI patients | STEMI wake up!
2016anaphylaxisAVIRcardiologistcathconsideredcontraindicationsdoctorfibrinolytichypertensiveiliacinterventionalocclusionpatientradiologistrisksbvtherapy
Evolution of PCI for STEMI | STEMI wake up!
Evolution of PCI for STEMI | STEMI wake up!
2016AVIRbasicallybiliarycoronarysbvstentstentsthrombectomythrombustools
Coronary Anatomy | STEMI wake up!
Coronary Anatomy | STEMI wake up!
2016anteriorarteryAVIRcagecircumflexcoronarydescendinglateralleftmarginalposteriorsbvsurgeonstravelsventricleventricular
ECG Interpretation | STEMI wake up!
ECG Interpretation | STEMI wake up!
2016anteriorAVIRgreenlateralleadsposteriorsbvseptum
CP proceeding Vfib arrest | Balloon, Stent | 74 | Male | STEMI wake up!
CP proceeding Vfib arrest | Balloon, Stent | 74 | Male | STEMI wake up!
2016anteriorAVIRballooncircumflexinterventionnormalocclusivesbvsegmentseptumstentvisceral
Syncope, Neck/arm pain, Diaphoresis&Nausea | Balloon,Nitrates, Stent | 78 | Female | STEMI wake up!
Syncope, Neck/arm pain, Diaphoresis&Nausea | Balloon,Nitrates, Stent | 78 | Female | STEMI wake up!
2016anteriorAVIRballooninghurtsoccludedocclusiveproximalsbvstentingsympatheticsyncopethromboticvessel
Intermitent CP for 12 hours, LED Vein| Bypass, Lesions,Balloon | 78  | STEMI wake up!
Intermitent CP for 12 hours, LED Vein| Bypass, Lesions,Balloon | 78 | STEMI wake up!
2016arteryautopsyAVIRcircumflexlateralmicronocclusionspatientprettysbvtypically
STEMI Complications & Management | STEMI wake up!
STEMI Complications & Management | STEMI wake up!
2016accessacutearteryAVIRballoonboluscardiologistcathclosurecommoncomplicationscontrastcoronarycreatininedissectionsdoctorsintravascularoccurquantitativeradialretroperitonealrisksbvstandardizestentvolumewire
Transcript

Good morning. Thank you Mike. It's a pleasure to speak you all. I realize you don't get a chance to see cardiologists here very often. Great. How many of you here have done intervention with a cardiologist in acute MI? Raise your hand.

Ok so not that many. So I tried to tailor my lecture to kind of cover some of the issues that those who do do it might see and might learn and for those you who do not to interest you to come to the dark side. Which is the cardiology world. I will say

that our patients tend to really love us and so it's it's a nice thing. I'm gonna run kind of quickly because I know I'm separating you from your break. This is essentially the common thread in almost every intervention that we do in

the vascular system. And its an occlusive thrombus. It may be a embolic it may be indigenous to a lesion within the arterial system. But fundamentally this is what we're dealing with. So the I took out the slide about

disclosures to minimize the size of your handout which appears to be very large. I'm a handout kind of guy because I usually take notes. Quickly we're gonna I'm gonna try and go over the need for urgency in the acute MI. I i think it very much

correlates with the acute stroke. I'm going to review some of the options for treatment. For those of you who are not familiar I'm going to go over some of the patterns that get us to an acute MI. Some of the anatomy and then of course the

intervention. I will go over common procedural complications if we have time. But this is fundamentally what we deal

with. This is a coronary artery developing plaque. This is all that bacon and eggs that you've been eating.

And this is probably the age of 30. Acute inflammation tends to occur at the site typically on border zones as in right there. And ultimately either due to shear stress inflammation we have plaque rupture. So arterial embolism occurs

with this same phenomenon. In the coronary circulation it typically occurs at branch points but not always. That acute thrombus results in an acute MI acute pain and loss of muscle. So ultimately the faster a patient arrives the faster we

can save the muscle. And these are this is a large kind of complicated slide to basically tell you that we have actually extended our reach out to the community to emergency medical services to get those patients to us quickly.

The faster we get them into the door the faster we get them into the cath lab and the faster we can open them up. There is a difference between those places that are PCI and non-PCI capable. Since we're in the interventional room we're

going to talk about interventions today. So as you know time is heart muscle & of course brain tissue and the stroke setting. And it all occurs early on. It turns out the role here is actually mostly EMS. Because once we get here into

the hospital into the emergency room its pretty much a fixed time. And that time is decreased from anywhere from 45 to 60 minutes at the early start of the game to less than 30 minutes at Riverside. Its about 22 minutes on average. Great. And so

this is a simply saying that the time from symptom onset to the time that you can inflate a balloon to improve coronary blood flow is directly related to mortality. And so the longer you move along these endpoints the worse the survival

is. Now these numbers may not seem very big. That is that you go from an average at Riverside of about 60 minutes. In some places it could be essentially a transfer into five percent. But oftentimes remember this is symptom onset. So this is when

they're at home and then they come in. So these are really very short numbers. Right these that I mean there's a time for them to call EMS and paramedics show up and then they load them on the gurney they get him to the

hospital there's transport time there's traffic. All this is included here. Right now 120 minutes is actually one of our benchmarks from first medical contact to opening a balloon. But notice how the curve starts really increasing up if

there's a delay in the patient activating EMS. This is one of our community goals. And I realize this is somewhat upstream to where you all are at but if you have to think about that heartburn that your uncle or your father

or your brother or you have when you come and you know after Thanksgiving Dinner and you're wondering whether it's an acute MI and you wait three hours. Well guess what happens you're way out here. And then you move the needle on.

Ok so the bottom line with this slide is PCI is better than lytics and that kind of goes without saying that in this day and mean age lytics in the cardiac world is infinitesimally small. We're looking at probably one out of every three hundred

patients are actually getting thrombolytics which is good. So step one

is that we are really looking at time of onset. We look at the risk of an infarct. Whether it's a large or small infarct. The risk to the patient. The risk of

fibrolytics and then the risk of the time it would take to get to the cath lab because we have to utilize you all. We need to get a team in there a doctor is nothing without you and I will tell you that's probably true for almost every

aspect of care that we do. So i'm just going to jump past this because I got more fun stuff to talk about. Ok so fibrinolytic therapy however is not out of the game. It's still an important piece and the

only reason I wanted to cover this is there are certain things that we do... somebody has known anaphylaxis associated with radio contrast... that's probably a contraindication. They should be considered for fibrinolytic therapy

because we do not get a chance to pretreat. And I think that this is one of those things that frankly usually the cath lab picks up. It is you all that pick it up. It's not the ED doctor and it's not the doctor it's not

the it's not the physician or cardiologist or the interventional radiologist they're not usually asking the patient. It is you all. If the patient or family or unwilling to consent consented momentum to get to the cath

lab is so great sometimes we don't get a chance to even ask the patient. Again tends to be that cath lab tech or that cath lab nurse that is actually asking the patient. Religious or personal preferences. Biases

for bleeding. Sean will be talking a bit about those people who are willing to take the risk of bleeding. Transfer times if somebody takes a long time to get to the lab it does matter. So fibrinolytic therapy

needs to be considered if somebody has known access issues they should be considered fibrinolytic therapy. So you know that the ED says oh this patient needs to go to the cath lab the cardiologist hasn't shown up and you

know they have no pulses in their feet. And they have a dialysis access site on the right and failed graph on the left. Well guess what that patient ain't going. Right they go nowhere. So I mean it takes too long to fix the chronic total occlusion just

through the iliac artery. They're not going to get any benefit from coronary PCI. Absolute or relative contraindications actually kind of have gone by the wayside. Hypertensive patients we used to have all these indications and

contraindications to PCI basically they've all kind of gone away.

grey hair it doesn't show I cut my hair short enough so you can't see it actually that's the reason....

Um but back in the day when I started this there was no stents. I remember putting in a biliary stent into the coronary artery. That was really exciting because it didn't really work. But by and large back in the balloon only age...

which is basically where I grew up... we didn't have all the tools that we have now. We are pretty it makes it pretty easy. I mean coronary...the coronary intervention is I believe easier than it

is the IR world because we deal with one set of arteries. And the number of variations is somewhat less. The number of tools that somewhat smaller. The difference is the price we pay for making a mistake is really big. So stents

drug-eluting stents thrombectomy thrombus extraction catheters. This is basically the only material that we need. So I'm going to go over the corner anatomy for those of you who are not familiar. But basically

the coronary arteries... I can't really well I'm a walker Mike I can't walk around I'm tied down I guess like walking out here. How did you walk Janine. Oh ok alright.

actually fairly simple. It's really really simple. So if you think of the heart extending outward you all. The right corner artery travels in the atrioventricular groove. The circumflex coronary travels in the left

atrioventricular groove. An artery comes off the front between the right and left ventricle - that's the left anterior descending. The posterior descending artery typically off the right three-quarters of the time comes off

the right coronary artery. And so what we have is a cage right. That's all it is. The diagonals come off the left-anterior descending artery. And if you actually think about what a surgeon would see when they crack the chest

they see a vertical artery that's the LAD and an artery that comes off at a diagonal. Okay so they're surgeons you know sorry for the surgeons in the back of the room but you know it's like that what else would you call it - diagonal. Ok so

the marginal branches are actually because they come around the rounded margins of the heart. The lateral wall comes off...The vessels that come off the circumflex usually supply the lateral wall and they are the obtuse

marginal branches. So they're marginal branches. There is a marginal branch on the right side. It's a right ventricular marginal branch. Or an acute marginal branch and the reason is the right ventricle is flat the left ventricle is

round. And so that's actually the simple anatomy. So you think of the cage the right coronary in the right AV groove. The left coronary artery in the left AV groove. The circumflex. Anterior descending posterior

descending artery marginal. That's it. Simple. Now the difference is however how do we correlate that with what happens when the patient shows up.

ask the question. Anybody here feel comfortable looking at a 12-lead EKG raise your hand. Good. For those of you who are not comfortable how many of you actually get a chance to

look at it before you actually get into the room. For those are going to STEMIs. And answer is probably not too many. You can predict what the doctors going to need by looking at that EKG. So that's the part of the reason I'm going to go over

this. Beyond the fact it's really cool because I'm a cardiologist. So this is a 12-lead EKG and I'm just going to go over these are the limb leads and these are the precordial leads. And fundamentally the leads tell us where

things need to go. So this is in your handout don't take any notes. Um just look. So the inferior wall... the red... supplies the back of the heart most of the posterior descending artery. And if you see changes in the EKG PQRST

wave the ST segment is where we hinge our therapy. So the lateral wall which is in blue... is actually not well seen out here... but it's on this margin right here. The anterior septum which is yellow here is in these leads v1 and v2 this is

the precordial leads. The anterior wall... so this is where usually the money is if you will cause of survival vessel... involves this green area here. Its the front of the heart the left anterior descending. So when they talk about the

"widow-maker" this is it. Lateral wall again is blue which is a little bit more of the lateral margin. Somewhere between green and red...I'm sorry green and yellow is going to be the other blue.

Ok so you're like I really don't understand that. Well let's take a look at some EKGs. So

this is actually...so every case I show I'm going to show you today was done in the last two months.

Actually I did my lecture 3 weeks ago so in the two months before. So this is all real. 70 year old gentleman who chest pain preceding a VF arrest he presents... Okay so everyone who works at Riverside

knows I usually ask people questions I won't do that to you today. I know that had that frightened look from Lauren just a second ago. And so because I usually actually I usually do do that. What we see here is in the anterior

leads. This is just to go over that. We see some unusual changes here. So the normal PQRS... which is there's nothing here normal...normal PQRST wave the ST segment is pulled up. ST segment pulled up. So those changes are kind of back of the

room I can see something's wrong there. And if you think about one thing you think about what we call tombstones right. And this is what this actually kinda looks like. Unusual tombstone but this is a tombstone nevertheless.

This is in the septum and the anterior leads so what vessel. Shout it out if you know. The LAD. So this is the patient and this is the coronary artery. This is a femoral approach. Dr. Vignen actually I think

did that really nicely. We do do the radial but not typically for STEMIs and I can talk about that later. But this is the left main. This is the circumflex traveling in the left AV groove. This is the obtuse marginal branches. This is the LAD and this is

the LAD that is missing. So very simply what happens is we pass a wire we pass a balloon we re-establish blood flow. It was particularly ugly that same point is right up in there. There's a lot of overlap in this vessel. And the

main reason why this view was chosen is because you can it lays out the normal or near normal or not so normal and the abnormal. That's the only reason the view's chosen and its not a great view. So we put in a stent. So the view actually

changes. This is actually... oh this is a because we were jailing a diagonal... this is actually what's called a kissing balloon. So I know we do this in the peripheral arterial world not so much in the visceral neuro world. A ballon

in the LAD a balloon in the diagonal. And the occlusive site was right here that looks pretty good. There's a stent there. The diagonal that's gotta overlap. So before and after. So that was easy. Because this is actually

the most common. This patient's survival without intervention went from over... I'm sorry mortality... without intervention at one year went from about 24% to about 8%. That's pretty good. So their mortality went from 24 to 8 in

one year with this intervention. So it's

a big intervention. Ok different EKG. 48 year old with new onset chest and jaw pain. Anybody see any abnormalities. Yes we got some ST segment elevation

1 and aVL a little bit in v2 and v3 maybe a little bit in v4. The difference here of course is you see it in a lot of leads. And that's that sometimes confusing but it's the greatest magnitude that matters. So

indeed it's the lateral leads that we're seeing those changes in mostly. A little bit in the anterior not so much in these lateral leads. So what vessel. Actually it is also the LAD but it includes a very large diagonal. So we see

the lesion here. Left main circumflex LAD this is a septal perforator. And we see a very tight stenosis. It is not occlusive. And so we take a long wire long balloon. And we make that look like that. And fortunately we've got some... this is a really

small vessel. It's a really funky little little vessel. Very typical of a diabetic. Seventy-eight year-old female presents with

syncope neck and arm pain diaphoresis and nausea. What's missing. Chest pain. So more common in a much more

common in women is an atypical presentation. So for those of you who've got moms and aunts and grandmothers who say that I don't feel good and my jaw hurts or my arm hurts and they start sweating. And remember diaphoresis...excessive sweating...

is a real marker the sympathetic system is being pushed. So when you see that patient on the table and they're just sweating like all get-out something's going wrong that patient.

And that's kind of one of the real good clinical clues that they're sympathetic system is being activated. So that's something that I do look at. They usually tells you something's wrong. Doesn't tell you what's wrong with them but it

tells you something's wrong. So in this particular instance we see some changes now the magnitude is where. Yeah its in the inferiorly leads. I heard somebody say that. We see big tombstone type EKG changes here here and here. These are

called reciprocal depressions right. They're the opposite direction. They're going down. Not so much in the anterior leads and we see reciprocal depressions in the lateral leads. So in this particular

instance we have what is and it will be termed an infralateral infarct. And we have occluded right coronary artery. So this is in the right AV groove. It's funny how the pictures all look the same regardless what vascular distribution it is right. Because

you know you see an occlusive or obstructive vessel and they all kinda look the same. Well that's that's the case here. A dialysis catheter in there unfortunately for this patient. So we get through there in this patient. We get a wire

down there and there's still no good flow. We do initial ballooning and unfortunately that vessel doesn't still look very good. Something is definitely going on all the way down in

here. So we give some nitrates. It turns out it has a thrombotic appearance. Whoops. Had a thrombotic appearance. We ended up stenting in the proximal segment up in here that looks great. The whole the rest of vessel does not. I actually think we're missing a

picture. This vessel does improve with nitrates. But I'm missing picture.

Alright so this is an old slide actually this is the patient that was not part of the... no actually this patient was in the past couple of months... so a different type of

patient seventy-year-old with intermittent chest pain for 12 hours. So the intermittency of chest pain... remember we saw that initial kind of animation actually was not an animation... I'll tell you how they did that's pretty cool. So

what they did is they took an artery and they actually sectioned it all the way up. It's the same patient so one artery...on autopsy obviously...and they sectioned the artery all the way up and they went from a normal segment to an abnormal

segment. That's actually how they got that picture. Those were like fifty hundred micron segments. So kind of cool how they got that picture. Pretty bad cause it's autopsy but that's the way it is to get great pictures. In this particular

patient we see some changes perhaps one in aVL. Very subtle. Right so this considered a lateral infarct. What's probably what would draw your eye to any EKG like this is that the depressions are greater magnitude than the lateral wall

the lateral EKG changes. And actually that is a pretty pathognomonic of a circumflex lesion. So in this patient left main. The LAD is actually a grafted vessel. This patient had bypass and the lesion's in the circumflex. So this

job was in the left AV groove. So therefore the marginals are the ones of the on the side of the heart the rounded side of the heart the left ventricle. And the changes will be in the lateral wall and that's why just changes are

seen in 1 and aVL. So kind of pretty typical for what we do this patient had a balloon and the final that was pretty. I gotta say so for myself. So pre and then the post. Even a grafted patient oftentimes has ungrafted

distributions and that's typically where see it. Vein graft occlusions interestingly enough are really complicated because they get competing flow. But in a native artery typically the changes are abrupt and

obvious. Ok so we look at targets... how far am I timewise...7 minutes...okay good. So this is the...actually I love that commercial where they're sending out the mask...you know the glasses and the

two deer in the woods. You guys don't know what I'm talking about right. Ok I love that commercial I'm trying to get a slide of that actually... and they kept saying those guys are dumb and its the two deer wearing the mask ok...

Anyway I want to go over some STEMI

complications because these are some of the things that I do believe that you all help us with. And I will say that the one thing I love about the cath lab that it's really it is a team.

I mean I can't do what I do without you all and the honest truth is that if you move into the admin world when we talk about standardization of care right that reduction of variance. The only way we really do that is we do

that with the sonographers the technicians those in the cath lab those in the in the CAT scan. We standardize care actually through you all. It's actually because the doctors do what doctors do right. You know they

can't... three doctors in a room and we get four opinions because they keep changing their mind. And so the fact is that we standardize care specifically in this instance reducing complications actually with you telling us that something is

going on. So there are there are three things that I want to talk about. One was the high risk contrast induce nephropathy. So we know that nephropathy can be defined by a

number of different ways but the ACCNCR - the American College of Cardiology Cath Registry - defines it a 0.3 rise and the creatinine. Which is actually I'm gonna tell ya not very much. Most people believe that if it's a twenty-five

percent rise its significant. But the highest risk patients interestingly enough... acute coronary syndromes chronic kidney disease volume depleted low cardiac output diabetics heart failure older patients hypertensives - this is the STEMI

patient. This is the STEMI all the...all factors. So what do we normally do well. We we prevent it with hydration we prevent NSAIDS we wait 48 hours for another

contrast load right. Because this is the ED did a CT scan already careful catheter wire manipulation. And guess what happens in a STEMI all that's out the door. We have no chance to pre hydrate we don't get a chance to stop

their Motrin or their Feldene that they took beforehand. And we are rushing to get this stuff done. So things are going very quickly. So STEMI patients unfortunately have a greater than two-time risk for having contrast-induced nephropathy. So

there are a couple of ways which is IV bolus therapy up front. Again sodium bicarb is not. But this is actually what I've been talking to the cardiologists about. Is that if you measure the filling pressure of the heart and I realized

most of you are not in the coronary world. I'm trying to get you here... talk to me.... is that we can bolus it based upon a measurement of intravascular volume and it will reduce the risk of contrast-induced nephropathy. So and there

are some guidelines for that. Obviously you want to minimize the bolus if they're volume overload but notice how there's still a volume bolus. And the reason is the heart is stiff after an acute MI. Pre-procedure high dose statins which

is actually part of our protocol is what we do. There is a maximum contrast dose that I'm just going to quickly go over. And I'll just tell you basically it's... there's a couple ways of calculating it... but probably the easiest way is if you know their

GFR are you can calculate that. There are there are levels at which point you should not exceed. There are weight-based contrast loads but it's not as accurate as the GFR right. Because if somebody is big and has a creatinine of 1.5 or

2 you can give them more contrast but that creatinine of 2 usurps their weight. So isn't just weight based. It should be based upon a GFR. And I will tell you unfortunate you go from risk of 6% if you go two and a half times to greater than

35% if you give them the maximal contrast dose. And I'll tell you the 5mL per kg we do that commonly. And I'll say that's probably more of a problem in the peripheral vascular world news in the coronary world. Ok access site complications that was a

great segue Dr. Vignen. Thank you. Basically yeah we get these ugly things that look like that. But we don't get that with radial access site... radial access. I'm not going to cover this. you all know how to get great access.

Unfortunately this is still a pretty common problem right. They hit the SFA they go to the external iliac. Its a problem. Hematomas retroperitoneal bleeding pseudoaneurysm. The rate of these are

actually still pretty high regardless of what kind of closure device you use. Closure devices unfortunately do not affect the rate of access site complications. A retroperitoneal bleed is going to occur regardless of what

kind of closure device you use. So radial site... radial artery access I won't cover that because that was covered by the last lecture... that was a great segue by the way... There is a bias against using radial arteries in the acute MI setting. And

that mainly is because we are under the gun for time. So if there is a conflicting interest. I wish there was going to be change in that there probably will not be. Abrupt closure dissection. Usually it's at the

balloon or stent edge. And I will tell you that it's not as obvious as it appears sometimes to the cardiologist because they are looking... and actually this is probably true across the board... this is really targeted therapy. You look at

what was bad and you look at what you did and you don't look what happened upstream or downstream. So this is where you want your eyes can really help us. This doesn't project really well but i'm going to I'm just going to tell you. This isn't

is going to project well. Okay so this is the initial lesion. This is the final. Unfortunately there's a problem right. Right at the take off of the septal and the diagonal ... it looked normal before... it doesn't look normal now.

So the doctor I am looking right here I go awesome high-five let's get out of the room. And there's something wrong right there. It's very easy to miss. You know where

you're going to figure this out. 30 minutes later when the patient occludes the artery they come back. So it's also actually... oh yeah so see I missed even in my own slide.. and so downstream here this caliber of the artery

is smaller than it was here. So there's a problem. It's easy to miss. And again I think part of it is because you know doctors being paged. They've got two other things to do and you know they're hungry. Actually we're all hungry. They gotta pee.

And then the next thing you know you're ready to get out of the room but there's a problem. So there are a couple of things. If you see something I want to hear something doesn't look right. One of the

hardest things is that when you're doing this and you're under the gun we don't do a lot of the quantitative measurements that we do do. I know the IR world you guys do a lot of quantitative measurements. How many times have you

seen a cardiologist actually say go out and measure that. The answer is none. Because it takes too long. Marginal dissections are very common the problem is it tends to occur at the edges.

It's not where your eyes are going ok. I'm going to move ahead because I'm at 9:58 yeah I'm gonna go right past here. So I'm going to tell you that intravascular ultrasound is actually one of the answers to this. Again it takes time and

skill. The other thing is if you you see something this is kind of what I want to hear is what do you think about that distal edge you know the flow is not as normal.

It doesn't look like it did before. That edge is hazy. Those are common findings that we tend to see after the fact. So we're reviewing this and it's some conference and almost always there is a clue. The question is can you get it ok. So

dissections and... I'm sorry... acute thrombus tends to occur with dissections. So you know you balloon an artery and it may look ok but unfortunately in this artery this is the first picture and then all of a sudden the artery disappears. So this is

the pre stent and then the artery is down. This abrput vessel closure usually in the stent is acute thombus. Inadequate anticoagulation or suboptimal expansion of the stent is the most common cause.

So when this happens unfortunately you don't want to ever want to lose wire right. Keep that wire down there. There's a tendency to kind of say things look really good and just start yanking everything out. And everyone starting to

feel that right because it looks good enough and so you start pulling out stuff. That's usually a problem. You have to reevaluate the degree of anticoagulation. And there's a variety of

different ways to do that. Its in your handout. Its 10 o'clock. Okay I know that was

kind of fast. It was intentional. It's a little bit of an overview but hopefully you get a little bit out of it and get you into the dark side.

Are there any questions.

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