Transcription
I will start with a simple case. This is a simple RCA angiogram. I want you to be able to identify those two branches proximally. This is an LEO view. The two branches approximately. And what is this branch going distally? You see this distal here long branch. What is that? And this is another view in a A P cranial. Again, the two proximal branches that you see here and that long slender branch distally. What are those? And this is the illustration of them. Those two and this long continuation and I will answer that.
So one is the cornis artery, which is the first RCA branch. It's very proximal. You can see it here filling off and on. It's very close to the oium of the RCA. The second RCA branch is the sinus node artery or sinoatrial branch. And in order to delineate it best, it's good to do an ao view. Ao view will show you that it's going toward the atria, not toward the ventricles. This is an AP cranial and you can already tell that sinoateral branch is navigating all the way up to the anterior part of the SVC where the sinus node lies.
Now distally, what is this branch going all the way up? This is actually the distal AV continuation of the RCA. So this is the AV groove. RCA going all the way up to the left AV groove. You can imagine this patient has a short left circumflex in the AV groove. So this is the answer to the three branches: cornis, sinoatrial branch, and AV continuation in the left AV groove in a patient with a short left circumflex.
Now I want to ask, where is the AV nodal arterial branch? Where does it lie usually and where is it in this particular case? This is the AV nodal branch. It usually arises in the distal RCA around the PDA, close to the crux, which is the intersection of the AV groove and the inferior septum, whether before it or after it. And this is the AV nodal branch. This one here, this is the AV nodal branch. And this is a distal AV RCA continuation. And this is the RCA running through the right AV groove and the left circumflex through the left AV groove. The longer the RCA is in that AV groove, the shorter the left circumflex is even in the left AV groove. The more the RCA gives PLB, the less the circumflex wraps down to the posterior left AV groove. And this is the left circumflex in this patient. You see it doesn't have much in the AV groove. It stops quickly. It gives one OM. It doesn't give much anymore beyond that point.
This is an illustration of where the AVAL branch arises. This is the PDA here. And the aoloral branch arises around the PDA, whether before it or after it. It can arise from the left circumflex distally only when the circumflex is dominant. When the circumflex goes all the way down, reaches the crux and gives a PDA. This is the case where the aviona branch could arise from the circle flex; otherwise, it arises from this area of the RCA around the right PDA. Rarely, it comes from the PDA itself, as you can see here. So the AV nodal artery, it comes from the RCA 90% of the time in the distal AV groove around the PDA. 10% of the time, it comes from the left circumflex distal AV groove, whichever is dominant. SA nodal artery, on the other hand, it can come from either the RC or or the circ, and it doesn't depend on the dominance because it comes approximately from those arteries. So it can come from the proximal right, as I showed here. It can come from the proximal left circumflex. 60% from the RCA, 40% from the circumflex, and usually it's the second branch of the RCA. It's important to know that the second branch after the corners. It's also important to know that the corners it frequently arises with a separate oium from the RCA. About a third of the time, it's a separate oium than the RCA.
And what does the cornis feed? What part of the heart does the cornis feed? Very important to know. It feeds the right ventricular outflow tract. This area of the heart. Both the left circumflex and the RCA give atrial branches on the other side of the AV groove. Well seen in a view. So this is the heart. This is an ao view, which looks straight in the AV groove, and it allows you to see branches that go to the ventricle, the marginal branches on one side, and branches that go to the atria on the other side, whether for the right AV groove RCA or when you're looking at the circumflex. So ao view for the RCA and for the circumflex will allow you to decide whether a branch is a ventricular branch, marginal branch, or whether it is an atrial branch. So the RCA in an ARO view will look like this. You'll see the acute marginal RV branches going this way, as well as the corners, and you'll see the atrial branches going on that other side of the AV groove. That includes the sinoatrial branch, which is usually the first atrial branch and which tends to go all the way up to the SVC.
Now remember Konis has a separate origin from the RCA in a third of the patients. This is another patient here. And you can see again, this is the cornis artery coming to the RV. And this is the sinoatrial branch going up. And this is the AV nodal branch here, coming just after the PDA. And the best way again is to do a view to separate those. And this is an AP cranial, not quite the audio, but it does show you. This is the cornis branch going to the right ventricle outflow tract. This is the syinoatrial branch. And look, this is the AV groove. Atrial branches are on this side. RV marginal branches are on that side. This is a circumflex. This is an ario codle. Again, aro any codal or not will split a groove on in the middle. Then you have the marginal to the ventricle, opt marginal on one side, and atrial branches on the other side. So this is the AV groove, and you can see an atrial branch. Very likely, if you pan toward this, this is likely a sinoatrial branch coming from the left circumflex.
I now I want to show another case. I want you to look at this RCA and tell me what is the true RCA. Point exactly to which one is the true RCA. You see two big branches here. So which one is it? That one, this arrow, or that arrow, which one is the true RCA? If you're not certain which one is the true RCA, the better view to delineate would be ARO. However, you should be able to tell on this view already. The RCA on an LEO view, it's an LEO with a little cranial. The RCA is the one that has two bands. It bends here. Then it bends again at what we call the crux of the heart, which is where the AV groove meets the inferior septum, which is this point. So I think looking at this view, this is a two RCA. It has one bend here and one bend there. And this is a probably the true PDA, which would make this branch an acute marginal branch. It is smooth and straight with no sharp bend distally. That's how an acute marginal looks like. Straight, no sharp band distally. This is an illustration from another patient. See this artery, smooth and straight with no sharp bend distally. Whenever you see this, this is an acute marginal. It's unlikely to be a true RCA.
Here is another view. The aio view is the one that helps you confirm, and you can see the artery that goes toward the margin of the heart is the acute marginal. The other one that is looping and giving two band, you see this is one band and this is another band over here. This is the crux of the heart, and this is the true PDA. This is actually an acute marginal. It's important to know the anatomy. Why? Because this branch has a tight lesion. So one should know, should I fix it or not? If this is a predominantly an acute marginal, we generally avoid fixing acute marginals. This is a special acute marginal. It's an acute marginal that feeds the RV. Then it wraps below the right ventricle on the inferior surface on the right of the right ventricle and reaches the PDA territory. It reaches the inferior septum. Here's an image. So this is the RCA. This is a standard acute marginal running on the border of the RV. This is a standard acute margin. It courses on the border of the RV. This is the special acute marginal that eventually takes a turn and reaches the inferior septum and supplies some of the PDA territory. And by the way, this artery, you know, in about 25% of patient with RCA dominance, there are significant anatomic variations in the origin of the PDA, and there is this variation here where you have partial supply of the distal PDA territory by a low-lying, that's what we call it, low-lying acute marginal branch that wraps around the inferior RV and reaches the inferior septum. So this is really an acute marginal. It's important to know in decision making because here's the question: Do we fix acute marginal and when do we fix them? So we do not usually uh do PCI of RV marginal stenosis or non-dominant RCA stenosis that only gives RV marginals because the RV rarely gets eskeemic. RV is thin, is able to increase its trans transoronary O2 extraction, which is at baseline 50%, unlike the LV, which is very high at baseline 75% with very little room to increase it. Uh, and the RV also easily recruits collaterals because of its low coronary microvascular resistance. So when RV gets eskeemic, it's usually because it's thick or dilated, in which cases it's more important to treat the RV hemodynamics than to treat RV marginal disease, like in pulmonary hypertension or big dilated failing right ventricle. So only rarely PCI of acute marginal may be considered, acute MI with RV shock from acute total occlusion of major acute marginal or non-dominant right colon, and those are the only cases we fix non-dominant right or acute marginal. Uh, another situation is something like what I just showed, but even what I just showed, it should be exceptional. It's an inferior RV marginal that supplies part of the PDA territory. So, it's supplying part of the left ventricle, not just the right ventricle. It's supplying part of the left ventricle. So, it can cause left ventricular eskeia, but it often doesn't. So you really need to prove he has very typical exertional severe angula and you have to have objective evidence hemodynamically IFR or FFR.
Question from the audience: Bottom line, when would you fix this acute marginal in this patient? If he's having RV shock, so he's having STEMI, STEMI typically with RV shock. In his in this case, he might have even a little inferior STEMI. So yes, STEMI or short of a STEMI, I would only fix it if you have this what I showed, severe typical exertional anga that is otherwise unexplained by any other disease and prove it is significant by AFR or FFR. All right, along those line, this is another case. This is a 59-year-old female. She had inferior STEMI at an outside hospital with recurrent VIB and RV shock. She got her RCA stented at the outside hospital. As you can see here, this is the stent. This is an acute fresh stent. But that strombosed during their procedure. She was transferred to another hospital where they reopened it, and they placed an impella RP. And this is what they got. The second operators. I want you to tell me here why did that scent thrombose just by looking at this image. This is their final image, by the way, or distal runoff. Excellent answer. Be specific. What is this artery? So they open, they put a stent here, and this is the runoff. What is this runoff that you're seeing where the wire is? Again, know those basic rules. This is an LEO view. The true RCA, if there's a dominant right, should have two band. One band here and one band at the crux. Look again. One band and another band at the crux. Okay, two bands, or here you can see you bend here at the margin of the heart and you bend again at the crux of the heart, intersection of AV groove and inferior septum. So when you see an RCA that looks smooth like this, beware. You're going into an acute marginal. It could be that this is a non-dominant right and that's all you get, or it could be you're missing the true right. So when you see something smooth like this, this is an acute marginal, whether that's all that RCA gives or you're missing something. So they open the RCA into one acute marginal. Seek is there a true RCA behind it? And actually, the late filling shows you this was probably missed, but you see late filling here. This is where the true RCA lies. Look again at this point. You see that? So the reason that sent thrombos is poor runoff. They open that RCA into one acute marginal. They did not open it into the much larger, probably distal territory. One of the big reasons tense thrombos, besides under expansion and dissections, is poor runoff. And here it's also poor recognition of anatomy. They open into one acute marginal, they miss the true runoff. And here you can do ARO view to confirm that what you see on an LAO view as a smooth straight structure with no bend is actually an acute marginal. On an ARO view, you'll see that acute marginal running on the margin of the right heart, whereas a true RCA will have bends distally.
Along those lines, this is a 71-year-old man. He had full metal jacket of his LED placed at an outside hospital two days before presenting to us. This stand, this full metal jacket, was unfortunately placed for stable CAD. Look at it. The full metal jacket ends here from proximal LED all the way distally. Now, just two days later, he presents to us with it's very similar to the prior case. Answer: no runoff. Okay, look at the here. We open that strombosis. The stent finishes here. Look how much runoff you have. So that distal stent is getting flow to a tiny territory. So that distal stent is receiving very little flow. So poor runoff is the cause of stance thrombosis in this patient. You can do IVIS, look for underexpansion and edge dissection, but it's very evident. That's one reason I avoid full metal jackets. You put stances that are way longer than the length of half of the vessel, you're predisposing the patient for thrombosis because the distal portion of that stent is having little runoff, is having little flow. It will thrombose, and the stent thrombosis will track backward. Eventually, the whole stented area will thrombose. Please don't stand vessels proximal to tip. It will thrombose. This is a poor man who had just a stable anga. He ended up with a massive anterior MI.
Now I want to move on to describe collateral formation types and grades. Collaterals form from branches in proximity in the neighborhood. So you need to understand collateral forming, and that will be important for you if one day you do CTO. So when you have LED or RCO occlusion, the septile branches come to the rescue. You get septal to septile collaterals. If you have, let's say, you have an RCOlusion, so you get LED subtile to RCA septile coming to the rescue. You can have distal circumflex to distal RCAV continuation collateral, again in the neighborhood, in proximity, you get those collateral forming, or you can get distal OM to right posterolateral branch collateral, or a very common one, distal apical led to PDA collateral, epicardial collateral this way. So remember this epicardial collateral led to PDA, or septile collateral LED to PDA, or epicardial collateral SER to distal right in the AV groove, or OM to posterolateral branch across the margin of the heart. Remember those four: one, two, three, four. Then you have the cougal. Then you have a bunch of other bridging collateral within the same coronary artery. For interventional fellows, this comes on board every other year. Kougal artery, you the classic scenario is that you have an occluded mid RCA, and you get an atrial branch, and this is an atrial view. This is atrial on this side of the AV groove, the posterior side of the AV groove. This is an atrial branch, and the atrial branch connects to the AV nodal branch. So atrial to AV nodal branch communication, right to right atrial to a nodal branch communication, and it navigates through the atrial septum all the way to the AV node at the bottom of the atrial septum. So atrial branch to AV nodal communication, it can come from the left circumflex, and actually, the first description by Dr. Google was atrial branch from the circumflex connecting to the a nodal branch of the RCA. Okay. So it's atrial to a nodal communication for an occluded mid RCA.
This is a case we have a coronary angiogram in a patient shows an oluded proximal LED, yet we don't see collaterals from the left coronary system, left circumflex, and we don't see collaterals from the RCA, yet the anterior apical wall is normal on echo, and we don't have a Q waves. So how come that LED must be having some collaterals? Where are the collaterals coming from? And is there any name for this situation? So we don't see collaterals anywhere from the right or circumflex, but there must be somewhere the collateral is coming from the cornis of the RCA. This is what we call the view sense ring or the viewense collateral. Keep in mind the cornis feeds the RVOT, which is in the neighborhood of the L, and collaterals always form in proximity. So when the LED is oluded, the cornis can come to the rescue. So we'll have a collateral from the cornis to the mid LED, and that's what we call the view sense ring. That's it here. Now, the cornis has a separate oium in a third of the cases. So what happened when you engaged the RCA in that patient? You did not see the cornis. The cornis had a separate oium. So you missed the fact that you had a collateral to the le. So in that case, you need to be aware of it. I don't see any collateral to the led. There must be a chronal collateral. I must see the corner. So what you do in this case? You do non-selective RCA in geography so that you can fill the cornis and see the view sense collateral, or disengage the RCA and try to engage selectively the cornice by aiming your catheter more anteriorly and making it point more upward, which is the opposite of what we try to do normally. We fall in the corners accidentally and we want to get out of it because we damp. So we try to disengage then engage by pulling more on the catheter to make it point down and by clocking more to make it go posteriorly. But when you want to go on the corners, you do the opposite. So you can try to make the catheter more point more anterior and more up to engage the corners and see that view sense collateral. This is from a case I did. This is a Vusense collateral for an oluded RCA. It can go both ways. It can go from a cornis to an oluded le, or it can go from le to an oluded proximal RCA. And this is a case I had where the patient had an oluded proximal RCA and he had a viewense collateral from the LED to the RCA.
And regarding collateral timing formation and classification, those are two landmark papers. This is the paper by Schwarz, and it basically shows that within 24 hours of an infar, half the patient have some collaterals, typically grade one or two. Beyond 24 hours to a few days, almost all patients have some collaterals. And beyond 2 weeks, this is when you start getting the collaterals grade three. Within one to few days, most of your collaterals are a grade one or two. And this is what you call raindrop. Grade three collateral is when the distal vessel is well opacified and well filled and delineated, as opposed to grade one collateral, which are like faint filling of branches of the vessel, and grade two, where there is faint filling of the distal vessel, but you don't see it clearly well delineated. And this is the CC classification of collateral. CC1, where you see continuous thread-like connection, and CC2, and there is continuous branch-like connection, more than a thread, and it's about half a millimeter or more in size. And the CC2 collaterals typically take over two weeks to form, even over 12 weeks to form those more advanced collaterals. So that gives you an idea about the classification and the timeline of collaterals.
I want to show another case. This case was shared by my prior great fellow Wasawat. So this is a 43-year-old man with no past medical history. He presents with chest pressure that has been going on at rest off and on for the last few days. This is his EKG. What's the diagnosis on that EKG? Could this be pericarditis? This is not pericarditis. This is a STEMI. So we see SC elevation in the interolateral lead, predominantly in V2 through V5. When you see that, go through the differential: STEMI, pericarditis, early reporization, or secondary to LVH or left bundle. The latter is not there. There is no LVH or left bundle. Could it be pericarditis? I don't think so. So this is, in my opinion, definitely an antilateral stemi. One hint is whenever you see that ST complex equal or bigger than the whole QRS, that's always very concerning to me. Okay, that's an early sign of a STEMI. So here, look at the SCT in those two leads. It's almost bigger than the QRS. That's very concerning. Another thing is when you have pericarditis or early reporization, you tend to have a big QRS, particularly in early parization, you do have a big QRS in those cases. Another thing when you have pericarditis, you have basically diffuse subepicardial injury, and therefore the ST elevation axis is parallel to the heart axis, which is this. So you tend to get most pronounced SC elevation in leads parallel to this, which is lead 2 and V5 V6, and you get SC depression in AVR and V1. Look at this patient. He has ST elevation in V1. When you have ST elevation in V1, it's very much against pericarditis. Also, when you're ST elevation, it's not predominant in lead 2 and V5 V6, again pericarditis. It's predominant in V2 to V4. So this is for all the reasons I explained, this is interrateral STEMI. They recognized it, and they took him to the Kath lab, and this is what the angiogram shows. And this is another view. So what's the diagnosis here? What's the finding? Is there a problem in that LED? So, you can see that this is the LED here. The other one is a diagonal running on the border of the card silhouette. But you can see the LED, and it's looping. It has a turn here and it goes there, and it oludes somewhat here, very distally. So there is a very dist occlusion. After it gives those distal septiles here, it occludes, which is not surprising. The STEMI EKG that mimics pericarditis is usually an apical STEMI. It's a STEMI that looks into all leads. When you have STEMI of this area, it will involve that part of the heart, that part of the heart. So all leads will have ST elevation. So it will mimic pericarditis. So the STEMI that mimics pericarditis is usually an apical STEMI, distal led STEMI. So it fits. It's a distal LED occlusion. Why did he occlude that LED? And you should think SCAD. And here are the reason you should think of SCAD. He's a man that doesn't that's not characteristic of scad. But he has all the other inographic features. He's relatively healthy. He has no calcium, no heavy atheroma in his vessels. No calcium. His vessels are very torturous. Look at that. Very torturous. And we know that heavy tortuosity is associated with scat. I mean, look at the LED and diagonal here. They overlap almost because they are so torturous. And in this view, it's hard to sort out the branches because you have so much overlap, and the disease is very long and smooth. In this case, it's so long. It starts here. It starts here where it's subtotally oluded. Then it occludes fully. It's a very long disease. Long and smooth distal disease. That's also scat feature. Remember those are the feature. Long smooth lesions more than 30 mm. Heavily torturous yet smooth nonatheromatus vessels. Non-calcified, a lot of overlap. Those are the four angographic features. And what type of scad this would be? There is a type one and type two. Type one is you see an a flap and a stain. Kind of what I showed here. This is atrogenic dissection, but that's kind of what type one scat could look like. You don't always see a stain in type one. You see either a double lumen and or a stain, but it would be something like this, except it would be longer if it is type one scad. Type two is where you see that diffuse long narrowing that is usually distal. And this is what this patient have. And when it's distal and extends all the way to the tip of the dissected artery, we call it type 2B. So this is type 2B scad. At least that's the inographic impression. He's a man. So data suggests registries suggests that about 10% of scad patients are men. So it can happen in man. Don't rule it out just because he's a man. He's a middle-aged man, which fits. And here is a registry, you know, describing the features of man with scad. It's fairly similar to the woman with scad. It tends to be more physical stress than emotional stress in men. Tend to be a little bit younger.
So what should you do for this patient here? If you think scad, what should be done? Should we wire it or leave it alone? The scad that is not olusive, not 100% olusive, where you have some distal flow ti 2 or three with no ongoing stemi on the EKG is left alone. However, scad with ongoing stemi and impaired distal flow ti one or zero, we should wire it and try to recanalyze it because you want to abort that effort, you want to revive that apex. And this is what was done here. So if you have total occlusion, in a way, it's even a little less important to make an initial diagnosis as you need to wire it anyway. So you need to wire it when it's total occlusion to abort the infire it and you try to do low pressure balloon inflation. That's the key idea. Don't stent it. Beside the fact that, as I explained earlier, you shouldn't stent tip of vessels anyway. They will thrombose, but wire it and balloon it. Even if it was proximal in scad, if it is totally occluded, try to be as limited as possible. If it's totally occluded, wire it and low pressure undersized balloon. Just reestablish flow aboard the infire need to stand if you can reestablish flow. So try to be minimalist, but you have to reestablish flow. And that's what they did here. They wire it and did a low pressure small size balloon inflation. And they did something else because he's a man and there is a question mark about SCAD. They did IVIS, and I want to show you. He wasawa shared with me. Those are excellent IVIS pictures. So you see this is your IIS catheter here. They are in the true lumen, and you see that here, dark banana shape. Dark banana shape. That is how scad looks like. That's how a subtimal plane looks like. Dark crescent shape or banana shape. This is from the lit literature. This is what OCT look how the scad looks like. So semi lunar or circumferential shape or banana shape. Well demarcated as in here, somewhat homogeneous, but it's usually darker DP. And by the way, when you're doing CTO and doing subintimal crossing, you you need to be familiar with that image, distinguish the true lumen from the subintima. So if you're doing CTO and you're going behind in the in the false lumen, your IVIS catheter will be here in that banana shape, and you will see usually that intima. It will look white because typically it's an occlusion. So you'll see your catheter here and you'll see a thick white plaque or band that you're pushing to the side. That's how being in the subintima will look like. You will be on this side with a collapsed white atheroma. These are images of CTO subintimal crossing. So here the wire went subintimally, and the IVIS is over that wire. So the IVIS is in the false lumen L, and the true lumen is that white compressed inima atheroma. This is another case here. Again, false lumen is that dark black one. It could be like in here, crescent shaped, or it could be here, round or more circumferentially shaped, and it's compressing the true lumen, the white inima atom. That's how you know you're in the false lumin. That black one is a false lumen. The compressed atoma is the true lumen. This is another illustration. You're in the false lumen with your ivis and wire. And this is the compressed white true lumen. Those are other examples from the lit literature of scad. This is the scad again, that crescent banana shape, somewhat dark area.
Question from the audience: How do you make a scad diagnosis when it is a total occlusion, and do you need to do ivvis? Here I have the hint. So if it is a total occlusion, and 30% plus of scad have total occlusion, and some call it scad type four, you think of scad like we thought here, based on the upstream segments, you know, the upstream segment in this patient were had no calcium, they were heavily torturous, a lot of vessel overlap, the occlusion looked long, so you had all those features. Then in total occlusion, you have to wire anyway. Anyway, you have to try to wire anyway. And when you wire, you may have further feature of scad. You may start to see a double lumen. You may see a wall stain. You don't need to do IVIS to prove scad. Guidelines try to tell you to avoid IVIS OCT if possible when you suspect scab because IVIS and OCT and extra manipulations can extend the dissection, and there is an 8% risk of extending the dissection by doing just IVIS or OCT. And in registries of SCAD, most patients do not receive confirmation by IVIS or OCT, less than 10% do.
Question from the audience: When it is a total occlusion, does it really matter to make a scad diagnosis since we have to wire it anyway? Yes, it's very important to make a scad diagnosis because if it is a scad, you can just wire it and balloon it, reestablish flow. You do not need to stent it. Also, scad has a very different long-term prognosis. With a scad, it will heal, and you may want to document healing with CT imaging at 6 weeks. Also, the treatment is different from atheroma. With atheroma, you need a statin and aggressive risk factor modification, and there is a higher risk of future MI events. Whereas SCAD, statin has no clear value, and dual antiplated therapy has no clear value. Probably just aspirin is administered.
I will move on to the next case. This is shared with me by my friend Neestor Bcaru. So this is a 35-year-old female, no prior cardiac history. She's a smoker. She presents with chest pain and non STEMI troponin elevation. And this is her inog. This is a shallow ario cranial. What's the diagnosis? So when you see this angagram, this is the LED here running to the apex, and you see a diagonal. So the LED has a long diffused smooth stenosis that's extending almost all the way distally. So when you see this, the top diagnosis is coronary epicardial vasospasm. So the first step is to give intracoronary nitroglycerin at least 200 200 to 400 microgram and consider even giving verapamil if it persists with nitroglycerin. So let's say we gave here in this case nitroglycerin, we gave even verapamil, and the same inographic appearance persisted. What's the diagnosis? Then the second diagnosis you need to consider in this middle-age women is scad spontaneous coronary artery dissection, specifically scad type two, okay, which gives you this inographic appearance exactly, which is intramural hematoma. It's a bleeding in the media that causes compression of the lumen, and it tends to have the appearance of that long smooth lesion over 30 mm, refractory to nitroglycerin, usually heavily torturous, although not in this particular case, and with no obvious calcium, middle-aged woman. So those patients tend to have a lot of vessel overlap and a lot of tuosity. This patient did not have that, but it had that long smooth appearance, refractory to nitroglycerin, without significant calcium. So you should think scad in this patient. Another possibility is long diffused atherosclerosis plus or minus plaque rupture. But this is the least likely diagnosis here. This is most likely scat type two. It's type 2 A because it doesn't extend all the way to the tip of the vessel. When the dissection extends all the way to the tip of the vessel, we call it type 2 B. This is probably scat type 2 A. And scat tends to involve distal vessels in 92% of the cases. It involves more proximal vessels in 8% of the cases. So this is most likely scar, and you really need to recognize it because this patient has uh tim 2 to three flow, and she's not having an ongoing ST elevation infar. Therefore, you should not touch it. You should not try to do PCI because there is PCI a risk of failure and complication of over 50% in those patients, and that's what my friend did here. So he did not intervene in this patient. One thing to do in those cases to prove scad beside the simple angographic appearance is to try to do peripheral inography like iortto iliac angography and see if you have FMD fibrouscular dysplasia, which is present in up to 70% of those patient that can indirectly corroborate your diagnosis, and do also CT carroted cerebral and abdominal iliac femoral CT to look for FMD fibrocular dysplasia, and that's what my friend did, and indeed this patient had carroted fibrouscular dysplasia, which in retrospect further corroborate the diagnosis. You can also do CTA six weeks later and prove that the patient has no longer significant obstruction of the LD. Even if you cannot tell for sure it's a scad, you can tell whether there is obstruction or not at 6 weeks. And in most scad over 80% up to 97%, they will recover spontaneously.