 I put some efforts into it, and I hope you all enjoy it. So the causes of myocardial infarction are non-athroscratic disease. If you look at non-athroscratic disease, coronary artery anomalies are one of the more common anomalies that are seen in the general population, and they affect equally men and women. Then comes the arthritis, granulomatous arthritis, tachyassus, Kawasaki's. Tachyassus certainly occurs in women, and Kawasaki's can occur equally in men and women. It starts in childhood. Polyaryte is Nadoza, again, much more common in women. I'm going to address mostly the ones I've listed here in blue to make it easier for all of you to understand. I'm going to talk about fibromastoid dysplasia, which is a very important disease. 90% of it occurring in women. Then just a little bit on coronary embolism can occur both from prosthetic valve as well as cocaine use. Thrombocytemia is another thing which actually can occur in men and women, and I'm not addressing that. Then I'm going to talk about spontaneous coronary artery dissection as well. So what we do at CVPath Registry, we have a huge autopsy registry. We've divided our registry into coronary artery disease secondary to atherosclerosis. So under that comes rupture, erosion, calcified nodule, that is the thrombotic lesions. Then the severe coronary artery disease, which have greater than 75% narrowing, but no acute thrombus. Then there is sudden coronary death, which is non-Atherosclerotic disease, like SCAD, that is spontaneous coronary artery dissection, intramural coronary artery thrombosis from other causes, et cetera. Then we have cardiac death, which is non-CAD. That is, curves from cardiomyopathies, myocarditis, infective endocarditis, valvular disease, congenital heart disease, hypertensive, amyloidosis, you name it, and all those diseases. Then we have the non-cardiac death, that is, occurs from pulmonary embolism, aortic dissections from any other unnatural causes, which also come to us. Then of course there is a group, which is the unknown cause. There are cases which is not that small a percent, good 5%, that's why genetics is very important. They may be individuals whose heart may be normal in terms of morphology, but actually not channelopathies, for example. They may not present with anything else, but arrhythmias. So we put them under unknown causes so that we can look into them. So here's what we've got. We've got 1582 adult females in our CV path registry. And amongst these, non-cardiac death accounts for 35%, 25% of cardiac death, 20% of coronary artery disease death, that is atherosclerosis, and again there is stents and cabbage. Another group, which is 16%, which I'm not gonna present. And then there is the unknown cause, which is good 4% of the cases. So when you look at coronary artery disease death, further divided, we have 3.3% are ruptures, 3.4% occurring at erosion, and then 0.6% is calcified nodule, but by far the most common amongst them is severe coronary artery disease. These are all ages. This is not young, less than 50, or older than 50 like I divided yesterday. Then SCAD forms 1% of the population and about 0.1% from embolic phenomenon. So I will address portions of this. Here I've taken from Dr. Shepard, who's Mary Shepard from the UK, she's a forensic pathologist, and a cardiac pathologist. She has done, reported on patients who are dying from relatively non-arthroscardic coronary pathology. She says anomalous coronary artery origin accounts for 48%, acute dissection 16%, vascularitis 12%, coronary spasm, which I don't think we can make the diagnosis. However, she has a category of 12%. Idiopathic arterial calcification, infancy another 6%, which is more common in boys than in girls. Fibromuscular dysplasia, benign lipoma of the heart, and then that's the total 100%. Accounting for only 3% total cases that are non-arthroscarotid. In our hands, it's a more higher. So let's talk of coronary artery anomalies. I think all of you know the symptoms more than I do since you see these patients. Angina, sycopy, congestive heart failure, myocardial infarction, sudden death. The incidence of sports related death among young patients with coronary artery anomalies is much higher. 12 to 19% as compared to non-sports related death, which is only 1.2%. So what are these anomalies? These anomalies are coronary arteries arising from the order. So here is the, we published some time ago, this is in 1992 with Dr. Taylor looking at the total number of cases. We are close to 230 cases or so, but these are the ones that are anomalous origin of greater than one coronary artery from the order. That is left main coronary, right coronary from the left main, left circumflex right, and the RCA from the right aortic sinus, right coronary from the left main, or from the posterior aortic sinus. And then this is the left, right and the left LAD from the right aortic sinus. Now overall here in our populations, only a third of the population occurs in women, but what has been reported is that in series that have done both male and female, mind you, these series came from the military in the, when I was at the Armed Forces Institute of Pathology, so it's obviously more male based. And then looking overall, it's 50% of women. So I try and show you what these are, just a glimpse of it. Coronary arteries arising from the aortic sinus, you can see the most fatal of them is the left main arising from the right coronary sinus passing between the order and the pulmonary trunk. And then the second most common is when the right arises from the left aortic sinus, and then passes between the order and the pulmonary trunk. This is the more common anomaly as compared to this, but the left main from the right is more fatal than is the right arising. And you can understand, because the left supplies the larger part of the heart. So here's an example of the 31 year old female who died suddenly after a negative stress echocardiogram for exertional syncope. And this arrow points to the, marks the position of the right osteum, you can see right here, and within the right coronary sinus, and the arrow is in the left osteum. And this tells you the right coronary sinus, the left coronary sinus, and the non-carnary sinus. And here is the membrane aseptum, so as to see what the difference is. You can see both arising. Here's the reverse, the right arising from the left, you can very clearly see here is the same heart, seen in the fresh, and this is after fixation, and we've unroofed the beginning of the right coronary artery, and you can see it seems to travel within the order. So you can understand what that order dilates. What's gonna happen is this orifice is going to close, because of the dilatation of the order in diastole. So you're going to see here, you can see this right coronary arising from the left, and here it is, the similar one showing in a 14 year old girl, a trained jogger, who had a sudden cardiac arrest while training. What I want to point out is, look at the way, in this case, ectopic right, you can see the artery is within the order itself, the osteum, same way here, ectopic left, you can see it is within the aortic wall, and you can understand why it would not fill during diastole, so well, especially during exercise. So now I'm going to switch to vasculitis. Vasculitis affects mostly women, especially large vessel vasculitis, as well as polyurethritis nodosa, and the large vessel vasculitis are tachyassus, giant cell arthritis, medium sized vessels which coronary falls into is the polyurethritis nodosa, and Kawasaki's disease. Although that occurs in children, but they may manifest as an adult, and usually beyond the 10, 12 years, between 10 and 40 years, if you see a coronary aneurysm, you can almost be rest assured that it is going to be Kawasaki's, or the other possibilities congenital, but I think congenital is overrated, most likely these were Kawasaki's disease. So let's talk a little bit on vasculitis as a general introduction. Vasculitis is characterized by inflammation of the vessel wall. Diagnosis of vasculitis can be challenging because of the signs, and symptoms are nonspecific, and can make other conditions such as infection, malignancy, thrombotic disorders, or connective tissue diseases. The clinical symptoms reflect affected vessel, that is the limb claudication, absin, pulses, unequal blood pressure, are typical symptoms of large vessel vasculitis, especially Takayasu's. Medium-sized vessels are defined as main visceral vessels and their initial branches, that is the proximal branches. Therefore, various symptoms occur during the involvement of these organs, and in the heart, as you can imagine, coronary involvement will lead to symptoms just like atherosclerosis, that is angina. Early death due to active disease, late death due to complications of the therapy can also occur. So large vessel Takayasu's, giant cell, medium, polyurethritis, Kawasaki's, these what I'm gonna talk about, and not the primary CNS. So large vessel Takayasu's, two million per year, more common in women than men, eight to one. Age ranges from 20 to 50 years, more common in individuals from Asian origin, that is Japanese, Southeast Asia, India, Mexico. Associated with HLA DRB 52 and B39. Acute phase, you see malaise, weakness, fever, arthralgia, myalgia, weight loss, pleurotic pain, anorexia, laboratory tests show us increased ESR, low grade leukocytosis, mononormic, normalcytic anemia, precedes the late phase by weeks up to six to eight years. Late phase diminish or absent pulses, all of you are familiar with, 96%. Bruise, hypertension, heart failure, also palpable pulse masses, emboli from the mural trombi, and sudden death. The four most common complications for classification are Takayasu's retinopathy, secondary hypertension, aortic regurgitation, and aneurysm formation, each being graded as mild, moderate, or severe. So we classify this, the type of environment into five different types. This is a newer classification, the old used to be grade one to four, four being when pulmonary involvement occurred. Now it is predominantly based upon the aortic involvement that is branches of the aortic arch, or type two or type two A or B, A being ascending aorta, aortic arch, and it's branches, and B being involving thoracic descending aorta also. Type three is thoracic descending aorta, abdominal aorta, and or renal aurease. This is the more common renal aurease hypertension being. The type four is abdominal aorta and renal aurease, and type five is any combination of two B to four. And according to this classification, wall metachartinary and pulmonary aurease should be designated C plus and P plus. This is now what is commonly now used. So if you look at the pathology of a Q phase, you see edema and necrosis as shown here. You can see medial necrosis. You can see scattered giant cells. It involves more the outer two thirds of the media, but it is well said that granulomates are doritis, which is common to both tachyacus as well as giant cell. It's not easy to separate them just based on morphology. We call it granulomates, and age is what helps us the most to differentiate. Age, in the case of tachyacus, less than 50 years, in case of giant cell, over 50 years. And you also see intimal proliferation of the vasovazorum, which is uncommon in the case of giant cell. So late phase, you'll see intimal adventitial thickening, your thickening and narrowing of the arch vessels you can see right here, illustrated arch vessels narrowing, and you can even see the coronary ostea involved in this case. You see scarring and revasorized in tree bark early on. This is at five to six years. You see the tree bark appearance. Skip areas of stenosis and aneurysm can also occur as shown here. So this is what it looks like. Intimal thickening. This is the media. This is the adventitia. You can see predominant involvement inflammation involving the outer two-thirds. And you can see the inflammation giant cells and even some idea of agranuloma foaming with the macrophage. Here's another case of tachyacus aeotitis in a 45-year-old woman, sudden debt due to hemopericardium. You can see the tear right here in the asinine order and the involvement just at the normal to the tree bark appearance in this case. And you can see even the arch vessel narrowing in these two arteries. So here's the histology showing intimal thickening, quite extensive. Scar formation within the aortic wall. Not much inflammation. Rare giant cells are seen, but you can see very well the media is destroyed. You can see the intimal. This is in the left common carotid. You can see the intimal thickening quite extensive. So tachyacus pathology, it is intimal hypercellular, intimal formation, focal disorganization and absence of elastic lamellae. You see at, see areas of necrosis which can persist. You can see adventitional fibrosis and you see high rate of coronary involvement. So if you look at all coronary lesions in this case, you can see greater than 50% in 23%. Osteal greater than 50% narrowing in 7.2%. Non-osteal greater than 50% in 10.8%. Overall, if you look at it, of these 28% had cardiac symptoms. So it's not small in patients who have tachyacus aotitis that they can have cardiac involvement as much as close to 30%. So what about giant cell arthritis affects older individuals, greater than 50 years, North European descent. New onset is localized, headaches, tenderness or decrease in pulses in the temporal artery. Although temporal arthritis may not be the right word to use, it's a giant cell arthritis. Just because it involves sometimes temporal artery, we should not call it temporal arthritis. We should call it because almost isolated never occurs. It is always with the aotitis. So that's why not to use the term, it is being discontinued, the term temporal arthritis. So giant cells is a granulomatous inflammation again of the large and medium sized arteries. Most common systemic in adults with a Western hemisphere eodic involvement is clodication upper and lower extremities, parasthesias, Reynolds phenomenon, Donald, Anjana, Karnes, Kimia, renal involvement, and of course, you know better therapy than I do. Overall, if you look at totally eodic aneurysms or dissections as high as close to 20%, whether it is by different people, but they're all in the same ballpark. So here's again showing the involvement in giant cell aotitis. Here, this is the lumen side. Here in this case, it involves more the luminal part of that is the inner half of the eodic rather than the outer. But based on that alone, you cannot make the diagnosis because both have granulomatous involvement, showing here the inflammatory infiltrate consisting of macrophage and lymphocytes, T lymphocytes. You can get giant cell aotitis as I said of the temporal arteries and rarely also of the coronary. This happens to be the coronary. You can see the involvement by the giant cells and the large number of inflammatory cells. So what about polyartritis and eodosa? Necrotizing inflammation of medium sized arteries and small arteries, but without luminal nephritis and or involvement of the arterioles, capillaries of vinyls. So it's limited to the arteries, the medium size and the small arteries. The peak incidence is five to six decade, two to 33 million people. Name derived from prominent visible or palpable nodules, which are, that's why it's called polyartritis, nodosa, the name. And it is usually especially common at branch points. Again, the presenting symptoms are systemic symptoms, which may be the same fatigue, weight loss, fever, arthralgia and signs, skin lesions, hypertension, renal insufficiency, CNS dysfunction, abdominal pain and other organs can be involved as well. And most cases, it is idiopathic, can be associated with hepatitis B and C and now more or less, we call it no longer polyartritis, but name it after the hepatitis saying, arteritis related to viral hepatitis B or C. So this is just to show you the segmental involvement of transmural inflammation of the muscular arteries. In this case, you can see the fibrin deposition, you can see the extensive inflammation that is present, which can be homogenous, can involve a large number of eosinols, but fibrinoid necrosis is the hallmark of this disease. And where do we see it? We see it at the branch points. And then this affects, you can see lesions which are healing as well as acute lesions in the same section. So activity can keep on going while healing is occurring in other areas. And again, there is association with intima proliferation, narrowing all the arteries leading to ischemia. What about Kawasaki's disease? All of you should know mucocritinous lymph node syndrome, pediatric age group, usually mean age 2.8 years. Typically it is self-limiting, but has vascular complications, 20 to 100,000 in Japan, four to five per 100,000 in the US. It's again, predominantly a disease of the Asian origin. Unknown, but linked to viruses, bacteria, autoimmune triggers. Outcome and survival rate is 62.7% at 30 years. So not unusual to see aneurysms of the coronary arteries which are being diagnosed as secondary to atherosclerosis, but really these are vascularities. Then post-MI ventricular tachycardia free rate of only 28.5 years at 25 years. So if you have the complication, it is going to be quite detrimental. 5% of coronary arteries, aneurysms likely due to Kawasaki's disease in childhood in patients under 40 years of age who underwent coronary angiography for suspected MI. So it should be in your differential diagnosis, Kawasaki's, you need to ask. Often patients don't remember because it occurred so long ago or it have occurred when they could not remember because they were less than three years of age. So clinical classification is type one, pancarditis progressing to coronary aneurysms. Type B is pancarditis progressing to diffuse intima proliferation without discreet aneurysms. Microvascular disease can also occur and healing without demonstrable sequelae also is known to occur. So you may have mucocotanias and you may never know that you had coronary involvement because there's no sequelae left. So here's to show an example. Here's a coronary artery aneurysm in an 11 year old kid that we saw at autopsy. You can see the large number with a history of mucocotanias lymph node syndrome, pancarditis, myocarditis, wide spread inflammation of medium and small arteries. Our coronaries, testicular, pulmonary, spleenic, iliac can all be involved. Panarteritis without fibroenoid necrosis. This one lacks the fibroenoid necrosis. It is more an inflammatory disease of the wall of the vessel, whether it is the odor or it's the coronary arteries. In this case more commonly coronary arteries. And of course there is destruction of the media with little inflammation can lead in the late stages. Completely you may not see much inflammation. So here's to show you an 11 year old girl sudden death, multiple coronary artery aneurysms. This is her coronary artery wall. You can hardly tell the difference where the media starts and the intima. This is intima, this is the media right here. This is the adventitial part. And you can see the inflammation, again showing complete destruction of the media with luminal traumas and chronic inflammation on the right. Rarely you can get just intima proliferation and this can present like total intima proliferation you could make the diagnosis of intima fibromuscular dysplasia but the age is what distinguishes. If it's a child you're more likely to call it mucocutaneous lymph node syndrome. If the person presents in the 40s you are likely to label it fibromuscular dysplasia with involving intima fibromuscular dysplasia rather than media. So this is just to show intima proliferation without much inflammation. So now I just want to mention some diseases like burgers disease since smoking is much more common in our younger population, especially women are smoking much more. Therefore I think we must remember burgers can, although it usually involves the lower extremities or even the upper extremities but coronary is not immune. I've seen cases of coronary burgers. So middle age smokers, inflammation of the arteries in the veins, clodication of extremities and treatment is cessation of smoking and sometimes amputations are required. Here's to show one case. You can see the media more or less intact. You can see intima proliferation and you see this necrosis with giant cells around it. Inflammation classic of burgers disease within the, it is not in the wall, is within the lumen that you see these giant cells with areas of necrosis. Now we mustn't forget we are with drug abuse still and cocaine abuse does cause coronary spasm and does lead to coronary thrombosis. Here are two cases, 30 year old and 42 year old showing these resemble black erosion as I talked about it yesterday but it is very important to look for cocaine abusers. Specifically must do both blood and urine tests to rule out that there is no cocaine on the patient who's come into your clinic asking complaining of chest pain. So I'm now switching to the most important topic, spontaneous coronary artery dissections. The definition is defined as spontaneous separation of coronary artery war that is not itrogenic or related to trauma. Contemporary usage of the term SCAD is typically reserved for non-athroscratic variants and most modern series exclude SCAD due to athroscratic disease. If there is athroscrosis that must be excluded. First report was reported in 1931 by Pretti, this was in a 42 year old woman who died unexpectedly following repetitive retching and vomiting. The epidemiology true incidents and prevalence of SCAD is general population is unknown but a significant diagnosis of this condition is due to significant causes. If you look at ACS cases only, SCAD accounts for about 4% of the cases in women. If you look at the incidence SCAD, it is not rare in women who are presenting with ACS. If you look at 24 to 35% just in women, this is overall population, this is just in women, especially related to those with pregnancy related MI. So SCAD affects women commonly accounting for 92 to 95% of the cases. I saw some cases when I was in the military in men as well. Those are young men similarly age group remains the same. Mean age 44 to 55 years, race in terms of racial distribution, all races are affected, nobody is exempt, who underwent percutaneous PCI in British Columbia. If you look at length, SCAD overall has about 45 millimeters but somehow I think this seems longer to me than necessarily but I'll show you cases which are much longer. So the symptoms are chest pain, radiation to arm, nausea, vomiting, radiation to neck, diaphoresis, dyspnea, back pain, dizziness, ventricular tachycardia, ventricular fibrillation, fatigue, headache and sin to be. So any of the symptoms are not typical for chest pain necessarily. If you look at the best way to diagnose is by coronary angiography and I'll come back to that. Intracoronary imaging has become very important but I think it has its own problems. Remember you have to enter an artery, you may be in the faults or the true lumen and therefore you could make it worse. So one of the things that I at least I'm very cautious if the patient is stable, I think you leave the patient alone. If the patient is unstable, that's the time you need to go in. You can see the entry wound, you can see here the hematoma, inside the plaque that is inside the media and by echocardiography also by IVAS. So these are the typical ones that I think type one, type two, type three, most of the patient are taken to the cath lab, done angiography to make the diagnosis, radial lucency flap linear, you can see right here, you can see tapering, diffuse, long diffuse smooth stenosis with subtle abrupt changes in the arterial caliber or you can get type three which is indistinguishable from focal atherosclerosis as shown here. This could be spasm, could be anything that you can make a mistake of thinking of it being atherosclerotic in origin. So I'm gonna show you a series of cases which we have seen, which I have seen, I probably have seen in my 40 years of being in cardiovascular pathology, probably close to 50 cases, which is a large number of cases anybody has seen. So here is a case of a 41 year old female, sudden death following presentation with seizure. You can see this left main LID left circumflex, you can clearly see the hematoma in the arterial wall, very clearly seen here, section you can see the lumen on one side here and the hematoma narrowing that lumen excessively, you can see right here. Similarly in the left ventricular apex, there was also the LID proximal was not involved, the distal LID was involved and here it is showing that LID again, showing the dissection and showing the hematoma outside in the medial wall itself. Here's another one, 30 year old female pregnant, 28 weeks, chest pain, sudden death. This is her distal LID again. You can very clearly see where the arrows are, that there's a hematoma in here and you can see that hematoma right here and the lumen is on one side, lumen here, lumen here, lumen here and you can see this small lumen in the LID, patient died suddenly. One of the things I will come back to it but note what I'm going to show you, majority of the cases are more proximal and most of the time, if you look at the angiographic features, people have talked about being not involving the proximal arteries. Maybe when there's proximal artery involvement, these are most uniformly fatal and that's why they come to our table and not to your tables. So if you look at this is a 43 year old female with headache, not feeling well, became unresponsive and died suddenly. Here's the left main artery, the left anterior descending is involved, not the distal arteries, here's the left main showing the dissection, here's the LID almost completely occluded from the surrounding hematoma. Here's a 36 year old female presenting a sudden death. You can see from the proximal, these are serial sections shown to show that the dissection continues and therefore you're likely to get long occlusions which look like atherosclerotic disease but are actually not. One of the things that many years ago I published which was in the 80s, I published a paper saying in spontaneous coronary artery dissection, could this be related to eosinophilic infiltrate in the adventitia? That is that a primary process? In fact, I was of the belief this could be a primary vasculitis and secondary dissections occur but Dr. Buya from here actually very nicely showed that actually most cases, not all cases show this. It depends when the patient dies. If the patient dies early, you don't see the inflammation. If the patient dies a few days later, you'll see the inflammation and this is just to show that inflammation in this 36 year old female who died I think three days after chest pain, 42 year old female, same way showing the adventitia, eosinophilic infiltrate, you can see these bright cells, these are all eosinophilic. Now this one is very tragic, 32 year old female, two weeks postpartum, chest pain, in fair myocardial infarction, she was taken to the cath lab and died in the cath lab. This is her arteries. She has left main, left anterior descending, left circumflex, right coronary artery, mid distal PDA, all involved. She had no chance if she had dissection in all arteries. So these are not the cases that are going to likely to come to your table. Now this is a case interesting that is one of the few cases we have with multiple spontaneous coronary artery dissections in this 49 year old female who was hypertensive and a smoker. She presented with a abdominal pain, admitted, small renal artery infarct, CT, angio and MRI were done, fibromuscle dysplasia was diagnosed, but she died. Pustia descending artery, here's the dissection, here's the celiac artery with the dissection, showing the area of the interruption of the medial wall, hepatic artery, right renal artery, all involved in this young woman. So what about our registry now, since I've been at CVPAT now, almost 12 years, we've been collecting cases. So what we've done is one of my fellows has put together these cases on SCAD and our registry. Here are SCAD patients, we've got 17, median age is 41 years, of these 15 are females. And if you look at the race, white, predominantly black, just as much and unknown in about 6%, heart rate is normal, no differences, diabetes no different, hypertension no different, hyperlipidemia no different, these are controlled patients that we selected non-CAD patients. And if you look at coronary artery disease, they're both don't have coronary disease because we wanted to match them and I'll show the reason we tried to match. The cause of death is coronary in this case and non-cardiac death in these. Now, multiple lesions involving within the coronary artery, seven of them had multiple lesions. So these patients don't have a chance if they have multiple coronary artery involvement specifically proximal. Look how many were proximal, 10 of them had proximal involvement. Left main in five cases and previous history of SCAD was only one case where the previous history of SCAD. So here are the vessels involved, left main, LAD predominantly, circumflex and right coronary arteries. And then where is it? Predominantly proximal and mid in three distal in four and branches. This obviously doesn't add to 17 since multiple arteries are involved in each patient. Our length is shorter, that is 15, nine to 24. Now this could be related to shrinkage, can be related to whatever you can think of. But ours are much shorter in involvement. And disruption of the media was only seen in one. So it's more like a hematoma rather than a true disruption. So what we did was we were interested in the thinnest portion of the media. Are they different? So we looked at the arteries that were dissected but had a normal media, like here for example. We measured that area where there was no dissection. Non-dissected artery that is a control artery in the same patient, again looking for the thinnest. If you look at, then we did the control arteries that were no dissection, nothing. So you can see these arteries are thicker in the control as compared to what we see in our SCAD patients. So that's something one should look for. Maybe that's a hallmark to distinguish whether these patients have the SCAD features or they don't. Where is the location of the dissection? We wanted to know whether it involved the inner media, middle media or the outer media that is EEL border. So if you look at predominantly it's at the EEL border. Outer media in a very 20% and very small are in the inner media. So predominantly that's why, in a way to think, why does it occur? So here's just to show the dissection. Here is to show the arc of involvement. Large number obviously will have 365 degrees or three quarters of the circumference is involved in large percent of the cases that is close to 95% of the case because these are all fatal cases. So the prevalence of plaque type, we see in the SCAD artery usually there is no interval proliferation of fibrocalsic is very rare at the site or dissection. If you look at other non-SCAD arteries, you will find fibrocalsic lesion, fibroathroma or pathologic intimal thickening but adaptive intimal thickening is the predominant feature of this disease. They don't have atherosclerotic process and this is in our non-SCAD cases showing that the prevalence is much greater even in patients who are not dying from coronary disease. So mechanisms, I think this is an important, they think it's a tear within, I think that's a very small percent. Predominantly I think it comes from the vasovazorum bleeding into the media, that's something to think about, how does it occur, why does it occur? People have done TEM transmission electron microscopy in nine of the cases and they showed that they had heavy basement membrane and covering by medial smooth muscle cells not just endothelial lining but medial. So suggesting that there's relative ischemia that may be the cause of why hemorrhage occurs, why there is likelihood of hemorrhage because they're necrotic vessels and therefore likely to rupture. So management of course you all know better than I do, this is stable, conservative therapy, high risk features, if it left main disease ongoing ischemia patient, VT or VF, cardiogenic shock, these are all patients that are taken to the cath lab, PCI success and in hospital death is very low, PCI success is high, follow up and I'll show you that I don't quite believe in PCI personally, I think these patients should be left alone but they don't have an option, those who are high risk, that's the only way you can save them. So here are two examples that we recently published showing that this is a 42 year old female recently postpartum, was admitted with chest pain, shortness of breath, proximal right coronary artery was occluded and an avaroloma saluting stent was placed, the patient remained in cardiogenic shock, despite insertion of intraioric balloon and temporary pacemaker, she died after cardiac arrest and you can see that this had dissected distally as well and that was the main reason why the death occurred in this particular patient. Here's another case is a patient who actually 40 year old female, she had dissection, she was in cardiogenic shock, she was taken to the cath lab, they put in a stent, she was stabilized intraioric balloon, she came off the balloon four months later, she had to transplant and this is the heart that we received that was taken out from her. The stent was placed in one order in the LID in the false lumen, not in the true lumen, that's why she didn't do so well and continued to be on life support for four months, she'd survived four months and then left circumflex was implanted in the true lumen but not that effective as you can see the false lumen is still present and the false lumen is showing large amount of new intramur proliferation. So predisposing fibromuscular dysplasia, that's become very important, majority of the people feel that scad is part and parcel of fibromuscular dysplasia but if you look at fibromuscular dysplasia how often can you diagnose scad or see abnormalities is only three or four percent. Here they say anywhere from 51 to 90 percent of cases will show you presence of fibromuscular dysplasia in other bands, that is if you look at renal, you look at cervical vertebra, these are the arteries that can be involved. So I'll touch a little bit on fibromuscular dysplasia, I hope I'm quite over my time and I'd like to and as you know fibromuscular dysplasia similarly is more common in women than in men and therefore why not the two being connected, it's genetics causes unknown, subset of fibromuscular carry a genetic predisposition because seven to 11 percent and the first degree relatives have fibromuscular dysplasia in very common in smokers, high among patients with fibromuscular compared to the control group 30 versus 18 percent. This was the first classification, actually it was McCormick who gave the first classification but what was published well was from the Mayo Clinic, they showed examples of it, Losha, Tom Losha who runs the editor of the European Heart Journal and Lee who did a lot of the work in Mayo Clinic showed that there was three types of fibromuscular dysplasia, this interval fibroplasia, medial fibroplasia and then there's periadventicial fibroplasia and this has been now made simpler in some ways, histologically we don't have many specimens, therefore we can't quite always say what it correlates with but angiographically multifocal or just focal only, these are the two main types that are being used, here's to show the classification FMD, this is the fibromuscular dysplasia, you find that the media is thinned focally very prominently in those that have the classic form and here is the focal intimal hyperplasia, that's the only change that is seen and rarely you can see adventitial but I have seen one case and that was when I was at the AFIP, I haven't seen another case so it's extremely rare if it really exists. Renal and the carotid arteries are the main arteries that are involved and coronary as I said in only 3% of the cases that they can show. This I just wanted to show some cases, 55 year old female with fibromus involving multiple arteries, you can see right external carotid, right renal artery, left renal artery highlighting the areas, this is a dysplasia, you can see that media is totally replaced by intima here and again, there is almost no media in this particular spot so showing fibromuscular dysplasia, the same lady also had left lesion involvement that is left internal carotid, left middle cerebral and left external carotid arteries and you can see how dysplastic this artery looks, this is the dysplastic artery which has also been described in the SA node, AV node by our group many years ago. This is a recent case that I got from actually Jacqueline, Ken from Vancouver, 34 year old female with FMD involving multiple arteries, you can see this number of arteries that are involved, you can see thoracoservical trunk, you can see the internal thoracic, proximal right vertebral, right vertebral artery which had a previous dissection as shown right here which is healed in this particular case and again on the left side the same way you can see a healed lesion of dissection and rupture and you can see here dissection of the right vertebral, no dissection but dysplastic vessel in the bifurcation region and left external carotid. So sudden death is not unusual, unfortunately close to 20% of cases and these are the same features, we have to rule out differential diagnosis, earless, dandless, tachyacus, cocaine, coronary vasospasm, myocardial bridging which I didn't address and then atherosclerotic plaque. And last of all, S curvature in the internal, in the carotid artery patients and the tortuosity of the carotid artery is also described in FMD is higher as compared to general population but although the S curve may not be specific for FMD, its presence in carotid duplex ultrasound is in an individual less than 70 years should suggest the diagnosis of FMD. So in summary I've shown you carotid artery anomalies, I've talked about vasculitis and then I've talked about SCAD and fibromuscular dysplasia, the true incidence prevalence SCAD in the general population is unknown due to significant underdiagnosing of this condition. Of patients presenting with ACS SCAD is seen in 4%. Incidents of SCAD is not rare in young women presenting with ACS. SCAD is associated with FMD in 52 to 91%. FMD most commonly involves renal carotid and SCAD is most frequent, 3.4 reported. First and second degree relatives are more effective than the general population. Thank you so much.