00:00 So other symptoms of ischemic heart disease, and basically, this has to do with a dysfunctional heart. 00:08 So if the heart is not squeezing appropriately. 00:10 It's got systolic dysfunction because of ischemia, you're going to have low flow and you will have symptoms of dyspnea. 00:14 you're going to have low flow and you will have symptoms of dyspnea. 00:17 So you will be short of breath. 00:19 You may have abnormal conduction through the heart. 00:22 That will give rise to palpitations. 00:24 You may have inadequate perfusion of the rest of the vasculature. 00:29 So you get dizziness. You can even have syncope. 00:33 There is a sense of restlessness and anxiety. 00:35 A feeling of doom and gloom, particularly, if you're having an acute myocardial infarct. 00:40 This is probably due to activation of a neurohumoral axis, but you actually feel like, "I'm going to die." Sometimes, you're right. 00:50 And then you can have other autonomic symptoms. 00:53 So diaphoresis, sweating, nausea and vomiting. 00:56 Those are typically associated with posterior wall ischemia, so that we are activating the vagal nerve. You can also have syncope. 01:04 If you activate the vagal nerve enough, you can go into bradycardia. 01:07 Alright. So some other interesting pathophysiology of atherosclerotic ischemic heart disease. 01:14 So this is just showing you a progression over years of an atherosclerotic plaque. 01:20 On the left-hand side is a normal coronary artery with a nice normal media and no intimal hyperplasia. 01:28 And you can grow that atherosclerotic plaque for a long time. 01:31 Up to that point shown there on the fourth circle where the luminal diameter hasn't changed. 01:40 It's the same blood flow through that vessel, even though I got more and more and more atherosclerotic plaque. 01:46 That's because there's outward remodeling of the vessel. 01:50 So even though I'm getting a thicker intima and the wall is getting thicker locally, the vessel is dilating and adapting. That's the Glagov phenomenon. 01:59 Now, there's an upper limit to this adaptation, and it occurs kind of right around when you have 70% stenosis. 02:07 At that point, the atherosclerotic plaque wins, and the ability of the vessel wall to expand is inadequate to keep up. 02:14 So now, with that critical stenosis, the 70% stenosis, you could potentially start becoming symptomatic. 02:21 And actually, if the atherosclerotic plaque progresses, you can develop now, anginal symptoms, even without an infarct, even at rest. 02:30 So the last one on the right is just showing you a very small pinpoint lumen, and that may be limiting even at rest in terms of providing adequate nutrition and oxygenation to the heart muscle. 02:43 So let's think about this looking in a slightly different way. 02:48 We're going to look at the lumen of a coronary artery, and over the course of decades as indicated at the top, you can have a progressive evolution of atherosclerosis. 03:02 Atherosclerosis has a very long timeline. 03:05 It doesn't in most people occur within weeks or months. It takes years and decades. 03:12 So you can have up to six decades before it begins to be a significant occlusion. 03:18 At that 70% stenosis, that's critical. 03:21 That will give - that critical stenosis will give you stable angina. 03:25 So running around the block pretty reliably gives you chest pain. 03:29 And then you can have plaque rupture. 03:32 And within minutes, you go from whatever degree of occlusion you had, to now, a completely occluded vessel. 03:39 Manifesting as an acute coronary syndrome, unstable angina and remember that the majority of such plaque ruptures occur on vessels that are less than critically stenotic. 03:53 So that are 20%, 30%, 40%, 50% chronically stenotic, alright? With that thrombus formation and complete occlusion of a vessel, then you can have a myocardial infarct.
The lecture Ischemic Heart Disease: Clinical Manifestations and Pathophysiology by Richard Mitchell, MD, PhD is from the course Ischemic Heart Disease.
What part of the heart is most likely affected by a myocardial infarction if the patient is experiencing autonomic symptoms like diaphoresis, nausea, and vomiting?
Which nerve activation is responsible for the syncope and bradycardia after a myocardial infarction?
What is the term that describes vascular remodeling to maintain constant flow despite increases in atherosclerotic lesion mass?
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