Ischemic Heart Disease: Plaque Changes and Adaptive Mechanisms

by Richard Mitchell, MD, PhD

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    00:01 So plaque changes.

    00:02 There are a variety of ways that the plaque can rupture, erode, whatever.

    00:07 So if you have inflammation that can cause endothelial cell erosion.

    00:12 If you have a toxic exposure from whatever that is.

    00:14 It could be various chemotherapies.

    00:16 It could even be infection, whatever.

    00:19 You can have endothelial cell injury and apoptosis that then leads to a plaque erosion.

    00:26 So I haven't really ruptured the atherosclerotic plaque, but now, I have a surface that is not covered with endothelium and that can be a source for thrombosis. Okay. There you go. Thrombosis.

    00:39 There can also be intrinsic factors that decide whether or not, or contribute to whether or not a plaque will rupture.

    00:47 So the plaque composition is really important.

    00:49 If you have a very thick-walled fibrous cap with a lot of connective tissue in it, that's not going to rupture. If you have a very fibro, fatty, if you're very fatty, atheromatous core, big old globule of fat and cholesterol and necrotic debris with a little tiny thin cap, that's going to be much more likely to rupture.

    01:09 So the plaque composition and structure actually makes a difference.

    01:11 Parenthetically, things like statins change the overall structure of a lot of plaques.

    01:18 They make them more fibrotic.

    01:20 So one of the other benefits of statins other than cholesterol lowering is that we get more fibrotic plaques.

    01:26 And even though we haven't changed particularly the size of the plaque, we make it less likely to rupture.

    01:32 Okay. Other extrinsic factors, blood pressure, platelet reactivity.

    01:37 So increased blood flow, increased heartrate.

    01:41 All those things will make a plaque more likely to rupture.

    01:46 And if there is increased platelet reactivity, we're more likely to form thrombus.

    01:50 Mechanical stresses, such as increased turbulent flow will drive the process, and we get an acute plaque rupture, which of course, will lead to thrombosis.

    02:03 We have ways to adapt and hopefully, prevent some of this.

    02:08 So normally, and we'll - I'll show you a diagram in a minute, but normally, for example, in the coronary circulation, you have the left anterior descending territory, the left circumflex territory, and the right coronary artery territory.

    02:23 Those territories have a zone in between that get perfusion from both, say, the left anterior descending and the right coronary artery.

    02:32 There is a watershed zone in there.

    02:34 And there is some interconnection between the arteries.

    02:37 That is a collateral flow. And if we have partial obstruction of one vessel, the collateral flow from the other vessel that can feed into that territory can takeover.

    02:50 In fact, it can become fairly much more robust.

    02:53 So if I have a progressive low-level occlusion that occurs in a coronary artery over years, the other coronary arteries can take over for that territory.

    03:06 And they can provide compensatory blood flow.

    03:09 And in fact, that collateral perfusion can even protect against an MI if the original vessel is totally obstructed.

    03:18 Okay, so just keep that in mind as well. With acute coronary blockage, however, there is no opportunity for the collateral flow to open.

    03:28 So then you will have an infarction.

    03:31 Alright, so this is just looking at a heart to make this point about the collateral circulation.

    03:37 This is showing you the left anterior descending.

    03:39 This is a heart that has been permeabilized with methyl salicylate.

    03:43 so you can see through the tissue.

    03:45 And then we've injected the coronaries with a red latex.

    03:49 So the left anterior descending, the LAD, is shown there.

    03:53 And the right coronary artery is shown there and that's the left circumflex.

    03:57 Now there are collaterals between those various territories that can allow collateral perfusion of the zones in between, the watershed zone.

    04:07 So even if I lose my LAD but I lose it slowly enough, the right coronary artery can take over for that territory.

    04:14 It may not take over entirely for all the left anterior descending territory but it can compensate.

    04:20 Similarly, between the left circumflex and the LAD, we also have another watershed zone.

    04:25 So there are compensatory mechanisms.

    04:27 All things considered, we really don't want to have atherosclerotic disease.

    04:30 And if you do, you probably want to get it treated.

    04:33 And with that, we'll conclude ischemic heart disease.

    About the Lecture

    The lecture Ischemic Heart Disease: Plaque Changes and Adaptive Mechanisms by Richard Mitchell, MD, PhD is from the course Ischemic Heart Disease.

    Included Quiz Questions

    1. Statins
    2. Nitroglycerin
    3. Beta-blockers
    4. Heparin
    5. Spironolactone
    1. Plaque composition
    2. Platelet reactivity
    3. Hypertension
    4. Hypotension
    5. Heart rate

    Author of lecture Ischemic Heart Disease: Plaque Changes and Adaptive Mechanisms

     Richard Mitchell, MD, PhD

    Richard Mitchell, MD, PhD

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    By Anadil F. on 20. March 2022 for Ischemic Heart Disease: Plaque Changes and Adaptive Mechanisms

    you make everything so so simple...loved your videos thank you for clearing the whole concept