IHD Patho 2012_Student Version (1)

Triggers of plaque rupture may occur spontaneously

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Triggers of Plaque Rupture May occur spontaneously Other factors that may serve as triggers: blood pressure shear force force of cardiac contraction coronary blood flow Plaque rupture collagen exposure platelet aggregation & coagulation cascade activation thrombus formation
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Photo adopted from: 101/F1 Vulnerable Plaque Plaque Rupture Thrombus ACS
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Thrombus Formation Fibrin & platelets form a clot on top of the ruptured plaque #1) Platelets aggregate and form a platelet plug Adhesion to disrupted endothelium Activation Release mediators (ADP, TXA 2 , thrombin) Activates surrounding platelets Aggregation Platelet activation leads to conformational change of glycoprotein IIb/IIIa (GPIIb/IIIa) surface receptors of platelets Fibrinogen binds to GPIIb/IIIa receptors Links platelets together Aggregation Tissue factor in ruptured plaque activates extrinsic coagulation pathway Formation of thrombin fibrin
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Platelet Aggregation Photo adopted from: von Willebrand factor (vWF) is a cell adhesion ligand, which under normal conditions, helps endothelial cells adhere to collagen in the basement membrane. When the BV is injured, collagen, vWF, and tissue factor from the subendothelium are exposed to the bloodstream. When platelets contact exposed collagen or wWf, they are activated causing platelet aggregation.
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Platelet Aggregation Photo adopted from: Platelet activators ADP: Adenosine diphosphate, TXA2: Thromboxane A2
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White vs. Red Clot White clot Contains more platelets than fibrin Platelets give the clot a “white” color Typically occurs in NSTE ACS Usually produces incomplete occlusion of coronary lumen Red clot Contains more fibrin and red blood cells than platelets Fibrin stabilize clots and trap red blood cells giving it a “red” appearance Typically occurs in STE MI Usually produces complete occlusion of coronary lumen
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Acute coronary syndrome Stable angina
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Pathogenesis of ACS Atherosclerotic plaque with a lipid-rich core and thin fibrous cap Plaque rupture Thrombus formation over lesion Acute coronary syndrome Shear forces, inflammation, apoptosis Platelet adhesion, activation, and aggregation; production of thrombin Acute in coronary blood flow
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Myocardial Infarction “Heart attack” Results from persistent ischemia (not quickly reversed) or from complete occlusion of a coronary artery Effect on myocardium Necrotic (nonviable) Often dysfunctional Often leads to heart failure Photo adopted from:
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Myocardial Ischemia Inadequate supply of O 2 to meet myocardial O 2 demand (MVO 2 ) O O 2 demand in face of fixed supply causes ischemia demand in face of fixed supply causes ischemia PAIN!
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