Non ST Elevation Myocardial Infarction: Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
As opposed to the original hypothesis that ACS is caused by gradual progression of coronary atherosclerosis to the point of a severe, fixed lesion, it has become clear that, in fact, ACS is usually caused by atherosclerotic plaque rupture at a site that previously had only mild to moderate stenosis. This plaque rupture exposes ligands (including collagen) for platelet adhesion which causes platelet aggregation and subsequent platelet activation. Platelets are activated by thrombin (found in blood clots), adenosine diphosphate (found in platelet granules), serotonin (also found in platelet granules) and thromboxane-A2. Upon activation, the glycoprotein IIb/IIIa receptor that in a non-active state is found in the cytosol is exteriorized and modified which enables additional platelet aggregation and cross-linking. The prothrombinase complex then binds to the activated platelet and starts to coagulation cascade. This entire process results in a thrombus which coalesces over the ruptured plaque. This thrombus may then embolize resulting in myonecrosis of the myocardium which is detected as a rise in troponin or CK-MB.
References
<biblio>
- Martinezref1 pmid=17100031
- Patronoref1 pmid=9296464
</biblio>