Unstable Angina / Non ST Elevation Myocardial Infarction: Pathophysiology & Etiology
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As opposed to the original hypothesis that acute coronary syndrome (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.Martinezref1 This plaque rupture exposes ligands (including collagen) for platelet adhesion which causes platelet aggregation and subsequent platelet activation.Patronoref1 Platelets are activated by thrombin (found in blood clots), adenosine diphosphate (found in platelet granules), serotonin (also found in platelet granules) and thromboxane-A2.Patronoref1 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.Martinezref1 The prothrombinase complex then binds to the activated platelet and starts to coagulation cascade.Martinezref1 This entire process results in a thrombus which coalesces over the ruptured plaque.
Although less common, ACS may also occur by other mechanisms. These include 1) coronary artery spasm as in Prinzmetal's angina, 2) severe narrowing alone without plaque rupture, as in the case of restenosis after percutaneous coronary intervention (PCI) or as with progressive atherosclerosis, 3) coronary artery dissection, 4) secondary ischemia in cases in which there is either increased myocardial oxygen demand as in tachycardia from fever, anemia, hypoxemia, thyrotoxicosis, or in cases of decreased supply such as in hypotension or anemia from hemorrhage. (Cannon & Braunwald, 2005).
Genetics
To date, there does not appear to be any single genetic marker predictive acute coronary syndrome (ACS).Anwaruddinref1 In a recent validation study of genetic variants associated with (which includes ST-elevation myocardial infarction (STEMI), NSTEMI and UA) none of the 85 genetic variants tested were shown to be correlated with ACS. The study chose the polymorphic genetic variants based on statistically significant findings of prior studies.Morganref1 Nonetheless, although no individual marker is likely to be predictive, in the future it is possible that a panel of markers may be used to assess risk.Anwaruddinref1
References
- Martinezref1 pmid=17100031
- Patronoref1 pmid=9296464
- Morganref1 pmid=17426274
- Anwaruddinref1 pmid=17239708
- Wilckenref1 pmid=12889664
Additional Resources
- Cannon, CP & Braunwald, E (2005). Unstable angina and non-ST-elevation myocardial infarction, pp 1444-1448. Harrison's Principles of Internal Medicine, 16th ed., Kasper, Braunwald et al., Eds. McGraw-Hill: NY. ISBN 0071402357.
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Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .