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Cardiovascular Pharmacology Concepts |
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The Pharmacologic Treatment of Angina cont.
Types of Angina
Variant (Printzmetal's) angina results from coronary vasospasm, which temporarily reduces coronary blood flow (i.e., produces ischemia by reducing oxygen supply; "supply ischemia"), thereby decreasing the oxygen supply/demand ratio. Enhanced sympathetic activity (e.g., during emotional stress), especially when coupled with a dysfunctional coronary vascular endothelium (i.e., reduced endothelial production of the vasodilators nitric oxide and prostacyclin) can precipitate vasospastic angina. Chronic stable angina is caused by a chronic narrowing of coronary arteries due to atherosclerosis. When a coronary artery is narrowed beyond a critical value (critical stenosis), the myocardial tissue perfused by the artery will not receive adequate blood flow (i.e., the tissue becomes ischemic and hypoxic), particularly during times of increased oxygen demand (e.g., during physical exertion). The relative ischemia occurs when the oxygen demand increases, so this is referred to as "demand ischemia." This will lead to anginal pain during physical exertion. The pain usually is associated with a predictable threshold of physical activity. Other conditions that cause myocardial oxygen demand to increase, such as a large meal or emotional stress, can also precipitate pain. Unstable angina is caused by transient formation and dissolution of a blood clot (thrombosis) within a coronary artery. The clots often form in response to plaque rupture in atherosclerotic coronary arteries; however, the clot may also form because diseased coronary artery endothelium is unable to produce nitric oxide and prostacyclin that inhibit platelet aggregation and clot formation. When the clot forms, coronary flow is reduced, leading to a reduction in the oxygen supply/demand ratio ("supply ischemia"). If the clot completely occludes the coronary artery for a sufficient period of time, the myocardium supplied by the vessel may become infarcted (acute myocardial infarction) and become irreversibly damaged.
Go to Next Page Revised 03/14/07 |
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DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice. © 2005-2007 Richard E. Klabunde, all rights reserved. |