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What Is the Connection between Aspirin and Platelets?

By Toni Henthorn
Updated May 17, 2024
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Aspirin is an oral medication that has both anti-inflammatory and blood-thinning properties. It inhibits the formation of blood clots by preventing platelets from producing a chemical called thromboxane A-2, which normally induces platelet clumping. When aspirin and platelets interact, the medication blocks the action of the enzyme cyclo-oxygenase-1 (COX-1) that forms thromboxane A-2. Without thromboxane A-2, platelets cannot stick together and join with fibrin to make a blood clot. While other agents also block the COX-1 enzyme, the antiplatelet effect of aspirin lasts for several days versus several hours for the other agents, making it a preferred choice according to many physicians for long-term prevention of heart attacks and strokes secondary to blood clots.

The connection between aspirin and platelets has been well studied in clinical trials. At doses of 325 milligrams per day, the greatest antiplatelet effect occurs within 30 minutes of ingestion. Low-dose aspirin, however, may take as long as several days to reach its most potent effect. For this reason, physicians recommend the regular dose of aspirin when patients are experiencing signs and symptoms of chest pain, heart attack, and stroke. Unlike other antiplatelet medications, aspirin only blocks the COX-1 pathway of thromboxane A-2 formation, allowing some normal platelet activity to occur.

Further demonstrating the relationship between aspirin and platelets, one large multi-center study of acute heart attack patients revealed a 23 percent reduction in mortality when aspirin was administered with 24 hours of the start of symptoms. The current recommendation for patients experiencing severe chest pain, shortness of breath with exercise, clamminess, nausea, and pain radiating into the jaw or arm is to take a regular aspirin as soon as the symptoms develop and to continue the aspirin each day for at least one month. Although aspirin will not open an blocked vessel with an existing blood clot, it will prevent growth of that clot and prevent the formation of more clots. In this way, aspirin limits the extent to which heart tissue becomes starved for oxygen and thereby limits the damage.

A cerebrovascular accident (CVA), or stroke, is an injury that occurs within the brain or body due to reduced blood flow. Common contributors to stroke include narrowing of the blood vessels due to cholesterol and damage from high blood pressure, as well as blood clots or cholesterol plaques traveling in the blood stream and becoming lodged in a small blood vessel. The link between treatment with aspirin and platelets for stroke patients is revealed in several studies that show that moderate aspirin administration within the first 48 hours of symptom onset dramatically increases survival, reduces the severity of neurological deficits, and prevent further strokes. Physicians recommend doses of 160 to 350 milligrams to be given as soon as patients notice the classic signs of stroke, including weakness, numbness, changes in vision, difficulty talking, and balance problems.

Although research continues on the connection between aspirin and platelets, aspirin is not always the best solution for blood clot problems. Significant side effects of aspirin include allergic reactions, asthma, bleeding ulcers, and hemorrhages within the brain. Poor candidates for aspirin therapy include pregnant or breast-feeding mothers, children, and patients with kidney or gastrointestinal diseases. On the other hand, most doctors prescribe low doses of aspirin for patients with severe atherosclerosis and a history of previous heart attacks, prior strokes or mini-strokes, chest pain with exercise, and reduced blood flow in the extremities.

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