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.
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.
There, fixed it.