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Heart Attack Treatment (cont.)

Anti-platelet agents

Anti-platelet agents are medications that prevent blood clots from forming by inhibiting the aggregation of platelets. Platelets are fragments of cells that circulate in the blood. Platelets begin the formation of blood clots by clumping together (a process called aggregation). Platelet clumps are then strengthened and expanded by the action of clotting factors (coagulants) that result in the deposition of protein (fibrin) among the platelets. Aggregation of platelets occurs at the site of any injury or laceration, but it also occurs at the site of rupture of cholesterol plaques in the walls of coronary arteries. Formation of clots at the site of an injury or laceration is desirable because it prevents excessive loss of blood, but formation of clots inside coronary arteries blocks the arteries and causes heart attacks.

There are three types of anti-platelet agents -- aspirin, thienopyridines, and the glycoprotein IIb/IIIa inhibitors. These agents differ in their mode of action, anti-platelet potency, speed of onset of action, and cost. For more, please read the Anti-Platelet Medication article.

Aspirin

Aspirin inhibits the activity of the enzyme cyclo-oxygenase inside platelets. Cyclo-oxygenase is an enzyme whose activity is necessary for the formation of a chemical, thromboxane A2, that causes platelets to aggregate. Aspirin, by inhibiting the formation of thromboxane A2, which prevents platelets from aggregating and thereby prevents the formation of blood clots.

Aspirin alone has its greatest impact on improving survival among patients with heart attacks. Numerous studies have shown that aspirin reduces mortality (by 25%) when given to patients with heart attacks. Aspirin is easy to use, safe at the low doses used for anti-platelet action, fast acting (with an onset of action within 30 minutes), and cheap. Aspirin is given at a dose of 160 mg to 325 mg immediately to almost all patients as soon as a heart attack is recognized. It also is continued on a daily basis indefinitely after the heart attack. The only reason for not using aspirin is a history of intolerance or allergy to aspirin.

Aspirin is taken daily following a heart attack to reduce the risk of another heart attack. (Preventing further heart attacks is called secondary prevention, while preventing the first heart attack is called primary prevention). The ideal daily dose of aspirin for secondary prevention has not been established. Some doctors recommend 160 mg; others recommend 81 mg. The reason for this difference has to do with aspirin's occasional long-term side effect of bleeding (for example from stomach ulcers). Even though the risk of major bleeding with long-term, moderate dose aspirin (325 mg/day) is low (less than 1one percent), this risk can be lowered slightly by using an even lower dose (160 or 81 mg/day).

Aspirin also benefits patients with forms of coronary heart disease other than an acute heart attack. Aspirin has been shown to reduce heart attacks and improve survival in the following patients:

  • Aspirin improves survival among patients with unstable angina. Patients with unstable angina experience chest pains at rest or with minimal exertion. These patients have critically narrowed coronary arteries and are at imminent risk of having a heart attacks.
  • Aspirin improves survival among patients with stable exertional angina. (These are patients who experience chest pain only with exertion.)
  • Aspirin prevents formation of blood clots at the site of the PTCA (see below).
  • Aspirin prevents the formation of blood clots that can occlude surgical bypass grafts. (Occlusion of bypass grafts can lead to heart attacks.)
  • Aspirin in low doses (81 mg/day) has been shown to prevent first heart attacks (primary prevention)


Next: Thienopyridines »

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