All About Aspirin

In previous blog posts (08/10/09, 08/16/09) I have reviewed the concept of antiplatelet drugs and their primary role in the protection of patients with coronary atherosclerotic heart disease from heart attack and death. They also serve to help prevent stent closure by clotting. In my next several blogs I will show how, although these concepts seem simple, they continue to engender controversy.

The first controversy again concerns aspirin. I find aspirin’s history compelling. This compound has been in use since ancient times. The active compound acetylsalicylic acid was first prepared by the French chemist Charles Gerhardt in 1853. The name was patented in 1899 after scientists at Bayer decided it was less irritating than salicylate alone. Aspirin soon became quite a hit and now an estimated 40,000 metric tons are used a year.

Two fun facts about aspirin: why is the dose of aspirin 325 mg? It’s because that was the amount of medicine in the tablet that withstood the manufacturing process including the stamping of the Bayer “cross” on the pill. Second, Germany was forced to give up the patent on aspirin in France, Russia, England and the United States after WW I as part of the war reparations.

You would think that since this substance has been around since Hippocrates that we would know how it worked. That piece of science waited until1971 when John Robert Vane showed that aspirin suppressed prostaglandin and thromboxane production. In 1982, he won the Nobel Prize in Medicine for this discovery and was knighted.

Aspirin has been further characterized as a COX-1 (cyclooxygenase enzyme) inhibitor which irreversibly blocks the formation of thromboxane A2 in platelets leading them to lose their ability to form clots. It is this action that we as cardiologists depend upon. The amount of aspirin to accomplish this is small — roughly 40mg a day, which is where the use of 81mg of aspirin gets its recommendation. This is a source of controversy among physicians and in many cases, more aspirin is needed to accomplish the clinical goal of preventing heart attacks, death from cardiovascular causes or stent closure. The more aspirin you take, the higher the likelihood of GI bleed; so that balance is what comes into play.

Next…the beginning of the trials.

Tags: acetylsalicylic acid, antiplatelet drugs, aspirin, coronary atherosclerotic heart disease, COX-1 (cyclooxygenase enzyme) inhibitor, prostaglandin, thromboxane

This entry was posted on Friday, September 18th, 2009 at 10:55 am and is filed under Atherosclerotic Heart Disease, Coronary Artery Disease, Heart Failure. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.