Aspirin and Heart Attacks

You would think by now the aspirin issue long ago had been put to rest. Yet the debate still continues with the primary care physician right in the center, trying to decide which tune to follow.

Three decades ago, right in the middle of my 23 year "tour of duty" as a family doctor, the general consensus, the tune to which we all danced, was that for all males over the age of 50 (and probably women as well), the benefits of a baby aspirin daily far outweighed possible risks.

Now, thanks to Joel Kauffman's critical review, we find that much has changed. First of all, the buffer coating on aspirin has proven to be critical for its vital magnesium content. Secondly, after critical appraisal of side effects and all cause death rates, the use of a low dose aspirin in primary prevention can no longer be supported.

Secondary prevention is quite another matter with very favorable outcomes for limited periods of times after the thrombotic event.

Thankfully, this still fits with our knowledge of relevant pathophysiology - the inhibition of platelet stickiness by aspirin. In secondary prevention you are dealing with an endothelial wound and aspirin during the healing period seems reasonable.

It seemed logical that inhibition of platelets, the proven mechanism of action of aspirin in men, would be helpful in both primary and secondary prevention of myocardial infarctions and although women may come from Venus and men from Mars, I never saw any strong reason to withhold this medication from women.

The problem here again is that fellow named Gauss and his frequency distribution curve. You give 81 mg of aspirin (baby aspirin dose) to a thousand people and 25 of them will likely bleed excessively into their tissues and return to the office looking like victims of physical assault, another 25 will have no effect on platelets whatsoever, demonstrating complete insensitivity to aspirin at that dose and the rest will be in the middle, some leaning right and some left.

That is what makes medicine an art rather than a science. Our DNA mandate is such that no two of us are alike and that goes for reactions to medicines of all kinds. So in public health as in primary and secondary prevention, you try to find the middle road when there is no such thing.

And now we find that the results of longitudinal studies of large numbers of people are not nearly as supportive of aspirin as we once thought. I have heard doctors say as they go off for their year of self-sacrifice into third world countries, "You give me all the salt, penicillin and aspirin I need and I can practice medicine anywhere." They have now taken away penicillin with threats of dire sensitivity reactions and limited spectrum of effectiveness. What if they take away aspirin? How much can you do with salt? Quite a lot actually, but that is another story.

In primary prevention there is no wound - this is a different kind of problem. So our challenge for rational aspirin use seems to be one of identifying those people at risk, those with open endothelial lesions or those very likely to have them.

Since we now understand better the vital role of inflammation in atherosclerosis we are in need of better markers of inflammation to guide our identification of those at risk. C-reactive protein (CRP) is a step in that direction but a much better marker is necessary. With such a marker physicians would have little doubt in determining which patients to place on aspirin and the super-aspirins, which surely will follow now that we are focusing on the true etiology of atherosclerosis.

On this subject of inflammation, we are indebted to Kauffman's suggestion of such aspirin substitutes as omega 3, Co-enzyme Q10, magnesium and even vitamin E all of which address inflammation at least as effectively as aspirin, if not more so, and do so with near absence of side effects.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

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