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Inflammation and Heart Attacks

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Updated November 30, 2003

Dateline: November 12, 2001

Two studies published this month add weight to the increasingly likely theory that inflammation within the bloodstream is a major factor in causing heart attacks.

In one study, increased blood levels of an enzyme called myeloperoxidase (MPO,) a protein made by white blood cells, was strongly associated with a high risk of coronary artery disease and heart attacks. In the second study, elevated blood levels of another protein, interleukin 6 (IL6,) was also associated with an increased risk of death in patients with heart disease. Both MPO and IL6 become increased in the bloodstream in response to inflammation. In these two studies, elevated levels of MPO and IL6 were both better predictors of cardiac events than the more commonly used risk factors.

What does this mean?

That both MPO and IL6 turn out to be predictors of cardiac events adds significantly to the growing body of evidence that inflammation in the blood vessels can precipitate the rupture of plaque, and thus the sudden closing off of coronary arteries. A heart attack (i.e., the death of heart muscle) is caused by the abrupt closure of the coronary arteries.

Clinicians have long been puzzled as to why many heart attacks occur from sudden blockages in coronary arteries that appear normal or near-normal when tested with coronary angiography (cardiac catheterization.) The most widely accepted explanation for such events has been the abrupt rupture of plaques that are either inapparent or that traditionally have been termed "non-significant" on angiography. Why such "small" plaques would suddenly rupture has been a mystery. It now appears likely - especially with this new evidence - that inflammation within the plaques may cause them to rupture. (Click here for a brief description of how rupture of a plaque - or ulcer formation on a plaque - can lead to abrupt closure of an artery.

Should you have your MPO and IL6 levels measured?

Despite the recent findings correlating elevated levels of MPO and IL6 with increased risk, for three reasons there is little or no reason for doctors to measure these enzyme levels in large numbers of patients. First, these two blood tests are research tools, and are not widely available. Second, both of these new studies are preliminary, and need to be confirmed in prospective trials in much larger numbers of patients. And third, there is no obvious course of action to be taken if the MPO or IL6 levels are found to be elevated.

The major impact of these new studies is that they add significantly to the body of evidence that inflammation is an important mediator of heart attacks, and thus they will spur funding - both by the government and by pharmaceutical companies - to find ways of reducing the inflammation that mediates fatal and potentially fatal cardiac events.

What does all this mean to you and your doctor?

Let's assume that the latest theory is right, and that inflammation can be an important factor in causing heart attacks. The best ways we know of at present to reduce factors of inflammation are aspirin and the statins.

As it turns out, both of these drugs ought to be taken already by the vast majority of patients who have coronary artery disease, or who have a high risk of developing coronary artery disease. While aspirin and statins are recommended for reasons other than their anti-inflammatory effects, those effects might turn out to be very important factors in why they work. If doctors and patients merely follow the current recommendations for risk reduction, then they will already be doing everything that is currently known to reduce inflammation.

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