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Do all NSAIDs Increase Cardiac Risk?
Two new studies suggest they do

By , About.com Guide

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Jun 15 2005
By DrRich

Two new studies add to the growing evidence that increased cardiac risk from non-steroidal anti-inflammatory drugs (NSAIDs) is NOT limited to the Cox-2 agents.

The first study, published in the British Medical Journal, studied over 9000 patients from the British Isles who had suffered heart attacks, and examined their usage of NSAIDs. They found that the risk of heart attack was increased for patients who were taking NSAIDs by as much as 20 - 50%. In this study, the association with a higher risk of heart attack was especially significant, statistically, for ibuprofen (Motrin, Advil,) diclofenac (Voltaren, Cataflam), and rofecoxib (Vioxx) - but there was at least a trend toward increased risk for all NSAIDs.

The second study was reported at the 2005 meetings of the European League Against Rheumatism scientific meetings in Vienna, Austria. In the largest study of NSAIDs reported so far - using a database that tracked over 1 million patients with arthritis treated with NSAIDs - investigators reported similar findings. Namely, there appeared to be an increase in the risk of heart attacks with NSAIDs - and further, the increase in risk was not obviously greater with the COX-2 drugs than for other NSAIDs. The average increase in risk for NSAIDs was approximately 12%.

DrRich Comments:

It is becoming difficult to ignore the evidence that NSAIDs as a class - and not just the COX-2 subgroup - increase the risk of heart attacks. This fact should now be taken into account when doctors prescribe these drugs, and when patients purchase them over the counter. However, this fact should not produce panic or unreasonable concern.

So far, there is no evidence that any of the NSAIDs causeheart attacks in otherwise normal hearts. More likely, these drugs act by increasing the stickiness of platelets, so that in patients who have pre-existing coronary artery plaques that rupture, the platelets are somewhat more likely to occlude the artery in patients on NSAIDs than in patients not on NSAIDS. However, in patients who have plaques waiting to rupture, a heart attack is reasonably likely whether they are taking NSAIDs or not. Statistically, the risk is somewhat increased on NSAIDs. We must remember, however, that fundamentally the risk of heart attack is determined by the sum of many things - age, weight, exercise levels, blood pressure, lipid levels, diabetes, and smoking. The use of NSAIDs, apparently, tweaks that risk somewhat.

Since NSAIDs produce much good, removing them from the market would obviously be a mistake. (Indeed, if it is true that the COX-2 inhibitors are no riskier than other NSAIDs, even they should remain on the market.) Instead, patients who have a pain-producing condition or an inflammatory disease like arthritis need to take this new information into account when estimating the risk vs. benefit of taking NSAIDs.

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