SSRIs but not TCAs are known to reduce the “stickiness” of plate

SSRIs but not TCAs are known to reduce the “stickiness” of platelets. This effect, although involving mechanisms somewhat distinct from those of aspirin, could result in n reduction in the risk of MI similar to that provided by aspirin.32,33 This does not, however, imply that the same mechanism involved in the prevention of MI in patients with no Inhibitors,research,lifescience,medical prior history of cardiac disease would be responsible for the reduction in mortality in patients given an SSRI following an MI, as suggested by the data from SADHART and ENRICHD. These post-MI patients, unlike the depressed patients with no known prior history of cardiac disease, will already be receiving

multiple antiplatelet drugs, and it is unlikely that the addition of another

antiplatelet compound would have a dramatic impact on mortality. Another interesting observation from Cohen’s study in hospital workers is related Inhibitors,research,lifescience,medical to the risk of developing heart disease among patients suffering depression.26 He observed that the 1653 workers who filled prescriptions for TCAs (and were presumably depressed) were more than 100% Inhibitors,research,lifescience,medical more likely to have an MI than those 55 000 individuals who were not taking TCAs. This compares with the Wulsin ten-study meta-analysis2 where depressed individuals had essentially a 65% increase in the risk of developing Selleckchem SCR7 coronary disease. Although the studies are not absolutely comparable, the major difference is that all of the studies in the Wulsin analysis controlled for

smoking as well as other cardiac risk factors, while Cohen had no data on, and could not control for, such risk factors. Both studies were based on large Inhibitors,research,lifescience,medical samples and, although this is not an ideal way to approach the issue, they illustrate two different points of view. Inhibitors,research,lifescience,medical The epidemiologist asks whether depression makes an independent contribution to the risk of heart disease, or if it is only an apparent increase accounted for by the fact that depressed patients are more likely Dipeptidyl peptidase to smoke, and smoking causes heart disease. Wulsin’s data says that there is a 65% increase beyond that accounted for by any known risk factors. The clinician faced with a depressed patient may ask how much more likely this person is to develop coronary artery disease than a similar person without depression. For the specific patient, there exists both the independent risk associated with depression plus those cardiac risk factors known to be associated with depression such as smoking, poor health behaviors, obesity, diabetes, reduced physical activity, etc. Thus, while Wulsin’s estimate of a 65% increase in risk may be scientifically more accurate, Cohen’s estimate of more than a 100% increase is likely to be a clinically more relevant assessment of the problem.