EMBARGOED FOR RELEASE UNTIL 8 P.M. EST, MARCH 13, 2000
Jill Bloom
410-601-5025
[email protected]
MARCH 13, 2000
ANTI-DEPRESSANTS MAY BENEFIT DEPRESSED PATIENTS
WITH ISCHEMIC HEART DISEASE BY INHIBITING PLATELETS
Preliminary results of a laboratory study, conducted by researchers at the Center for Thrombosis Research at Sinai Hospital in Baltimore and Duke University, indicate that anti-depressants may be beneficial in patients with ischemic heart disease by having a previously undiscovered inhibitory effect on platelets. The study will be presented at the American College of Cardiology Meetings in Anaheim, California on Monday, March 13, 2000.
"Patients who become depressed after a myocardial infarction just don't do as well as non-depressed patients," said Paul A. Gurbel, M.D., executive director of the Sinai Center for Thrombosis Research and co-investigator of the study. "They experience a threefold increase of subsequent death and an increased risk of recurrent infarction." The underlying reasons for these increased risks remain unclear.
Recurrent coronary events and death are caused by the formation of clots in the blood vessels in the heart. The major determinant of clot formation is platelets. These components, found in blood, stick together when they are active, causing clots to form.
In an effort to understand the potential benefits of anti-depressants for these patients, investigators at the Sinai Center for Thrombosis Research took blood voluntarily donated by patients and healthy people, and mixed it with the antidepressant sertraline (trade name Zoloft) or its neurologically inert metabolite, N-desmethylsertraline. The results were that the platelets became less sticky. Both of these agents appeared to prevent clots from forming, thus potentially reducing the chance of a second heart attack or subsequent stroke.
"The potential explanation for adverse events in depressed patients following myocardial infarction, may be the platelet," said Gurbel. "We have learned a great deal about the role of platelets in heart attack the last several years, and this may be a very important piece of the large puzzle."
"The anti-platelet properties of setraline is on an order similar in strength to a super aspirin in our studies," said Victor L. Serebruany, M.D., Ph.D., co-investigator and research director of the Sinai Center for Thrombosis. "Here we have a drug that treats depression, is extremely safe, and has antiplatelet effects that no one else has looked at before." Serebruany says the most exciting discovery is that the neurologically inactive metabolite also has important anti-platelet effects. " Thus we also have a new anti-platelet agent without the potential neurologic effects of the parent drug."
Sertraline is believed to work in depression by selectively inhibiting the reuptake of an important biochemical, serotonin. By increasing the levels of this important neurotransmitter in the brain, depression is thereby relieved.
In addition to this laboratory investigation, the final results of a large, worldwide, clinical study of sertraline, conducted under the direction of Christopher M. O'Conner, M.D., also a co-investigator of this laboratory investigation and a cardiologist at Duke University, will be released later this year. The Sinai Center for Thrombosis Research served as the core platelet laboratory for the soon-to-be released worldwide clinical study.
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