Antidepressants Benefit Heart Health?

Reported April 28, 2010

(Ivanhoe Newswire) -- A class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs) may boost cardiovascular health by affecting the way platelets -- small blood cells involved in clotting -- clump together.

Researchers at the Loyola University Medical Center in Maywood, Ill. found that platelets were slower to clump together in participants who were taking an SSRI to treat depression. As depression is associated with an increased risk of cardiovascular disease, this finding could indicate a beneficial side effect for people who take SSRIs to treat depression, study author Evangelos Litinas, MD, Research Associate in the Center's Pathology Department, was quoted as saying.

Neurotransmitters, like serotonin, are messages sent across the gap between nerve cells in the brain called the synapse. The cell sending the message, called the pre-synaptic cell, releases serotonin into the synapse. Either the serotonin is taken in by the receiving, post-synaptic cell, or it can be taken back by the pre-synaptic cell.

In a depressed patient, the post-synaptic cell doesn't take in enough serotonin and the message gets lost. To treat the depression, SSRIs inhibit the ability of the pre-synaptic cell to reuptake the serotonin, leaving the message in the synapse longer and giving the post-synaptic cell a better chance of receiving the serotonin.

This blocking activity of SSRIs may have an effect on other cells in the body that require serotonin uptake. Platelets, which are involved in blood clotting, absorb serotonin only once and use it to activate in response to injury. This kind of platelet activation also occurs when blood vessel walls become inflamed in atherosclerosis or "hardening of the arteries."

Once activated, the platelets release the contents of small packages that they carry called delta granules. These packages contain various molecules, including serotonin. When the delta granules are released by activated platelets, the serotonin works to amplify the coagulation response.

Dr. Litinas and his team believe that in depressed patients who have an associated risk of cardiovascular problems, the blocking activity of SSRIs may have the side-effect of preventing the serotonin uptake by platelets, making them less responsive to aggregation and thereby improving the patients' cardiovascular health.

The researchers recruited 50 volunteers, 25 who were not taking antidepressant medications and 25 who were being treated for depression with an SSRI. The team collected blood samples from each volunteer at the beginning of the protocol and again at the study's fourth week and eighth week.

When the platelets from healthy volunteers were treated with platelet-activating substances at the 4-week time point, 95 percent of the cells aggregated. In contrast, the platelets of participants taking an SSRI showed only 37 percent aggregation, indicating that the SSRI had inhibited or changed the platelets' ability to clump together.

As the study progressed, the researchers noticed that platelets taken from SSRI-treated patients at the 8-week mark aggregated more than those drawn at the 4-week mark, suggesting that SSRIs have the greatest impact on preventing platelet activation early in treatment.

"The reason we're doing this is to better the lives of depressed patients," said Dr. Litinas. "There is clear evidence that depressed patients have a higher risk of cardiovascular disease, and we want to eliminate that. Since depression can be treated with an SSRI, maybe the cardiovascular disease risk can also be decreased. We want our patients to live longer and happier lives, without depression or the risk of heart problems."

SOURCE: Presented at the American Physiological Society's annual Experimental Biology conference, Anaheim, CA, April 24-28, 2010.