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    Incidents of heart attack and stroke, some fatal, in a small number of men taking the drug Viagra have remained a puzzle.
    After all, Viagra, commonly prescribed for erectile dysfunction, was originally developed to prevent these conditions -- not only by dilating blood vessels but also by stopping platelets in the blood from clumping.
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    In fact, the drug does just the opposite, according to researchers at the University of Illinois at Chicago College of Medicine.
    They found that Viagra, by elevating levels of a compound in cells called cyclic guanosine monophosphate, or cGMP, actually encourages platelets to aggregate.
    The study, to be published in the Jan.
    Cell, amends 20 years of scientific claims that cGMP acts to prevent platelet aggregation.
    While platelet aggregation helps minimize the loss of blood when injury occurs, it can also lead to clotting that blocks a blood vessel -- a life-threatening condition called thrombosis that can cause heart attack and stroke.

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    Du said he and his coworkers had not set out to investigate the cause of fatalities in Viagra patients when they began their research about five years ago.
    Rather, as a basic research scientist, he was hoping to illuminate the highly complex series of molecular steps that control platelet aggregation.
    Platelets are disk-shaped cells that freely circulate in the blood.
    When a blood vessel is injured, the platelets form sticky surfaces, adhering to one another and to the damaged area to plug the hole.
    Using recombinant DNA techniques, the researchers forced standard laboratory cells to manufacture two proteins key to platelet aggregation: one that helps the platelets clump together and stick to the surface of broken blood vessels, and another that activates the first.

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