Washington, Jan 5 : Cholesterol-lowering drugs, statins, turns off a molecular pathway that leads to abnormal blood clotting in arteries that could cause heart attack and stroke, according to a new study.

People with high cholesterol are at risk of heart attack and stroke because atherosclerotic plaques within their arteries can rupture triggering the formation of a blood clot called an occlusive thrombus that cuts off the blood supply to their heart or brain.

For years, scientists have studied the cause of this abnormal clotting.

Now, this new study led by researchers from the University of North Carolina at Chapel Hill School of Medicine, has finnaly identified the molecular pathway that leads to this abnormal blood clotting and successfully turned it off using simvastatin, a popular class of statins.

The research was performed using humans, monkeys and mice with highly elevated blood lipid levels. It indicated that elevated levels of oxidized low density lipoprotein (LDL) induces a molecule called "tissue factor" that triggers clotting.

"Statins have been shown to have antithrombotic activity in several previous studies. However, I believe our study is the first to elucidate how statins reduce the activation of the blood clotting process independently of their lipid lowering activity," said senior study author Nigel Mackman, PhD, FAHA.

Additionally, Mackman noted that statins "only target the `bad and inducible tissue factor', not the good one used in normal clotting, and therefore should not be associated with the increased bleeding risk that is a typical side effect of anticoagulant drugs currently on the market."

Mackman and his colleagues analysed humans, monkeys and mice with high cholesterol. They found that all three groups have elevated levels of tissue factor in the circulation. Then the researchers treated the mice and monkeys with simvastatin, a drug widely used to treat high blood cholesterol levels.

They found that simvastatin reduced levels of oxidized low-density lipoprotein and circulating tissue factor, which normalized coagulation without altering plasma cholesterol levels.

These results suggest that oxidized low-density lipoproteins induce tissue factor expression on monocytes and this contributes to formation of an occlusive thrombus after plaque rupture.

"Though statin therapy is primarily prescribed to lower cholesterol, some added benefits are its anti-inflammatory and antithrombotic activities," said Mackman.

The study appeared online in the January 3, 2012 issue of the Journal of Clinical Investigation. (ANI)