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Heart Center at Sinai Conducts Landmark Study on Aspirin Resistance

With coronary artery disease the single leading cause of death in the western world, aspirin is used by millions of patients as a prevention and treatment regiment for this deadly disease.// In the largest study to date on the effectiveness of aspirin, researchers at Sinai Hospital of Baltimore recently demonstrated that aspirin resistance is rare, less than 5 percent, at all doses (81 mg, 162 mg and 325 mg) in patients with heart disease.

Most coronary artery disease deaths are caused by platelets sticking together and forming blood clots (thrombosis) that block blood flow within arteries, resulting in a heart attack. By inhibiting clotting, aspirin keeps platelets from sticking together by specifically blocking an important enzyme, COX-1.

“The occurrence of clotting in patients taking aspirin therapy has been attributed to the failure of aspirin blocking its target and is a hot topic in cardiovascular disease today,” said Paul Gurbel, MD, lead investigator for the study and the Helen Dalsheimer director of the Division of Cardiology and director of the Center for Thrombosis Research at Sinai Hospital of Baltimore. “However, our data suggest that aspirin blocks COX-1 with high efficiency.”

The team at the Center for Thrombosis Research at Sinai Hospital studied 120 patients with a history of coronary artery disease treated with aspirin. All patients were randomly placed on 81 mg, 162 mg and 325 mg of aspirin daily for four weeks each for a total of 12 weeks. Then the response to aspirin was tested by multitude methods. When measuring the ability of aspirin to block its target, COX-1, it was found highly effective at all dose levels.

“The research also shows that aspirin may be effective at blocking other pathways that promote platelet activation, independent of COX-1. Further research is now under way to better understand these additional pathways that may cause clotting in patients in an effort to continue to improve patient outcomes,” said Gurbel.


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