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Cholesterol Particle May Encourage Heart Attacks By Promoting Clots

May 24, 1989

NEW YORK (AP) _ A cholesterol-carrying particle in the blood that appears to promote heart attacks may do so by hampering the body’s ability to destroy clots, two new studies suggest.

Clots trigger heart attacks by plugging narrowed arteries, and one researcher said clots may encourage the narrowing of the arteries in the first place.

The new studies of the particle, called lipoprotein (a), appear in Thursday’s issue of the British journal Nature.

Lipoprotein (a) resembles the better-known low-density lipoprotein, the so- called ″bad cholesterol″ that contributes to atherosclerosis, the buildup of material on artery walls. The buildup narrows the vessels and sets the stage for heart attacks.

Lipoprotein (a) is also associated with atherosclerosis and heart attacks, scientists from the Research Institute of Scripps Clinic in La Jolla, Calif., and the University of Chicago noted in their Nature paper.

They followed up on the earlier discovery that one component of the lipoprotein (a) particle strongly resembles a blood protein called plasminogen.

Plasminogen plays a key role in the destruction of blood clots, once it binds to other proteins called receptors. The receptors appear on blood cells and the lining of blood vessels.

Researchers found that in the test tube, lipoprotein (a) also bound to those receptors, interfering with the plasminogen binding. So in the body, that interference may hamper the destruction of clots, they suggested.

The same result was reported in the second Nature paper, by scientists from Cornell University Medical College and Rockefeller University in New York. They also found evidence of lipoprotein (a) accumulations in the atherosclerotic build-up in blood vessels. Katherine Hajjar, study co- author from Cornell, said in an interview that some scientists suspect that repeated clot formation may predispose a blood vessel to atherosclerosis. So high levels of lipoprotein (a) may encourage atherosclerosis by hampering a vessel’s ability to fight clot formation, she said.

The test-tube results make it logical to suspect that lipoprotein (a) may hamper clot destruction in humans, said John Albers of the University of Washington School of Medicine.

For more evidence, scientists should follow people with different levels of lipoprotein (a) to see if they show different rates of clot-induced heart attacks and strokes, he said.

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