Platelets are tiny, cell-like components in the blood that aggregate to form clots. They’re indispensable for closing wounds, but after injury caused by atherosclerosis in an artery, their automatic response can clog the vessel.
Scientists now report that people with platelets that tend to stick together are more likely to suffer complications from a common heart procedure than are those with less sticky platelets. In another study, researchers reveal that a genetic trait induces some people to make sticky platelets. The studies, which appear in the July 10 Circulation, could change how physicians treat people for heart disease.
In the first study, researchers tested how readily platelets aggregated in blood from 112 heart patients and compared the results with the patients’ symptoms after a surgical procedure. The scientists first measured platelet reactions to adenosine diphosphate, a compound that abets platelet clumping. Then, they divided the group into the half with the more sticky, or reactive, platelets and the half with less reactive ones.
All the study volunteers underwent angioplasty, in which a balloon-tipped catheter opens a blocked coronary artery.
Three months after the procedure, 15 of the patients with sticky platelets had experienced complications such as chest pain or a heart attack. Only 4 of the patients with less-reactive platelets had such complications. During these first 3 months, 10 people with sticky platelets needed another angioplasty, compared with only 2 in the other group, says study coauthor Samer S. Kabbani, a cardiologist at the University of Vermont and Fletcher Allen Health Care in Burlington.
People undergoing angioplasty take aspirin indefinitely and usually get other anticlotting drugs for a month or more. Using the platelet-reactivity test, “we can basically predict which people are going to have complications” and adjust medication accordingly, Kabbani says.
In the second study, researchers investigated the effect of genetic variations in a molecule on platelets that acts as a docking device. When a protein called fibrinogen docks, it links platelets together and gets converted into a protein called fibrin, which can form a blood clot.
Scientists have probed the docking device, a glycoprotein dubbed GPIIb/IIIa, for weaknesses that might be exploited to counter clotting and thus prevent heart attack and stroke. In the new study, blood samples from 1,340 people revealed that 72 percent had inherited from both parents a gene for a version of GPIIb/IIIa called PlA1, while 28 percent had inherited one or two copies of a gene encoding a version called PlA2.
The researchers mixed the blood samples with epinephrine, which catalyzes clotting. The blood from the group with two copies of PlA1 clotted less readily than the other blood did, says study coauthor James E. Muller, a cardiologist at Massachusetts General Hospital and Harvard Medical School in Boston.
The clotting also depended on fibrinogen concentrations in the blood, which vary among people. In patients with unusually high fibrinogen, PlA1 glycoprotein seemed to make their blood clot more readily than PlA2 did, Muller says. This contrasts with the overall finding.
Testing for platelet stickiness and a patient’s GPIIb/IIIa status could determine which people need anticlotting drugs beyond aspirin–and for how long–after undergoing heart procedures, says Pascal J. Goldschmidt, a cardiologist at Duke University in Durham, N.C.