Platelet reactivity linked to outcome after percutaneous coronary intervention

המידע לקוח מתוך מדיקונטקסט
Last Updated: 2001-07-09 16:00:19 EDT (Reuters Health)

WESTPORT, CT (Reuters Health) – In patients undergoing percutaneous coronary intervention (PCI), platelet reactivity appears to be predictive of subsequent complications, according to a report in Circulation: Journal of the American Heart Association for July 10.

In addition, a separate study in the same issue of the journal found an apparent genotype-specific association between the ability of platelets to aggregate and fibrinogen levels.

"In previous studies, we found that there is a marked difference between the platelet reactivity of individuals," Dr. Samer S. Kabbani, from the University of Vermont College of Medicine in Burlington, told Reuters Health. "Some people have very sensitive platelets, which we call high platelet reactivity. Other people have low platelet reactivity; these people do not bind fibrinogen easily."

Dr. Kabbani and colleagues hypothesized that people with increased platelet reactivity might be more inclined to have complications after PCI. "If we can predict complications based on a blood test, it would be a powerful tool to determine which patients are at high risk," he said.

The researchers found that for patients with high platelet reactivity, 26.8% reached the composite endpoint of myocardial infarction, urgent revascularization, or repeat revascularization compared with 7.1% of the patients with low platelet reactivity. This difference, Dr. Kabbani's group notes, was "most striking during the 30- to 90-day interval after PCI (16.7% versus 1.9%)." They also found that repeat revascularization was more frequent among patients with high platelet activity (17.9%) than patients without high platelet activity 3.6%.

"For patients with high platelet reactivity, we should be as aggressive as we can during the first 24 hours with antiplatelet agents. Then these patients should be put on long-term antiplatelet therapy after discharge to prevent recurrent events," Dr. Kabbani advised.

In the second report, Dr. Christopher J. O'Donnell from Massachusetts General Hospital in Boston and colleagues collected data on glycoprotein IIIa P1A genotype, fibrinogen, and platelet aggregation for 1340 subjects in the Framingham Offspring Study.

"Higher fibrinogen levels were associated with increased epinephrine-induced aggregation and a trend for ADP-induced aggregation," Dr. O'Donnell's group reports.

However, the researchers note that this was a genotype-specific fibrinogen effect. Increased platelet aggregation with high fibrinogen "was present for the P1A¹/A¹ genotype but not for the P1A²-positive genotype."

Dr. O'Donnell and colleagues believe that studies are needed to examine fibrinogen levels and P1A polymorphisms and their link to cardiovascular disease.

"If individuals with the P1A² variant or P1A¹ homozygotes with high fibrinogen levels have a higher incidence of cardiovascular disease, they may benefit from more aggressive measures for prevention and treatment with antiplatelet agents such as glycoprotein IIb/IIIa receptor antagonists," Dr. O'Donnell and colleagues suggest.

Circulation 2001;104:000-000.

-Westport Newsroom 203 319 2700

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