People with specific variations of the cyclooxygenase-2 gene have an associated lower risk for myocardial infarction and ischemic stroke, according to an article in the May 12th issue of the Journal of the American Medical Association.

Although myocardial infarction and thrombotic ischemic stroke are thought to be caused by rupture of vulnerable atherosclerotic plaques, they are recognized as complex disorders that probably result from interactions between genetic makeup and environmental factors, according to information in the article. The relation between variations in the cyclooxygenase-2 (COX-2) gene and the risk of myocardial infarction and ischemic stroke has not been clear.

Francesco Cipollone, MD, and his Italian colleagues conducted a study to determine if there was a relationship between a specific variation in the COX-2 gene (-765GC polymorphism) and clinically evident plaque rupture. The study was conducted between March 2002 and October 2003 among 864 patients with first myocardial infarction or atherothrombotic ischemic stroke and 864 hospitalized controls. The groups were matched for age, sex, body mass index, smoking, hypertension, hypercholesterolemia, and diabetes.

The prevalence of the specific genetic variation (-765GC) was 2.41 times higher among the controls than among the myocardial infarction and stroke patients. The prevalence of a different variation (-765CC) was 5.81 times higher among controls than among patients. Patients with the -765GC or -765CC genotype had a reduction in relative risk of myocardial infarction and ischemic stroke of 52 percent and 67 percent, respectively, after adjustment for age, sex, smoking status, body mass index, hypercholesterolemia, hypertension, and diabetes.

"We found that the -765GC polymorphism of the COX-2 gene is associated with a reduction in the risk of myocardial infarction and stroke, suggesting that this [variation] may offer protection against clinical events related to atherosclerotic plaque rupture," the authors wrote.