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Atherosclerosis. 2000 May;150(1):143-8.

T102C polymorphism of the serotonin (5-HT) 2A receptor gene in patients with non-fatal acute myocardial infarction.

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  • 1The First Department of Internal Medicine, Kobe University School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, Japan.


Serotonin (5-HT), released from activated platelets, has been implicated in the pathogenesis of acute myocardial infarction (AMI). 5-HT induces platelet aggregation and vascular contraction through 5-HT2A receptor activation at sites of coronary atherosclerosis, leading to thrombus formation. Recently, a 5-HT2A receptor gene T102C polymorphism has been reported to be associated with clinical response to 5-HT2A receptor antagonist in patients with schizophrenia, suggesting this polymorphism of the gene affects the 5-HT2A receptor function. To investigate the relationship between the T102C polymorphism and AMI, we conducted a case-control study of 255 non-fatal AMI patients and 255 control subjects. Among the patients, the prevalence of TT genotype was significantly higher than in controls (32.5 vs. 24.3%; P<0.05). In male patients (n=216), the prevalence was much higher than in control subjects (33.8 vs. 24. 1%, P<0.03). In multiple logistic regression models, odds ratio of TT genotype was 1.45 (95% CI 0.96-2.20) in all and 1.61 (95% CI 1. 03-2.53) (P<0.05) in males. The association of T102C polymorphism of the 5-HT2A receptor gene with non-fatal AMI was statistically significant and independent of other risk factors in males. The TT genotype of the 5-HT2A receptor gene may enhance susceptibility to AMI. Our observations suggest that the T102C polymorphism of the 5-HT2A receptor gene can serve as a new genetic marker for AMI.

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