Influence of Serotonin Transporter Gene Polymorphism on Depressive Symptoms and Future Cardiac Events After Acute Myocardial Infarction

Accession number;05A0202012
Title;Influence of Serotonin Transporter Gene Polymorphism on Depressive Symptoms and Future Cardiac Events After Acute Myocardial Infarction
Author; NAKATANI DAISAKU (Osakadai Daigakuin'igakukeikenkyuka Byotaijohonaikagaku) SATO HIROSHI (Osakadai Daigakuin'igakukeikenkyuka Byotaijohonaikagaku) SAKATA YASUHIKO (Osakadai Daigakuin'igakukeikenkyuka Byotaijohonaikagaku) SHIOTANI ISSEI (Osakadai Daigakuin'igakukeikenkyuka Byotaijohonaikagaku) KINJO KUNIHIRO (Osakadai Daigakuin'igakukeikenkyuka Byotaijohonaikagaku) MIZUNO HIROYA (Osakadai Daigakuin'igakukeikenkyuka Byotaijohonaikagaku) ITO HIROSHI (Div. Cardiology Sakurabashi Watanabe Hospital, JPN) KORETSUNE YUKIHIRO (Kokuritsubyoinkiko Osakairyose) HIRAYAMA ATSUSHI (Osakakeisatsubyoin)
Journal Title;J Cardiol
Journal Code:Y0264A
ISSN:0914-5087
VOL.45;NO.2;PAGE.92-93(2005)
Figure&Table&Reference;
Pub. Country;Japan
Language;Japanese
Abstract;Objectives. We sought to determine impacts of the serotonin transporter gene-linked polymorphic region (5-HTTLPR)on depressive symptoms and future cardiac events in patients with acute myocardial infarction. Background. Depressive symptoms are associated with an increased risk of cardiac events after acute myocardial infarction. Although it is known that the S allele of 5-HTTLPR reduces transcription and therefore serotonin reuptake, and is linked with psychiatric disease, the influence of the S allele of 5-HTTLPR on depressive symptoms or future cardiac events after acute myocardial infarction is unclear. Methods. We prospectively examined depressive symptoms and new cardiac events in 1,501 genotyped patients after acute myocardial infarction. Results. Depressive symptoms were more frequent in patients with than without the S allele (48.6% vs 30.0%, p=0.01). Multivariate analysis revealed that the S allele was independently associated with depressive symptoms (odds ratio 2.34, 95% confidence interval 1.17-4.66, p=0.02). Cardiac events (cardiac death, revascularization, heart failure, reinfarction, arrhythmia, or unstable angina) were more frequent in patients with than without the S allele (26.3% vs 12.7%, p=0.03). The unadjusted hazard ratio of S allele for cardiac events was 2.15 (95% confidence interval 1.07-4.33, p=0.03). After adjustment for depressive symptoms, the hazard ratio was smaller and the association was not significant (hazard ratio 1.98, 95% confidence interval 0.92-4.26, p=0.08), suggesting that depressive symptoms interacted as a confounder. After full adjustment, the hazard ratio was unchanged and the association was not significant (hazard ratio 1.80, 95% confidence interval 0.79-4.10, p=0.16). Conclusions.... (author abst.)