Melatonin is a circadian hormone with antioxidant properties that protects against myocardial ischemia-reperfusion injury. Genetic variations of the melatonin receptor 1B gene (MTNR1B) play an important role in the development of type 2 diabetes, a risk factor for cardiovascular diseases. Accordingly, MTNR1B polymorphisms are crucial in numerous disorders of the cardiovascular system. Therefore, the aim of the present study was to investigate a possible association of MTNR1B polymorphisms with chronotype and susceptibility to myocardial infarction. The present case-control study included 199 patients with myocardial infarction (MI) (57% men) and 198 control participants (52% men) without previous cardiovascular diseases who underwent genotyping for the MTNR1B polymorphisms rs10830963, rs1387153, and rs4753426 from peripheral blood samples. Chronotype was determined using the Morningness-Eveningness Questionnaire (MEQ). As estimated by the chi-square test, no significant association was found in the distribution of alleles and genotypes between myocardial infarction patients and controls. In addition, there was no association between MTNR1B polymorphisms and chronotype in MI patients. As some previous studies have shown, the present negative results do not exclude the role of the MTNR1B polymorphisms studied in the development of myocardial infarction. Rather, they may indicate that MTNR1B polymorphisms are a minor risk factor for myocardial infarction.

Background and Objectives: Cardiovascular diseases (CVDs) are among the leading causes of death worldwide, although CVD mortality has decreased in developed countries. Numerous pathophysiological processes lead to the development of CVDs. The circadian rhythm coordinates many physiological processes, and its disruption can lead to many pathophysiological changes. One of the significant circadian rhythm genes is the CLOCK gene, whose polymorphisms are associated with CVD risk factors. Research findings of the association between CLOCK gene polymorphism and CVDs and its comorbidities are not consistent. This meta-analysis was conducted to quantify the associations between T3111C polymorphism and the risk of CVDs. Materials and Methods: The PubMed and Scopus databases were searched for studies reporting onthe association between T3111C (rs1801260) in the circadian CLOCK gene and cardiovascular disease and its comorbidities such as obesity, hypertension, insulin resistance, and coronary artery disease. A fixed-effect model was used to calculate the pooled odds ratio and 95% confidence interval by comprehensive meta-analysis software. Results: Five independent studies, including case-control, cross-sectional, and cohort research methods, were analyzed with 3123 subjects in total. The meta-analysis revealed a significant association between T3111C polymorphism and cardiovascular disease (OR = 1.32, 95% CI: 1.16–1.50, p < 0.001) with significant heterogeneity (I² = 91.1%, p < 0.001) and no publication bias. The subgroup analysis on comorbidity related to CVDs revealed that hypertension was associated with T3111C polymorphism (OR = 2.02, 95% CI: 1.60–2.54, p < 0.001). Conclusions: Our meta-analysis based on available studies using a fixed model shows that T3111C polymorphism in the CLOCK gene is associated with CVD susceptibility.