AIM: To define a role of connexin37 (Cx37) C1019T and endothelial nitric oxide synthase (eNOS) G894T polymorphisms in the development of myocardial infarction (MI) in subjects without a history of coronary artery disease. SUBJECTS AND RESULTS: The investigation enrolled 183 male patients, of whom 56 (18.1%) developed MI in the presence of clinically and instrumentally verified coronary heart disease (CHD) (except MI) and 127 (81.9%) patients did without any previous clinical signs of CHD. The gene polymorphisms were identified using polymerase chain reaction and restriction fragment length polymorphism analysis. RESULTS: The spread of the G allele in the eNOS gene was 59.8% in the patients with MI in the presence of CHD and 75.6% in those with MI without a history of coronary artery disease (p<0.01). The GG genotype was found in 32.1 and 54.3%, respectively (p=0.01; the odds ratio (OR) was 2.5 with 95% confidence interval (CI) 1.3 to 4.9). The spread of the mutant T allele in the Cx37 gene was 29.5% in the patients with MI in the presence of CHD and 59.8% in those with MI without a history of coronary artery disease (p<0.01). The TT genotype was encountered in 7.1 and 42.5% of cases, respectively (p=0.01; OR 9.6 with 95% CI 3.3 to 28.4). There was no case of a combination of GG and TT genotypes among the patients with MI in the presence of CHD whereas this was found in 23.6% of the MI cases without a history of coronary artery disease (p<0.01). CONCLUSION: Determination of Cx37 C1019T and eNOS G894T polymorphisms may be used to detect a genetic predisposition to the development of MI in patients with hemodynamically insignificant atherosclerosis and in apparently healthy individuals.
AIM: To define a role of connexin37 (Cx37) C1019T and endothelial nitric oxide synthase (eNOS) G894T polymorphisms in the development of myocardial infarction (MI) in subjects without a history of coronary artery disease. SUBJECTS AND RESULTS: The investigation enrolled 183 male patients, of whom 56 (18.1%) developed MI in the presence of clinically and instrumentally verified coronary heart disease (CHD) (except MI) and 127 (81.9%) patients did without any previous clinical signs of CHD. The gene polymorphisms were identified using polymerase chain reaction and restriction fragment length polymorphism analysis. RESULTS: The spread of the G allele in the eNOS gene was 59.8% in the patients with MI in the presence of CHD and 75.6% in those with MI without a history of coronary artery disease (p<0.01). The GG genotype was found in 32.1 and 54.3%, respectively (p=0.01; the odds ratio (OR) was 2.5 with 95% confidence interval (CI) 1.3 to 4.9). The spread of the mutant T allele in the Cx37 gene was 29.5% in the patients with MI in the presence of CHD and 59.8% in those with MI without a history of coronary artery disease (p<0.01). The TT genotype was encountered in 7.1 and 42.5% of cases, respectively (p=0.01; OR 9.6 with 95% CI 3.3 to 28.4). There was no case of a combination of GG and TT genotypes among the patients with MI in the presence of CHD whereas this was found in 23.6% of the MI cases without a history of coronary artery disease (p<0.01). CONCLUSION: Determination of Cx37C1019T and eNOS G894T polymorphisms may be used to detect a genetic predisposition to the development of MI in patients with hemodynamically insignificant atherosclerosis and in apparently healthy individuals.