Purpose: the pathogenetic mechanism of acute myocardial infarction (AMI) in young patients remains unknown. We explored the impact of homocysteine and its main genetic modulator
Table 2
methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism in patients who sustained AMI under the age of 36 years.
Methods: we recruited 136 consecutive patients who had survived their first AMI before the age of 36 years (mean age=32 ± 3.1 years, range 23–35 years, 121 men). Blood was taken for lipids and homocysteine levels within 12 hours from admission. The MTHFR C677T polymorphism was also determined with polymerase chain reaction. All patients underwent cardiac catheterization. One hundred-three healthy individuals without a family history of coronary heart disease (CHD), matched for age and sex served as controls.
Results: coronary angiogram revealed significant CHD in 104 patients while 32 (23.5%) had no significant CHD. The prevalence of homozygotes for C677T polymorphism [T/T genotype] was 27.2% in patients and 14.6% in controls (p=0.02). In the subgroup of patients who had AMI and “normal” coronary arteries the frequency of homozygotes was 43.8% (p=0.001 versus controls and p=0.02 versus patients with significant CHD). The table presents lipids and homocysteine levels in AMI patients with “normal” coronary arteries and controls. Logistic regression model showed that the odds ratio for a young individual with T/T genotype to develop AMI with “normal” coronary arteries was 5.2 (confidence interval 1.2–23, p=0.03) adjusted for smoking habits, body mass index, hypertension and diabetes mellitus.
Conclusions: the presence of homozygocity for MTHFR C677T polymorphism is associated with 5-fold higher risk for premature AMI with “normal” coronary arteries. This suggests that homocysteine may be involved in the formation of an obstructive thrombus in coronary arteries, especially in young individuals without significant underlying atheromatic burden.
eNOS Gene Variants and the Risk of Premature Myocardial Infarction
