Increase in the risk of ST elevation myocardial infarction is associated with homocysteine level.

BACKGROUND AND AIMS

The present study aimed to investigate the relationship between coagulation defects and ST elevation myocardial infarction (STEMI) in patients without any known coronary artery risk factors and considered low risk according to the Framingham risk classification.

METHODS

This study included 76 (73.6% male) STEMI patients without any known risk factors for coronary artery disease and 56 healthy controls (67.8% male) with similar characteristics.

RESULTS

Factor V Leiden mutation was noted in two patients and in one control. There were no significant differences in protein C, protein S, or antithrombin 3 values between the patient and control groups (p = 0.405, p = 0.476, and p = 0.221, respectively). None of the participants had antiphospholipid syndrome, factor V deficiency, or factor VII deficiency. Plasma homocysteine level was significantly higher in the patient group (19.0 ± 3.6) μmol/L than in the control group (15.8 ± 4.2) μmol/L (p = 0.008). Homocysteine levels in both groups were higher in males without a statistically significant difference. Vitamin B12 and folate levels, which are directly related to homocysteine metabolism, did not differ significantly between groups. Correlation analysis showed that the homocysteine level was not correlated with lipid parameters, folate, or vitamin B12.

CONCLUSION

Homocysteine level was significantly higher in acute MI in patients without any risk factors and were considered low risk according to the Framingham risk score. The findings support the hypothesis that homocysteine level may be an independent risk factor for coronary artery disease.