Background: Fasting hyperhomocysteinemia is positively associated with atherothrombosis and acute myocardial infarction in several prospective and retrospective studies. In India folic acid deficiency is not uncommon, and subclinical folic acid deficiency is known to cause hyperhomocysteinemia without thrombocytopenia.
Objective: To observe the prevalence of plasma hyperhomocysteinemia in a cohort of patients with acute myocardial infarction after 2 weeks of oral folic acid therapy.
Material and methods: A cohort of 120 consecutive patients with acute myocardial infarction below the age of 40 years was tested for fasting hyperhomocysteinemia 8-10 weeks after AMI. Five hundred age and sex matched unrelated controls and 50 family controls were also studied for two mutations, MTHFR C677T and cystathionine Beta synthase (CBS) T833C mutations Parents of the AMI patients were also tested to see hyperhomocysteinemia in the family. The patients were given two weeks of oral folic acid therapy (folviteR - 5mg once daily) and fasting plasma homocysteine levels were measured again and the pattern of response was noted. Patients who responded partially or not responded at all to oral folic acid therapy received intramuscular injection of 1 mg of cyanoco-balamin ( NeurobionR,) and their level of plasma homocysteine were noted 1 week later.
Results: Sixty three out of 120 patients showed hyperhomocysteinemia compared to 9% of the age and sex matched controls. Fifty seven therapy percent of hyperhomocysteinemia patients responded completely to oral folvite. Subsequent vitamin B12 & B6 therapy normalized homocysteine levels in only 2/12 partial responders with less than 50 microg/l of plasma homocysteine levels, but none of the folate non responders and partial responders having plasma homocysteine levels above 50 microgm/l responded to the therapy.
Conclusion: Hyperhomocysteinemia is common amongst young acute myocardial infarction patients from western India. The major cause of hyperhomocysteinemia in young myocardial infarction cases is folic acid deficiency. However a fair number of patients who did not respond to folic acid, also did not respond to vitamin B12 and B6 parenterally suggesting existence of defect in other pathways of homocysteine metabolism in a subset of our patients.