title: Plasma homocysteine in acute myocardial infarction: homocysteine-lowering effect of folic acid.
abstract: OBJECTIVE
  Moderate hyperhomocysteinaemia is an independent risk factor for cardiovascular disease which may be causal. We investigated whether the concentration of plasma homocysteine changes between the acute phase of myocardial infarction and follow-up, and whether treatment with oral folic acid was effective in lowering homocysteine levels in patients with myocardial infarction.
  
  
  METHODS
  Plasma total homocysteine levels 24-36 h (baseline) after onset of acute myocardial infarction were compared with the levels obtained at 6 weeks' follow-up and with the levels in the controls. In the same patients, we studied the effect on plasma homocysteine of 6 weeks' treatment with daily oral folic acid doses of 2.5 or 10 mg compared to no treatment.
  
  
  RESULTS
  At baseline, 12 of 68 patients (18%) had moderate hyperhomocysteinaemia (> 17.3 mumol L-1; P < 0.05). Between baseline and follow-up, plasma homocysteine levels increased from 13.1 +/- 4.6 to 14.8 +/- 4.8 mumol L-1 (mean +/- SD; P < 0.001). Treatment with nitroglycerin, streptokinase, beta blockers, or acetylsalicylic acid seemed not to have caused this change. Folic acid lowered plasma homocysteine in all but two of 33 treated patients with a mean decrease of 4.4 mumol L-1 (-27%; P < 0.001). There was no difference between the effect of 2.5 and 10 mg of folic acid. In the untreated group (n = 20), plasma homocysteine increased with a mean increase of 0.6 mumol L-1 (+4%; P < 0.05).
  
  
  CONCLUSIONS
  Plasma homocysteine seems to increase in the post myocardial infarction period, the cause of which warrants further study. Folic acid appears to be an effective treatment for the reduction of both normal and increased plasma homocysteine concentrations in patients with myocardial infarction. This suggests that folic acid should be used for intervention when studying the effect of homocysteine-lowering therapy on the risk on myocardial infarction.
authors.affiliation: Department of Medicine, County Hospital, Kalmar, Sweden.
authors.forename: F
authors.initials: F
authors.lastname: Landgren
authors.forename: B
authors.initials: B
authors.lastname: Israelsson
authors.forename: A
authors.initials: A
authors.lastname: Lindgren
authors.forename: B
authors.initials: B
authors.lastname: Hultberg
authors.forename: A
authors.initials: A
authors.lastname: Andersson
authors.forename: L
authors.initials: L
authors.lastname: Brattström
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D005492:Folic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D006710:Homocysteine / Q000097:blood* / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy*; D016896:Treatment Outcome
chemical_list: D006710:Homocysteine; D005492:Folic Acid