F. Landgren et al., PLASMA HOMOCYSTEINE IN ACUTE MYOCARDIAL-INFARCTION - HOMOCYSTEINE-LOWERING EFFECT OF FOLIC-ACID, Journal of internal medicine, 237(4), 1995, pp. 381-388
Objectives. Moderate hyperhomocysteinaemia is an independent risk fact
or for cardiovascular disease which may be causal. We investigated whe
ther the concentration of plasma homocysteine changes between the acut
e 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, Design and subjects. Plasma total
homocysteine levels 24-36 h (baseline) after onset of acute myocardia
l infarction were compared with the levels obtained at 6 weeks' follow
-up and with the levels in the controls. In the same patients, we stud
ied 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. Resul
ts. At baseline, 12 of 68 patients (18%) had moderate hyperhomocystein
aemia (>17.3 mu mol L(-1); P < 0.05), Between baseline and follow-up,
plasma homocysteine levels increased from 13.1 +/- 4.6 to 14.8 +/- 4.8
mu mol L(-1) (mean +/- SD; P < 0.001). Treatment with nitroglycerin,
streptokinase, beta blockers, or acetylsalicylic acid seemed not to ha
ve caused this change. Folic acid lowered plasma homocysteine in all b
ut two of 33 treated patients with a mean decrease of 4.4 mu mol 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 homoc
ysteine increased with a mean increase of 0.6 mu mol L(-1) (+4%; P < 0
.05). Conclusions. Plasma homocysteine seems to increase in the post m
yocardial 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 patie
nts with myocardial infarction. This suggests that folic acid should b
e used for intervention when studying the effect of homocysteine-lower
ing therapy on the risk on myocardial infarction.