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Association of Elevated Homocysteine Levels With a Higher Risk of Recurrent Coronary Events and Mortality in Patients With Acute Myocardial Infarction
Shlomi Matetzky, MD;
Dov Freimark, MD;
Sela Ben-Ami, PhD;
Ilan Goldenberg, MD;
Jonathan Leor, MD;
Ram Doolman, MSc;
Ilya Novikov, PhD;
Michael Eldar, MD;
Hanoch Hod, MD
Arch Intern Med. 2003;163:1933-1937.
Background Despite the prothrombotic and proinflammatory effects associated with elevated homocysteine levels, only limited data exist regarding the effect of homocysteine levels on outcome of patients with acute myocardial infarction.
Methods Homocysteine levels were determined within 24 hours of presentation in 157 consecutive patients with acute myocardial infarction. Patients were allocated to 2 groups: those with homocysteine levels of 2.7 mg/L (20 µmol/L) or more (n = 22 [14%]) and those with homocysteine levels of less than 2.7 mg/L (n = 135 [86%]).
Results Female and diabetic patients had significantly lower homocysteine levels than males (P<.01) and nondiabetic patients (P = .005), respectively, with no significant correlation with age (r = 0.07, P = .42) or other risk factors. Patients with homocysteine levels greater than or equal to 2.7 mg/L and less than 2.7 mg/L did not differ significantly regarding extent of coronary artery disease as reflected by prevalence of multivessel disease (54% vs 61%; P = .87), and their in-hospital course. However, in a mean ±SD follow-up of 30 ± 10 months, patients with homocysteine levels greater than or equal to 2.7 mg/L had a higher incidence of recurrent coronary events (36% vs 17%; P = .04) and death (18% vs 5%; P<.05). Homocysteine levels greater than or equal to 2.7 mg/L remain a significant determinant of recurrent coronary event and/or death after controlling for potential cofounders by multivariate analysis (odds ratio, 3.8; 95% confidence interval, 1.3-11.0).
Conclusions In patients with acute myocardial infarction, elevated homocysteine levels are associated with a higher risk of recurrent coronary events and death, independent of other risk factors and the extent of coronary artery disease.
From the Heart Institute, Sheba Medical Center, Tel Hashomer, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel (Drs Matetzky, Freimark, Goldenberg, Leor, Novikov, Eldar, and Hod); and Institute of Chemical Pathology, Sheba Medical Center, Tel Hashomer, Israel (Dr Ben-Ami and Mr Doolman). The authors have no relevant financial interest in this article.
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