Abstract
BackgroundHomocysteine has been long considered a risk factor for atherosclerosis. However, cardiovascular events cannot be reduced through homocysteine lowering by B vitamin supplements. Although several association studies have reported an elevation of serum homocysteine levels in cardiovascular diseases, the relationship of homocysteine with ST-segment elevation myocardial infarction (STEMI) is not well established.MethodsWe prospectively enrolled STEMI patients who were consecutively admitted to an intensive care unit following coronary intervention in a single medical center in Taiwan. Control subjects were individuals who presented to the outpatient or emergency department with acute chest pain but subsequently revealed patent coronary arteries by coronary arteriography. The association between serum homocysteine levels and STEMI was investigated. A culture system using human coronary artery endothelial cells was also established to examine the toxic effects of homocysteine at the cellular level.ResultsPatients with chest pain were divided into two groups. The STEMI group included 56 patients who underwent a primary percutaneous coronary intervention. The control group included 17 subjects with patent coronary arteries. There was no difference in serum homocysteine levels (8.4 ± 2.2 vs. 7.6 ± 1.9 μmol/L, p = 0.142). When stratifying STEMI patients by the Killip classification into higher (Killip III-IV) and lower (Killip I-II) grades, CRP (3.3 ± 4.1 vs. 1.4 ± 2.3 mg/L, p = 0.032), peak creatine kinase (3796 ± 2163 vs. 2305 ± 1822 IU/L, p = 0.023), and SYNTAX scores (20.4 ± 11.1 vs. 14.8 ± 7.6, p = 0.033) were significantly higher in the higher grades, while serum homocysteine levels were similar. Homocysteine was not correlated with WBCs, CRP, or the SYNTAX score in STEMI patients. In a culture system, homocysteine at even a supraphysiological level of 100 μmol/L did not reduce the cell viability of human coronary artery endothelial cells.ConclusionsHomocysteine was not elevated in STEMI patients regardless of Killip severity, suggesting that homocysteine is a bystander instead of a causative factor of STEMI. Our study therefore supports the current notion that homocysteine-lowering strategies are not essential in preventing cardiovascular disease.
Highlights
Homocysteine has been long considered a risk factor for atherosclerosis
The serum level of homocysteine is significantly elevated in areas with dietary folate and B vitamin deficiencies as well as in subjects with the MTHFR 677 TT genotype [2], which can be lowered by B vitamins, including folic acid, B6, and B12
When serum homocysteine levels were compared to various factors, we found that there was no correlation with White blood cell (WBC), C-reactive protein (CRP), or the SYNTAX score (Fig. 1a-c)
Summary
Homocysteine has been long considered a risk factor for atherosclerosis. cardiovascular events cannot be reduced through homocysteine lowering by B vitamin supplements. Several association studies have reported an elevation of serum homocysteine levels in cardiovascular diseases, the relationship of homocysteine with ST-segment elevation myocardial infarction (STEMI) is not well established. Serum levels were correlated with long-term outcomes in patients with documented coronary artery disease (CAD) or acute coronary syndrome [11, 12]. Recent studies disclosed that even though serum homocysteine levels were reduced by B vitamins in patients with stable CAD, acute coronary syndrome, or stroke, the rate of major adverse cardiac events was not reduced [13,14,15,16,17]. There was no difference in early and late cardiovascular mortality among the tertiles of serum homocysteine levels in patients with ST-segment elevation myocardial infarction (STEMI) or non-ST-segment elevation acute coronary syndrome [18]. We tried to clarify the role of homocysteine in STEMI, an extreme entity of acute coronary syndrome, by making comparisons with subjects presenting with chest pain but proven to have patent or non-significant coronary arteries
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