Homocysteine is a bystander for ST-segment elevation myocardial infarction: A case-control study
Journal
BMC Cardiovascular Disorders
Journal Volume
18
Journal Issue
1
Date Issued
2018
Author(s)
Abstract
Background: Homocysteine 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. Methods: We 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. Results: Patients 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±1.9μmol/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±2.3mg/L, p=0.032), peak creatine kinase (3796±2163 vs. 2305±1822IU/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 100μmol/L did not reduce the cell viability of human coronary artery endothelial cells. Conclusions: Homocysteine 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. ? 2018 The Author(s).
SDGs
Other Subjects
C reactive protein; creatine kinase; homocysteine; biological marker; homocysteine; adult; amino acid blood level; Article; case control study; cell viability; controlled study; coronary artery endothelial cell; coronary artery occlusion; creatine kinase blood level; disease association; disease severity; endothelium cell; female; human; human cell; leukocyte count; major clinical study; male; middle aged; percutaneous coronary intervention; priority journal; prospective study; ST segment elevation myocardial infarction; SYNTAX score; Taiwan; thorax pain; vascular patency; aged; blood; cell culture; cell survival; coronary blood vessel; drug effect; pathology; ST segment elevation myocardial infarction; Aged; Biomarkers; Case-Control Studies; Cell Survival; Cells, Cultured; Coronary Vessels; Endothelial Cells; Female; Homocysteine; Humans; Male; Middle Aged; Prospective Studies; ST Elevation Myocardial Infarction; Taiwan
Publisher
BioMed Central Ltd.
Type
journal article