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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
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Homocysteine is a bystander for ST-segment elevation myocardial infarction: a case-control study
Ching-Yu Julius Chen1,2, Tzu-Ching Yang3, Christopher Chang4
1Cardiovascular Center and Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, 100, Taipei, Taiwan.
BMC Cardiovascular Disorders
|February 14, 2018
Summary
Serum homocysteine levels are not elevated in patients with ST-segment elevation myocardial infarction (STEMI). This suggests homocysteine is not a cause of STEMI, and lowering it may not be essential for cardiovascular disease prevention.
Area of Science:
- Cardiology
- Biochemistry
- Vascular Biology
Background:
- Homocysteine is a suspected risk factor for atherosclerosis, but B vitamin supplements have not reduced cardiovascular events.
- The relationship between homocysteine and ST-segment elevation myocardial infarction (STEMI) remains unclear despite associations with other cardiovascular diseases.
Purpose of the Study:
- To investigate the association between serum homocysteine levels and STEMI.
- To examine the cellular effects of homocysteine on human coronary artery endothelial cells.
Main Methods:
- Prospective enrollment of STEMI patients and controls with patent coronary arteries.
- Measurement of serum homocysteine levels and correlation with clinical parameters (Killip classification, CRP, peak creatine kinase, SYNTAX score).
- In vitro culture system to assess homocysteine's toxicity on endothelial cells.
Main Results:
- No significant difference in serum homocysteine levels between STEMI patients and controls.
- Homocysteine levels did not correlate with STEMI severity (Killip classification) or inflammatory markers.
- Supraphysiological homocysteine concentrations did not reduce human coronary artery endothelial cell viability in vitro.
Conclusions:
- Homocysteine is not elevated in STEMI patients, indicating it is likely a bystander, not a causative factor.
- The findings support the current understanding that homocysteine-lowering strategies may not be crucial for preventing cardiovascular disease.
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