Chen Ching-Yu Julius, Yang Tzu-Ching, Chang Christopher, Lu Shao-Chun, Chang Po-Yuan
Cardiovascular Center and Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, 100, Taipei, Taiwan.
Division of Cardiology, Department of Internal Medicine, National Taiwan University College of Medicine, No.1, Ren-Ai Road Section 1, 100, Taipei, Taiwan.
BMC Cardiovasc Disord. 2018 Feb 13;18(1):33. doi: 10.1186/s12872-018-0774-8.
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.
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.
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 ± 1.9 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.
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.
同型半胱氨酸长期以来被认为是动脉粥样硬化的一个风险因素。然而，通过补充B族维生素降低同型半胱氨酸水平并不能减少心血管事件。尽管多项关联研究报告了心血管疾病患者血清同型半胱氨酸水平升高，但同型半胱氨酸与ST段抬高型心肌梗死（STEMI）之间的关系尚未明确。
我们前瞻性纳入了在台湾某单一医疗中心接受冠状动脉介入治疗后连续入住重症监护病房的STEMI患者。对照对象是因急性胸痛就诊于门诊或急诊科但随后冠状动脉造影显示冠状动脉通畅的个体。研究了血清同型半胱氨酸水平与STEMI之间的关联。还建立了一个使用人冠状动脉内皮细胞的培养系统，以在细胞水平上研究同型半胱氨酸的毒性作用。
胸痛患者分为两组。STEMI组包括56例行直接经皮冠状动脉介入治疗的患者。对照组包括17例冠状动脉通畅的受试者。血清同型半胱氨酸水平无差异（8.4±2.2对7.6±1.9μmol/L，p = 0.142）。根据Killip分级将STEMI患者分为较高（Killip III-IV）和较低（Killip I-II）级别时，较高级别患者的CRP（3.3±4.1对1.4±2.3mg/L，p = 0.032）、肌酸激酶峰值（3796±2163对2305±1822IU/L，p = 0.023）和SYNTAX评分（20.4±11.1对14.8±7.6，p = 0.033）显著更高，而血清同型半胱氨酸水平相似。在STEMI患者中，同型半胱氨酸与白细胞、CRP或SYNTAX评分均无相关性。在培养系统中，即使同型半胱氨酸水平达到超生理水平100μmol/L，也不会降低人冠状动脉内皮细胞的细胞活力。
无论Killip严重程度如何，STEMI患者的同型半胱氨酸水平均未升高，这表明同型半胱氨酸是旁观者而非STEMI的致病因素。因此，我们的研究支持当前的观点，即降低同型半胱氨酸水平的策略对于预防心血管疾病并非必不可少。
