Homocysteine is a bystander for ST-segment elevation myocardial infarction: a case-control study.
Homocysteine is a bystander for ST-segment elevation myocardial infarction: a case-control study.
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DOI：
10.1186/s12872-018-0774-8
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发表时间：
2018-02-13
影响因子：
2.1
通讯作者：
Chang PY
中科院分区：
文献类型：
--
作者：
Chen CJ;Yang TC;Chang C;Lu SC;Chang PY
同型半胱氨酸长期以来一直被认为是动脉粥样硬化的危险因素。然而，补充 B 族维生素不能通过降低同型半胱氨酸来减少心血管事件。尽管一些关联研究报告了心血管疾病中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) 的关系尚未明确。我们前瞻性地招募了在台湾一家医疗中心进行冠状动脉介入治疗后连续入住重症监护室的 STEMI 患者。对照受试者是因急性胸痛而到门诊或急诊科就诊但随后通过冠状动脉造影显示冠状动脉开放的个体。研究了血清同型半胱氨酸水平与 STEMI 之间的关联。还建立了使用人冠状动脉内皮细胞的培养系统，以在细胞水平上检查同型半胱氨酸的毒性作用。胸痛患者被分为两组。 STEMI 组包括 56 名接受直接经皮冠状动脉介入治疗的患者。对照组包括 17 名冠状动脉开放的受试者。血清同型半胱氨酸水平没有差异（8.4±2.2 vs. 7.6±1.9 μmol/L，p=0.142）。当按 Killip 分类将 STEMI 患者分为较高级别 (Killip III-IV) 和较低级别 (Killip I-II) 时，CRP（3.3 ± 4.1 vs. 1.4 ± 2.3 mg/L，p = 0.032）、峰值肌酸激酶（3796 ± 2163 vs.高年级学生的 2305 ± 1822 IU/L，p = 0.023）和 SYNTAX 评分（20.4 ± 11.1 vs. 14.8 ± 7.6，p = 0.033）显着较高，而血清同型半胱氨酸水平相似。 STEMI 患者的同型半胱氨酸与 WBC、CRP 或 SYNTAX 评分不相关。在培养体系中，即使超生理水平的同型半胱氨酸达到 100 μmol/L，也不会降低人冠状动脉内皮细胞的细胞活力。无论 Killip 的严重程度如何，STEMI 患者的同型半胱氨酸均未升高，这表明同型半胱氨酸是 STEMI 的旁观者而不是致病因素。因此，我们的研究支持当前的观点，即降低同型半胱氨酸的策略对于预防心血管疾病并不重要。
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.
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影响因子：
10.8
作者：
Chang, Po-Yuan;Chen, Yi-Jie;Chen, Chu-Huang
通讯作者：
Chen, Chu-Huang
影响因子：
39.3
作者：
D'Ascenzo, Fabrizio;Iannaccone, Mario;Gaita, Fiorenzo
通讯作者：
Gaita, Fiorenzo
影响因子：
37.8
作者：
Doshi, SN;McDowell, IFW;Goodfellow, J
通讯作者：
Goodfellow, J
影响因子：
120.7
作者：
Armitage, Jane M.;Bowman, Louise;Collins, Rory
通讯作者：
Collins, Rory
影响因子：
3.5
作者：
Foussas, Stefanos G.;Zairis, Michael N.;Argyrakis, Spyros K.
通讯作者：
Argyrakis, Spyros K.