Huang Shao-Sung, Huang Po-Hsun, Chen Ying-Hwa, Sung Shih-Hsien, Chiang Kuang-Hsing, Chen Jaw-Wen, Lin Shing-Jong
Department of Internal Medicine, Division of Cardiology, Taipei Veterans General Hospital, Taipei, Taiwan.
Coron Artery Dis. 2008 Dec;19(8):597-602. doi: 10.1097/MCA.0b013e3283155579.
This study tested the hypothesis that plasma heparin cofactor II (HCII) activity independently predicts cardiovascular events in patients after acute myocardial infarction (AMI) and attempted to elucidate the role of HCII in atherothrombosis.
HCII inhibits thrombin activity by binding to dermatan sulfate and has been shown to be a novel and independent risk factor for atherosclerosis. However, there is limited data on the relation between plasma levels of HCII after AMI and future cardiovascular events.
A total of 110 consecutive patients (aged 63+/-11 years) with AMI were followed up for 42+/-12 months. Plasma HCII activity was determined from blood samples collected immediately after hospitalization. The primary end point was the combined occurrence of major adverse cardiovascular events (MACE), including rehospitalization because of unstable angina, nonfatal MI, revascularization with either percutaneous coronary intervention or coronary artery bypass grafting, ischemic stroke, and cardiovascular death.
All patients were divided into three groups: a high-HCII group (>122%, n=35), a normal-HCII group (>98% and <or=122%, n=41), and a low-HCII group (<or=98%, n=34). The high-HCII group had reduced MACE compared with the other groups, although the difference was not significant (P=0.150). Enhanced plasma HCII activity was, however, significantly associated with decreased MACE in the nondiabetic patients (P=0.034). In a Cox multivariate regression analysis that included all patients, plasma HCII activity was an independent predictor of future MACE (P=0.029).
The results indicate a potential association between plasma HCII activity and future cardiovascular events after AMI. Moreover, HCII activity seems to play a pivotal role in atherothrombosis.
本研究检验了以下假设,即血浆肝素辅因子II(HCII)活性可独立预测急性心肌梗死(AMI)患者的心血管事件,并试图阐明HCII在动脉粥样硬化血栓形成中的作用。
HCII通过与硫酸皮肤素结合来抑制凝血酶活性,并且已被证明是动脉粥样硬化的一个新的独立危险因素。然而,关于AMI后血浆HCII水平与未来心血管事件之间关系的数据有限。
连续纳入110例AMI患者(年龄63±11岁),随访42±12个月。血浆HCII活性通过住院后立即采集的血样进行测定。主要终点是主要不良心血管事件(MACE)的联合发生情况,包括因不稳定型心绞痛再次住院、非致命性心肌梗死、经皮冠状动脉介入治疗或冠状动脉旁路移植术的血管重建、缺血性卒中以及心血管死亡。
所有患者被分为三组:高HCII组(>122%,n = 35)、正常HCII组(>98%且≤122%,n = 41)和低HCII组(≤98%,n = 34)。高HCII组的MACE发生率低于其他组,尽管差异不显著(P = 0.150)。然而,在非糖尿病患者中,血浆HCII活性增强与MACE减少显著相关(P = 0.034)。在纳入所有患者的Cox多变量回归分析中,血浆HCII活性是未来MACE的独立预测因子(P = 0.029)。
结果表明血浆HCII活性与AMI后未来心血管事件之间存在潜在关联。此外,HCII活性似乎在动脉粥样硬化血栓形成中起关键作用。