High plasma heparin cofactor II activity is associated with reduced incidence of in-stent restenosis after percutaneous coronary intervention
High plasma heparin cofactor II activity is associated with reduced incidence of in-stent restenosis after percutaneous coronary intervention
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DOI：
10.1161/01.cir.0000109695.39671.37
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发表时间：
2004-02-03
期刊：
影响因子：
37.8
通讯作者：
Matsumoto, T
中科院分区：
文献类型：
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作者：
Takamori, N;Azuma, H;Matsumoto, T
背景-凝血酶在经皮冠状动脉介入治疗后动脉粥样硬化和再狭窄的发展中起重要作用。由于肝素辅助因子II （HCII）在硫酸皮肤聚糖存在时抑制凝血酶的作用，而硫酸皮肤聚糖大量存在于动脉壁中，HCII可能通过调节凝血酶的作用影响血管重塑。我们假设血浆HCII活性高的患者可能会降低支架内再狭窄（ISR）的发生率。方法和结果：对134例经皮冠状动脉介入治疗前、后、6个月置入NIR支架（波士顿科学公司）的患者进行序贯冠状动脉（n = 166）评估。将患者分为高HCII组（大于等于110%，36例45个病变）、正常HCII组（大于等于80%，< 110%，66例81个病变）、低HCII组（< 80%，32例40个病变）。高hcii组随访时内径狭窄率（18.7%）明显低于正常hcii组（30.3%）或低hcii组（29.0%）（P = 0.046）。高hcii组的ISR率（6.7%）显著低于低hcii组（30.0%）（P = 0.0039）。此外，多因素分析显示高血浆HCII活性是降低血管造影再狭窄发生率的独立因素（优势比，0.953/1% HCII升高；95% CI, 0.911 ~ 0.998）。结论-结果表明，HCII可能具有迄今未被认识到的抑制ISR的作用。HCII的作用可能是通过使损伤动脉凝血酶失活，从而抑制血管平滑肌细胞的迁移和增殖来介导的。
Background - Thrombin plays an important role in the development of atherosclerosis and restenosis after percutaneous coronary intervention. Because heparin cofactor II (HCII) inhibits thrombin action in the presence of dermatan sulfate, which is abundantly present in arterial wall, HCII may affect vascular remodeling by modulating thrombin action. We hypothesized that patients with high plasma HCII activity may show a reduced incidence of in-stent restenosis (ISR).Methods and Results - Sequential coronary arteries (n = 166) with NIR stent ( Boston Scientific Corp) implantation in 134 patients were evaluated before, immediately after, and at 6 months after percutaneous coronary intervention. Patients were divided into the following groups: high HCII ( greater than or equal to 110%, 45 lesions in 36 patients), normal HCII ( greater than or equal to 80% and < 110%, 81 lesions in 66 patients), and low HCII ( < 80%, 40 lesions in 32 patients). Percent diameter stenosis at follow-up in the high-HCII group (18.7%) was significantly lower ( P = 0.046) than that in the normal-HCII group (30.3%) or the low-HCII group (29.0%). The ISR rate in the high-HCII group (6.7%) was significantly lower than that in the low-HCII group (30.0%) ( P = 0.0039). Furthermore, multivariate analysis demonstrated that high plasma HCII activity is an independent factor in reducing the incidence of angiographic restenosis ( odds ratio, 0.953/1% increase of HCII; 95% CI, 0.911 to 0.998).Conclusions - The results demonstrate that HCII may have a hitherto unrecognized effect in inhibiting ISR. The effect of HCII may be mediated by inactivating thrombin in injured arteries, thereby inhibiting vascular smooth muscle cell migration and proliferation.