尚不清楚高剂量他汀类药物对心血管事件的有益作用是否因慢性冠脉综合征(CCS)患者的血栓形成风险而异。方法和结果:冠心病患者使用匹伐他汀的积极或中度降脂治疗的随机评估(REAL-CAD)研究是一项比较CCS患者中4mg和1mg匹伐他汀的随机试验。这项研究根据CREDO-Kyoto血栓形成风险评分将12,413例患者分为3层:低风险(N=9,434;4mg:N=4,742和1mg:N=4,692),中等风险(N=2,415;4mg:N=1,188和1mg:N=1,227);和高风险(N=564;4mg:N=269和1mg:N=295)。主要终点是心血管死亡,非致死性心肌梗死,非致死性缺血性卒中,或者不稳定型心绞痛.主要终点的累积4年发病率在高危层明显高于中危层和低危层(11.0%,6.3%,和4.5%,P<0.0001)。在低风险阶层,4mg组的主要终点的累积4年发生率显着低于1mg组(4.0%和4.9%,P=0.02),而在中高风险阶层,4mg组的数值低于1mg组。对于主要终点,没有明显的治疗-亚组交互作用(P交互作用=0.77)。
高剂量匹伐他汀治疗与低剂量匹伐他汀治疗相比,与CCS患者的血栓风险无关,具有降低心血管事件风险的趋势。
It is unknown whether beneficial effects of higher-dose statins on cardiovascular events are different according to the thrombotic risk in patients with chronic coronary syndrome (CCS).
The Randomized Evaluation of Aggressive or Moderate Lipid-Lowering Therapy with Pitavastatin in Coronary Artery Disease (REAL-CAD)
study is a randomized
trial comparing 4 mg and 1 mg pitavastatin in patients with CCS. This
study categorized 12,413 patients into 3 strata according to the CREDO-Kyoto thrombotic risk score: low-risk (N=9,434; 4 mg: N=4,742, and 1 mg: N=4,692), intermediate-risk (N=2,415; 4 mg: N=1,188, and 1 mg: N=1,227); and high-risk (N=564; 4 mg: N=269, and 1 mg: N=295). The primary endpoint was a composite of cardiovascular death, non-fatal myocardial infarction, non-fatal ischemic stroke, or unstable angina. Cumulative 4-year incidence of the primary endpoint was significantly higher in the high-risk stratum than in the intermediate- and low-risk strata (11.0%, 6.3%, and 4.5%, P<0.0001). In the low-risk stratum, the cumulative 4-year incidence of the primary endpoint was significantly lower in the 4 mg than in the 1 mg group (4.0% and 4.9%, P=0.02), whereas in the intermediate- and high-risk strata, it was numerically lower in the 4 mg than in the 1 mg group. There was no significant treatment-by-subgroup interaction for the primary endpoint (P-interaction=0.77).
High-dose pitavastatin therapy compared with low-dose pitavastatin therapy was associated with a trend toward lowering the risk for cardiovascular events irrespective of the thrombotic risk in patients with CCS.