Reed Grant W, Horr Samuel, Young Laura, Clevenger Joshua, Malik Umair, Ellis Stephen G, Lincoff A Michael, Nissen Steven E, Menon Venu
Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH
Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH.
J Am Heart Assoc. 2017 Jun 6;6(6):e005672. doi: 10.1161/JAHA.117.005672.
The time-sensitive hazard of perioperative cardiac troponin T (cTnT) elevation and whether long-term mortality differs by mechanism of myocardial injury are poorly understood.
In this observational study of 12 882 patients who underwent noncardiac vascular surgery, patients were assessed for cTnT sampling within 96 hours postoperatively. Mortality out to 5-years was stratified by cTnT level and mechanism of myocardial injury. During a median follow-up of 26.9 months, there were 2149 (16.7%) deaths. By multivariable Cox proportional hazards analysis, there was a graded increase in mortality with any detectable cTnT compared to <0.01 ng/mL; cTnT 0.01 to 0.029 ng/mL hazard ratio (HR) 1.54 (95% CI 1.18-2.00, =0.002), 0.03 to 0.099 ng/mL HR 1.86 (95% CI 1.49-2.31, <0.001), 0.10 to 0.399 ng/mL HR 1.83 (95% CI 1.46-2.31, <0.001), ≥0.40 ng/mL HR 2.62 (95% CI 2.06-3.32, <0.001). Mortality for each mechanism of injury was greater than for patients with normal cTnT; baseline cTnT elevation HR 1.71 (95% CI 1.31-2.24; <0.001), Type 2 myocardial infarction HR 1.88 (95% CI 1.57-2.24; <0.001), Type 1 MI HR 2.56 (95% CI 2.56, 1.82-3.60; <0.001). On Kaplan-Meier analysis, long-term survival did not differ between mechanisms. The hazard of mortality was greatest within the first 10 months postsurgery. Consistent results were obtained in confirmatory propensity-score matched analyses.
Any detectable cTnT ≥0.01 ng/mL is associated with increased long-term mortality after vascular surgery. This risk is greatest within the first 10 months postoperatively. While short-term mortality is greatest with Type 1 myocardial infarction, long-term mortality appears independent of the mechanism of injury.
围手术期心肌肌钙蛋白T（cTnT）升高的时间敏感性危害以及长期死亡率是否因心肌损伤机制而异，目前了解甚少。
在这项对12882例接受非心脏血管手术患者的观察性研究中，对患者在术后96小时内进行cTnT采样评估。根据cTnT水平和心肌损伤机制对5年死亡率进行分层。在中位随访26.9个月期间，有2149例（16.7%）死亡。通过多变量Cox比例风险分析，与<0.01 ng/mL相比，任何可检测到的cTnT都会使死亡率分级增加；cTnT为0.01至0.029 ng/mL时，风险比（HR）为1.54（95%可信区间[CI] 1.18 - 2.00，P = 0.002），0.03至0.099 ng/mL时HR为1.86（95% CI 1.49 - 2.31，P < 0.001），0.10至0.399 ng/mL时HR为1.83（95% CI 1.46 - 2.31，P < 0.001），≥0.40 ng/mL时HR为2.62（95% CI 2.06 - 3.32，P < 0.001）。每种损伤机制的死亡率均高于cTnT正常的患者；基线cTnT升高时HR为1.71（95% CI 1.31 - 2.24；P < 0.001），2型心肌梗死时HR为1.88（95% CI 1.57 - 2.24；P < 0.001），1型心肌梗死时HR为2.56（95% CI 1.82 - 3.60；P < 0.001）。根据Kaplan - Meier分析，不同机制之间的长期生存率没有差异。术后前10个月内死亡风险最高。在验证性倾向评分匹配分析中获得了一致的结果。
任何可检测到的cTnT≥0.01 ng/mL与血管手术后长期死亡率增加相关。这种风险在术后前10个月内最大。虽然1型心肌梗死的短期死亡率最高，但长期死亡率似乎与损伤机制无关。
