Associations Between Cardiac Troponin, Mechanism of Myocardial Injury, and Long-Term Mortality After Noncardiac Vascular Surgery.

Associations Between Cardiac Troponin, Mechanism of Myocardial Injury, and Long-Term Mortality After Noncardiac Vascular Surgery.
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DOI:
10.1161/jaha.117.005672
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发表时间:
2017-06-06
影响因子:
5.4
通讯作者:
Menon V
Menon V
中科院分区:
医学2区
文献类型:
--
作者:
Reed GW;Horr S;Young L;Clevenger J;Malik U;Ellis SG;Lincoff AM;Nissen SE;Menon V

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围术期心肌肌钙蛋白T(CTnT)升高的时间敏感性风险以及长期死亡率是否因心肌损伤的机制而不同,目前还知之甚少。在这项对12882名接受非心脏血管手术的患者进行的观察性研究中,对患者在术后96小时内进行了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26.9个月的中位随访期间,有2149人(16.7%)死亡。多变量COX比例风险分析显示,cTnT与cTnT0.01~0.029 ng/mLHR1.54(95%CI1.18~2.00,P=0.002)、0.03~0.099 ng/mLHR1.86(95%CI1.49~2.31,P<0.001)、0.10~0.399 ng/mLHR1.83(95%CI1.46~2.31,P<;0.001),≥0.40 ng/mLHR 2.62(95%可信区间2.06~3.32,P<0.001)。两种损伤机制的死亡率均高于cTnT正常者,cTnT升高时HR1.71(95%CI1.31-2.24;P<0.001),2型心肌梗死HR1.88(95%CI1.57-2.24;P<0.001),1型心肌梗死HR2.56(95%CI2.56,1.82-3.60;P<0.001)。在Kaplan-Meier分析中,长期存活率在不同机制之间没有差别。死亡风险在术后前10个月内最大。验证性倾向-得分匹配分析得到了一致的结果。任何可检测到的cTnT≥都与血管手术后长期死亡率的增加有关。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。
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, P=0.002), 0.03 to 0.099 ng/mL HR 1.86 (95% CI 1.49–2.31, P<0.001), 0.10 to 0.399 ng/mL HR 1.83 (95% CI 1.46–2.31, P<0.001), ≥0.40 ng/mL HR 2.62 (95% CI 2.06–3.32, P<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; P<0.001), Type 2 myocardial infarction HR 1.88 (95% CI 1.57–2.24; P<0.001), Type 1 MI HR 2.56 (95% CI 2.56, 1.82–3.60; P<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.