Associations between cardiac troponin, mechanism of myocardial injury, and long-term mortality after noncardiac vascular surgery

Abstract

Background-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. Methods and Results-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. Conclusions-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.