Dataset Information

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.

SUBMITTER: Reed GW

PROVIDER: S-EPMC5669177 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature

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Publications

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

Reed Grant W GW Horr Samuel S Young Laura L Clevenger Joshua J Malik Umair U Ellis Stephen G SG Lincoff A Michael AM Nissen Steven E SE Menon Venu V

Journal of the American Heart Association 20170606 6

<h4>Background</h4>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.<h4>Methods and results</h4>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-u ...[more]

PMID: 28588090

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Project description:BackgroundIncreased postoperative cardiac troponin (cTn) independently predicts short-term mortality. Previous studies suggest that preoperative cTn also predicts major adverse cardiovascular events (MACE) and mortality after noncardiac surgery. The value of preoperative and perioperative changes in cTn as a prognostic tool for adverse outcomes has been sparsely investigated.Methods and findingsA systematic review and meta-analysis of the prognostic value of cTns for adverse outcome was conducted. Adverse outcome was defined as short-term (in-hospital or <30 days) and long-term (>30 days) MACE and/or all-cause mortality, in adult patients undergoing noncardiac surgery. The study protocol (CRD42018094773) was registered with an international prospective register of systematic reviews (PROSPERO). Preoperative cTn was a predictor of short- (OR 4.3, 95% CI 2.9-6.5, p<0.001, adjusted OR 5.87, 95% CI 3.24-10.65, p<0.001) and long-term adverse outcome (OR 4.2, 95% CI 1.0-17.3, p = 0.05, adjusted HR 2.0, 95% CI 1.4-3.0, p<0.001). Perioperative change in cTn was a predictor of short-term adverse outcome (OR 10.1, 95% CI 3.2-32.3, p<0.001). It was not possible to conduct pooled analyses for adjusted estimates of perioperative change in cTn as predictor of short- (a single study identified) and long-term (no studies identified) adverse outcome. Further, it was not possible to conduct pooled analyses for unadjusted estimates of perioperative change in cTn as predictor of long-term adverse outcome, since only one study was identified. Bivariate analysis of sensitivities and specificities were performed, and overall prognostic performance was summarized using summary receiver operating characteristic (SROC) curves. The pooled sensitivity and specificity for preoperative cTn and short-term adverse outcome was 0.43 and 0.86 respectively (area under the SROC curve of 0.68). There were insufficient studies to construct SROCs for perioperative changes in cTn and for long-term adverse outcome.ConclusionOur study indicates that although preoperative cTn and perioperative change in cTn might be valuable predictors of MACE and/or all-cause mortality in adult noncardiac surgical patients, its overall prognostic performance remains uncertain. Future large, representative, high-quality studies are needed to establish the potential role of cTns in perioperative cardiac risk stratification.

Dataset Information

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

Background

Methods and results

Conclusions

Publications

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

Similar Datasets

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