Revascularization in response to identification of elevated high sensitivity troponin in stable patients does not improve outcomes

Among patients presenting with an acute coronary syndrome, cardiac troponin assays are the standard method for the identification of patients at high risk who benefit from early revascularization.  With advances in technology, high-sensitivity troponin (hsTn) assays are now available to identify levels of circulating troponin that were previously undetectable.  In this study, the authors sought to determine the impact of prompt revascularization on outcomes among patients with type 2 diabetes and stable ischemic heart disease. Utilizing patients from the BARI 2D study, a total of 2285 patients with stable ischemic heart disease and type 2 diabetes had hsTn measurements taken at baseline and 12 months.  Patients with an elevated hsTn were randomized to prompt revascularization or to ongoing medical therapy.  Over 5 years of follow-up from the point of revascularization, the primary composite end point was death from cardiovascular causes, myocardial infarction, or stroke.  A total of 897 (39.3%) patients were found to have a hsTn above the normal range (≥14 ng/l).  Compared with patients with normal hsTn levels, patients with elevated hsTn levels had a significantly increased risk for adverse events (27.1% vs 12.9% for the composite outcome; P<0.001) Early revascularization in response to elevated hsTn did not improve patient outcomes in this population of patients with stable ischemic heart disease.

Conclusions

Elevated hsTn in patients with stable coronary artery disease was associated with increased risk of adverse cardiovascular outcomes and death.  However, revascularization in response to the identification of elevated hsTn did not improve patient outcomes.

Summarized by Hussain Contractor and Steven M. Bradley

Everett BM, Brooks MM, Vlachos HE, Chaitman BR, Frye RL, Bhatt DL; BARI 2D Study Group. Troponin and Cardiac Events in Stable Ischemic Heart Disease and Diabetes. N Engl J Med. 2015 Aug 13;373(7):610-20.

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