Circulating cardiac troponin has been associated with adverse prognosis in the acute respiratory distress syndrome in small and single-center studies; however, comprehensive studies of myocardial injury in acute respiratory distress syndrome using modern high-sensitivity troponin assays, which can detect troponin at much lower circulating concentrations, have not been performed.
We performed a prospective cohort study.
We included patients enrolled in previously completed trials of acute respiratory distress syndrome.
One thousand fifty-seven acute respiratory distress syndrome patients were included.
To determine the association of circulating high-sensitivity troponin I (Abbott ARCHITECT), with acute respiratory distress syndrome outcomes, we measured high-sensitivity troponin I within 24 hours of intubation. The primary outcome was 60-day mortality.
Detectable high-sensitivity troponin I was present in 94% of patients; 38% of patients had detectable levels below the 99th percentile of a healthy reference population (26 ng/L), whereas 56% of patients had levels above the 99th percentile cut point. After multivariable adjustment, age, cause of acute respiratory distress syndrome, temperature, heart rate, vasopressor use, Sequential Organ Failure Assessment score, creatinine, and PCO2 were associated with higher high-sensitivity troponin I concentration. After adjustment for age, sex, and randomized trial assignment, the hazard ratio for 60-day mortality comparing the fifth to the first quintiles of high-sensitivity troponin I was 1.61 (95% CI, 1.11–2.32; p trend = 0.003). Adjusting for Sequential Organ Failure Assessment score suggested that this association was not independent of disease severity (hazard ratio, 0.95; 95% CI, 0.64–1.39; p = 0.93).
Circulating troponin is detectable in over 90% of patients with acute respiratory distress syndrome and is associated with degree of critical illness. The magnitude of myocardial injury correlated with mortality.
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1Division of Cardiology, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD.
2Department of Epidemiology, Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.
3Department of Medicine, Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.
4Department of Pathology, Johns Hopkins Hospital, Baltimore, MD.
5Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA.
6Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
7Department of Emergency Medicine, University of Michigan Medical School, Ann Arbor, MI.
Drs. Metkus, Guallar, Morrow, Brower, Schulman, and Korley contributed to study design. All the authors contributed to analysis and interpretation and drafting the article for intellectual content.
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Dr. Metkus’s institution received funding from Abbott Laboratories and the National Institutes of Health (NIH)/National Heart, Lung, and Blood Institute (salary support from grant number T32-HL007227-40, 2014–2016); he received funding from BestDoctors (consulting [unrelated to subject matter]), Oakstone/EBIX (consulting [unrelated to subject matter]), and McGraw-Hill Publishing (royalties, unrelated to this subject matter); he disclosed that Abbott Laboratories provided reagents and financial support for the study, but the study was designed and executed solely by the study investigators without industry involvement; he received support for article research from the NIH, and he disclosed off-label product use of high sensitivity troponin assays, which are not yet approved or have just recently been approved for clinical use in the United States (these assays are in routine clinical use in Europe). Dr. Sokoll’s institution received funding from Abbott Laboratories and disclosed reagent support from Abbott Laboratories. Dr. Morrow received funding from consulting for Abbott Laboratories, Roche Diagnostics, diaDexus; he reports grants to the Thrombolysis in Myocardial Infarction Study Group (for studies other than the one in this article) from Abbott Laboratories, Amgen, AstraZeneca, Daiichi Sankyo, Eisai, GlaxoSmithKline, Merck, Novartis, Roche Diagnostics, and Singulex, and he received consultant fees from Abbott Laboratories, AstraZeneca, diaDexus, GlaxoSmithKline, Merck, Peloton, Roche Diagnostics, and Verseon. Dr. Tomaselli received support for article research from the NIH. Dr. Brower received funding from Applied Clinical Intelligence and Global Therapeutics. Dr. Korley’s institution received funding from Abbott Laboratories, and he disclosed funding from prior consulting for Abbott Laboratories and Roche Diagnostics. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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