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Biomarker evidence of myocardial cell injury is associated with mortality in acute respiratory distress syndrome*

Bajwa, Ednan K. MD; Boyce, Paul D. MD, MPH; Januzzi, James L. MD; Gong, Michelle N. MD, MS; Thompson, B Taylor MD; Christiani, David C. MD, MPH

doi: 10.1097/01.CCM.0000281852.36573.22
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Objective: Although a number of studies have reported elevated levels of markers of myocardial necrosis among critically ill patients, the association between these markers and outcome remains poorly studied in patients with lung injury. We investigated the association of elevated troponin and creatine phosphokinase isoenzyme levels with mortality and organ failure in subjects with acute respiratory distress syndrome.

Design: Retrospective study.

Setting: Tertiary academic medical center.

Patients: A total of 305 subjects with acute respiratory distress syndrome enrolled in a prospective intensive care unit cohort.

Intervention: None.

Measurements and Main Results: Cardiac biomarker data were available on 248 of 305 patients with acute respiratory distress syndrome (81%), of which 89 patients had at least one elevated cardiac marker level (35%). The presence of an elevated cardiac marker was associated with significantly higher mortality (p = .01) and was an independent predictor of mortality (p = .02) among patients with lower severity of illness (Acute Physiology and Chronic Health Evaluation III, <79). Patients with at least one elevated cardiac marker also had significantly more organ system derangement, including noncardiovascular organ system failures (p = .02).

Conclusions: Patients with acute respiratory distress syndrome have a high prevalence of elevated cardiac markers. The presence of elevated cardiac markers is independently associated with increased 60-day mortality and increased organ failure. This association is most pronounced among patients with lower severity of illness. These results indicate that occult myocardial injury may be an important factor in acute respiratory distress syndrome morbidity and mortality. Further study of the relevant causal relationships and mechanisms is warranted.

From the Pulmonary and Critical Care Unit (EKB, PDB, BTT, DCC) and Cardiology Unit (JLJ), Massachusetts General Hospital, Harvard Medical School, Boston, MA; Pulmonary and Critical Care Division, Mount Sinai School of Medicine, New York, NY (MNG); and Department of Environmental Health, Harvard School of Public Health, Boston, MA (DCC).

The authors have not disclosed any potential conflicts of interest.

Supported, in part, by grants HL60710, HL67197, and HL07874 from the National Heart, Lung, and Blood Institute, National Institutes of Health.

For information regarding this article, E-mail: dchristi@hsph.harvard.edu

© 2007 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins