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Troponin elevation predicted mortality in acute dyspnea patients

Issue: November 2011

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Heart Failure Society of America 15th Annual Scientific Meeting

Troponin elevation had a better rate at predicting mortality in patients with acute dyspnea due to both cardiac and pulmonary etiologies than B-type natriuretic peptide, acute HF and chronic obstructive pulmonary disease, according to an abstract from the 15th Annual Scientific Meeting of the Heart Failure Society of America.

There were 1,641 patients enrolled in the Biomarkers in Acute Heart Failure trial to evaluate troponin as a prognostic biomarker in patients with acute dyspnea. Biomarkers were measured during the patients’ initial visit, and then were followed up to 90 days for all-cause mortality, according to the abstract. At each enrolling site, researchers defined elevated troponin as levels at the upper limit of normal.

Researchers found that of 1,162 patients, there was an association between elevated troponin and increased mortality (P<.001). Troponin (P=.009; HR=1.84) and mid-region pro-adrenomedullin (P.001; HR=16.83) were significant predictors of mortality vs. acute HF, chronic obstructive pulmonary disease and B-type natriuretic peptide. Researchers also found that troponin elevation was a predictor of mortality when looking at cardiac (P<.001; HR=3.63) and pulmonary (P=.003; HR=4.86) diagnoses. But when researchers compared troponin elevation and B-type natriuretic peptide with cardiac and pulmonary diagnoses, B-type natriuretic peptide elevations were greater predictors of mortality with cardiac diagnoses (P=.001; HR=2.46) vs. troponin (P<.001 HR=2.46), and troponin elevation was a greater predictor of mortality among patients with pulmonary diagnosis (P=.015; HR=4.07) vs. B-type natriuretic peptide (P=.41).

“This will be very important in clinical practice [for two reasons]. One, if troponin rises during admission, these are patients that you would consider cardiac cath on vs. low and stable or declining, and two, new anti-ischemic drugs could be specifically targeted to this troponin rise, as it likely represents subendocardial ischemia,” Alan Maisel, MD, Professor of Medicine at the University of California, told Cardiology Today.

Disclosure: Drs. Maisel and Xue report no relevant financial disclosures.

For more information:

• Xue Y. #185. Presented at: 15th Annual Scientific Meeting of the Heart Failure Society of America; Sept. 18-21, 2011; Boston.

I think trying to find better prognostic markers for heart failure critically important. It is no surprise to me that a marker of myocyte demise might do this best. The wide spread applicability of this needs exploration.

–James B. Young, MD
Cardiology Today Editorial Board Section Editor

Disclosure: Dr. Young reports no relevant financial disclosures.

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