SAN FRANCISCO — Patients seen in the emergency department for acute decompensated heart failure fared much worse if they had elevated serum troponin, W. Frank Peacock IV, M.D., said in a poster at the annual meeting of the American College of Emergency Physicians.
The results should have a profound impact on controversy about the clinical implications of elevating troponin in patients with heart failure, several speakers said at the meeting.
The analysis of data on 67,924 patients in the Acute Decompensated Heart Failure National Registry (ADHERE) showed that 6% had elevated troponin levels, and the rest were considered troponin negative. Patients with elevated serum troponin were more likely than troponin-negative patients to develop systolic heart failure (61% vs. 51%) or undergo coronary artery bypass grafting (4% vs. 1%), intra-aortic balloon counterpulsation (3% vs. less than 1%), mechanical ventilation (11% vs. 4%), or cardioversion (3% vs. 2%), said Dr. Peacock of the Cleveland Clinic and his associates.
Patients with acute decompensated heart failure and elevated serum troponin also had longer hospitalizations (median 5.1 vs. 4.1 days) and longer ICU stays (a median of 2.9 vs. 2.3 days) and were more likely to die in the hospital (8% vs. 3%) compared with troponin-negative patients.
The study defined elevated serum troponin as a level of at least 1 ng/ml for troponin I or at least 0.1 ng/ml for troponin T. Patients with levels below those cutoffs were considered troponin-negative.
“This [study] is important, because cardiologists everywhere—particularly our heart failure cardiologists—tend to pooh-pooh troponin leaks,” said Judd E. Hollander, M.D., professor of emergency medicine at the University of Pennsylvania, Philadelphia.
Elevated troponin in heart failure does not necessarily indicate underlying coronary disease, he said. “What this doesn't tell us is whether there's something we can fix in the hospital to decrease that mortality” associated with elevated troponin, he added.
Particularly in older patients, elevated troponin has been a marker for sick patients in studies of sepsis, shock, chest pain, or congestive heart failure. “It's a worrisome marker and should be treated as such,” said Charles V. Pollack, Jr., M.D., chair of emergency medicine at the University of Pennsylvania.
Troponin is a structural protein, and elevated levels are produced by cell death, noted Brian J. O'Neil, M.D., of Wayne State University, Detroit. “These are not 'leaks,' “ he said.
In a separate interview, cardiologist Christopher P. Cannon, M.D., agreed that some of his colleagues have been misled by the common use of elevated troponin levels as a marker for acute coronary syndrome. When catheterizations found no arterial blockage in some patients with elevated troponin, the marker gained a reputation for false positives.
“We've learned that there are other things that cause elevations in troponin. We're all learning how to use this in these other patient groups. People are realizing it's a good marker of high-risk patients independent of whether the arteries have blockages or not,” said Dr. Cannon of Brigham and Women's Hospital, Boston.
Previous studies have shown that troponin is a biomarker for myocardial injury. In earlier studies of patients hospitalized for heart failure, troponin elevations have been associated with lower ejection fractions, worse functional status, repeat hospitalizations for heart failure, and death. Studies on the clinical implications of troponin in heart failure are few, however, and have been plagued by methodological problems.
Although speakers at the meeting lauded the current study for the number and breadth of patients in the database, Jerome R. Hoffman, M.D., pointed out one major limitation: possible incorporation bias. Higher rates of procedures and longer hospitalizations may be due to physicians' reactions.
“When somebody tells you a patient has a high troponin level, you might keep them in the hospital or ICU a little longer. It may be a self-fulfilling prophecy” and not necessarily an appropriate step, said Dr. Hoffman of the University of California, Los Angeles.
Sorin J. Brener, M.D., called the study “important and well executed” but agreed with Dr. Hoffman's criticism. A multivariate logistic regression analysis controlling for the differences between patients in the two troponin groups would be necessary to isolate the independent effect of elevated troponin on outcomes, he said in a separate interview.
“Elevated troponin levels are indeed a marker of adverse prognosis and cannot be ignored. Unfortunately, more often than not there is no specific intervention tailored to this finding in patients with decompensated heart failure that one would not apply in patients without elevated troponin,” said Dr. Brener, director of the angiography core laboratory at the Cleveland Clinic.