Medscape Medical News 2009. © 2009 Medscape
Elevated levels of troponin are associated with a nearly 50% increase in mortality risk among severely ill noncardiac patients, and one-fifth of noncardiac patients in medical intensive care units (ICUs) have high troponin levels.
High troponin levels “may represent secondary cardiac injury in medical patients,” which could, in turn, increase mortality. Treatment of patients with very high levels of troponin may decrease the risk for mortality, investigators announced here at the Society of Critical Care Medicine 38th Critical Care Congress.
Vipin Koshal, MD, Chief Cardiology Fellow at the University of Cincinnati, Ohio, presented his team’s findings from a database of 43,415 ICU patients hospitalized in 116 Veterans Administration hospitals between 2005 and 2006 with recorded troponin levels.
Patients were divided into 3 groups: those with negative or undetectable levels of troponin; those with intermediate levels, or below 10% of the coefficient variance; and those with high levels, at or above 10% of the coefficient variance. Cases were then stratified into quintiles according to predicted mortality.
In all, 45% of cases were negative for troponin, 35% had intermediate levels, and 20% had high levels.
The odds ratio (OR) for mortality was not significantly increased in patients with intermediate levels of troponin, with an OR = 1.071 (95% confidence interval [CI], 1.004 – 1.143).
But mortality was increased significantly in patients with high troponin levels, with an OR = 1.464 (95% CI, 1.364 – 1.572).
The proportion of patients with high troponin levels increased with severity of illness. Among those with a predicted mortality below 2.5%, 11% had high troponin levels. Among those with a greater than 30% chance of mortality, 34% had high troponin levels.
Approximately 45% of patients with intermediate or high troponin levels were treated with beta-blockers, Dr. Koshal reported.
Nontreatment among those with high levels increased the OR for mortality by 40% (OR, 1.140; 95% CI, 1.025 – 1.268). Nontreatment did not increase mortality risk in those with intermediate troponin levels (OR, 1.066; 95% CI, 0.972 – 1.169).
“There appears to be a protection of myocardium in patients with high troponin levels that does not happen in patients with intermediate levels,” Dr. Koshal told Medscape Critical Care.
“It’s important to keep in mind that these are noncardiac patients,” he added. “We don’t know how this happens. There may be a small leak in troponin. Even the high levels [in these patients] were lower than in cardiac patents. This is not the same scenario as in cardiac patients, who would probably already be on beta-blockers.”
“The clinical message is that in the absence of contraindications, such as hypotension, beta-blockers could be beneficial for the noncardiac patient with high troponin levels,” Dr. Koshal said in an interview with Medscape Critical Care after his presentation.
“A main limitation of these findings is that many noncardiac patients with elevated troponins have hemodynamic compromise, in particular low blood pressure, and are therefore not treated” and are not candidates for treatment, Robert Duncan Hite, MD, FCCP, associate professor and director of medical intensive care and critical care research at Wake Forest University School of Medicine in Winston-Salem, North Carolina, told Medscape Critical Care.
Dr. Hite commented that the retrospective design of Dr. Koshal’s study is a major limitation. “A finding that those who are not treated vs those who are treated in this retrospective manner may simply identify those who were sicker. It is unlikely that this study will change practice.”
Dr. Hite said that “a potentially more important question for this clinical scenario is whether these patients should have more formal studies of their cardiac disease, such as stress tests or cardiac catheterization, after they recover from their acute illness. That is not the current standard in practice.”
Randomized studies of noncardiac ICU patients with high troponin levels randomized to beta-blockers or placebo are needed, he said.
Dr. Hite and Koshal have disclosed no relevant financial relationships.
Society of Critical Care Medicine (SCCM) 38th Critical Care Congress: Abstract 226. Presented February 3, 2009.