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J Am Coll Cardiol, 2002; 40:2065-2071 © 2002 by the American College of Cardiology Foundation |
,*
* Department of Internal Medicine, Cleveland Clinic Foundation, Cleveland, Ohio, USA
Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio, USA
Department of Clinical Pathology, Cleveland Clinic Foundation, Cleveland, Ohio, USA
Department of Emergency Medicine, Cleveland Clinic Foundation, Cleveland, Ohio, USA
Manuscript received April 1, 2002; revised manuscript received June 18, 2002, accepted August 26, 2002.
* Reprint requests and correspondence: Dr. Gary S. Francis, Cleveland Clinic Foundation, Department of Cardiovascular Medicine, 9500 Euclid Avenue, F25, Cleveland, Ohio 44195, USA.
francig{at}ccf.org
Patients with renal insufficiency may have increased serum troponins even in the absence of clinically suspected acute myocardial ischemia. While cardiovascular disease is the most common cause of death in patients with renal failure, we are just beginning to understand the clinical meaning of serum troponin elevations. Serum troponin T is increased more frequently than troponin I in patients with renal failure, leading clinicians to question its specificity for the diagnosis of myocardial infarction. Many large-scale trials demonstrating the utility of serum troponins in predicting adverse events and in guiding therapy and intervention in acute coronary syndromes have excluded patients with renal failure. Despite persistent uncertainty about the mechanism of elevated serum troponins in patients with reduced renal function, data from smaller groups of renal failure patients have suggested that troponin elevations are associated with added risk, including an increase in mortality. It is possible that increases in serum troponin from baseline in patients with renal insufficiency admitted to hospital with acute coronary syndrome may signify myocardial necrosis. Further studies are needed to clarify this hypothesis.
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