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J Am Coll Cardiol, 1999; 33:471-478 © 1999 by the American College of Cardiology Foundation |
a Department of Clinical Pathology, The Department of Cardiology, The Division of Nursing, and The Department of Emergency Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
Manuscript received June 2, 1998; revised manuscript received August 24, 1998, accepted October 2, 1998.
Reprint requests and correspondence: Dr. Frederick Van Lente, PhD., Department of Clinical Pathology/L11, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, Ohio 44195
vanlenf{at}cesmtp.ccf.org
Objectives
The purpose of this study was to investigate the utility of cardiac troponin T and troponin I for predicting outcomes in patients presenting with suspected acute coronary syndromes and renal insufficiency relative to that observed in similar patients without renal disease.
Background
Cardiac troponin T and troponin I have shown promise as tools for risk stratification of patients with acute coronary syndromes. However, there is uncertainty regarding their cardiac specificity and utility in patients with renal disease.
Methods
We measured troponin T, troponin I and creatine kinase MB in 51 patients presenting with suspected acute coronary syndromes and renal insufficiency and in 102 patients without evidence of renal disease matched for the same peak troponin T or I value, selected from a larger patient cohort. Blood samples were obtained at presentation to an emergency room 4 hours, 8 hours and 16 hours later. The ability of biochemical markers to predict adverse outcomes in both groups including infarction, recurrent ischemia, bypass surgery, heart failure, stroke, death or positive angiography/angioplasty during hospitalization and at six months was assessed by receiver-operator curve analysis. The performance of both troponins was compared between groups.
Results
Thirty-five percent of patients in the renal group and 45% of patients in the nonrenal group experienced an adverse initial outcome; over 50% of patients in all groups had experienced an adverse outcome by 6 months, but these differences were not significant. The area under the curve (AUC) for the ROC curve for troponin T as predictor of initial outcomes was significantly lower in the renal group than in the nonrenal group: 0.56 ± 0.07 and 0.75 ± 0.07, respectively. The area under the curve was also significantly lower in the renal group compared with the nonrenal group for troponin T as predictor of six month outcomes: 0.59 ± 0.07 and 0.74 ± 0.07, respectively. The area under the curve was also significantly lower in the renal group compared to the nonrenal group for troponin I as predictor of both initial and six month outcomes: 0.54 ± 0.06 vs. 0.71 ± 0.07 and 0.53 ± 0.06 vs. 0.65 ± 0.07, respectively. The sensitivity of troponin T for both initial and six month adverse outcomes was significantly lower in the renal group than in the nonrenal group at a similar level of specificity (0.87): 0.29 vs. 0.60 and 0.45 vs. 0.56, respectively. Troponin I also exhibited similar differences in sensitivity in the renal group (0.29 vs. 0.50 and 0.33 vs. 0.40, respectively).
Conclusions
The ability of cardiac troponin T and troponin I to predict risk for subsequent adverse outcomes in patients presenting with suspected acute coronary syndromes is reduced in the presence of renal insufficiency.
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