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Cardiac troponins have no prognostic value for acute and chronic cardiac events in asymptomatic patients with end-stage renal failure.
Clinical Nephrology 2001 July
BACKGROUND: Cardiovascular diseases determine overall mortality in patients with end-stage renal failure. Therefore, testing for myocardial ischemia is important. Elevation of cardio-specific troponins have been frequently measured in patients with end-stage renal failure. Thus, we studied systematically whether patients on chronic intermittent hemodialysis without overt coronary heart disease have increased serum levels of cardiac troponin T and cardiac troponin I. After 2 years, the patients were screened again for cardiac events.
METHODS AND RESULTS: The patients had no history of angina during the previous 3 months or myocardial infarction (MI) within the previous 2 years. For analysis we used two cardio-specific assays for troponin T as well as for troponin I and compared the results with the CK-MB concentration. In a number of patients serum concentrations were elevated above the reference range as follows: troponin T rapid bedside assay: 41 of 100 patients, troponin I rapid bedside assay: 27 of 100 patients, quantitative measurement oftroponin T: 22 of 100 patients, quantitative measurement oftroponin I: 7 of 100 patients, CK-MB: 2 of 100 patients. The increased serum levels of cardiac troponins were neither the result of uremic perimyocarditis (pericardial effusion), changes in the hemodialysis regimen, pulmonary congestion nor were they consistent with the etiology of renal failure. None of the patients with an elevated troponin level in either of the test suffered from any acute cardiac event initially. Within 2 years 18 of 100 patients died, 13 out of them because of cardiac events. Fourteen patients had a myocardial infarction and 19 patients developed angina pectoris. Sensitivity and specificity (0.75 and 0.67) of troponin T rapid bedside assay for MACE (angina pectoris, MI, cardiac death) was lower compared to studies in patients with normal renal function. Correlation between troponin elevation and late outcome was low or absent.
CONCLUSION: Patients on chronic intermittent hemodialysis frequently present with elevated TnT and TnI levels which cannot be used as predictors of acute and chronic cardiac events. Rapid bedside assays have a lower specificity than quantitative assays.
METHODS AND RESULTS: The patients had no history of angina during the previous 3 months or myocardial infarction (MI) within the previous 2 years. For analysis we used two cardio-specific assays for troponin T as well as for troponin I and compared the results with the CK-MB concentration. In a number of patients serum concentrations were elevated above the reference range as follows: troponin T rapid bedside assay: 41 of 100 patients, troponin I rapid bedside assay: 27 of 100 patients, quantitative measurement oftroponin T: 22 of 100 patients, quantitative measurement oftroponin I: 7 of 100 patients, CK-MB: 2 of 100 patients. The increased serum levels of cardiac troponins were neither the result of uremic perimyocarditis (pericardial effusion), changes in the hemodialysis regimen, pulmonary congestion nor were they consistent with the etiology of renal failure. None of the patients with an elevated troponin level in either of the test suffered from any acute cardiac event initially. Within 2 years 18 of 100 patients died, 13 out of them because of cardiac events. Fourteen patients had a myocardial infarction and 19 patients developed angina pectoris. Sensitivity and specificity (0.75 and 0.67) of troponin T rapid bedside assay for MACE (angina pectoris, MI, cardiac death) was lower compared to studies in patients with normal renal function. Correlation between troponin elevation and late outcome was low or absent.
CONCLUSION: Patients on chronic intermittent hemodialysis frequently present with elevated TnT and TnI levels which cannot be used as predictors of acute and chronic cardiac events. Rapid bedside assays have a lower specificity than quantitative assays.
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