Elevation of serum cardiac troponin I in noncardiac and cardiac diseases other than acute coronary syndromes.

This study evaluated the role of serum cardiac troponin I as a biochemical marker for the diagnosis of acute coronary syndromes in the presence of noncardiac diseases. Diagnostic characteristics were examined in 102 consecutive patients who were found to have serum cardiac troponin I levels higher than the upper reference limit of 0.6 ng/mL. Of 102 patients with cardiac troponin I levels of >0.6 ng/mL, 35 did not have the final diagnoses of acute coronary syndromes (myocardial infarction or unstable angina) but had various other final diagnoses, including nonischemic dilated cardiomyopathy, muscular disorders, central nervous system disorders, HIV disease, chronic renal failure, sepsis, lung diseases, and endocrine disorders. The mean value of serum cardiac troponin I in the patients with diseases other than acute coronary syndromes was significantly lesser than in those with acute coronary syndromes (2.0+/-1.9 [SD] v. 24.7+/-28.2 ng/mL; P<.0001). There were significantly fewer histories of chest pain and prior myocardial infarction in patients with diseases other than acute coronary syndromes than in those with acute coronary syndromes (history of chest pain, 3 v. 48 patients [P<.001]; history of prior myocardial infarction, 0 v. 30 patients [P<.001]). In conclusion, elevated serum levels of cardiac troponin I, especially in the lower ranges, should be interpreted with caution, particularly in patients suffering from acute illnesses who lack other diagnostic features suggestive of acute coronary ischemic events.

Increased regional and transmyocardial dispersion of ventricular repolarization in end-stage renal disease.

BACKGROUND: Approximately half of patients with end-stage renal disease die because of cardiac disease, and ventricular arrhythmias are the common terminal events. Increased dispersion of the repolarization phase of the myocardial action potential can predispose patients to ventricular tachycardia and fibrillation causing cardiac death. OBJECTIVE: To determine the existence of increased regional and transmyocardial dispersion of ventricular repolarization in end-stage renal disease. STUDY DESIGN: Case-control prospective study. PATIENTS AND METHODS: The QT dispersion and the interval between the peak of the T wave (Tp) and the end of the T wave (Te) on a surface electrocardiogram represent regional and transmyocardial dispersion in ventricular repolarization, respectively. The prehemodialysis QT dispersions and Tp-Te intervals of 94 consecutive patients with end-stage renal disease were determined and compared with those of age- and sex-matched healthy controls. RESULTS: Both the QT and the QTc dispersion were significantly higher in the end-stage renal disease group than in the control group (QT dispersion 46 +/- 17 ms [mean +/- SD] versus 26 +/- 16 ms, P < 0.001; QTc dispersion 51 +/- 20 ms versus 30 +/- 20 ms, P < 0.001). Similarly, both the corrected average Tp-Te and the corrected maximum Tp-Te intervals were significantly higher in the end-stage renal disease group than in the control group (corrected average Tp-Te interval 99 +/- 19 ms versus 87 +/- 19 ms, P = 0.023; corrected maximum Tp-Te interval 114 +/- 23 ms versus 103 +/- 23 ms, P = 0.023). CONCLUSIONS: Increased regional and transmyocardial dispersion of ventricular repolarization in end-stage renal disease was demonstrated. This increased dispersion may be a contributory factor in the high cardiac mortality in patients with end-stage renal disease.

Specificity of cardiac troponin I and creatine kinase-MB isoenzyme in asymptomatic long-term hemodialysis patients and effect of hemodialysis on these cardiac markers.

OBJECTIVES: The objectives of this study were: (1) to evaluate the specificity of cardiac troponin I and creatine kinase-MB isoenzyme in ambulatory asymptomatic chronic renal failure patients on long-term hemodialysis, and (2) to evaluate the effect of hemodialysis on the serum levels of cardiac troponin I and creatine kinase-MB isoenzyme. METHODS: One hundred and forty-four consecutive ambulatory asymptomatic chronic renal failure patients on hemodialysis for a minimum of 1 year were evaluated clinically. Serum cardiac troponin I and creatine kinase-MB isoenzyme levels were measured with specific monoclonal antibodies before and after dialysis using ACCESS Troponin I and ACCESS CK-MB assays. RESULTS: The specificity of serum cardiac troponin I was 83% with a cutoff level of 0.03 ng/ml, which is an expected level for healthy population, but it rose to 100% with a cutoff level of 0.15 ng/ml, which is a reference level for patients with acute myocardial infarction. Twenty-four (17%) patients had borderline elevation in cardiac troponin I (>0.03 to <0.15 ng/ml). A history of angina pectoris was more common in the borderline-elevated cardiac troponin I subgroup. In 28% of the patients, serum creatine kinase-MB isoenzyme levels were increased with a specificity of 72% at a cutoff level of 4 ng/ml, which is the upper limit of normal, but the specificity rose to 98% by increasing the cutoff level value to 10 ng/ml. There were no statistically significant differences in serum levels of cardiac troponin I and creatine kinase-MB isoenzyme before and after dialysis. CONCLUSIONS: Cardiac troponin I is highly specific in ambulatory asymptomatic chronic renal failure patients on long-term hemodialysis; borderline elevations in cardiac troponin I may represent microinjury to the myocardium. A serum level of creatine kinase-MB isoenzyme >2.5 times of the normal upper limit may be highly specific in this patient population. Hemodialysis per se does not significantly change the serum levels of cardiac troponin I and creatine kinase-MB isoenzyme.