Relationship between elevated serum troponin values in end-stage renal disease patients and abnormal isotopic cardiac scans following stress.
One hundred asymptomatic high-risk renal transplant candidates were screened for asymptomatic coronary artery disease using stress cardiac isotopic imaging. The cardiac markers, serum cTnT, cTnI, and CKMB, were collected pre and post stress testing. Of the 99 patients whose cardiac scans were technically satisfactory, 32 were normal, 49 had a definite imaging abnormality and the scan was indeterminate in the remaining 18 patients. Based on these results, patients were stratified into either normal, indeterminate or abnormal scan groups. They then were analyzed to detect any correlations between cardiac perfusion defects and either elevated pre-stress cardiac markers or consistent changes 24h after stress testing. While the mean pre-stress serum values for both cardiac troponin T (0.117 +/- 0.12 microgram/L) and cardiac troponin I (0.235 +/- 0.89 microgram/L) were increased in the abnormal cardiac scan group, only the cTnT value proved to differ significantly from the normal group (p < 0.01). For the indeterminate group neither marker was different from the normal scan group. Only an elevated serum cTnT > 0.1 microgram/L (OR 3.042, p = 0.030) proved to discriminate an abnormal scan in this population. It is concluded that the increase in pre-stress serum cTnT encountered in patients with chronic renal failure, with or without evidence of overt, symptomatic coronary artery disease, may represent a combination of subclinical myocardial damage and a prolonged half-life of the marker in the serum. Because of the frequency of elevated serum concentrations of cTnT and, to a lesser degree cTnI, the physician should exercise caution when interpreting a single elevated Troponin value during the evaluation of chest pain in patients with end-stage renal disease. A cTnT > 0.1 microgram/L increases the likelihood of finding significant coronary artery disease three fold in high-risk ESRD patients being evaluated for renal transplantation.
Porter
George A
GA
Division of Nephrology, Hypertension and Clinical Pharmacology, PP 262 Department of Medicine, Oregon Health Sciences University, Portland, Oregon, USA.
Norton
Theadore L
TL
Lindsley
Jessie
J
Stevens
Jeffrey S
JS
Phillips
David S
DS
Bennett
William M
WM
D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D005080:Exercise Test; D005260:Female; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000628:therapy; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood / Q000150:complications; D015425:Myocardial Reperfusion; D009922:Oregon; D011237:Predictive Value of Tests; D006435:Renal Dialysis; D013223:Statistics as Topic; D014336:Troponin / Q000097:blood*
D015415:Biomarkers; D007527:Isoenzymes; D014336:Troponin; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form