Clinical findings in patients with cardiac troponin T elevation and end-stage renal disease without acute coronary syndrome

NO signaling, which manifest clinically as endothelial dysfunction. Although at baseline there were no significant differences in NO metabolites, the present study showed that healthy control subjects produced excess urinary NO metabolites when given supplemental L-arginine. In contrast, in transplant patients, supplemental L-arginine did not lead to increased urinary NO metabolites but decreased serum H2O2 production, suggesting an increase in bioavailability of NO. Therefore, in young transplant patients, possible mechanisms for NO impairment include inadequate substrate for endothelial NO synthase, insufficient endothelial NO synthase production, inhibition of endothelial NO synthase function, or increased scavenging of NO by oxygen-derived free radicals. This study and its implications are clearly limited by a small number of subjects. However, this study’s findings support continued investigation into L-arginine’s effect on systemic arterial pressure and endothelial function in cardiac transplant patients, including free radical production and diurnal blood pressure variations. L-arginine supplementation may prove beneficial in cardiac transplant patients with medically refractory hypertension. 1. Bode-Boger SM, Boger RH, Kielstein JT, Loffler M, Schaffer J, Frolich JC.

Role of endogenous nitric oxide in circadian blood pressure regulation in healthy

humans and in patients with hypertension or atherosclerosis. J Investig Med 2000;48:125–132. 2. Navarro-Antolin J, Rey-Campos J, Lamas S. Transcriptional induction of endothelial nitric oxide gene by cyclosporine A. A role for activator protein-1. J Biol Chem 2000;275:3075–3080. 3. Kojda G, Harrison D. Interactions between NO and reactive oxygen species: pathophysiological importance in atherosclerosis, hypertension, diabetes and heart failure. Cardiovasc Res 1999;43:562–571. 4. Drexler HFT, Pinto FJ, Chenzbraun A, Botas J, Cooke JP, Alderman EL. Effect of L-arginine on coronary endothelial function in cardiac transplant recipients. Circulation 1994;89:1615–1623. 5. Celermajer DS, Sorensen KE, Gooch VM, Spiegelhalter DJ, Miller OI, Sullivan ID, Lloyd JK, Deanfield JE. Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Lancet 1992;340: 1111–1115. 6. Corretti MC, Anderson TJ, Benjamin EJ, Celermajer D, Charbonneau F, Creager MA, Deanfield JE, Drexler HFT, Gerhard-Herman M, Herrington D, Vallance P, Vita J, Vogel R. Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery. J Am Coll Cardiol 2002;39:257–265. 7. National Heart L, and Blood Institute. Report of the Second Task Force on Blood Pressure Control in Children—1987. Pediatrics 1987;79:1–25. 8. Clarkson P, Adams MR, Powe AJ, Donald AE, McCredie R, Robinson J, McCarthy SN, Keech A, Celermajer DS, Deanfield JE. Oral L-arginine improves endothelium-dependent dilation in hypercholesterolemic young adults. J Clin Invest 1996;97:1989 –1994. 9. Blum A, Hathaway L, Mincemoyer R, Schenke WH, Kirby M, Csako G, Waclawiw MA, Panza JA, Cannon RO III. Effects of oral L-arginine on endothelium-dependent vasodilation and markers of inflammation in healthy postmenopausal women. J Am Coll Cardiol 2000;35:271–276. 10. Mullen MJ, Wright D, Donald AE, Thorne S, Thomson H, Deanfield JE. Atorvastatin but not L-arginine improves endothelial function in type I diabetes mellitus: a double-blind study. J Am Coll Cardiol 2000;36:410 – 416. 11. Oriji GK, Keiser HR. Role of nitric oxide in cyclosporine A-induced hypertension. Hypertension 1998;32:849 – 855. 12. Sigfusson G, Fricker FJ, Bernstein D, Addonizio LJ, Baum D, Hsu DT, Chin C, Miller SA, Boyle GJ, Miller J, et al. Long-term survivors of pediatric heart transplantation: a multicenter report of sixty-eight children who have survived longer than five years. J Pediatr 1997;130:862– 871.

Clinical Findings in Patients With Cardiac Troponin T Elevation and End-Stage Renal Disease Without Acute Coronary Syndrome Doo-Soo Jeon, MD, Man-Young Lee, MD, Chong-Jin Kim, MD, Jin-Man Cho, MD, Keon-Woong Moon, MD, Byung-Soo Kim, MD, Seung-Hun Lee, MD, Ki-Bae Seung, MD, Jae-Hyung Kim, MD, Soon-Jo Hong, MD, and Kyu-Bo Choi, MD Clinical, echocardiographic, and carotid ultrasound parameters were compared according to the level of cardiac tropopin T (cTnT) (cTnT <0.04 vs >0.04 ␮g/L; cTnT <0.1 vs >0.1 ␮g/L) in patients with end-stage renal disease without acute coronary syndrome. Left atrial size, left ventricular mass index, the ratio of transmitral early left ventricular filling velocity to early diastolic Doppler tissue imaging velocity of the mitral annulus, and the prevalence of left ventricular dysfunction and diabetes mellitus were higher in the groups with cTnT >0.04 and >0.1 ␮g/L. Diabetes was an independent correlate of cTnT elevation of From the Department of Internal Medicine, Our Lady of Mercy Hospital, College of Medicine, The Catholic University of Korea, Inchon, Korea. Dr. Lee’s address is: Department of Cardiology, Our Lady of Mercy Hospital #665, Pupyoungdong, Pupyounggu, Inchon, 403-016, Korea. E-mail: [email protected]. Manuscript received February 9, 2004; revised manuscript received and accepted May 22, 2004. ©2004 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 94 September 15, 2004

>0.04 and >0.1 ␮g/L. Left ventricular mass index and left atrial size were independent predictors of cTnT elevations of >0.04 and >0.1 ␮g/L, respectively. 䊚2004 by Excerpta Medica, Inc. (Am J Cardiol 2004;94:831– 834)

patients with end-stage renal disease (ESRD), troponin T (cTnT) elevation is found Ievenncardiac in the absence of clinically suspected acute coronary syndrome, and it predicts long-term, allcause mortality and cardiovascular mortality.1–5 In this study, we investigated clinical, transthoracic echocardiographic (TTE), and carotid ultrasound characteristics in relation to cTnT elevation in patients with ESRD on maintenance dialysis without acute coronary syndrome. •••

Ninety-nine patients with ESRD (56 men, 43 women) receiving regular dialysis (51 hemodialysis, 48 peritoneal dialysis) for ⱖ3 months (median 0002-9149/04/$–see front matter doi:10.1016/j.amjcard.2004.05.074

831

TABLE 1 Baseline Characteristics Parameters Age (yrs) Men Hemodialysis Duration of dialysis (mo) Hypercholesterolemia Hypertension Smoker Diabetes mellitus Left atrial size (cm) LV mass index (g/m2.7) LV ejection fraction E/Ea Plaque in carotid artery Thickest IMT (mm)

cTnT ⬍0.04 ␮g/L (n ⫽ 57)

cTnT ⱖ0.04 ␮g/L (n ⫽ 42)

p Value

cTnT ⬍0.1 ␮g/L (n ⫽ 81)

cTnT ⱖ0.1 ␮g/L (n ⫽ 19)

p Value

51 ⫾ 11 38.6% 42.1% 37 ⫾ 34 29.8% 64.9% 10.5% 22.8% 4.05 ⫾ 0.56 61 ⫾ 23 63 ⫾ 10% 8.33 ⫾ 2.77 27.3% 1.11 ⫾ 0.60

56 ⫾ 14 50.0% 64.3% 40 ⫾ 38 9.5% 76.2% 19.0% 52.4% 4.47 ⫾ 0.89 79 ⫾ 26 57 ⫾ 12% 10.33 ⫾ 4.34 40.0% 1.27 ⫾ 0.77

0.029 0.307 0.042 0.791 0.024 0.272 0.256 0.003 0.002 ⬍0.0001 0.014 0.014 0.268 0.483

52 ⫾ 12 39.5% 48.1% 38 ⫾ 36 24.7% 67.9% 12.3% 27.2% 4.12 ⫾ 0.68 66 ⫾ 27 62 ⫾ 11% 8.77 ⫾ 3.49 35.1% 1.22 ⫾ 0.78

58.61 ⫾ 13 61.1% 66.7% 42 ⫾ 35 5.6% 77.8% 22.2% 72.2% 4.71 ⫾ 0.85 79 ⫾ 20 53 ⫾ 11% 11.10 ⫾ 3.79 22.2% 0.99 ⫾ 0.45

0.92 0.118 0.196 0.611 0.109 0.573 0.277 0.001 0.005 0.027 0.013 0.002 0.406 0.34

Values are expressed as means ⫾ SD or as a percentage. LV ⫽ left ventricular.

TABLE 2 Univariate Predictors of cTnT ⱖ0.04 ␮g or cTnT ⱖ0.1 ␮g/L cTnT ⱖ0.04 ␮g/L Odds Ratio (95% CI) Age (yrs) Men Hemodialysis Duration of dialysis (mo) Hypercholesterolemia Hypertension Smoking Diabetes Left atrial size (cm) LV mass index (g/m2.7) LV ejection fraction ⬍45% E/Ea ⬎10 Plaque in carotid artery

1.035 1.591 2.475 1.003 0.248 1.730 2.000 3.723 2.237 1.030 4.231 3.223 1.778

(1.002–1.070) (0.710–3.563) (1.088–5.628) (0.992–1.014) (0.076–0.803) (0.707–4.230) (0.637–6.279) (1.566–8.849) (1.231–4.065) (1.011–1.050) (1.049–17.057) (1.350–7.698) (0.742–4.232)

cTnT ⱖ0.1 ␮g/L p Value 0.04 0.259 0.031 0.63 0.02 0.230 0.235 0.003 0.008 0.002 0.043 0.008 0.194

Odds Ratio (95% CI) 1.044 2.406 2.154 1.003 0.180 1.655 2.028 6.972 3.130 1.018 4.808 2.672 0.529

(0.999–1.090) (0.844–6.856) (0.737–6.295) (0.989–1.017) (0.023–1.435) (0.496–5.522) (0.556–7.393) (2.226–21.837) (1.446–6.776) (0.999–1.058) (1.278–18.085) (0.921–7.752) (0.158–1.767)

p Value 0.053 0.10 0.161 0.671 0.105 0.413 0.284 0.001 0.004 0.066 0.02 0.071 0.301

CI ⫽ confidence interval; other abbreviation as in Table 1.

duration 31) without a history of acute coronary syndrome, at electrocardiography, or cTnI ⱖ0.1 ␮g/L, were eligible for the study. In the patients on hemodialysis, blood was sampled for cTnT (Elecys 2010; Roche Diagnostics, Mannheim, Germany) and cardiac troponin I (cTnI; Diagnostic Products Corporation, California) just before dialysis, and TTE was performed within 1 hour after dialysis. In the patients on peritoneal dialysis, blood was sampled for cTnT and cTnI just before TTE. Patients with mitral valvular disease and atrial fibrillation were excluded. Subjects were divided into 2 groups according to the upper reference limit (0.04 ␮g/L) or the recommended clinical threshold value (0.1 ␮g/L) of cTnT. Hypercholesterolemia was defined as total serum cholesterol ⱖ220 mg/dl or current use of cholesterollowering agents, hypertension as systolic blood pressure ⱖ140 mm Hg and/or diastolic blood pressure ⱖ90 mm Hg or current use of antihypertensive medication, diabetes mellitus as fasting plasma glucose ⱖ126 mg/dl or current use of hypoglycemic agents, and smoking status was defined by current or past smoking ⱖ10 pack-years. 832 THE AMERICAN JOURNAL OF CARDIOLOGY姞

VOL. 94

The TTE measurements using Sequoia C 256 (Acuson, Mountain View, California) were performed according to the recommendation of the American Society of Echocardiography. Left ventricular mass was calculated by the Devereux formula and indexed to height2.7 to minimize any potential distortion attributable to expansion of extracellular volume.6,7 In the apical 4-chamber view, a sample volume (size 2 mm) of the pulse-wave Doppler was placed between the tips of the mitral leaflets, and early transmitral flow velocity (E) was obtained. A pulse-wave Doppler tissue image was also obtained at the septal side of the mitral annulus in the apical 4-chamber view. Early diastolic mitral annulus velocity (Ea) was measured; the Nyquist limit of 20 cm/s was set, with the lowest filter settings and the minimum optimum gain, to minimize noise. The mean values of 3 consecutive cardiac cycles were obtained by 1 investigator and averaged, and the ratio of E to Ea (E/Ea) was calculated. High resolution B-mode carotid sonography was performed with an 8.0-MHz linear-type probe on the same machine. Longitudinal images of the left and right carotid arteries were acquired. Intima media thickness (IMT) was measured with an electronic calSEPTEMBER 15, 2004

TABLE 3 Independent Predictors in the Stepwise Multiple Logistic Regression Analysis

cTnT ⱖ0.04 ␮g/L LV mass index (g/m2.7) Diabetes cTnT ⱖ0.1 ␮g/L Left atrial size (cm) Diabetes

Odds Ratio (95% CI)

p Value

1.025 (1.006–1.045) 3.293 (1.312–8.267)

0.005 0.011

2.889 (1.247–6.691) 5.168 (1.552–17.208)

0.013 0.007

Abbreviation as in Tables 1 and 2.

iper on the frozen frame and evaluated as the distance between the luminal-intimal interface and the medialadventitial interface. IMT was measured at its thickest point on the far wall of the carotid bulb and at the distal 10 mm of the common carotid artery, and the measured IMTs were averaged. Plaque was considered present if the protruding IMT was ⬎1.2 mm. Numerical values are given as mean ⫾ SD or as a proportion of the sample size. Comparisons between the groups were made by the chi-square test for categorical data, and Mann-Whitney test for continuous data. Stepwise multiple logistic regression analysis used entry of a p value ⬍0.05 and exit criteria of a p value ⬍0.1. Data analysis was performed using the SPSS statistical package (version 10.0, SPSS Inc., Chicago, Illinois). In clinical parameters, compared with the cTnT ⬍0.04 ␮g/L group, the cTnT ⱖ0.04 ␮g/L group was more likely to be older, to have diabetes, and to receive hemodialysis. In contrast, the prevalence of hypercholesterolemia was lower in the cTnT ⬍0.04 ␮g/L group. There were no significant differences in these clinical parameters except prevalence of diabetes between the cTnT ⬍0.1 ␮g/L group and the cTnT ⱖ0.1 ␮g/L group. In TTE parameters, left atrial size and left ventricular mass index were significantly higher in the cTnT ⱖ0.04 ␮g/L group as well as the cTnT ⱖ0.1 ␮g/L group. In addition, left ventricular ejection fraction and the prevalence of E/Ea ⬎10 were significantly higher in the cTnT ⱖ0.04 ␮g/L group and the cTnT ⱖ0.1 ␮g/L group. In the mean IMT at the thickest portion and the prevalence of plaque in the carotid artery, no significant differences were found according to the elevation of cTnT ⱖ0.04 ␮g/L or cTnT ⱖ0.1 ␮g/L (Table 1). Univariate predictors of cTnT ⱖ0.04 or ⱖ0.1 ␮g/L are listed in Table 2. With these univariate predictors, we used stepwise multiple logistic regression analysis to assess independent predictors of cTnT ⱖ0.04 or ⱖ0.1 ␮g/L. Diabetes proved to be an independent correlate of cTnT elevation of ⱖ0.04 and ⱖ0.1 ␮g/L. Left ventricular mass index and left atrial size were independent predictors of cTnT elevation of ⱖ0.04 and ⱖ0.1 ␮g/L, respectively (Table 3). •••

The mechanism underlying elevated cTnT concentrations in renal failure is unclear. In experimental renal failure, cardiac function is impaired in association with abnormal cardiac energies and increased

susceptibility to ischemic damage caused by microvascular change,8 –10 and left ventricular hypertrophy is not accompanied by a commensurate increase in capillaries.11,12 These functional and anatomic changes may contribute to the increased susceptibility to ischemic injury. In clinical studies, a positive correlation between elevated concentrations of cTnT and an increase in left ventricular mass has also been reported.4,11,13 Elevated serum cTnT was associated with recent acute myocardial infarction/microinfarct, a healing microinfarct, heart failure/degenerative changes, or other myocardial damage in autopsied ESRD cases.12 Thus, the increased cTnT in ESRD may point to ongoing pathologic changes leading to functional and anatomic impairment rather than an acute coronary syndrome. Measurement of IMT by carotid ultrasound is a very useful method for screening for atherosclerosis.14,15 In this study there was no difference in the average maximum IMT or the prevalence of plaque between the high and low cTnT groups. Thus, atherosclerosis may not be centrally involved in cTnT elevation in ESRD. In addition to a coronary risk factor, diabetes results in functional, biochemical, and morphologic abnormalities independent of myocardial ischemia.16 These abnormalities, not atherosclerosis, may contribute to the elevation of cTnT in ESRD. Our study is limited in that the dialysis method may affect the TTE parameters. TTE was performed within 1 hour after hemodialysis. Because the left ventricular filling pressure was lowest at that time, we may have measured the lowest level of E in the ESRD patients on hemodialysis and this may have introduced some error into the measurements of E/Ea, indicating a pulmonary capillary wedge pressure. In a further study, direct measurements of filling pressure of left ventricular or B-type natriuretic peptide may be needed. 1. Dierkes J, Domrose U, Westphal S, Ambrosch A, Bosselmann HP, Neumann KH, Luley C. Cardiac troponin T predicts mortality in patients with end-stage renal disease. Circulation 2000;102:1964 –1969. 2. Ooi DS, Zimmerman D, Graham J, Wells GA. Cardiac troponin T predicts long-term outcomes in hemodialysis patients. Clin Chem 2001;47:412– 417. 3. Apple FS, Murakami MM, Pearce LA, Herzog CA. Predictive value of cardiac troponin I and T for subsequent death in end-stage renal disease. Circulation 2002;106:2941–2945. 4. Mallamaci F, Zoccali C, Parlongo S, Tripepi G, Benedetto FA, Cutrupi S, Bonanno G, Fatuzzo P, Rapisarda F, Seminara G, et al. Troponin is related to left ventricular mass and predicts all-cause and cardiovascular mortality in hemodialysis patients. Am J Kidney Dis 2002;40:68 –75. 5. Wood GN, Keevil B, Gupta J, Foley R, Bubtana A, McDowell G, Ackrill P. Serum troponin T measurement in patients with chronic renal impairment predicts survival and vascular disease: a 2 year prospective study. Nephrol Dial Transplant 2003;18:1610 –1615. 6. de Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, de Divitiis O, Alderman MH. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight. J Am Coll Cardiol 1992;20:1251–1260. 7. Zoccali C, Benedetto FA, Mallamaci F, Tripepi G, Giacone G, Cataliotti A, Seminara G, Stancanelli B, Malatino LS, CREED Investigators. Prognostic impact of the indexation of left ventricular mass in patients undergoing dialysis. J Am Soc Nephrol 2001;12:2768 –2774. 8. Raine AE, Seymour AM, Roberts AF, Radda GK, Ledingham JG. Impairment of cardiac function and energetics in experimental renal failure. J Clin Invest 1993;92:2934 –2940. 9. Tornig J, Gross ML, Simonaviciene A, Mall G, Ritz E, Amann K. Hypertrophy of intramyocardial arteriolar smooth muscle cells in experimental renal failure. J Am Soc Nephrol 1999;10:77– 83.

BRIEF REPORTS

833

10. Amann K, Wiest G, Zimmer G, Gretz N, Ritz E, Mall G. Reduced capillary density in the myocardium of uremic rats—a stereological study. Kidney Int 1992;42:1079 –1085. 11. Lowbeer C, Ottosson-Seeberger A, Gustafsson SA, Norrman R, Hulting J, Gutierrez A. Increased cardiac troponin T and endothelin-1 concentrations in dialysis patients may indicate heart disease. Nephrol Dial Transplant 1999;14: 1948 –1955. 12. Ooi DS, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem 2000;46:338 –344. 13. Mallamaci F, Zoccali C, Parlongo S, Tripepi G, Benedetto FA, Cutrupi S, Bonanno G, Fatuzzo P, Rapisarda F, Seminara G, et al. Cardiovascular risk

extended evaluation in dialysis investigators. Diagnostic value of troponin T for alterations in left ventricular mass and function in dialysis patients. Kidney Int 2002;62:1884 –1890. 14. Bots ML, Hoes AW, Koudstaal PJ, Hofman A, Grobbee DE. Common carotid intima-media thickness and risk of stroke and myocardial infarction: the Rotterdam Study. Circulation 1997;96:1432–1437. 15. Chambless LE, Heiss G, Folsom AR, Rosamond W, Szklo M, Sharrett AR, Clegg LX. Association of coronary heart disease incidence with carotid arterial wall thickness and major risk factors: the Atherosclerosis Risk in Communities (ARIC) Study, 1987–1993. Am J Epidemiol 1997;146:483– 494. 16. Taegtmeyer H, McNulty P, Young ME. Adaptation and maladaptation of the heart in diabetes: part I: general concepts. Circulation 2002;105:1727–1733.

Ability of Troponin T to Predict Angiographic Coronary Artery Disease in Patients With Chronic Kidney Disease Chamberlain I. Obialo, MD, Shalini Sharda, MD, Smriti Goyal, MD, Elizabeth O. Ofili, MD, Adefisayo Oduwole, MD, and Nancy Gray, BS, An association between angiographic coronary artery disease and cardiac troponin T levels has been observed in patients with normal kidney function; however, this association remains unsettled in patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD). Over a 12-month period we retrospectively reviewed coronary angiograms (CAs) performed in 194 hospitalized patients with presumed acute myocardial injury. About 50% of the ESRD and 30% of the CKD patients had normal CAs. Troponin T levels significantly correlated with CAs in patients with normal kidney function (r ⴝ 0.4, p ⴝ 0.005) but not in ESRD and CKD patients (r ⴝ 0.2, p ⴝ NS, respectively). 䊚2004 by Excerpta Medica, Inc. (Am J Cardiol 2004;94:834 – 836)

ardiac troponin T and troponin I have emerged as sensitive predictors of mortality in patients with C end-stage renal disease (ESRD). Troponin T levels 1,2

above the diagnostic threshold for acute myocardial injury have been observed in patients with ESRD with no evidence for myocardial injury.2,3 Thus, the sensitivity of troponin T for predicting angiographic coronary artery disease (CAD) in patients with chronic kidney disease (CKD) or ESRD remains subjective. A recent study in asymptomatic hemodialysis patients reported that increasing troponin T levels showed an association with diffuse CAD.4 We observed that some of our patients with ESRD admitted to the From the Department of Medicine, and Nephrology and Cardiology Sections, Morehouse School of Medicine, and Cardiac Catheterization Laboratory, Grady Memorial Hospital, Atlanta, Georgia. This study was supported in part by Grant no. NIHCRC, 1P20-RR 1110404-RCR11 from the Morehouse School of Medicine Clinical Research Center, Atlanta, Georgia. Dr. Obialo’s address is: Department of Medicine, Morehouse School of Medicine, 720 West View Drive, SW, Atlanta, Georgia 30310. E-mail: [email protected]. Manuscript received January 30, 2004; revised manuscript received and accepted May 5, 2004.

834

©2004 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 94 September 15, 2004

RT

hospital with presumed myocardial infarction and elevated troponin T levels had normal coronary angiograms (CAs); hence, the initiation of this retrospective review, which was designed to evaluate the relation between troponin T levels at and above the diagnostic threshold for myocardial injury, renal function, and angiographic CAD. •••

We retrospectively reviewed all CAs performed at the Grady Memorial Hospital, Atlanta, Georgia, over a 12-month period (January 2001 to December 2001). Through an integrated computer system, all patients who had cardiac troponin assays were identified for data abstraction from hard copies of their charts. Only hospitalized patients with acute coronary syndromes or presumed acute myocardial injury who had emergency CAs were included in this study. Patients with troponin T levels ⬍0.10 ng/ml were excluded. Patients with a history of coronary angioplasty, stent placement, or coronary artery bypass graft surgery were also excluded from analysis. Of the 950 CAs reviewed, 194 cases met the inclusion criteria and are presented in this report. Angiographic CAD was classified into 4 categories: normal, mild (⬍50% stenosis), moderate (50% to 69% stenosis), and severe (ⱖ70% stenosis of any major epicardial coronary artery). Renal function was classified into 3 groups according to the glomerular filtration rate: normal renal function was defined as glomerular filtration rate ⱖ90 ml/min/1.73 m2, CKD (glomerular filtration rate ⬍90 ml/min/1.73 m2 and the patient not on maintenance dialysis), and ESRD if the patient is already on maintenance dialysis. The glomerular filtration rate was determined with the Modification of Diet in Renal Disease Study equation: glomerular filtration rate ⫽ 170 ⫻ (creatinine)⫺0.999 ⫻ (blood urea nitrogen)⫺0.170 ⫻ (albumin)⫺0.176 ⫻ 0.762 (if female) ⫻ 1.180 (if black). Data are reported as mean ⫾ SD where applicable. The relation between troponin T levels and angiographic CAD was evaluated with Spearman’s rank 0002-9149/04/$–see front matter doi:10.1016/j.amjcard.2004.05.075