Context
Cardiac troponin T (cTnT) and C-reactive protein (CRP) are prognostic markers in acute coronary syndromes. However, for patients with end-stage renal disease (ESRD) the ability of combinations of these markers to predict outcomes, and their association with cardiac pathology, are unclear.
Objective
To investigate the association between levels of cardiac troponin T (cTnT) and C-reactive protein (CRP) and long-term risk of cardiac pathology and death in patients with ESRD.
Design, Setting, and Participants
A prospective cohort study initiated February through June 1998 and enrolling 224 patients with ESRD from 5 hemodialysis centers in the Houston-Galveston region of Texas. Levels of cardiac troponin T (cTnT) and C-reactive protein (CRP) were analyzed at study entry in patients without ischemic symptoms.
Main Outcome Measures
All-cause mortality during a mean follow-up of 827 (range, 29-1327) days. Secondary outcomes in predefined substudies were coronary artery disease (CAD), decreased (40%) left ventricular ejection fraction (LVEF), and presence of left ventricular hypertrophy (LVH).
Results
One hundred seventeen (52%) patients died during follow-up. For levels of cardiac troponin T (cTnT) and C-reactive protein (CRP), progressively higher levels predicted increased risk of death compared with the lowest quartile (for cTnT quartile 2: unadjusted hazard ratio [HR], 2.2; 95% confidence interval [CI], 1.2-4.1; quartile 3: HR, 2.7; 95% CI, 1.5-4.9; quartile 4: HR, 3.0; 95% CI, 1.6-5.3. For CRP quartile 2: HR, 0.9; 95% CI, 0.5-1.6; quartile 3: HR, 1.8; 95% CI, 1.1-3.1; quartile 4: HR, 1.8; 95% CI, 1.1-3.2). Both cTnT and CRP remained independent predictors of death after adjusting for a number of potential confounders. The combination of cTnT and CRP results provided prognostic information when patients were divided into groups at or above and below the biomarker medians (high cTnT/high CRP levels vs low cTnT/low CRP levels for risk of death: HR, 2.5; 95% CI, 1.5-4.0). Elevated levels of cTnT, but not CRP, were strongly associated with diffuse CAD (n = 67; 0%, 25%, 50%, and 62% prevalence of multivessel CAD across progressive cTnT quartiles, P<.001). An LVEF of 40% or less was identified in 4 (9%), 3 (8%), 10 (27%), and 7 (19%) of patients across cTnT quartiles (P = .07). No trend for cTnT levels was found among patients with LVH (P = .45); similarly, no trend for CRP was found among patients with LVH (P = .65) or an LVEF of 40% or less (P = .75).
Conclusions
Among stable patients with ESRD, increasing levels of cardiac troponin T (cTnT) and C-reactive protein (CRP) are associated with increased risk of death. Furthermore, higher levels of cTnT may identify patients with severe angiographic coronary disease.
Showing posts with label coronary artery disease. Show all posts
Showing posts with label coronary artery disease. Show all posts
Monday
Cardiac-Specific Troponin I Levels and Risk of Coronary Artery Disease and Graft Failure Following Heart Transplantation
Context
Previous studies have yielded conflicting data regarding whether a relationship exists between elevated cardiac troponin levels and acute allograft rejection in patients who have received heart transplants.
Objective
To determine whether cardiac troponin I levels after heart transplantation were associated with a procoagulant microvasculature and long-term allograft outcome.
Design
Prospective cohort study with a mean (SE) follow-up of 45.1 (2.5) months. Serum troponin I levels were measured 9.9 (0.2) times per patient during the first 12 months after heart transplantation.
Setting
Heart transplant center in the United States.
Patients
A total of 110 consecutive patients who received a heart transplant between 1989 and 1997 and survived at least 1 year after transplantation.
Main Outcome Measures
Histological and immunohistochemical biopsy findings, development of coronary artery disease (CAD), and graft failure in patients with vs without elevated serum cardiac troponin I levels.
Results
All recipients had elevated troponin I levels during the first month after transplantation. Troponin I levels remained persistently elevated during the first 12months in 56 patients (51%) and became undetectable in 54 patients (49%). Persistently elevated troponin I levels were associated with increasing fibrin deposits in microvasculature and cardiomyocytes (P<.001). Patients with persistently elevated levels of troponin I had significantly increased risk for subsequent development of CAD (odds ratio [OR], 4.3; 95% confidence interval [CI], 1.8-10.1; P<.001) and graft failure (OR, 3.4; 95% CI, 1.2-9.7; P = .02), and also developed more severe CAD (OR, 4.2; 95% CI, 1.9-9.3; P<.001) and showed more disease progression (OR, 3.7; 95% CI, 1.3-10.4; P = .009).
Conclusion
In this study, elevated cardiac troponin I levels, which are considered to be a noninvasive surrogate marker of a procoagulant microvasculature, identified a subgroup of patients with high risk for developing CAD and graft failure after cardiac transplantation.
Previous studies have yielded conflicting data regarding whether a relationship exists between elevated cardiac troponin levels and acute allograft rejection in patients who have received heart transplants.
Objective
To determine whether cardiac troponin I levels after heart transplantation were associated with a procoagulant microvasculature and long-term allograft outcome.
Design
Prospective cohort study with a mean (SE) follow-up of 45.1 (2.5) months. Serum troponin I levels were measured 9.9 (0.2) times per patient during the first 12 months after heart transplantation.
Setting
Heart transplant center in the United States.
Patients
A total of 110 consecutive patients who received a heart transplant between 1989 and 1997 and survived at least 1 year after transplantation.
Main Outcome Measures
Histological and immunohistochemical biopsy findings, development of coronary artery disease (CAD), and graft failure in patients with vs without elevated serum cardiac troponin I levels.
Results
All recipients had elevated troponin I levels during the first month after transplantation. Troponin I levels remained persistently elevated during the first 12months in 56 patients (51%) and became undetectable in 54 patients (49%). Persistently elevated troponin I levels were associated with increasing fibrin deposits in microvasculature and cardiomyocytes (P<.001). Patients with persistently elevated levels of troponin I had significantly increased risk for subsequent development of CAD (odds ratio [OR], 4.3; 95% confidence interval [CI], 1.8-10.1; P<.001) and graft failure (OR, 3.4; 95% CI, 1.2-9.7; P = .02), and also developed more severe CAD (OR, 4.2; 95% CI, 1.9-9.3; P<.001) and showed more disease progression (OR, 3.7; 95% CI, 1.3-10.4; P = .009).
Conclusion
In this study, elevated cardiac troponin I levels, which are considered to be a noninvasive surrogate marker of a procoagulant microvasculature, identified a subgroup of patients with high risk for developing CAD and graft failure after cardiac transplantation.
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