scholarly journals TROPONIN T IS A STRONG MARKER FOR CARDIOVASCULAR DISEASE IN DIALYSIS PATIENTS, DESPITE HIGH BACKGROUND LEVELS OF SERUM TROPONIN T

2014 ◽  
Vol 63 (12) ◽  
pp. A1545
Author(s):  
Maurits Buiten ◽  
Joris Rotmans ◽  
Arnoud van der Laarse ◽  
Johan Jukema
1997 ◽  
Vol 43 (6) ◽  
pp. 976-982 ◽  
Author(s):  
Mary D McLaurin ◽  
Fred S Apple ◽  
Ellen M Voss ◽  
Charles A Herzog ◽  
Scott W Sharkey

Abstract Serum cardiac troponin T (cTnT) concentrations are frequently increased in chronic dialysis patients as measured by the first-generation ELISA immunoassay, as is creatine kinase (CK) MB mass in the absence of acute ischemic heart disease. We designed this study to compare four serum markers of myocardial injury [CK-MB mass, first-generation ELISA cTnT, second-generation Enzymun cTnT, and cardiac troponin I (cTnI)] in dialysis patients without acute ischemic heart disease. We also evaluated skeletal muscle from dialysis patients as a potential source of serum cTnT. No patients in the clinical evaluation group (n = 24) studied by history and by physical examination, electrocardiography, and two-dimensional echocardiography had evidence of ischemic heart disease. Biochemical markers were measured in serial predialysis blood samples with specific monoclonal antibody-based immunoassays. For several patients at least one sample measured above the upper reference limit: CK-MB, 7 of 24 (30%); ELISA cTnT, 17 of 24 (71%); Enzymun cTnT, 3 of 18 (17%); and cTnI, 1 of 24 (4%). In a separate group of dialysis patients (n = 5), expression of cTnT, but not cTnI, was demonstrated by Western blot analysis in 4 of 5 skeletal muscle biopsies. Chronic dialysis patients without acute ischemic heart disease frequently had increased serum CK-MB and cTnT. The specificity of the second-generation cTnT (Enzymun) assay was improved over that of the first-generation (ELISA) assay; cTnI was the most specific of the currently available biochemical markers. cTnT, but not cTnI, was expressed in the skeletal muscle of dialysis patients.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
David Berg ◽  
Stephen D Wiviott ◽  
Eugene Braunwald ◽  
David A Morrow ◽  

Background: Circulating biomarkers reflecting pathways implicated in heart failure (HF) may improve HF risk assessment in patients with stable atherosclerotic cardiovascular disease (ASCVD). Hypothesis: We aimed to evaluate the performance of circulating biomarkers of hemodynamic stress, myocardial injury, and inflammation for the prediction of hospitalization for HF (HHF) in a large well-characterized cohort with stable ASCVD followed for a median of 4.1 years. Methods: HPS3/TIMI 55-REVEAL was a randomized, double-blind, placebo-controlled trial of the CETP inhibitor anacetrapib in patients with stable ASCVD. We performed a nested prospective biomarker study, measuring high-sensitivity troponin T (hsTnT), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and growth differentiation factor-15 (GDF-15) (all Roche Diagnostics) at randomization (n=29,673). Hazard ratios were adjusted for covariates of a priori clinical relevance to HHF risk: age, prior HF, hypertension, diabetes mellitus, eGFR <60, body-mass index, and polyvascular disease. Discrimination was assessed using Harrell’s c-index. Results: A significant graded risk of HHF was observed with increasing deciles of hsTnT, NT-proBNP, and GDF-15 (p-trend <0.001 for each) ( Figure ). These associations remained significant after multivariable adjustment for clinical risk factors (p<0.001 for each). When added to a multivariable Cox regression model of clinical risk indicators (c-index 0.74), these 3 biomarkers significantly improved the prognostic performance of the model (c-index 0.85; p<0.001). There was no treatment interaction with anacetrapib. Conclusions: In patients with stable ASCVD, biomarkers of myocardial injury, hemodynamic stress, and inflammation provide incremental information for prediction of HHF. Future studies should address whether these patients are more likely to benefit from emerging HF preventive therapies.


2017 ◽  
Author(s):  
John K. Roberts ◽  
John P. Middleton

Cardiovascular disease is a common cause of death and disease in patients with end-stage renal disease (ESRD). Registry data show that 41% of deaths in ESRD patients are due to a variety of cardiovascular causes, such as acute myocardial infarction, congestive heart failure, arrhythmia/sudden cardiac death, and stroke. In the general population, each of these disease entities in isolation can be effectively managed according to evidence from large clinical trials and evidence-based guidelines. However, many of these trials did not include patients with ESRD, limiting the transferability of this evidence to the care of patients on dialysis. To complicate matters, cardiovascular events in ESRD patients are likely augmented from a unique interplay of cardiac risk due to both reduced kidney function and the necessity for artificial renal replacement therapies. In this light, the patient on dialysis is subjected to a series of unique factors: the continued presence of the metabolic perturbations of uremia and the peculiar environment of the dialysis treatment itself. Since the ESRD heart is under a considerable amount of strain due to chronic volume overload, rapid electrolyte and fluid shifts, and accelerated vascular calcification, management can be complex and outcomes multifactorial. In this review, we summarize the current evidence regarding management of acute myocardial infarction, heart failure, sudden cardiac death, and atrial fibrillation. We also address modifiable risk factors related to the dialysis procedure itself and highlight recent randomized controlled trials that included dialysis patients and measured important cardiovascular outcomes. 


2017 ◽  
Author(s):  
John K. Roberts ◽  
John P. Middleton

Cardiovascular disease is a common cause of death and disease in patients with end-stage renal disease (ESRD). Registry data show that 41% of deaths in ESRD patients are due to a variety of cardiovascular causes, such as acute myocardial infarction, congestive heart failure, arrhythmia/sudden cardiac death, and stroke. In the general population, each of these disease entities in isolation can be effectively managed according to evidence from large clinical trials and evidence-based guidelines. However, many of these trials did not include patients with ESRD, limiting the transferability of this evidence to the care of patients on dialysis. To complicate matters, cardiovascular events in ESRD patients are likely augmented from a unique interplay of cardiac risk due to both reduced kidney function and the necessity for artificial renal replacement therapies. In this light, the patient on dialysis is subjected to a series of unique factors: the continued presence of the metabolic perturbations of uremia and the peculiar environment of the dialysis treatment itself. Since the ESRD heart is under a considerable amount of strain due to chronic volume overload, rapid electrolyte and fluid shifts, and accelerated vascular calcification, management can be complex and outcomes multifactorial. In this review, we summarize the current evidence regarding management of acute myocardial infarction, heart failure, sudden cardiac death, and atrial fibrillation. We also address modifiable risk factors related to the dialysis procedure itself and highlight recent randomized controlled trials that included dialysis patients and measured important cardiovascular outcomes. 


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