Article

High-sensitive troponin T in chronic heart failure correlates with severity of symptoms, left ventricular dysfunction and prognosis independently from N-terminal pro-b-type natriuretic peptide

Department of Cardiology, Klinik und Poliklinik fuer Innere Medizin II, Universitätsklinikum Regensburg, Regensburg, Germany.
Clinical Chemistry and Laboratory Medicine (Impact Factor: 2.96). 09/2011; 49(11):1899-906. DOI: 10.1515/CCLM.2011.251
Source: PubMed

ABSTRACT Troponin T is an established marker of myocardial ischemia. We speculated that the role of the new high-sensitive troponin T (hs-cTnT) might expand towards non-ischemic myocardial disease, indicate disease severity and allow for prognostication in chronic heart failure.
Hs-cTnT (Roche Diagnostics, Mannheim, Germany) was assessed in 233 individuals with chronic heart failure (n=149) or healthy controls (n=84).
Hs-cTnT was significantly elevated in patients with chronic heart failure [0.018 ng/mL, interquartile range (IQR) 0.009-0.036 ng/mL, vs. controls 0.003 ng/mL, 0.003-0.003 ng/mL, p<0.001] and positively correlated with N-terminal pro-b-type natriuretic peptide (NT-proBNP) (r=0.79, p<0.001). Hs-cTnT increased stepwise and signitificantly according to clinical (NYHA stage) as well as functional (LV ejection fraction, fluid retention) severity (each p<0.001). At a binary cutpoint of 0.014 ng/mL, hs-TropT was a significant predictor of all-cause mortality and all-cause mortality or rehospitalization for congestive heart failure (each p≤0.01). Of note, the prognostic value of hs-TropT was independent and additive to that of NT-proBNP.
Hs-cTnT increases stepwise with the severity of symptoms and LV dysfunction and offers important prognostic information in chronic heart failure, independently from and additive to NT-proBNP. The utility of hs-cTnT expands beyond acute myocardial ischemia and towards chronic heart failure.

0 Followers
 · 
104 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: -Clinical trials in heart failure have focused on the improvement in symptoms or decreases in the risk of death and other cardiovascular events. Little is known about the effect of drugs on the risk of clinical deterioration in surviving patients. -We compared the angiotensin-neprilysin inhibitor LCZ696 (400 mg daily) with the angiotensinconverting enzyme inhibitor enalapril (20 mg daily) in 8399 patients with heart failure and reduced ejection fraction in a double-blind trial. The analyses focused on prespecified measures of nonfatal clinical deterioration. In comparison with the enalapril group, fewer LCZ696-treated patients required intensification of medical treatment for heart failure (520 versus 604; hazard ratio, 0.84; 95% confidence interval, 0.74-0.94; P=0.003) or an emergency department visit for worsening heart failure (hazard ratio, 0.66; 95% confidence interval, 0.52-0.85; P=0.001). The patients in the LCZ696 group had 23% fewer hospitalizations for worsening heart failure (851 versus 1079; P<0.001) and were less likely to require intensive care (768 versus 879; 18% rate reduction, P=0.005), to receive intravenous positive inotropic agents (31% risk reduction, P<0.001), and to have implantation of a heart failure device or cardiac transplantation (22% risk reduction, P=0.07). The reduction in heart failure hospitalization with LCZ696 was evident within the first 30 days after randomization. Worsening of symptom scores in surviving patients was consistently more common in the enalapril group. LCZ696 led to an early and sustained reduction in biomarkers of myocardial wall stress and injury (N-terminal pro-Btype natriuretic peptide and troponin) versus enalapril. -Angiotensin-neprilysin inhibition prevents the clinical progression of surviving patients with heart failure more effectively than angiotensin-converting enzyme inhibition. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01035255.
    Circulation 11/2014; DOI:10.1161/CIRCULATIONAHA.114.013748 · 14.95 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The aim was to evaluate the cardio-protective effect of atorvastatin in combination with standard chronic heart failure (CHF) therapy that might improve cardiac function, remodeling, and further delay the progression of CHF in patients and rats.Methods and resultsCHF patients (n = 20 per group) with left ventricular ejection fraction (LV-EF) <45% were randomized into: standard anti-failure treatment alone (controls) and standard anti-failure treatment plus atorvastatin (40 mg/day) for 6 weeks. After 6 weeks, the patients were assessed using echocardiography. Laboratory evaluation for lipid profiles, high sensitive C-reactive protein (hs-CRP), cardiac troponin-T (cTnT) and malondialdehyde (MDA) were performed in all patients. In parallel, rats (n = 10 per group) received treatment for 4 weeks and were divided as follows: saline treated (control, 1 ml intraperitoneal, IP), doxorubicin treated (2.5 mg/kg, IP), atorvastatin–doxorubicin treated (10 mg/kg, orally), and digoxin–doxorubicin treated (0.02 mg/kg, orally). The same laboratory analysis including histopathology of heart tissues was performed on the rats.In patients, atorvastatin improved heart function (increased LV-EF%, LV-fraction shorting (LV-FS%), and E/A velocity ratio; decreased LV-end diastolic diameter (LV-EDD) and LV-end systolic diameter (LV-ESD)) and significantly reduced serum lipid profiles, cTnT, hs-CRP and MDA versus patient controls. In rats, atorvastatin improved signs of CHF, systolic blood pressure, reduced serum lipid profiles, cTnT, hs-CRP and tissue MDA; less cardiac necrosis and fibrosis with enhancement of neo-vascularization versus other doxorubicin-treated rats.Conclusions Atorvastatin with standard CHF therapy improved cardiac function and remodeling. Cardio-protective “pleiotropic” actions of atorvastatin are anti-inflammatory, anti-fibrotic and anti-oxidative. Thus, atorvastatin has a potential therapeutic value in the management of CHF patients.
    11/2014; DOI:10.1016/j.ehj.2014.11.003
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Cardiac troponin levels offer prognostic information for patients with heart failure. Highly sensitive assays detect levels of cTn much lower than the 99th percentile of standard cTn assays. We hypothesize that cardiac troponin (cTn) levels measured by a high sensitivity assay provide better prognostic value compared to cTn levels measured by a standard assay in patients with chronic heart failure. Methods We measured high sensitivity cTnT (hs-cTnT) and standard cTnI levels, as well as aminoterminal pro B-type natriuretic peptide (NT-proBNP) in 504 sequential stable patients with a history of heart failure who underwent elective coronary angiography, without acute coronary syndrome, and with 5-year follow-up of all-cause mortality. Results The median hs-cTnT level was 21.2 [interquartile range 12.3, 40.9] ng/L and 170 subjects died over 5-years. In a head-to-head overall comparison, hs-cTnT provided increased prognostic utility compared to cTnI (area under the curve [AUC] 66.1% and AUC 69.4%, respectively, p=0.03; 9.0% integrated discrimination improvement, p<.001; and 13.6% event-specific reclassification, p<.001), and was independent of NT-proBNP and renal function. Even within the subset of patients where cTn levels by both assays were above the limit of quantification, higher hs-cTnT is associated with a 2-fold increase in 5-year mortality risk after adjusting for traditional risk factors (tertile 1 vs. 3: Hazard ratio [95% confidence interval] 2.0 [1.3-3.2]; p=0.0002). Conclusion Cardiac troponin can be detected by the high sensitivity assay in more patients with chronic heart failure than the standard assay, and may yield independent and better prognostic accuracy for mortality prediction than standard assay.
    The American Journal of Medicine 10/2014; 128(3). DOI:10.1016/j.amjmed.2014.09.029 · 5.30 Impact Factor