Troponin T levels in patients with acute heart failure: clinical and prognostic significance of their detection and release during hospitalisation

Metra, Marco; Bettari, Luca; Pagani, F.; Lazzarini, Valentina; Lombardi, Carlo; Carubelli, Valentina; Bonetti, Graziella; Bugatti, Silvia; Parrinello, Giovanni; Caimi, Luigi; Felker, G. Michael; Dei, Livio

doi:10.1007/s00392-012-0441-5

Cited by 39 publications

(15 citation statements)

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“…In this analysis of a large clinical trial population, cTnI levels were associated with in‐hospital outcomes but not post‐discharge outcomes in a large cohort of patients with ADHF. Given that these results differ from those of other recent analyses,, they will require confirmation in other data sets. Further research with contemporary assays is needed to define the appropriate role of troponin as a biomarker in the clinical care of patients with HF.…”

Section: Discussioncontrasting

confidence: 64%

Troponin I in acute decompensated heart failure: insights from the ASCEND‐HF study

Felker

Hasselblad

Tang

et al. 2012

European J of Heart Fail

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104

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AimsWe examined the prognostic importance of cardiac troponin I (cTnI) in a cohort of patients enrolled in the ASCEND-HF study of nesiritide in acute decompensated heart failure (ADHF). Circulating troponins are a prognostic marker in patients with ADHF. Contemporary assays with greater sensitivity require reassessment of the significance of troponin elevation in HF. Methods and resultsCardiac troponin I was measured in a core laboratory in 808 ADHF patients enrolled in the ASCEND-HF biomarkers substudy using a sensitive assay (VITROS Trop I ES, Ortho Clinical Diagnostics) with a lower limit of detection of 0.012 ng/mL and a 99th percentile upper reference limit (URL) of 0.034 ng/mL. Patients with clinical evidence of acute coronary syndrome or troponin .5× the URL were excluded. Multivariable modelling was used to assess the relationship between log(cTnI) and in-hospital and post-discharge outcomes. Baseline cTnI was undetectable in 22% and elevated above the 99th percentile URL in 50% of subjects. cTnI levels did not differ based on HF aetiology. After multivariable adjustment, higher cTnI was associated with worsened in-hospital outcomes such as length of stay (P ¼ 0.01) and worsening HF during the index hospitalization (P ¼ 0.01), but was not associated with worsened post-discharge outcomes at 30 or 180 days. The relationship between cTnI and outcomes was generally linear and there was no evidence of a threshold effect at any particular level of cTnI.Conclusion cTnI is elevated above the 99th percentile URL in 50% of ADHF patients and predicts in-hospital outcome, but is not an independent predictor of long-term outcomes.--

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Section: Discussioncontrasting

confidence: 64%

Troponin I in acute decompensated heart failure: insights from the ASCEND‐HF study

Felker

Hasselblad

Tang

et al. 2012

European J of Heart Fail

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104

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“…A steep rise in aldosterone levels is also seen in the setting of acute myocardial injury,– and is associated with worse outcomes . Myocardial injury has also been postulated to occur in AHF, with elevated troponin levels being associated with worse outcomes ,…”

Section: Introductionmentioning

confidence: 99%

Serum aldosterone is associated with mortality and re‐hospitalization in patients with reduced ejection fraction hospitalized for acute heart failure: analysis from the EVEREST trial

Girerd

Pang²,

Swedberg

et al. 2013

European J of Heart Fail

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AimsPost-discharge morbidity and mortality for acute heart failure (AHF) patients remains high. Although the adverse effects of neurohormonal activation are well known in chronic HF, the prognostic significance of serum aldosterone in patients hospitalized for AHF has not been well studied. Methods and resultsA secondary analysis was carried out of the placebo arm (n ¼ 1850) from the EVEREST trial which had aldosterone measured at baseline. All patients were hospitalized for worsening HF and had an LVEF ,40%. The median follow-up was 9.9 months. The association between serum aldosterone levels at baseline and the independently adjudicated outcomes [allcause mortality (ACM) and the combined outcome of cardiovascular mortality (CVM) and HF re-hospitalization] were explored with multivariable Cox models. Median aldosterone levels increased during the hospital stay from 11 ng/dL at baseline to 15 ng/dL at discharge (P , 0.001) and remained increased after discharge (16 ng/dL at 24 weeks, P , 0.001). After adjusting for potential confounders, higher baseline aldosterone levels were associated with an increased risk for ACM and CVM or HF re-hospitalization [hazard ratio (HR) 1.49, 95% confidence intrerval (CI) 1.11-1.99; and HR 1.40, 95% CI 1.11 -1.78, respectively, in the highest quartile when compared with the lowest]. ConclusionIn patients with LVEF ,40% hospitalized for AHF and receiving standard therapy, serum aldosterone levels correlated with worse post-discharge outcomes. Aldosterone levels increase during AHF hospitalization and remain increased long after discharge. These results suggest that further modulation of the renin-angiotensin -aldosterone system in patients admitted with worsening HF might favourably improve post-discharge outcomes.--

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“…Although the hypothesis was that electrical remodeling takes place before visible left ventricular (LV) remodeling, and this consequently reduced sudden cardiac death (SCD), interestingly the readmission rate was also reduced to a similar extent as SCD with early MRA (and only with early MRA) [18], implying that there are other acute protective effects beyond antiarrhythmic properties with early MRA in AHF. Considering that AHF is associated with acute cardiac damage, as evidenced by detectable troponin release in~50 % in recent cohorts with sensitive assays, which in turn adversely affected outcomes [19][20][21]22•], MRAs could have an immediate protective effect in the early post-AHF period both for SCD and arrhythmias.…”

Section: Benefits From Early Mra Administrationmentioning

confidence: 99%

Mineralocorticoid Receptor Antagonism in Acute Heart Failure

Brown

Chee

Kyung

et al. 2015

Curr Treat Options Cardio Med

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Heart failure (HF) remains a tremendous burden to health care systems and patients worldwide. The cornerstone neurohormonal disruption that leads to the debilitating sequelae in HF patients revolves primarily around aldosterone and the renin-angiotensin-aldosterone system (RAAS). Aldosterone plays a detrimental role in tissue remodeling by inducing inflammation and fibrosis within the cardiovascular and renal systems, leaving mineralocorticoid receptor antagonists (MRAs) as key pharmacological tools to slow pathogenesis and improve patient outcomes. The role of MRA in improving morbidity and mortality in outpatients with chronic HF and low ejection fraction is well established and supported by large randomized controlled trials. However, evidence-based data relating to the use of MRA in acute HF (AHF) remain somewhat limited, and therefore, the use of MRA is not ubiquitously considered in the acute setting. Current studies for the use of MRA in AHF are limited by small sample size as well as safety concerns relating to the dose-dependent effects on electrolyte homeostasis and renal function. Here, we discuss the imperative need for additional trials elucidating the potential benefits of MRA in AHF as an adjunct diuretic therapy. We not only discuss the role of MRA in neurohormonal regulation of aldosterone but also highlight a potential dose-dependent role for MRA in natriuresis. Furthermore, we showcase existing and recent evidence-based data demonstrating the effectiveness of MRA in AHF and on long-term outcomes. Finally, we look at several treatment strategies and safety concerns as they relate to MRA use so as to aid in avoidance of MRA-related complications while facilitating achievement of treatment goals.

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Troponin T levels in patients with acute heart failure: clinical and prognostic significance of their detection and release during hospitalisation

Abstract: Increased cTnT levels are a frequent finding in patients with AHF. They are more likely to occur in patients with comorbidities and are associated with poorer outcomes. cTnT release is an independent predictor of poorer outcomes.

Cited by 39 publications

References 54 publications

Troponin I in acute decompensated heart failure: insights from the ASCEND‐HF study

Troponin I in acute decompensated heart failure: insights from the ASCEND‐HF study

Serum aldosterone is associated with mortality and re‐hospitalization in patients with reduced ejection fraction hospitalized for acute heart failure: analysis from the EVEREST trial

Mineralocorticoid Receptor Antagonism in Acute Heart Failure

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