Minor Myocardial Damage is a Prevalent Condition in Patients With Acute Heart Failure Syndromes and Preserved Systolic Function With Long-Term Prognostic Implications. A Report From the CIAST-HF (Collaborative Italo-Argentinean Study on Cardiac Troponin T in Heart Failure) Study

Perna, Eduardo R.; Aspromonte, Nadia; Canella, Juan P. Címbaro; Tano, Giuseppe Di; Macin, Stella M.; Feola, Mauro; Coronel, María Lorena; Milani, L.; Parras, Jorge I.; Milli, Massimo; García, Edgar; Valle, Roberto

doi:10.1016/j.cardfail.2012.10.008

Cited by 26 publications

(24 citation statements)

References 41 publications

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“…Although elevated troponin is now well described in HFrEF, 3 prior studies on the relationship between troponin and HFpEF have concentrated on patients who are hospitalized or acutely decompensated. [8][9][10] Our population was similar to other trials of patients with HFpEF 18 but generally younger with fewer comorbidities than community-based cohorts of patients with HFpEF. 19 We found that 58% had a hs-TnT level in the myocardial injury range, a result similar to that observed in HFrEF.…”

Section: Discussionmentioning

confidence: 58%

“…7 Heart November 2014 failure with preserved ejection fraction (HFpEF) accounts for up to 50% of cases of heart failure. While elevated troponin has been detected in hospitalized patients with HFpEF, [8][9][10] whether troponin is detectable in stable outpatients with HFpEF, and whether elevations in troponin are related to abnormalities of cardiac structure and function, is unknown. [10][11][12][13] The Prospective comparison of angiotensin receptor neprilysin inhibitor with angiotensin receptor blocker on Management Of heart failUre with preserved ejectioN fracTion (PARAMOUNT) trial was a phase II trial testing the safety and efficacy of LCZ696 in stable outpatients with HFpEF.…”

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confidence: 99%

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Elevation in High-Sensitivity Troponin T in Heart Failure and Preserved Ejection Fraction and Influence of Treatment With the Angiotensin Receptor Neprilysin Inhibitor LCZ696

Jhund

Claggett

Voors

et al. 2014

Circ: Heart Failure

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Background-Elevated high-sensitivity troponin is associated with increasing disease severity in patients with stable heart failure with reduced ejection fraction, but less is known about the association in heart failure with preserved ejection fraction. Methods and Results-We examined the prevalence of elevated high-sensitivity troponin T (hs-TnT) in 298 patients with heart failure with preserved ejection fraction enrolled in the Prospective comparison of angiotensin receptor neprilysin inhibitor with angiotensin receptor blocker on Management Of heart failUre with preserved ejectioN fracTion (PARAMOUNT) trial, in which the angiotensin receptor neprilysin inhibitor LCZ696 reduced markers of heart failure severity compared with valsartan. We assessed the association between hs-TnT and cardiac structure and function, and the effect of LCZ696, compared with valsartan, on hs-TnT over 36 weeks. Elevated hs-TnT in the myocardial injury range (>0.014 μg/L) was found in 55% of patients and was associated with older age, history of diabetes mellitus, higher N-terminal pro-brain natriuretic peptide, lower estimated glomerular filtration rate, and larger left atrial size, left ventricular volume, and mass. LCZ696 treatment reduced hs-TnT to a greater extent at 12 weeks (12% reduction; P=0.05) and at 36 weeks (14% reduction; P=0.03) compared with valsartan. Conclusions-Troponin T was elevated in a substantial number of patients enrolled in a heart failure with preserved ejection fraction clinical trial and was associated with abnormalities of cardiac structure, function, and elevated baseline N-terminal pro-brain natriuretic peptide. Decreases in hs-TnT with LCZ696 in parallel with improvement in N-terminal pro-brain natriuretic peptide and left atrial size suggest that the angiotensin receptor neprilysin inhibitor LCZ696 may reduce this measure of myocardial injury in heart failure with preserved ejection fraction. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT00887588.(Circ Heart Fail. 2014;7:953-959.)

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Section: Discussionmentioning

confidence: 58%

mentioning

confidence: 99%

Elevation in High-Sensitivity Troponin T in Heart Failure and Preserved Ejection Fraction and Influence of Treatment With the Angiotensin Receptor Neprilysin Inhibitor LCZ696

Jhund

Claggett

Voors

et al. 2014

Circ: Heart Failure

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“…32 In another study involving a cohort of patients with an ejection fraction ≥40 %, a cTnT level ≥0.02 ng/ml was associated with worse clinical outcomes of death and rehospitalisation at 6 months with a HR of 1.8 compared with patients whose cTnT was <0.02. 33 A study of patients with preserved ejection fraction showed an elevated cTn level to correlate with left ventricular end-diastolic dimension and tissue Doppler Ea wave peak velocity. 34 Overall, these studies clearly show that an elevated cTn level in patients with AHF portends poor short-and longterm outcomes regardless of heart failure characteristics.…”

Section: Prognostic Value Of Troponin With Conventional Assaysmentioning

confidence: 99%

Role of Cardiac Troponin Levels in Acute Heart Failure

Wettersten

Maisel

2015

Cardiac Failure Review

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Cardiac troponin (cTn) is the primary biomarker for the diagnosis of myocardial necrosis in an acute coronary syndrome (ACS). cTn levels can also be elevated in many other conditions, including heart failure, with significant prognostic value. An elevated cTn level can be found in both acute and chronic heart failure and its presence is believed to be due to multiple different pathophysiological processes. In acute decompensated heart failure (AHF), an elevated cTn level has been repeatedly shown to correlate with increased short- and long-term mortality and, to a lesser extent, readmission rates. These associations have been demonstrated with both I and T isoforms of cTn, as well as when troponin is measured with conventional assays or new high-sense assays. In multimarker models, cTn has repeatedly been found to be an independent predictive variable enhancing prognostic ability of the model. cTn is therefore an important biomarker for prognosis in AHF.

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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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Minor Myocardial Damage is a Prevalent Condition in Patients With Acute Heart Failure Syndromes and Preserved Systolic Function With Long-Term Prognostic Implications. A Report From the CIAST-HF (Collaborative Italo-Argentinean Study on Cardiac Troponin T in Heart Failure) Study

Cited by 26 publications

References 41 publications

Elevation in High-Sensitivity Troponin T in Heart Failure and Preserved Ejection Fraction and Influence of Treatment With the Angiotensin Receptor Neprilysin Inhibitor LCZ696

Elevation in High-Sensitivity Troponin T in Heart Failure and Preserved Ejection Fraction and Influence of Treatment With the Angiotensin Receptor Neprilysin Inhibitor LCZ696

Role of Cardiac Troponin Levels in Acute Heart Failure

Mineralocorticoid Receptor Antagonism in Acute Heart Failure

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