The health and economic burden of heart failure is significant, and continues to grow each year. Loop diuretics are an integral part of symptom management in heart failure. Furosemide is used disproportionately compared to other loop diuretics and there is currently no guidance for physicians regarding which agent to choose. However, there exist pharmacologic differences as well as other mechanistic differences that appear to favor torsemide use over furosemide. Compared to furosemide, torsemide improves surrogate markers of heart failure severity such as left ventricular function, plasma brain natriuretic peptide levels, and New York Heart Association functional class and may also reduce hospitalizations, readmissions, and mortality. Data suggest these benefits could be mediated through torsemide’s ability to positively affect the renin-angiotensin-aldosterone system. Specifically, torsemide has been shown to inhibit aldosterone secretion, synthesis, and receptor binding in vitro, as well as decrease transcardiac extraction of aldosterone, myocardial collagen production and cardiac fibrosis in patients with heart failure. We identified pertinent literature using keyword MEDLINE searches and cross-referencing prior bibliographies. We summarize the available data suggesting potential benefits with torsemide over furosemide, and call attention to the need for a reappraisal of diuretic use in heart failure patients and also for a well powered, randomized control trial assessing torsemide versus furosemide use.

AimsWhile abnormal resting LV GLS has been described in patients with chronic heart failure with preserved ejection fraction (HFpEF), its prognostic significance when measured during an acute heart failure hospitalization remains unclear. We assessed the association between left ventricular global longitudinal strain (LV GLS) and outcomes in patients hospitalized with acute HFpEF.Methods and resultsWe studied patients discharged alive for acute HFpEF from Duke University Medical Center between 2007 and 2010. Among patients with measurable LV GLS, we performed 2D, speckle‐tracking analysis and Cox proportional hazards models assessed the association between continuous LV GLS and outcomes. Baseline characteristics were stratified by normal (≤−16%) or abnormal (>−16%) LV GLS for comparison. Among 463 patients, the median LV GLS was −12.8% (Interquartile range, −15.8 to −10.8%) and was abnormal in 352 (76%). Overall patients in the cohort were generally elderly, female and had hypertension. After multivariable adjustment, worse outcomes were noted between LV GLS and mortality (HR 1.19 per 1% increase; 95% CI 1.00–1.42; P = 0.046) and a composite endpoint of mortality or rehospitalization at 30 days (HR 1.08 per 1% increase; 95% CI 0.99–1.18; P = 0.08). There was no association between LV GLS and mortality or a composite of mortality or rehospitalization at 1 year.ConclusionsA high prevalence of patients hospitalized with acute HFpEF have abnormal LV GLS suggesting unrecognized myocardial systolic dysfunction. Furthermore, worse LV GLS is associated with worse clinical outcomes at 30 days but not by1 year.

Although overall myocarditis accounts for a minority of cardiomyopathy and heart failure presentations, the clinical presentation is variable and the pathophysiology of myocardial damage is unique. Cardiac MRI has significantly improved diagnostic abilities, but endomyocardial biopsy remains the gold standard. However, current treatment strategies are still focused on routine heart failure pharmacotherapies and supportive care or cardiac transplantation/mechanical support for those with end-stage heart failure.

Heart failure (HF) is an increasingly common syndrome associated with high mortality and economic burden, and there has been a paucity over the past decade of new pharmacotherapies that improve outcomes. However, recent data from a large randomized controlled trial compared the novel agent LCZ696, a dual-acting angiotensin receptor blocker and neprilysin inhibitor (ARNi), with the well established angiotensin-converting enzyme (ACE) inhibitor enalapril and found significant reduction in mortality among the chronic reduced ejection fraction HF population. Preclinical and clinical data suggest that neprilysin inhibition provides beneficial outcomes in HF patients by preventing the degradation of natriuretic peptides and thereby promoting natriuresis and vasodilatation and counteracting the negative cardiorenal effects of the up-regulated renin-angiotensin-aldosterone system. Agents such as omapatrilat combined neprilysin and ACE inhibition but had increased rates of angioedema. Goals of an improved safety profile provided the rationale for the development of the ARNi LCZ696. Along with significant reductions in mortality and hospitalizations, clinical trials suggest that LCZ696 may improve surrogate markers of HF severity. In this paper, we review the preclinical and clinical data that led to the development of LCZ696, the understanding of the underlying mechanistic action, and the robust clinical impact that LCZ696 may have in the near future. (J Cardiac Fail 2015;21:741e750)

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