1,721,282 research outputs found
Reply to the letter regarding the article ‘Head‐to‐head comparison between recommendations by the ESC and ACC/AHA/HFSA heart failure guidelines’
Full text linkBiomarkers of inflammation in heart failure: from risk prediction to possible treatment targets
Full text linkDifferent Effects on Protein Expression of CDR132L, an Antisense Inhibitor of miR-132, and Standard Therapies for Myocardial Infarction
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Empagliflozin in heart failure with preserved and mildly reduced ejection fraction: prognostic benefit confirmed with different endpoint definitions
Full text linkDo we need to EVALUATE multiple biomarkers and/or the same biomarkers multiple times in patients with heart failure?
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Management of heart failure with preserved ejection fraction: from neurohormonal antagonists to empagliflozin
Full text link: Heart failure with preserved ejection fraction (HFpEF) is a highly prevalent syndrome with multifaceted pathophysiology. All approaches to neurohormonal modulation were shown not to improve survival in HFpEF, despite their well-established efficacy in heart failure with reduced ejection fraction (HFrEF). This might be attributed to suboptimal study design, inadequate diagnostic criteria, or statistical power, but is also likely to reflect a lack of consideration for its clinical heterogeneity. The attention then shifted to the phenotypic heterogeneity of HFpEF, with the ultimate goal of developing therapies tailored to individual patient phenotypes. Recently, the sodium-glucose co-transporter-2 inhibitor (SGLT2i) empagliflozin has been found to reduce the combined risk of cardiovascular death or hospitalization for HF in patients with HFpEF, a result driven by a reduction in HF hospitalizations. This paper recapitulates the journey from the failure of trials on neurohormonal antagonists to the attempts of personalized approaches and the new perspectives of SGLT2i therapy for HFpEF
Treatment of cardiac fibrosis: from neuro-hormonal inhibitors to CAR-T cell therapy
Full text linkCardiac fibrosis is characterized by the deposition of extracellular matrix proteins in the spaces between cardiomyocytes following both acute and chronic tissue damage events, resulting in the remodeling and stiffening of heart tissue. Fibrosis plays an important role in the pathogenesis of many cardiovascular disorders, including heart failure and myocardial infarction. Several studies have identified fibroblasts, which are induced to differentiate into myofibroblasts in response to various types of damage, as the most important cell types involved in the fibrotic process. Some drugs, such as inhibitors of the renin–angiotensin–aldosterone system, have been shown to be effective in reducing cardiac fibrosis. There are currently no drugs with primarily anti-fibrotic action approved for clinical use, as well as the evidence of a clinical efficacy of these drugs is extremely limited, despite the numerous encouraging results from experimental studies. A new approach is represented by the use of CAR-T cells engineered in vivo using lipid nanoparticles containing mRNA coding for a receptor directed against the FAP protein, expressed by cardiac myofibroblasts. This strategy has proved to be safe and effective in reducing myocardial fibrosis and improving cardiac function in mouse models of cardiac fibrosis. Clinical studies are required to test this novel approach in humans
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