English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Heart failure (HF) is common after acute myocardial infarction (MI) with an estimated one in five individuals aged 65 years or older who experience a first MI subsequently developing HF over the next 5 years.1 While a temporal trend towards reduction in HF hospitalizations post-MI has been noted, survival remains poor even in the era of primary reperfusion therapy, multiagent neurohormonal modulation and device implantation, with a 1-year mortality for patients hospitalized for HF after MI of over 45%.2Complex changes in ventricular geometry ensue within hours of MI—particularly for transmural infarcts—and progress well beyond the acute episode in a process termed ventricular remodelling.3 The degree of ventricular remodelling—described by parameters such as left ventricular (LV) end-systolic volume—has emerged as a key predictor of long-term survival post-MI.4 All therapies proved to beneficially alter HF clinical outcomes, including renin–angiotensin–aldosterone system (RAAS) inhibition, beta-adrenergic receptor blockade, cardiac resynchronization therapy, and LV assist devices, have been associated with LV reverse remodelling, highlighting it as a therapeutic target.5Modern definitions of cardiac remodelling6 build on earlier, largely morphological descriptions of infarct expansion, progressive ventricular dilatation, and eccentric hypertrophy culminating in systolic failure.3 These reflect complex changes in: gene expression, molecular response (altered expression of proteins resulting in impaired sarcoplasmic calcium cycling and abnormal excitation–contraction coupling, increased AT1 receptor expression, and altered β-adrenoceptor function),5,7,8 cellular adaptations (altered myocyte shape, size, and increased levels of apoptosis),9 and interstitial [matrix metalloproteinase (MMP)-mediated extracellular matrix remodelling, RAAS- and TGF-β-mediated fibrosis, activation and recruitment of inflammatory and progenitor cells, and reduced capillary density]10,11 in the pathogenesis and progression of post-MI HF. The ability of current evidence-based therapies to induce reverse remodelling depends on their ability to favourably alter some of these pathological changes, …

Potentiating mitochondrial aldehyde dehydrogenase 2 to treat post-infarction heart failure