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What's new in the Fourth Universal Definition of Myocardial infarction? Prognostic Significance of Complex Ventricular Arrhythmias Complicating ST-Segment Elevation Myocardial Infarction Left Main Revascularization in 2017 Coronary Artery Bypass Grafting or Percutaneous Coronary Intervention? Patterns and associations between DAPT cessation and 2-year clinical outcomes in left main/proximal LAD versus other PCI: Results from the Patterns of Non-Adherence to Dual Antiplatelet Therapy in Stented Patients (PARIS) registry Comparison of double kissing crush versus Culotte stenting for unprotected distal left main bifurcation lesions: results from a multicenter, randomized, prospective DKCRUSH-III study Relation between door-to-balloon times and mortality after primary percutaneous coronary intervention over time: a retrospective study Respiratory syncytial virus infection and risk of acute myocardial infarction Improvement of Clinical Outcome in Patients With ST-Elevation Myocardial Infarction Between 1999 And 2016 in China : The Prospective, Multicenter Registry MOODY Study In Vivo Calcium Detection by Comparing Optical Coherence Tomography, Intravascular Ultrasound, and Angiography Recurrent Cardiovascular Events in Survivors of Myocardial Infarction with St-Segment Elevation (From the AMI-QUEBEC Study)

Review Article2018 Jun 13.[Epub ahead of print]

JOURNAL:Eur Heart J. Article Link

Heart failure with preserved ejection fraction: from mechanisms to therapies

Lam CSP, Voors AA, de Boer RA et al. Keywords: HFpEF; mechanisms; therapy

ABSTRACT


This review aims to provide a translational perspective on recent developments in heart failure with preserved ejection fraction (HFpEF), linking mechanistic insights to potential therapies. A key concept in this review is that HFpEF is a haemodynamic condition wherein the heart fails to keep up with the circulatory demands of the body, or does so at the expense of raised left ventricular filling pressures. We, therefore, propose that the 'final common pathway' for development of congestion, i.e. basic haemodynamic mechanisms of increased left ventricular end-diastolic pressure, left atrial hypertension, pulmonary venous congestion, and plasma volume expansion, represents important initial targets for therapy in HFpEF. Accordingly, we group this review into six mechanisms translating into potential therapies for HFpEF: beginning with three haemodynamic mechanisms (left atrial hypertension, pulmonary hypertension, and plasma volume expansion), and working backward to three potential molecular mechanisms [systemic microvascular inflammation, cardiometabolic functional abnormalities, and cellular (titin)/extracellular (fibrosis) structural abnormalities].