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Revascularization in Patients With Left Main Coronary Artery Disease and Left Ventricular Dysfunction Extracellular Vesicles From Epicardial Fat Facilitate Atrial Fibrillation Proteomics to Improve Phenotyping in Obese Patients with Heart Failure with Preserved Ejection Fraction Percutaneous Coronary Intervention Versus Coronary Artery Bypass Grafting in Patients With Left Main and Multivessel Coronary Artery Disease: Do We Have the Evidence? Single Versus Dual Antiplatelet Therapy Following TAVR: A Systematic Review and Meta-Analysis of Randomized Controlled Trials Usefulness of intravascular ultrasound to predict outcomes in short-length lesions treated with drug-eluting stents Combined use of OCT and IVUS in spontaneous coronary artery dissection 1-Year Outcomes After Edge-to-Edge Valve Repair for Symptomatic Tricuspid Regurgitation: Results From the TriValve Registry Coronary Access After TAVR With a Self-Expanding Bioprosthesis: Insights From Computed Tomography Management of Antithrombotic Therapy in Atrial Fibrillation Patients Undergoing PCI: JACC State-of-the-Art Review

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].