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Dynamic atrioventricular delay programming improves ventricular electrical synchronization as evaluated by 3D vectorcardiography Early Diagnosis of Myocardial Infarction With Point-of-Care High-Sensitivity Cardiac Troponin I Heart Failure With Preserved, Borderline, and Reduced Ejection Fraction: 5-Year Outcomes Association Between Living in Food Deserts and Cardiovascular Risk Impact of Optimal Medical Therapy on 10-Year Mortality After Coronary Revascularization Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association The Astronaut Cardiovascular Health and Risk Modification (Astro-CHARM) Coronary Calcium Atherosclerotic Cardiovascular Disease Risk Calculator 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC) Canadian Multicenter Chronic Total Occlusion Registry: Ten-Year Follow-Up Results of Chronic Total Occlusion Revascularization Long-Term Outcomes of Biodegradable Versus Second-Generation Durable Polymer Drug-Eluting Stent Implantations for Myocardial Infarction

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].