CBS 2019
CBSMD教育中心
中 文

Congestive Heart Failure

Abstract

Recommended Article

Positive recommendation for angiotensin receptor/neprilysin inhibitor: First medication approval for heart failure without "reduced ejection fraction" Angiotensin–Neprilysin Inhibition in Heart Failure with Preserved Ejection Fraction Myofibroblast Phenotype and Reversibility of Fibrosis in Patients With End-Stage Heart Failure Association of Reduced Apical Untwisting With Incident HF in Asymptomatic Patients With HF Risk Factors The Management of Atrial Fibrillation in Heart Failure: An Expert Panel Consensus Ranolazine in High-Risk Patients With Implanted Cardioverter-Defibrillators - The RAID Trial Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association Cardiovascular Aging and Heart Failure: JACC Review Topic of the Week

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].