CBS 2019
CBSMD教育中心
中 文

充血性心力衰竭

Abstract

Recommended Article

Angiotensin–Neprilysin Inhibition in Heart Failure with Preserved Ejection Fraction Heart Failure Outcomes With Volume-Guided Management Unexpectedly Low Natriuretic Peptide Levels in Patients With Heart Failure Universal Definition and Classification of Heart Failure: A Report of the Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology, Japanese Heart Failure Society and Writing Committee of the Universal Definition of Heart Failure Frequency, predictors, and prognosis of ejection fraction improvement in heart failure: an echocardiogram-based registry study Percutaneous Atriotomy for Levoatrial–to–Coronary Sinus Shunting in Symptomatic Heart Failure: First-in-Human Experience Impact of Myocardial Scar on Prognostic Implication of Secondary Mitral Regurgitation in Heart Failure Mechanical circulatory support devices for acute right ventricular failure

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].