CBS 2019
CBSMD教育中心
English

充血性心力衰竭

科研文章

荐读文献

Aliskiren, Enalapril, or Aliskiren and Enalapril in Heart Failure Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction Lifestyle Modifications for Preventing and Treating Heart Failure A Randomized Controlled Trial to Evaluate the Safety and Efficacy of Cardiac Contractility Modulation When and how to use SGLT2 inhibitors in patients with HFrEF or chronic kidney disease Efficacy and Safety of Dapagliflozin in Heart Failure With Reduced Ejection Fraction According to Age: Insights From DAPA-HF From ACE Inhibitors/ARBs to ARNIs in Coronary Artery Disease and Heart Failure (Part 2/5) H2FPEF Score for Predicting Future Heart Failure in Stable Outpatients With Cardiovascular Risk Factors SGLT-2 Inhibitors and Cardiovascular Risk: An Analysis of CVD-REAL Longitudinal Change in Galectin-3 and Incident Cardiovascular Outcomes
|<<... 9 10 11 12 13 14 15 ...>>|

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].

>CBS CBS 2019

> CBS 2019

> CBS 2019 注册

> CBS 2019 会议日程

> CBS 2019 学术征集

> CBS 2019 热点

 CBSMD

> CBSMD 网站注册

> 教育中心

> 荐读文献

> Top 10 阅读文献

> 文献导读
CBS 2019 CBS 2019 主席团 教育中心 科研动态
Copyright ⓒ CBS MD Nanjing China. All rights reserved. 京ICP备16025898号-11
联系我们| Top