CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

Does Risk of Premature Discontinuation of Dual-Antiplatelet Therapy Following PCI Attenuate With Increasing Age? Lipoprotein(a) in Alzheimer, Atherosclerotic, Cerebrovascular, Thrombotic, and Valvular Disease: Mendelian Randomization Investigation Trial Design Principles for Patients at High Bleeding Risk Undergoing PCI: JACC Scientific Expert Panel Clinical Outcomes and Cost-Effectiveness of Fractional Flow Reserve-Guided Percutaneous Coronary Intervention in Patients With Stable Coronary Artery Disease: Three-Year Follow-Up of the FAME 2 Trial (Fractional Flow Reserve Versus Angiography for Multivessel Evaluation) Statin Effects on Vascular Calcification: Microarchitectural Changes in Aortic Calcium Deposits in Aged Hyperlipidemic Mice Sox17 Controls Emergence and Remodeling of Nestin-Expressing Coronary Vessels Endocardium Minimally Contributes to Coronary Endothelium in the Embryonic Ventricular Free Walls 2010 ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Empagliflozin, Health Status, and Quality of Life in Patients with Heart Failure and Preserved Ejection Fraction: The EMPEROR-Preserved Trial Impact of bleeding during dual antiplatelet therapy in patients with coronary artery disease
|<<... 129 130 131 132 133 134 135 ...>>|

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