CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

Long-term effects of intensive glucose lowering on cardiovascular outcomes The Evolution of β-Blockers in Coronary Artery Disease and Heart Failure (Part 1/5) Prior Balloon Valvuloplasty Versus Direct Transcatheter Aortic Valve Replacement: Results From the DIRECTAVI Trial Cardiac resynchronization therapy with a defibrillator (CRTd) in failing heart patients with type 2 diabetes mellitus and treated by glucagon-like peptide 1 receptor agonists (GLP-1 RA) therapy vs. conventional hypoglycemic drugs: arrhythmic burden, hospitalizations for heart failure, and CRTd responders rate Relationship Between Hospital Surgical Aortic Valve Replacement Volume and Transcatheter Aortic Valve Replacement Outcomes Usefulness of intravascular ultrasound guidance in percutaneous coronary intervention with second-generation drug-eluting stents for chronic total occlusions (from the Multicenter Korean-Chronic Total Occlusion Registry) Intravascular Ultrasound Assessment of In-Stent Restenosis in Saphenous Vein Grafts Negative Risk Markers for Cardiovascular Events in the Elderly Meta-Analysis of Effectiveness and Safety of Transcatheter Aortic Valve Implantation Versus Surgical Aortic Valve Replacement in Low-to-Intermediate Surgical Risk Cohort Short-Term Progression of Multiterritorial Subclinical Atherosclerosis

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].