CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

A Meta-Analysis of Contemporary Lesion Modification Strategies During Percutaneous Coronary Intervention in 244,795 Patients From 22 Studies Drug-Coated Balloon Treatment for Femoropopliteal Artery Disease: The IN.PACT Global Study De Novo In-Stent Restenosis Imaging Cohort Rotational Atherectomy Followed by Drug-Coated Balloon Dilation for Left Main In-Stent Restenosis in the Setting of Acute Coronary Syndrome Complicated with Right Coronary Chronic Total Occlusion SGLT2 Inhibitors in Patients With Heart Failure With Reduced Ejection Fraction: A Meta-Analysis of the EMPEROR-Reduced and DAPA-HF Trials Aggressive lipid-lowering therapy after percutaneous coronary intervention – for whom and how? Can the Vanishing Stent Reappear? Fix the Technique, or Fix the Device? AIM2-driven inflammasome activation in heart failure Coronary Artery Calcium Is Associated with Left Ventricular Diastolic Function Independent of Myocardial Ischemia Disrupting Fellow Education Through Group Texting: WhatsApp in Fellow Education? Screening for Atrial Fibrillation With Electrocardiography US Preventive Services Task Force Recommendation Statement

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].