CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

Coronary Angiography after Cardiac Arrest — The Right Timing or the Right Patients? Alirocumab Reduces Total Nonfatal Cardiovascular and Fatal Events in the ODYSSEY OUTCOMES Trial Optimal medical therapy improves clinical outcomes in patients undergoing revascularization with percutaneous coronary intervention or coronary artery bypass grafting: insights from the Synergy Between Percutaneous Coronary Intervention with TAXUS and Cardiac Surgery (SYNTAX) trial at the 5-year follow-up Healthy Behavior, Risk Factor Control, and Survival in the COURAGE Trial Changes in high-sensitivity troponin after drug-coated balloon angioplasty for drug-eluting stent restenosis Effect of Side Branch Predilation in Coronary Bifurcation Stenting With the Provisional Approach - Results From the COBIS (Coronary Bifurcation Stenting) II Registry Transverse partial stent ablation with rotational atherectomy for suboptimal culotte technique in left main stem bifurcation Positive remodelling of coronary arteries on computed tomography coronary angiogram: an observational study Prevention of Bleeding in Patients with Atrial Fibrillation Undergoing PCI Effects of Liraglutide on Cardiovascular Outcomes in Patients With Diabetes With or Without Heart 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].