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Hs-cTroponins for the prediction of recurrent cardiovascular events in patients with established CHD - A comparative analysis from the KAROLA study Shock Team Approach in Refractory Cardiogenic Shock Requiring Short-Term Mechanical Circulatory Support: A Proof of Concept SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019 Large-Bore Radial Access for Complex PCI: A Flash of COLOR With Some Shades of Grey Association of Coronary Anatomical Complexity With Clinical Outcomes After Percutaneous or Surgical Revascularization in the Veterans Affairs Clinical Assessment Reporting and Tracking Program Development and validation of a simple risk score to predict 30-day readmission after percutaneous coronary intervention in a cohort of medicare patients Invasive Coronary Physiology After Stent Implantation: Another Step Toward Precision Medicine Mechanisms and diagnostic evaluation of persistent or recurrent angina following percutaneous coronary revascularization Prevalence, Presentation and Treatment of 'Balloon Undilatable' Chronic Total Occlusions: Insights from a Multicenter US Registry Dynamic Myocardial Ultrasound Localization Angiography

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].