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Comparison of Coronary Intimal Plaques by Optical Coherence Tomography in Arteries With Versus Without Internal Running Vasa Vasorum Volumetric characterization of human coronary calcification by frequency-domain optical coherence tomography Meta-Analysis of Death and Myocardial Infarction in the DEFINE-FLAIR and iFR-SWEDEHEART Trials Mortality after coronary artery bypass grafting versus percutaneous coronary intervention with stenting for coronary artery disease: a pooled analysis of individual patient data The Relation Between Optical Coherence Tomography-Detected Layered Pattern and Acute Side Branch Occlusion After Provisional Stenting of Coronary Bifurcation Lesions Reply: Will Pulmonary Artery Denervation Really Have a Place in the Armamentarium of the Pulmonary Hypertension Specialist? Two-year outcomes of everolimus vs. paclitaxel-eluting stent for the treatment of unprotected left main lesions: a propensity score matching comparison of patients included in the French Left Main Taxus (FLM Taxus) and the LEft MAin Xience (LEMAX) registries Left main coronary artery disease: importance, diagnosis, assessment, and management Histopathological validation of optical coherence tomography findings of the coronary arteries Diagnostic accuracy of fractional flow reserve from anatomic CT angiography
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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].

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