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Management of two major complications in the cardiac catheterisation laboratory: the no-reflow phenomenon and coronary perforations Advances in Coronary No-Reflow Phenomenon-a Contemporary Review A Randomized Trial Comparing the NeoVas Sirolimus-Eluting Bioresorbable Scaffold and Metallic Everolimus-Eluting Stents Homeostatic Chemokines and Prognosis in Patients With Acute Coronary Syndromes Management of Patients With NSTE-ACS: A Comparison of the Recent AHA/ACC and ESC Guidelines A Randomized Trial to Assess Regional Left Ventricular Function After Stent Implantation in Chronic Total Occlusion The REVASC Trial Long-Term Effect of Ultrathin-Strut Versus Thin-Strut Drug-Eluting Stents in Patients With Small Vessel Coronary Artery Disease Undergoing Percutaneous Coronary Intervention: A Subgroup Analysis of the BIOSCIENCE Randomized Trial Better Prognosis After Complete Revascularization Using Contemporary Coronary Stents in Patients With Chronic Kidney Disease Radionuclide Image-Guided Repair of the Heart Optimal Stenting Technique for Complex Coronary Lesions Intracoronary Imaging-Guided Pre-Dilation, Stent Sizing, and Post-Dilation

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].