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Myocardial Blood Flow and Coronary Flow Reserve During 3 Years Following Bioresorbable Vascular Scaffold Versus Metallic Drug-Eluting Stent Implantation: The VANISH Trial Coronary Artery Intraplaque Microvessels by Optical Coherence Tomography Correlate With Vulnerable Plaque and Predict Clinical Outcomes in Patients With Ischemic Angina Joint consensus on the use of OCT in coronary bifurcation lesions by the European and Japanese bifurcation clubs Management of pulmonary hypertension from left heart disease in candidates for orthotopic heart transplantation Local Low Shear Stress and Endothelial Dysfunction in Patients With Nonobstructive Coronary Atherosclerosis Classification and treatment of coronary artery bifurcation lesions: putting the Medina classification to the test Left ventricular remodelling and changes in functional measurements in patients undergoing transcatheter vs surgical aortic valve replacement: a head-to-head comparison Diagnostic accuracy of intracoronary optical coherence tomography-derived fractional flow reserve for assessment of coronary stenosis severity T and small protrusion (TAP) vs double kissing crush technique: Insights from in-vitro models ‘Small bifurcation?’ CT myocardial mass volume measurements change therapeutic strategy in coronary artery disease

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].