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The pyruvate-lactate axis modulates cardiac hypertrophy and heart failure Association of Smoking Status With Long‐Term Mortality and Health Status After Transcatheter Aortic Valve Replacement: Insights From the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry Mechanical complications of everolimus-eluting stents associated with adverse events: an intravascular ultrasound study Cardiac Resynchronization Therapy in Inotrope-Dependent Heart Failure Patients - A Systematic Review and Meta-Analysis Plaque composition by intravascular ultrasound and distal embolization after percutaneous coronary intervention Circulating sST2 and catestatin levels in patients with acute worsening of heart failure: a report from the CATSTAT-HF study Meta-analysis of outcomes after intravascular ultrasound-guided versus angiography-guided drug-eluting stent implantation in 26,503 patients enrolled in three randomized trials and 14 observational studies Fluid Volume Overload and Congestion in Heart Failure: Time to Reconsider Pathophysiology and How Volume Is Assessed Role of Proximal Optimization Technique Guided by Intravascular Ultrasound on Stent Expansion, Stent Symmetry Index, and Side-Branch Hemodynamics in Patients With Coronary Bifurcation Lesions Optical frequency-domain imaging findings to predict good stent expansion after rotational atherectomy for severely calcified coronary lesions

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].