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Heart Failure With Preserved Ejection Fraction in the Young Treatment strategies for coronary in-stent restenosis: systematic review and hierarchical Bayesian network meta-analysis of 24 randomised trials and 4880 patients Intravascular ultrasound-guided implantation of drug-eluting stents to improve outcome: a meta-analysis In vivo intravascular ultrasound-derived thin-cap fibroatheroma detection using ultrasound radiofrequency data analysis Left Main Revascularization With PCI or CABG in Patients With Chronic Kidney Disease: EXCEL Trial Economic and Quality-of-Life Outcomes of Natriuretic Peptide–Guided Therapy for Heart Failure Non-obstructive High-Risk Plaques Increase the Risk of Future Culprit Lesions Comparable to Obstructive Plaques Without High-Risk Features: The ICONIC Study Use of Intravascular Ultrasound Imaging in Percutaneous Coronary Intervention to Treat Left Main Coronary Artery Disease Patient Selection and Clinical Outcomes in the STOPDAPT-2 Trial: An All-Comer Single-Center Registry During the Enrollment Period of the STOPDAPT-2 Randomized Controlled Trial Clinical impact of intravascular ultrasound-guided chronic total occlusion intervention with zotarolimus-eluting versus biolimus-eluting stent implantation: randomized study

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].