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Outcomes with drug-coated balloons in small-vessel coronary artery disease Bare metal or drug-eluting stent versus drug-coated balloon in non-ST-elevation myocardial infarction: the randomised PEPCAD NSTEMI trial Chronic Total Occlusion Interventions: Update on Current Tips and Tricks Treating Bifurcation Lesions: The Result Overcomes the Technique Multicenter Registry of Real-World Patients With Severely Calcified Coronary Lesions Undergoing Orbital Atherectomy: 1-Year Outcomes Impact of stent deformity induced by the kissing balloon technique for bifurcating lesions on in-stent restenosis after coronary intervention The Hybrid Approach to Chronic Total Occlusion Percutaneous Coronary Intervention: Update From the PROGRESS CTO Registry Applications of left ventricular strain measurements to patients undergoing chemotherapy Percutaneous coronary intervention with drug-coated balloon-only strategy in stable coronary artery disease and in acute coronary syndromes: An all-comers registry study Percutaneous coronary interventional strategies for treatment of in-stent restenosis: a network meta-analysis

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].