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Association of Sustained Blood Pressure Control with Multimorbidity Progression Among Older Adults 5-Year Outcomes Comparing Surgical Versus Transcatheter Aortic Valve Replacement in Patients With Chronic Kidney Disease 中国肺动脉高压诊断与治疗指南（2021版） 5-Year Outcomes After TAVR With Balloon-Expandable Versus Self-Expanding Valves: Results From the CHOICE Randomized Clinical Trial Stress Echocardiography and PH: What Do the Findings Mean? Randomized trial of simple versus complex drug-eluting stenting for bifurcation lesions: the British Bifurcation Coronary Study: old, new, and evolving strategies Short Length of Stay After Elective Transfemoral Transcatheter Aortic Valve Replacement Is Not Associated With Increased Early or Late Readmission Risk Extracellular Myocardial Volume in Patients With Aortic Stenosis Change in Kidney Function and 2-Year Mortality After Transcatheter Aortic Valve Replacement Glycemic Index, Glycemic Load, and Cardiovascular Disease and Mortality
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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].

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