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Cardiovascular risk prediction in type 2 diabetes: a comparison of 22 risk scores in primary care settings Flow-Regulated Endothelial S1P Receptor-1 Signaling Sustains Vascular Development Impact of large periprocedural myocardial infarction on mortality after percutaneous coronary intervention and coronary artery bypass grafting for left main disease: an analysis from the EXCEL trial Feasibility and efficacy of the ultrashort side branch dedicated balloon in coronary bifurcation stenting Fractional flow reserve-guided PCI versus medical therapy in stable coronary disease Coronary Optical Coherence Tomography and Cardiac Magnetic Resonance Imaging to Determine Underlying Causes of Myocardial Infarction With Nonobstructive Coronary Arteries in Women Instantaneous Wave-free Ratio versus Fractional Flow Reserve to Guide PCI Outcomes of patients with and without baseline lipid-lowering therapy undergoing revascularization for left main coronary artery disease: analysis from the EXCEL trial Left main coronary angioplasty: early and late results of 127 acute and elective procedures Long-term safety and effectiveness of unprotected left main coronary stenting with drug-eluting stents compared with bare-metal stents
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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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