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Hemodynamic, Functional, and Clinical Responses to Pulmonary Artery Denervation in Patients With Pulmonary Arterial Hypertension of Different Causes Evolving insights into the role of local shear stress in late stent failure from neoatherosclerosis formation and plaque destabilization Management and outcomes of patients with left atrial appendage thrombus prior to percutaneous closure Systematic Review and Network Meta‐Analysis Comparing Bifurcation Techniques for Percutaneous Coronary Intervention Rivaroxaban for Thromboprophylaxis in High-Risk Ambulatory Patients With Cancer 2015 ACC/HRS/SCAI Left Atrial Appendage Occlusion Device Societal Overview Long-Term Outcomes of Patients With Mediastinal Radiation–Associated Coronary Artery Disease Undergoing Coronary Revascularization With Percutaneous Coronary Intervention and Coronary Artery Bypass Grafting Implications of the local hemodynamic forces on the formation and destabilization of neoatherosclerotic lesions Transseptal puncture versus patent foramen ovale or atrial septal defect access for left atrial appendage closure Alcohol consumption, cardiac biomarkers, and risk of atrial fibrillation and adverse outcomes
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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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