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Anticoagulation After Surgical or Transcatheter Bioprosthetic Aortic Valve Replacement Anticoagulation with or without Clopidogrel after Transcatheter Aortic-Valve Implantation Dual Antiplatelet Therapy Duration in Medically Managed Acute Coronary Syndrome Patients: Sub-Analysis of the OPT-CAD Study Post-stenting fractional flow reserve vs coronary angiography for optimisation of percutaneous coronary intervention: TARGET-FFR trial Comparison of Outcomes of Percutaneous Coronary Intervention on Native Coronary Arteries Versus on Saphenous Venous Aorta Coronary Conduits in Patients With Low Left Ventricular Ejection Fraction and Impella Device Implantation Achieved or Attempted (from the PROTECT II Randomized Trial and the cVAD Registry) 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk: The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) A Controlled Trial of Rivaroxaban After Transcatheter Aortic-Valve Replacement Extended antiplatelet therapy with clopidogrel alone versus clopidogrel plus aspirin after completion of 9- to 12-month dual antiplatelet therapy for acute coronary syndrome patients with both high bleeding and ischemic risk. Rationale and design of the OPT-BIRISK double-blinded, placebo-controlled randomized trial Effect of the PCSK9 Inhibitor Evolocumab on Total Cardiovascular Events in Patients With Cardiovascular DiseaseA Prespecified Analysis From the FOURIER Trial Long-Term Outcomes After PCI or CABG for Left Main Coronary Artery Disease According to Lesion Location
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Review Article2017 Oct 24;70(17):2186-2200.

JOURNAL：J Am Coll Cardiol. Article Link

Biological Phenotypes of Heart Failure With Preserved Ejection Fraction

Lewis GA, Schelbert EB, Miller CA et al. Keywords: diastolic dysfunction; ejection fraction; heart failure; heart failure with preserved ejection fraction; myocardial fibrosis; titin

ABSTRACT

Heart failure with preserved ejection fraction (HFpEF) involves multiple pathophysiological mechanisms, which result in the heterogeneous phenotypes that are evident clinically, and which have potentially confounded previous HFpEF trials. A greater understanding of the in vivo human processes involved, and in particular, which are the causes and which are the downstream effects, may allow the syndrome of HFpEF to be distilled into distinct diagnoses based on the underlying biology. From this, specific interventions can follow, targeting individuals identified on the basis of their biological phenotype. This review describes the biological phenotypes of HFpEF and therapeutic interventions aimed at targeting these phenotypes.



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