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Ten-Year All-Cause Death According to Completeness of Revascularization in Patients With Three-Vessel Disease or Left Main Coronary Artery Disease: Insights From the SYNTAX Extended Survival Study A Prospective, Multicenter, Randomized, Open-label Trial to Compare Efficacy and Safety of Clopidogrel vs. Ticagrelor in Stabilized Patients with Acute Myocardial Infarction after Percutan eous Coronary Intervention: rationale and design of the TALOS-AMI trial 5-Year Outcomes Comparing Surgical Versus Transcatheter Aortic Valve Replacement in Patients With Chronic Kidney Disease Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel Pulmonary artery denervation for treatment of a patient with pulmonary hypertension secondary to left heart disease EXCELling in Left Main Intervention The contribution of tissue-grouped BMI-associated gene sets to cardiometabolic-disease risk: a Mendelian randomization study Higher neutrophil-to-lymphocyte ratio (NLR) increases the risk of suboptimal platelet inhibition and major cardiovascular ischemic events among ACS patients receiving dual antiplatelet therapy with ticagrelor Global Approach to High Bleeding Risk Patients With Polymer-Free Drug-Coated Coronary Stents: The LF II Study 2020 ACC Expert Consensus Decision Pathway on Management of Conduction Disturbances in Patients Undergoing Transcatheter Aortic Valve Replacement A Report of the American College of Cardiology Solution Set Oversight Committee
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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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