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Subcutaneous Selatogrel Inhibits Platelet Aggregation in Patients With Acute Myocardial Infarction Short Sleep Duration, Obstructive Sleep Apnea, Shiftwork, and the Risk of Adverse Cardiovascular Events in Patients After an Acute Coronary Syndrome Complete Revascularization During Primary Percutaneous Coronary Intervention Reduces Death and Myocardial Infarction in Patients With Multivessel Disease-Meta-Analysis and Meta-Regression of Randomized Trials Stent Thrombosis Risk Over Time on the Basis of Clinical Presentation and Platelet Reactivity: Analysis From ADAPT-DES Restenosis, Stent Thrombosis, and Bleeding Complications - Navigating Between Scylla and Charybdis In-Hospital Coronary Revascularization Rates and Post-Discharge Mortality Risk in Non–ST-Segment Elevation Acute Coronary Syndrome Ticagrelor versus Clopidogrel in Patients with STEMI Treated with Fibrinolytic Therapy: TREAT Trial An EAPCI Expert Consensus Document on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary Pathophysiology & Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group The association between body mass index and obesity with survival in pulmonary arterial hypertension Evaluation and Management of Nonculprit Lesions in STEMI

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].