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Proportion and Morphological Features of Restenosis Lesions With Acute Coronary Syndrome in Different Timings of Target Lesion Revascularization After Sirolimus-Eluting Stent Implantation Appropriate Use Criteria and Health Status Outcomes Following Chronic Total Occlusion Percutaneous Coronary Intervention: Insights From the OPEN-CTO Registry Clinician’s Guide to Reducing Inflammation to Reduce Atherothrombotic Risk Impact of Coronary Lesion Complexity in Percutaneous Coronary Intervention: One-Year Outcomes From the Large, Multicentre e-Ultimaster Registry Pharmacotherapy in the Management of Anxiety and Pain During Acute Coronary Syndromes and the Risk of Developing Symptoms of Posttraumatic Stress Disorder Intensive Care Utilization in Stable Patients With ST-Segment Elevation Myocardial Infarction Treated With Rapid Reperfusion The Prognostic Significance of Periprocedural Infarction in the Era of Potent Antithrombotic Therapy: The PRAGUE-18 Substudy A Test in Context: E/A and E/e' to Assess Diastolic Dysfunction and LV Filling Pressure Linking Spontaneous Coronary Artery Dissection, Cervical Artery Dissection, and Fibromuscular Dysplasia: Heart, Brain, and Kidneys Selection of stenting approach for coronary bifurcation lesions

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].