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Uncovered Culprit Plaque Ruptures in Patients With ST-Segment Elevation Myocardial Infarction Assessed by Optical Coherence Tomography and Intravascular Ultrasound With iMap Consensus standards for acquisition, measurement, and reporting of intravascular optical coherence tomography studies: a report from the International Working Group for Intravascular Optical Coherence Tomography Standardization and Validation Covering our tracks – optical coherence tomography to assess vascular healing Double-Kiss-Crush Bifurcation Stenting: Step-by-Step Troubleshooting Chronic thromboembolic pulmonary hypertension Device specificity of vascular healing following implantation of bioresorbable vascular scaffolds and bioabsorbable polymer metallic drug-eluting stents in human coronary arteries: the ESTROFA OCT BVS vs. BP-DES study Elaborately Engineering a Self-Indicating Dual-Drug Nanoassembly for Site-Specific Photothermal-Potentiated Thrombus Penetration and Thrombolysis Meta-Analysis of Death and Myocardial Infarction in the DEFINE-FLAIR and iFR-SWEDEHEART Trials Incidence of Adverse Events at 3 Months Versus at 12 Months After Dual Antiplatelet Therapy Cessation in Patients Treated With Thin Stents With Unprotected Left Main or Coronary Bifurcations Refined balloon pulmonary angioplasty for inoperable patients with chronic thromboembolic pulmonary hypertension

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].