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A Randomized Trial Evaluating Online 3-Dimensional Optical Frequency Domain Imaging-Guided Percutaneous Coronary Intervention in Bifurcation Lesions Optical Coherence Tomography-Guided Percutaneous Coronary Intervention in ST-Segment-Elevation Myocardial Infarction: A Prospective Propensity-Matched Cohort of the Thrombectomy Versus Percutaneous Coronary Intervention Alone Trial Experimental basis of determining maximum coronary, myocardial, and collateral blood flow by pressure measurements for assessing functional stenosis severity before and after percutaneous transluminal coronary angioplasty Retrospective Comparison of Long-Term Clinical Outcomes Between Percutaneous Coronary Intervention and Medical Therapy in Stable Coronary Artery Disease With Gray Zone Fractional Flow Reserve - COMFORTABLE Retrospective Study Left main coronary artery compression in pulmonary hypertension Robustness of Fractional Flow Reserve for Lesion Assessment in Non-Infarct-Related Arteries of Patients With Myocardial Infarction Rotational Atherectomy in acute STEMI with heavily calcified culprit lesion is a rule breaking solution Technical aspects of the culotte technique Optimal threshold of postintervention minimum stent area to predict in-stent restenosis in small coronary arteries: An optical coherence tomography analysis PCI for obstructive bifurcation lesions the 14th consensus document from the european bifurcation club

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].