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Association of the PHACTR1/EDN1 Genetic Locus With Spontaneous Coronary Artery Dissection Long-Term Incremental Prognostic Value of Cardiovascular Magnetic Resonance After ST-Segment Elevation Myocardial Infarction A Study of the Collaborative Registry on CMR in STEMI Oxidative Stress and Cardiovascular Risk: Obesity, Diabetes, Smoking, and Pollution: Part 3 of a 3-Part Series MR-proADM as a Prognostic Marker in Patients With ST-Segment-Elevation Myocardial Infarction-DANAMI-3 (a Danish Study of Optimal Acute Treatment of Patients With STEMI) Substudy Preventing Coronary Obstruction During Transcatheter Aortic Valve Replacement From Computed Tomography to BASILICA The Aging Cardiovascular System: Understanding It at the Cellular and Clinical Levels Randomized Trial Evaluating Percutaneous Coronary Intervention for the Treatment of Chronic Total Occlusion: The DECISION-CTO Trial Impact of Off-Hours Versus On-Hours Primary Percutaneous Coronary Intervention on Myocardial Damage and Clinical Outcomes in ST-Segment Elevation Myocardial Infarction Late Survival Benefit of Percutaneous Coronary Intervention Compared With Medical Therapy in Patients With Coronary Chronic Total Occlusion: A 10-Year Follow-Up Study Correlation between frequency-domain optical coherence tomography and fractional flow reserve in angiographically-intermediate coronary 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].