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Clinical impact of PCSK9 inhibitor on stabilization and regression of lipid-rich coronary plaques: a near-infrared spectroscopy study Coronary Access After TAVR Comparison of safety and periprocedural complications of transfemoral aortic valve replacement under local anaesthesia: minimalist versus complete Heart Team Usefulness of minimum stent cross sectional area as a predictor of angiographic restenosis after primary percutaneous coronary intervention in acute myocardial infarction (from the HORIZONS-AMI Trial IVUS substudy) Clinical Impact of Valvular Heart Disease in Elderly Patients Admitted for Acute Coronary Syndrome: Insights From the Elderly-ACS 2 Study Impaired Retinal Microvascular Function Predicts Long-Term Adverse Events in Patients with Cardiovascular Disease Increased Risk of Valvular Heart Disease in Systemic Sclerosis: An Underrecognized Cardiac Complication Intravascular Ultrasound and Angioscopy Assessment of Coronary Plaque Components in Chronic Totally Occluded Lesions From Detecting the Vulnerable Plaque to Managing the Vulnerable Patient CT Angiographic and Plaque Predictors of Functionally Significant Coronary Disease and Outcome Using Machine Learning

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].