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High-Risk Coronary Plaque Regression After Intensive Lifestyle Intervention in Nonbstructive Coronary Disease: A Randomized Study Differential prognostic impact of treatment strategy among patients with left main versus non-left main bifurcation lesions undergoing percutaneous coronary intervention: results from the COBIS (Coronary Bifurcation Stenting) Registry II 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure Comparison of newer generation self-expandable vs. balloon-expandable valves in transcatheter aortic valve implantation: the randomized SOLVE-TAVI trial Mechanisms of in-stent restenosis after drug-eluting stent implantation: intravascular ultrasound analysis The Year in Cardiovascular Medicine 2020: Coronary Prevention: Looking back on the Year in Cardiovascular Medicine for 2020 in the field of coronary prevention is Professor Ramon Estruch, Dr Luis Ruilope, and Professor Francesco Cosentino. Mark Nicholls meets them Two-year outcomes following unprotected left main stenting with first vs new-generation drug-eluting stents: the FINE registry. EuroIntervention. Edoxaban versus Vitamin K Antagonist for Atrial Fibrillation after TAVR Value of Coronary Artery Calcium Scanning in Association With the Net Benefit of Aspirin in Primary Prevention of Atherosclerotic Cardiovascular Disease Effects of Icosapent Ethyl on Total Ischemic Events: From REDUCE-IT
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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].

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