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Long-Term Outcomes of Patients With Late Presentation of ST-Segment Elevation Myocardial Infarction Prevalence of Coronary Vasospasm Using Coronary Reactivity Testing in Patients With Spontaneous Coronary Artery Dissection Impact of Percutaneous Coronary Intervention for Chronic Total Occlusion in Non-Infarct-Related Arteries in Patients With Acute Myocardial Infarction (from the COREA-AMI Registry) Interleukin-1 Beta as a Target for Atherosclerosis Therapy: Biological Basis of CANTOS and Beyond Comparison of Stenting Versus Bypass Surgery According to the Completeness of Revascularization in Severe Coronary Artery Disease: Patient-Level Pooled Analysis of the SYNTAX, PRECOMBAT, and BEST Trials 4-Step Protocol for Disparities in STEMI Care and Outcomes in Women Triage Considerations for Patients Referred for Structural Heart Disease Intervention During the Coronavirus Disease 2019 (COVID-19) Pandemic: An ACC /SCAI Consensus Statement Multimodality imaging in cardiology: a statement on behalf of the Task Force on Multimodality Imaging of the European Association of Cardiovascular Imaging Early Natural History of Spontaneous Coronary Artery Dissection Prasugrel versus clopidogrel in patients with acute coronary syndromes

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].