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Superficial Calcium Fracture After PCI as Assessed by OCT Long-Term Clinical Outcomes and Optimal Stent Strategy in Left Main Coronary Bifurcation Stenting Transthoracic echocardiography for the evaluation of children and adolescents with suspected or confirmed pulmonary hypertension. Expert consensus statement on the diagnosis and treatment of paediatric pulmonary hypertension. The European Paediatric Pulmonary Vascular Disease Network, endorsed by ISHLT and D6PK Medical Therapy for CTEPH: Is There Still Space for More? Autologous CD34+ Stem Cell Therapy Increases Coronary Flow Reserve and Reduces Angina in Patients With Coronary Microvascular Dysfunction Sotatercept for the Treatment of Pulmonary Arterial Hypertension Machine Learning Using CT-FFR Predicts Proximal Atherosclerotic Plaque Formation Associated With LAD Myocardial Bridging Self-expandable sirolimus-eluting stents compared to second-generation drug-eluting stents for the treatment of the left main: A propensity score analysis from the SPARTA and the FAILS-2 registries Dual Antiplatelet Therapy after PCI in Patients at High Bleeding Risk Pancoronary Plaque Characteristics in STEMI Caused by Culprit Plaque Erosion Versus Rupture: 3-Vessel OCT Study

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].