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Systematic Review for the 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines No causal effects of plasma homocysteine levels on the risk of coronary heart disease or acute myocardial infarction: A Mendelian randomization study Pulmonary Artery Pressure-Guided Management of Patients With Heart Failure and Reduced Ejection Fraction Comparison of Accuracy of One-Use Methods for Calculating Fractional Flow Reserve by Intravascular Optical Coherence Tomography to That Determined by the Pressure-Wire Method Impact of percutaneous coronary intervention extent, complexity and platelet reactivity on outcomes after drug-eluting stent implantation Novel functions of macrophages in the heart: insights into electrical conduction, stress, and diastolic dysfunction Invasive Versus Medical Management in Patients With Prior Coronary Artery Bypass Surgery With a Non-ST Segment Elevation Acute Coronary Syndrome: A Pilot Randomized Controlled Trial Systems of Care for ST-Segment–Elevation Myocardial Infarction: A Policy Statement From the American Heart Association Outcome of Applying the ESC 0/1-hour Algorithm in Patients With Suspected Myocardial Infarction Incidence, predictors, and outcomes of DAPT disruption due to non-compliance vs. bleeding after PCI: insights from the PARIS Registry

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].