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Optimal Fluoroscopic Projections of Coronary Ostia and Bifurcations Defined by Computed Tomographic Coronary Angiography Comparison of intravascular ultrasound-guided with angiography-guided double kissing crush stenting for patients with complex coronary bifurcation lesions: rationale and design of a prospective, randomized and multicenter DKCRUSH VIII trial Long-term outcomes after treatment of bare-metal stent restenosis with paclitaxel-coated balloon catheters or everolimus-eluting stents: 3-year follow-up of the TIS clinical study Atrial Fibrillation: JACC Council Perspectives Optical coherence tomography-guided percutaneous coronary intervention in ST-segmentelevation myocardial infarction: a prospective propensity-matched cohort of the thrombectomy versus percutaneous coronary intervention alone trial The Natural History of Nonculprit Lesions in STEMI: An FFR Substudy of the Compare-Acute Trial Sex Differences in Instantaneous Wave-Free Ratio or Fractional Flow Reserve–Guided Revascularization Strategy Optical Coherence Tomography to Optimize Results of Percutaneous Coronary Intervention in Patients with Non-ST-Elevation Acute Coronary Syndrome: Results of the Multicenter, Randomized DOCTORS Study (Does Optical Coherence Tomography Optimize Results of Stenting) Physiology-Based Revascularization: A New Approach to Plan and Optimize Percutaneous Coronary Intervention: State-of-the-Art Review Prognostic Implication of Functional Incomplete Revascularization and Residual Functional SYNTAX Score in Patients With Coronary Artery Disease

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].