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Randomized study on simple versus complex stenting of coronary artery bifurcation lesions: the Nordic bifurcation study Contemporary techniques in percutaneous coronary intervention for bifurcation lesions Drug-Coated Balloons for Coronary Artery Disease: Third Report of the International DCB Consensus Group Treatment of Very Small De Novo Coronary Artery Disease With 2.0 mm Drug-Coated Balloons Showed 1-Year Clinical Outcome Comparable With 2.0 mm Drug-Eluting Stents Clinical and angiographic outcomes of coronary dissection after paclitaxel-coated balloon angioplasty for small vessel coronary artery disease Influence of Local Myocardial Damage on Index of Microcirculatory Resistance and Fractional Flow Reserve in Target and Nontarget Vascular Territories in a Porcine Microvascular Injury Model Adaptive development of concomitant secondary mitral and tricuspid regurgitation after transcatheter aortic valve replacement Long-term efficacy and safety of drug-coated balloons versus drug-eluting stents for small coronary artery disease (BASKET-SMALL 2): 3-year follow-up of a randomised, non-inferiority trial Drug-Coated Balloon-Only Percutaneous Coronary Intervention for the Treatment of De Novo Coronary Artery Disease: A Systematic Review Optical Coherence Tomography–Defined Plaque Vulnerability in Relation to Functional Stenosis Severity and Microvascular Dysfunction

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].