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State of the Art in Noninvasive Imaging of Ischemic Heart Disease and Coronary Microvascular Dysfunction in Women: Indications, Performance, and Limitations Derivation and Validation of a Chronic Total Coronary Occlusion Intervention Procedural Success Score From the 20,000-Patient EuroCTO Registry：The EuroCTO (CASTLE) Score Long-Term Follow-Up of Complete Versus Lesion-Only Revascularization in STEMI and Multivessel Disease: The CvLPRIT Trial Major infections after bypass surgery and stenting for multivessel coronary disease in the randomised SYNTAX trial TACIT (High Sensitivity Troponin T Rules Out Acute Cardiac Insufficiency Trial): An Observational Study to Identify Acute Heart Failure Patients at Low Risk for Rehospitalization or Mortality Thin Composite-Wire-Strut Zotarolimus-Eluting Stents Versus Ultrathin-Strut Sirolimus-Eluting Stents in BIONYX at 2 Years Routinely reported ejection fraction and mortality in clinical practice: where does the nadir of risk lie? Myocardial Infarction in Young Women Treatment of higher-risk patients with an indication for revascularization: evolution within the field of contemporary percutaneous coronary intervention Older Adults in the Cardiac Intensive Care Unit: Factoring Geriatric Syndromes in the Management, Prognosis, and Process of Care: A Scientific Statement From the American Heart Association
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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].

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