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充血性心力衰竭

科研文章

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Age-Related Characteristics and Outcomes of Patients With Heart Failure With Preserved Ejection Fraction Heart Failure Outcomes With Volume-Guided Management Natriuretic Peptide-Guided Heart Failure Therapy After the GUIDE-IT Study In acute HF and iron deficiency, IV ferric carboxymaltose reduced HF hospitalizations, but not CV death, at 1 y Nuclear Imaging of the Cardiac Sympathetic Nervous System: A Disease-Specific Interpretation in Heart Failure The pyruvate-lactate axis modulates cardiac hypertrophy and heart failure SPECT and PET in ischemic heart failure Association of Abnormal Left Ventricular Functional Reserve With Outcome in Heart Failure With Preserved Ejection Fraction Unexpectedly Low Natriuretic Peptide Levels in Patients With Heart Failure Is Acute heart failure a distinctive disorder? An analysis from BIOSTAT-CHF

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].