Inflammation in HFpEF: Key or circumstantial?

V. van Empel, H.P. Brunner-La Rocca

Research output: Contribution to journalEditorialAcademic

Abstract

Heart failure (HF) can be split into HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Currently the pathophysiologic mechanisms involved in HFpEF remain largely unknown. The neurohumoral and sympathetic nervous systems seem not to play a crucial role in HFpEF, as treatments targeting these pathways do not show beneficial effects in HFpEF patients, in contrast to HFrEF patients. A better understanding of the pathophysiological processes involved in HFpEF is needed, as there is no proven treatment for this disease at the moment. Recent data have yielded growing attention to the role of inflammation in HFpEF. In this review we discuss increased inflammation in HFpEF as demonstrated in translational animal models and human studies. This review evaluates whether inflammation plays a key role in HFpEF or is just a by-product of various comorbidities. Additionally, we analyze the involvement of oxidative stress and endothelial dysfunction and lastly we outline potential therapeutic targets. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)259-263
Number of pages5
JournalInternational Journal of Cardiology
Volume189
DOIs
Publication statusPublished - 15 Jun 2015

Keywords

  • Heart failure
  • Heart failure with preserved ejection fraction
  • Heart failure with reduced ejection fraction
  • Inflammation
  • Endothelial dysfunction
  • Oxidative stress
  • PRESERVED EJECTION FRACTION
  • CHRONIC HEART-FAILURE
  • C-REACTIVE PROTEIN
  • DIASTOLIC DYSFUNCTION
  • HYPERTENSIVE-RATS
  • EXERCISE CAPACITY
  • MYOCARDIAL FIBROSIS
  • CARDIAC-HYPERTROPHY
  • METABOLIC SYNDROME
  • BODY-COMPOSITION

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