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Inter-twinned relationship between heart failure and atrial fibrillation
  1. Giuseppe Rosano1,
  2. Gianluigi Savarese2
  1. 1 Department of Medical Sciences, IRCCS San Raffaele, Rome, Italy
  2. 2 Department of Medicine, Karolinska Institute, Stockholm, Sweden
  1. Correspondence to Professor Giuseppe Rosano, Department of Medical Sciences, IRCCS San Raffaele, Rome 00163, Italy; giuseppe.rosano{at}

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In the recent few years new treatment options have been added to the life-saving evidence-based treatments already available for heart failure (HF) with reduced ejection fraction (HFrEF). Conversely, no treatment has demonstrated any prognostic benefit in HF with preserved EF (HFpEF).1 Post-hoc analyses of randomised controlled trials focussing mainly on HFrEF but also partially embracing the heart failure with mid range ejection fraction (HFmrEF) population have suggested that patients with HFmrEF may benefit, although to a lesser extent, by the same treatments which are effective in HFrEF.2 Phenotyping HFmrEF and HFpEF is key to identify new therapeutic targets and preventive strategies and to implement trial design.

Atrial fibrillation (AF) and HF are both age-related diseases and represent global pandemics.3 4 AF predisposes to HF and vice versa, and, therefore, these diseases are highly co-prevalent.5 What is not currently completely understood is the association between AF and the individual HF subtypes, that is, HFpEF, HFmrEF and HFrEF. One currently proposed HF paradigm claims that HFpEF would be the consequence of comorbidities-induced microvascular inflammation and endothelial activation, which foster fibrosis and concentric left ventricular remodelling and thus overt HFpEF.5 6 On the other hand, HFrEF (and HFmrEF) would be linked to direct myocardial injury (eg, myocardial infarction), leading to eccentric left ventricular remodelling and thus overt …

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  • Contributors The two authors have provided significant contributions to the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests GS reports grants and personal fees from Vifor, grants and non-financial support from Boehringer Ingelheim, personal fees from Societa' Prodotti Antibiotici, grants from MSD, grants and personal fees from AstraZeneca, personal fees from Roche, personal fees from Servier, grants from Novartis, personal fees from GENESIS, personal fees from Cytokinetics, personal fees from Medtronic, outside the submitted work.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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