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NAFLD and increased risk of cardiovascular disease: clinical associations, pathophysiological mechanisms and pharmacological implications
  1. Giovanni Targher1,
  2. Christopher D Byrne2,
  3. Herbert Tilg3
  1. 1Endocrinology and Metabolism, University of Verona Department of Medicine, Verona, Veneto, Italy
  2. 2Southampton National Institute for Health Research Biomedical Research Centre, University Hospital Southampton, Southampton, UK
  3. 3Department of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology & Metabolism, Medical University of Innsbruck, Innsbruck, Tirol, Austria
  1. Correspondence to Professor Giovanni Targher, Endocrinology and Metabolism, University of Verona Department of Medicine, Verona 37126, Italy; giovanni.targher{at}univr.it

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a public health problem, affecting up to a third of the world’s adult population. Several cohort studies have consistently documented that NAFLD (especially in its more advanced forms) is associated with a higher risk of all-cause mortality and that the leading causes of death among patients with NAFLD are cardiovascular diseases (CVDs), followed by extrahepatic malignancies and liver-related complications. A growing body of evidence also indicates that NAFLD is strongly associated with an increased risk of major CVD events and other cardiac complications (ie, cardiomyopathy, cardiac valvular calcification and cardiac arrhythmias), independently of traditional cardiovascular risk factors. This narrative review provides an overview of the literature on: (1) the evidence for an association between NAFLD and increased risk of cardiovascular, cardiac and arrhythmic complications, (2) the putative pathophysiological mechanisms linking NAFLD to CVD and other cardiac complications and (3) the current pharmacological treatments for NAFLD that might also benefit or adversely affect risk of CVD.

  • nonalcoholic steatohepatitis
  • cardiovascular disease
  • cardiovascular complications
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Footnotes

  • GT, CDB and HT contributed equally.

  • Correction notice This article has been corrected since it published Online First. The ORCID ID's have been added and table 2 has been corrected.

  • Contributors All authors contributed equally to write 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 None declared.

  • 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; externally peer reviewed.

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