Concomitant Obesity and Metabolic Syndrome Add to the Atrial Arrhythmogenic Phenotype in Male Hypertensive Rats

Mathias Hohl, Dennis H. Lau, Andreas Mueller, Adrian D. Elliott, Benedikt Linz, Rajiv Mahajan, Jeroen M. L. Hendriks, Michael Boehn, Ulrich Schotten, Prashanthan Sanders, Dominik Linz*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Background-Besides hypertension, obesity and the metabolic syndrome have recently emerged as risk factors for atrial fibrillation. This study sought to delineate the development of an arrhythmogenic substrate for atrial fibrillation in hypertension with and without concomitant obesity and metabolic syndrome.

Methods and Results-We compared obese spontaneously hypertensive rats (SHR-obese, n=7-10) with lean hypertensive controls (SHR-lean, n=7-10) and normotensive rats (n=7-10). Left atrial emptying function (MRI) and electrophysiological parameters were characterized before the hearts were harvested for histological and biochemical analyses. At the age of 38 weeks, SHR-obese, but not SHR-lean, showed increased body weight and impaired glucose tolerance together with dyslipidemia compared with normotensive rats. Mean blood pressure was similarly increased in SHR-lean and SHR-obese when compared with normotensive rats (178 +/- 9 and 180 +/- 8 mm Hg [not significant] versus 118 +/- 5 mm Hg, P

Conclusions-In addition to hypertension alone, concomitant obesity and metabolic syndrome add to the atrial arrhythmogenic phenotype by impaired left atrial emptying function, local conduction abnormalities, interstitial atrial fibrosis formation, and increased propensity for atrial fibrillation.

Original languageEnglish
Article number006717
Number of pages12
JournalJournal of the American Heart Association
Volume6
Issue number9
DOIs
Publication statusPublished - Sept 2017

Keywords

  • atrial fibrillation
  • hypertension
  • metabolic syndrome
  • obesity
  • ADIPOSE-TISSUE
  • CATHETER ABLATION
  • SODIUM-ABSORPTION
  • CARDIAC FIBROSIS
  • PERICARDIAL FAT
  • ANGIOTENSIN-II
  • HEART-FAILURE
  • FIBRILLATION
  • OSTEOPONTIN
  • INHIBITION

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