Dynamics of Atrial Fibrillation Mechanisms and Comorbidities

J. Heijman*, D. Linz, U. Schotten

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

18 Citations (Web of Science)

Abstract

Atrial fibrillation (AF) contributes to morbidity and mortality of millions of individuals. Its molecular, cellular, neurohumoral, and hemodynamic pathophysiological mechanisms are complex, and there is increasing awareness that a wide range of comorbidities can contribute to AF-promoting atrial remodeling. Moreover, recent research has highlighted that AF risk is not constant and that the temporal variation in concomitant conditions contributes to the complexity of AF dynamics. In this review, we provide an overview of fundamental AF mechanisms related to established and emerging comorbidities or risk factors and their role in the AF-promoting effects. We focus on the accumulating evidence for the relevance of temporally dynamic changes in these risk factors and the consequence for AF initiation and maintenance. Finally, we highlight the important implications for future research and clinical practice resulting from the dynamic interaction between AF risk factors and mechanisms.
Original languageEnglish
Pages (from-to)83-106
Number of pages24
JournalAnnual Review of Physiology
Volume83
DOIs
Publication statusPublished - 1 Jan 2021

Keywords

  • atrial fibrillation
  • catheter ablation
  • comorbidities
  • dose-response relationship
  • dynamics
  • epicardial adipose-tissue
  • heart-failure
  • mechanisms
  • molecular-mechanisms
  • nerve activity
  • risk factors
  • sleep-apnea severity
  • stellate ganglion
  • stress kinase jnk
  • time-course
  • STRESS KINASE JNK
  • TIME-COURSE
  • EPICARDIAL ADIPOSE-TISSUE
  • DOSE-RESPONSE RELATIONSHIP
  • HEART-FAILURE
  • NERVE ACTIVITY
  • SLEEP-APNEA SEVERITY
  • CATHETER ABLATION
  • MOLECULAR-MECHANISMS
  • STELLATE GANGLION

Cite this