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Electrical Ventricular Remodeling in Dilated Cardiomyopathy

Christine Mages1,2,3, Heike Gampp1,2, Pascal Syren1,2

  • 1Department of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.

Cells
|October 23, 2021
PubMed

Insights

Ventricular arrhythmias in heart failure (HF) stem from fibrosis and ion channel changes. This review explores dilated cardiomyopathy (DCM) mechanisms and potential therapies for these life-threatening heart rhythm disorders.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Electrophysiology

Background:

  • Ventricular arrhythmias are a major cause of death in heart failure (HF) patients.
  • Myocardial fibrosis and ion channel remodeling in ventricular cardiomyocytes contribute to arrhythmogenesis in structural heart disease.
  • Ion channel dysregulation is linked to cardiomyopathy and arrhythmia development, with molecular signaling pathways becoming clearer.

Purpose of the Study:

  • To review the clinical and cellular electrophysiologic characteristics of dilated cardiomyopathy (DCM) related to ventricular ionic and structural alterations.
  • To highlight potential translational strategies and therapeutic options for ventricular arrhythmias in DCM.

Main Methods:

  • Literature review focusing on clinical studies and cellular electrophysiology research.
  • Analysis of molecular signaling pathways involved in ion channel dysregulation and cardiac remodeling.
  • Synthesis of information on therapeutic targets and translational approaches.

Main Results:

  • Dilated cardiomyopathy (DCM) exhibits specific ionic and structural alterations at the ventricular level that promote arrhythmias.
  • Understanding molecular signaling pathways is crucial for elucidating the mechanisms of arrhythmogenicity in HF.
  • Various potential therapeutic strategies targeting ion channels and fibrosis are being investigated.

Conclusions:

  • Ventricular arrhythmias in DCM are driven by complex electrophysiologic and structural changes.
  • Targeting molecular pathways offers promising avenues for novel therapeutic interventions.
  • Further research into translational strategies is essential for improving outcomes in HF patients with arrhythmias.

Keywords:
dilated cardiomyopathyion channelremodelingsudden cardiac deathventricular arrhythmia

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