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Nicotine Exacerbates Arrhythmogenesis in Rabbit Right Ventricular Outflow Tract Triggered by Chronic Obstructive

Chao-Shun Chan1,2, Feng-Zhi Lin3,4, Yao-Chang Chen4

  • 1Division of Cardiology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Journal of Cellular and Molecular Medicine
|June 19, 2025
PubMed
Summary

Nicotine worsens ventricular tachycardia (VT) in chronic obstructive pulmonary disease (COPD) by increasing electrical and structural changes in the right ventricular outflow tract (RVOT). These effects were reversed by specific drug treatments.

Keywords:
chronic obstructive pulmonary diseasenicotineright ventricular outflow tractventricular tachycardia

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Area of Science:

  • Cardiology
  • Pulmonary Medicine
  • Pharmacology

Background:

  • Cigarette smoke contains nicotine, a known risk factor for ventricular tachycardia (VT).
  • Chronic obstructive pulmonary disease (COPD) and the right ventricular outflow tract (RVOT) are primary risk factors and origins for VT, respectively.
  • Understanding nicotine's role in COPD-related VT is crucial for patient management.

Purpose of the Study:

  • To investigate the arrhythmogenic effects of nicotine in the context of COPD-induced RVOT changes.
  • To explore the potential of specific signaling pathway inhibitors (H89, KN93, KB-R7943) in mitigating nicotine-exacerbated VT.

Main Methods:

  • Induction of COPD in rabbits using human leukocyte elastase.
  • Tachypacing and isoproterenol administration to induce VT.
  • Treatment with nicotine, H89, KN93, and KB-R7943.
  • Patch clamp electrophysiology and Masson's trichrome staining for fibrosis assessment.

Main Results:

  • COPD rabbits exhibited higher VT incidence and increased RVOT fibrosis compared to controls.
  • Nicotine exposure exacerbated VT and increased fibrosis in COPD rabbits.
  • Drug treatments (H89, KN93, KB-R7943) suppressed VT in both COPD and nicotine-treated COPD groups.
  • Nicotine altered action potentials, L-type Ca2+ currents, NCX currents, and late Na+ currents in COPD RVOT myocytes.

Conclusions:

  • COPD intensifies RVOT VT through electrical and structural remodeling, and calcium dysregulation via PKA, CaMKII, and NCX pathways.
  • Nicotine significantly exacerbates VT in the setting of COPD by further worsening these electrical and structural changes.