Heart Rhythm
Volume 7, Issue 7 , Pages 953-961, July 2010

Tunnel propagation following defibrillation with ICD shocks: Hidden postshock activations in the left ventricular wall underlie isoelectric window

  • Jason Constantino, BS

      Affiliations

    • Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland
  • ,
  • Yun Long, MS

      Affiliations

    • Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland
  • ,
  • Takashi Ashihara, MD, PhD

      Affiliations

    • Department of Cardiovascular Medicine, Shiga University of Medical Science, Otsu, Japan
  • ,
  • Natalia A. Trayanova, PhD, FHRS

      Affiliations

    • Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland
    • Corresponding Author InformationAddress reprint requests and correspondence: Dr. Natalia Trayanova, 3400 North Charles Street, CSEB 216, Baltimore, Maryland 21218

Received 27 January 2010; accepted 20 March 2010. published online 29 March 2010.

Background

After near-defibrillation threshold (DFT) shocks from an implantable cardioverter-defibrillator (ICD), the first postshock activation that leads to defibrillation failure arises focally after an isoelectric window (IW). The mechanisms underlying the IW remain incompletely understood.

Objective

The goal of this study was to provide mechanistic insight into the origins of postshock activations and IW after ICD shocks, and to link shock outcome to the preshock state of the ventricles. We hypothesized that the nonuniform ICD field results in the formation of an intramural excitable area (tunnel) only in the left ventricular (LV) free wall, through which both pre-existing and new shock-induced wavefronts propagate during the IW.

Methods

Simulations were conducted using a realistic three dimensional (3D) model of defibrillation in the rabbit ventricles. Biphasic ICD shocks of varying strengths were delivered to 27 different fibrillatory states.

Results

After near-DFT shocks, regardless of preshock state, the main postshock excitable area was always located within LV free wall, creating an intramural tunnel. Either pre-existing fibrillatory or shock-induced wavefronts propagated during the IW (duration of up to 74 ms) in this tunnel and emerged as breakthroughs on LV epicardium. Preshock activity within the LV played a significant role in shock outcome: a large number of preshock filaments resulted in an IW associated with tunnel propagation of pre-existing rather than shock-induced wavefronts. Furthermore, shocks were more likely to succeed if the LV excitable area was smaller.

Conclusion

The LV intramural excitable area is the primary reason for near-DFT failure. Any intervention that decreases the extent of this area will improve the likelihood of defibrillation success.

Keywords: Ventricular defibrillation, Bidomain model, Postshock activations, Internal cardioverter-defibrillator, Excitable area

Abbreviations: 3D, three dimensional, Ca, calcium, Cai, intracellular calcium, DFT, defibrillation threshold, DFT90, DFT with 90% probability of defibrillation success, ICD, implantable cardioverter-defibrillator, IW, isoelectric window, LV, left ventricle/ventricular, PA, postshock activation, RV, right ventricle/ventricular, SS, shock strength, VEP, virtual electrode polarization, VF, ventricular fibrillation

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 Supported by National Institutes of Health grants R01-HL082729 and R01-HL067322 to Dr. Trayanova.

 Constantino and Long contributed equally to this work.

PII: S1547-5271(10)00268-7

doi:10.1016/j.hrthm.2010.03.026

Heart Rhythm
Volume 7, Issue 7 , Pages 953-961, July 2010