title: Ventricular fibrillation induced by stretch pulse: implications for sudden death due to commotio cordis.
abstract: BACKGROUND
  Nonpenetrating chest wall impact (commotio cordis) may lead to sudden cardiac death due to the acute initiation of ventricular fibrillation (VF). VF may result from sudden stretch during a vulnerable window, which is determined by repolarization inhomogeneity.
  
  
  METHODS
  We examined action potential morphologies and VF inducibility in response to sudden myocardial stretch in the left ventricle (LV). In six Langendorff perfused rabbit hearts, the LV was instrumented with a fluid-filled balloon. Increasing volume and pressure pulses were applied at different times of the cardiac cycle. Monophasic action potentials (MAPs) were recorded simultaneously from five LV epicardial sites. Inter-site dispersion of repolarization was calculated in the time and voltage domains.
  
  
  RESULTS
  Sudden balloon inflation induced VF when pressure pulses of 208-289 mmHg were applied within a window of 35-88 msec after MAP upstroke, a period of intrinsic increase in repolarization dispersion. During the pressure pulse, MAPs revealed an additional increase in repolarization dispersion (time domain) by 9 +/- 6 msec (P < 0.01). The maximal difference in repolarization levels (voltage domain) between sites increased from 19 +/- 3% to 26 +/- 3% (P < 0.05). Earliest stretch-induced activation was observed near a site with early repolarization, while sites with late repolarization showed delayed activation.
  
  
  CONCLUSIONS
  Sudden myocardial stretch can elicit VF when it occurs during a vulnerable window that is based on repolarization inhomogeneity. Stretch pulses applied during this vulnerable window can lead to nonuniform activation. Repolarization dispersion might play a crucial role in the occurrence of fatal tachyarrhythmias during commotio cordis.
authors.affiliation: Medical University Luebeck, Luebeck, Germany. bodef@t-online.de
authors.forename: Frank
authors.initials: F
authors.lastname: Bode
authors.forename: Michael R
authors.initials: MR
authors.lastname: Franz
authors.forename: Iris
authors.initials: I
authors.lastname: Wilke
authors.forename: Hendrik
authors.initials: H
authors.lastname: Bonnemeier
authors.forename: Heribert
authors.initials: H
authors.lastname: Schunkert
authors.forename: Uwe K H
authors.initials: UK
authors.lastname: Wiegand
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D002404:Catheterization / Q000009:adverse effects / Q000379:methods; D016757:Death, Sudden, Cardiac / Q000209:etiology; D005260:Female; D006335:Heart Injuries / Q000150:complications / Q000503:physiopathology*; D006352:Heart Ventricles / Q000293:injuries; D066298:In Vitro Techniques; D008297:Male; D011311:Pressoreceptors / Q000502:physiology*; D011817:Rabbits; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology*; D016276:Ventricular Function; D014949:Wounds, Nonpenetrating / Q000150:complications / Q000503:physiopathology*