Mechanically Induced Ectopy via Stretch-Activated Cation-Nonselective Channels Is Caused by Local Tissue Deformation and Results in Ventricular Fibrillation if Triggered on the Repolarization Wave Edge (Commotio Cordis)

Figures

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  Figure 1.. Subcontusional local epicardial mechanical stimulation. A, Images of a typical epicardial mechanical stimulus (from Movie I in the Data Supplement). B, Mechanical stimulation characteristics, showing: (i) probe velocity (blue lines indicate period of probe acceleration; green, red, and purple lines show time of initial tissue contact [0 ms in A], full probe deceleration [7 ms in A] followed by reversal of probe direction initially by tissue recoil, and subsequently by retractor arm activation [16 ms in A, dashed outline showing resting arm position]), along with calculated precontact probe acceleration, velocity, and kinetic energy; peak and mean force; peak negative acceleration; mean stress; and extent and mean rate of tissue deformation (Methods in the Data Supplement for calculations); (ii) surface ECG showing mechanically induced premature ventricular excitation; and (iii) intraventricular balloon pressure, along with impact-induced pressure surge amplitude and rise/fall times.

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  Figure 2.. Left ventricular excitation visualized by epicardial optical mapping. Representative recordings during sinus rhythm (A) and mechanically (B) or electrically induced (C) excitation (from Movies II through IV in the Data Supplement) and maps of activation time (0 ms represents earliest epicardial activation in the associated map). Mechanical and electric stimulations were triggered at the same midlevel left ventricular (mid-LV) freewall location (green dots). Isochrones represent 2 ms steps. Note that the dark region at the mechanical stimulation location is an artifact caused by the probe entering the field of view, and the notch at the LV apex is caused by the surface ECG electrode.

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  Figure 3.. Mechanically induced ventricular fibrillation (VF). A, Surface ECG showing mechanical stimulation in early T wave, resulting in instantaneous VF (Movie V in the Data Supplement). B, Spatial interrelation of stimulation site and 50% repolarization isochrone (green). C, Comparison with previously published computational 2-dimensional modeling predictions,27 showing mechanically induced premature ventricular excitation (PVEM; red) arising directly adjacent to inexcitable tissue (yellow), forming a region of functional block (black rectangle) around which sustained reentry occurs. Adapted from Garny and Kohl27 with permission of the publisher. Copyright © 2004, John Wiley and Sons. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

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  Figure 4.. Mechanically induced premature ventricular excitation (PVEM) thresholds. Box-and-whisker plots of mechanical stimulation characteristics (precontact kinetic energy, mean deformation rate, peak force, mean stress, intraventricular pressure surge amplitude, and local tissue deformation) at PVEM threshold with varying combinations of freewall contact location (midleft ventricular [mid-LV; blues boxes] and midright ventricular freewall [mid-RV; red boxes]) and contact area (3.1 mm2 [lighter boxes] and 28.3 mm2 [darker boxes]). Only local tissue indentation (far right) forms a uniform predictor of PVEM threshold across the various stimulation protocols. Measurements from 7 hearts. P values are for comparison of contact location and area by 2-way ANOVA with Tukey–Kramer post hoc tests.

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  Figure 5.. Intraventricular volume pulses. A, Relationship between intraventricular balloon volume pulse and peak pressure, averaged from 6 hearts. Red points indicate volumes assessed in the standard experiments (which were not associated with elevated creatine kinase release; Figure III in the Data Supplement), whereas a mechanically induced premature ventricular excitation (PVEM)–inducing excessive volume pulse (200 μL) is shown in green. The gray horizontal band indicates the range of pressure amplitudes measured during PVEM-inducing epicardial mechanical stimulation. B, Representative pressure surges measured during epicardial mechanical stimulation (black) and with active injection/retraction of 20 μL (left) or 130 μL (right) intraventricular volume pulses (red). C, Representative optical mapping data for 90% repolarization time (0 ms represents earliest repolarization in the associated map) in sinus rhythm during (i) control and application of (ii) 15 mm Hg or (iii) 124 mm Hg pressure surges (using stimuli shown in B) applied at the peak of the T wave. Isochrones represent 5 ms steps. Note that the notch at the left ventricular (LV) apex is caused by the surface ECG electrode in the…