Commotio Cordis -- Sudden Cardiac Death With Chest Wall Impact

Christopher Madias, M.D.; Barry J. Maron, M.D.; Jonathan Weinstock, M.D.; N. A. Mark Estes III, M.D.; Mark S. Link, M.D.

Disclosures

J Cardiovasc Electrophysiol. 2007;18(1):115-122. 

In This Article

Cellular Mechanisms

The cellular mechanisms that underlie the initiation of VF in CC remain incompletely understood, but appear to be multifactorial. The induction of electrical events by mechanical stimulation of the myocardium has been well described under such circumstances as catheter-induced ectopic beats and thumping of the chest wall during asystole to produce premature ventricular depolarizations.[12,27] This phenomenon, termed mechano-electric coupling, has been attributed to the presence of mechano-sensitive ion channels that are activated by deformation of the myocardial cell membrane. In CC, rapid rise of ventricular pressure immediately following the chest impact may cause VF mediated through resultant myocardial stretch and the activation of ion channels via mechano-electric coupling.

Myocardial ischemia and CC appear to share certain electrical similarities, including ST-segment elevation and the risk of R on T causing VF.[11,28] The K+ ATP channel is primarily responsible for the ST-segment elevation and contributes to the risk of VF in myocardial ischemia.[11,28] In addition, mechano-sensitivity of the K+ATP channel has been previously demonstrated in a rat atrial model.[29] In our swine model of CC, infusion of glibenclamide, a sulfonylurea that primarily acts by inhibiting the K+ATP channel, reduced the magnitude of ST elevation and the incidence of VF.[11] Our results suggest that the immediate activation of the mechano-sensitive K+ATP channel by chest wall impacts is in part responsible for the induction of VF in CC. Other stretch-sensitive ion channels might also be involved. Blockade of the nonselective cation stretch-activated channel (SAC) has been shown to suppress stretch-induced depolarizations.[30,31] However, in our model, blockade of SAC with streptomycin did not prevent induction of VF.[20]

The data suggest that chest wall impacts in CC generate inward current through the opening of mechano-sensitive ion channels, which is the likely cause of premature ventricular depolarizations that, in turn, trigger development of VF. However, depolarization of a single beat is not sufficient to result in reentrant arrhythmia that underlies the mechanism of VF.[4] Thus, initiation of VF in CC appears to require at least two features: (1) a trigger—a premature ventricular depolarization—occurring in the setting of (2) a susceptible myocardial substrate. Evidently, both features are created by a chest wall blow occurring in the vulnerable portion of the cardiac cycle. Illustrating this point of the necessity of trigger and substrate is the fact that in our experiments of impact velocity, premature ventricular depolarizations were observed in nearly 70% of impacts that did not result in VF.[4] Thus, the trigger was produced, but VF was not, presumably because the proper substrate was not present.

The second necessary feature for the production of CC—the susceptible myocardial substrate—is likely related to the dispersion of repolarization that is present during the vulnerable period of the cardiac cycle when the chest impact occurs.[11] Recent data by Bode et al. support this hypothesis.[32] Using a fluid-filled balloon placed in the LV of six Langendorff-perfused rabbit hearts, increasing volume and pressure pulses were applied at different times of the cardiac cycle. Five epicardial electrodes placed evenly across the LV were used to measure monophasic action potentials and repolarization time. Pressure pulses induced VF only when balloon inflation occurred within a vulnerable window of 35-88 ms after the initiation of an action potential. This vulnerable window corresponded with the time of spontaneous increase in repolarization dispersion—the difference in the degree of local repolarization measured across the five LV electrodes after each corresponding area had depolarized. Even more interesting was the observation that pressure pulses that induced VF resulted in an increase in repolarization dispersion as compared to baseline.[32] Thus, it appears that for the induction of VF in CC, the upstroke of the T wave might signify a window of potential vulnerability due to an innate, spontaneous increase in repolarization dispersion. The potential vulnerability for the induction of VF is realized when chest impact results in sudden elevation in myocardial pressure leading to further increase in repolarization dispersion. A correlate to this hypothesis is seen in the well-documented R on T phenomenon.[33] In nonischemic situations, such as continuous ventricular pacing (VOO), premature depolarizations during the vulnerable portion of the T wave do not generally cause VF. However, in the setting of ischemia, the potential for induction of VF can be realized when a premature ventricular contraction falls on the vulnerable portion of the T wave.[4,33,34]

In addition, the experiments by Bode et al. provide further insight into the mechanism by which increase in repolarization dispersion might result in VF in CC. In their model, it was observed that the LV myocardium was not excited simultaneously by a global pressure pulse.[32] Instead, it was noted that the earliest activation occurred at the LV site with the shortest repolarization time and occurred considerably later at sites with longer repolarization times. On the basis of these findings, it was suggested that VF is induced when an electrical gradient is sufficient to activate myocardium with early local recovery of excitability, but fails to activate less-repolarized myocardium because of local refractoriness. Nonuniform excitation might thus form the basis for the initiation of reentry and the induction of VF in CC.

In addition, as had been shown in our swine model, a lower and upper limit of vulnerability was observed for pressure pulses that resulted in VF. Thus, VF occurred instantaneously after 11% of pressure pulses (ranging from 208 to 289 mmHg; mean 252 ± 30) that fell within the narrow vulnerable window of early repolarization.[32] Premature beats, but absence of VF could be observed with pressure pulses above or below this range. While not necessarily mechanistically similar, an analogous association is seen in the initiation of VF with electrical T wave shocks during implantable cardioverter-defibrillator testing. Electrical shocks can induce VF during early repolarization if they surpass a lower limit but do not exceed an upper limit of shock strength.[32,35] In addition, induction of VF with T wave shocks also correlates with shock-induced dispersion of repolarization.[32,35]

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