It is now apparent that CC is a primary electrical event, with sudden death resulting from the instantaneous induction of VF initiated by a chest wall blow. Autopsy data generally has not revealed any underlying congential or acquired heart disease in victims. Available evidence suggests that the pathophysiology of impact-induced VF is multi-factorial and requires the precise confluence of several variables. Development of an experimental animal model has allowed for a deeper understanding of the underlying mechanisms. This model attempts to mimic the clinical profile of CC, and entails propelling projectiles commonly used in sport (baseballs and lacrosse balls) at the chest wall of anesthetized juvenile swine [1
]. Release and subsequent impact of the balls are gated to the cardiac cycle by a cardiac stimulator with triggering from the surface electrocardiogram of the swine (). Initial experiments involving this animal model defined a narrow window of vulnerability within the cardiac cycle that is critical for the development of CC. When impacts occurred precisely within 10 to 30 milliseconds before the peak of the T wave, VF was consistently produced (). VF was instantaneous and was not preceded by premature ventricular contractions (PVC), ST-segment changes, or heart block. Chest impacts occurring in other portions of the cardiac cycle produced various other electrophysiologic effects - including ST-segment elevation, PVC, transient heart block, and left bundle branch block - but never resulted in VF.
Figure 2 Laboratory and study design for the commotio cordis model. An anesthetized and intubated animal is positioned prone in a sling. Under echocardiographic guidance, a ball affixed to an aluminum shaft is impacted on the chest directly over the base of the (more ...)
Figure 3 Six lead electrocardiogram and intraventricular pressure measurement from and 11 kg swine undergoing a 48 km/h (30 mph) chest wall impact with an object the shape and weight of a standard baseball. Ventricular fibrillation is produced immediately upon (more ...)
Several other factors have also been identified as crucial to the development of VF in this model of CC. Using echocardiographic guidance, the importance of impact location directly over the anatomic position of the heart was revealed [9
]. VF occurred most commonly with blows directly over the center of the cardiac silhouette (30% of impacts) versus those over the left ventricular base (13% of impacts) or apex (4% of impacts). Thoracic impacts not overlaying the heart did not result in VF or other electrophysiologic effects. In addition, a relationship between the hardness of the impact object and the likelihood of inducing VF was also identified. Impacts with softer safety baseballs were associated with a lower incidence of VF than impacts with harder standard balls [10
]. Finally, the importance of the velocity of chest wall impacts was also systematically evaluated [11
]. Baseballs were propelled with velocities ranging from 32 to 113 km/h (20 to 70 mph) and timed to impact on the vulnerable 20 ms window on the upstroke of the T wave. The plot of impact velocity relative to incidence of VF exhibited a Gaussian distribution. The threshold velocity to cause VF was 40 to 48 km/h (25 to 30 mph) and as impact velocity increased, the incidence of VF rose to a peak of nearly 70% of impacts at 64 km/h (40 mph). At velocities > 80 km/h (50 mph), however, the likelihood of VF decreased (). This observation is consistent with the observed clinical scenario of CC in youth baseball, where baseball velocities are estimated to range between 48 to 80 km/h (30 to 50 mph).
Figure 4 Incidence of ventricular fibrillation (VF) induced by chest wall impacts at the vulnerable period of repolarization (10-30 ms prior to the peak of the T-wave) with a regulation baseball propelled at velocities ranging from 32 to 113 km/h (20 to 70 mph) (more ...)
The importance of the location, hardness, and velocity of chest wall impacts in CC relate to the effects of these variables on induction of a critical left ventricular (LV) pressure that is necessary to produce VF. In experiments of impact velocity, higher velocities correlated with the generation of greater peak instantaneous LV pressures. As with impact velocities, the risk of VF correlated with the LV pressure rise created by the chest wall blow in a Gaussian distribution () [8
]. The highest incidence was evident with peak LV pressures of 250 to 450 mmHg and decreased with pressures above and below this range. Thus, these data suggest that there is a lower and upper limit of vulnerability of LV pressures resulting in VF and that the instantaneous LV pressure rise produced by the chest blow mediates the electrophysiologic consequences of CC.
Figure 5 The probability of ventricular fibrillation (VF) relative to the peak left ventricular (LV) pressure and LV pressure over time (dP/dt) in 8-12 kg swine undergoing 48 km/h (30 mph) chest wall impacts with a baseball. The data exhibit a Gaussian distribution (more ...)
Mechanical stimulation of the myocardium resulting in electrical events is well-described, occurring in such circumstances as catheter induced ectopic beats and thumping of the chest wall during asystole to produce PVCs [5
]. 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 chest impact results in VF mediated through resultant myocardial stretch and the activation of ion channels. CC appears to share certain electrical similarities with myocardial ischemia, including ST-segment elevation and the phenomenon of R on T causing VF [13
]. Activation of the K+ATP
channel is primarily responsible for ST-segment elevation noted in myocardial infarction, and contributes to the increased risk of VF associated with ischemia. In addition, mechano-sensitivity of the K+ATP
channel has been previously demonstrated in a rat model [15
]. In our model of CC, infusion of glibenclamide, a K+ATP
channel inhibitor, reduced the magnitude of ST-elevation and the incidence of VF following chest blows [13
]. 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 are also likely to be involved. Interestingly, however, blockade of the non-selective cation stretch-activated channel (SAC) with streptomycin did not prevent induction of VF in our model [12
In CC, the inward current generated through the opening of mechano-sensitive ion channels results in ventricular depolarizations that in turn, trigger development of VF. However, ventricular depolarization alone is not sufficient to result in reentrant arrhythmia that underlies the mechanism of VF. Thus, initiation of VF in CC appears to require at least two features: (i) a trigger
- premature ventricular depolarization - occurring in the setting of (ii) a susceptible myocardial substrate
]. The necessity of both trigger and substrate is illustrated in experiments of impact velocity [8
]. PVCs were observed in nearly 70% of impacts that did not result in VF. Thus, a trigger (ventricular depolarization) was produced, but did not result in VF, presumably due to the absence of appropriate substrate.
Interestingly, both trigger for CC and the susceptible myocardial substrate are in part created by a chest wall blow occurring in the vulnerable portion of the cardiac cycle. Susceptibility to development of CC relates to dispersion of repolarization that is present during the vulnerable period of the cardiac cycle when chest impact occurs. Recent data by Bode et al support this hypothesis [16
]. Fluid-filled balloons were placed in the LV of Langendorff perfused rabbit hearts and increasing volume and pressure pulses were applied at different points of the cardiac cycle. VF was induced only when balloon inflation occurred within a vulnerable window of 35ms to 88ms after the initiation of an action potential. This vulnerable window corresponded to the time of spontaneous increase in repolarization dispersion. Even more interesting was the observation that as compared to baseline, pressure pulses that induced VF resulted in a further increase
in repolarization dispersion. Thus, it appears that the upstroke of the T wave signifies a window of potential
vulnerability for development of VF in CC, due to spontaneous increase in repolarization dispersion. The potential vulnerability for the induction of VF is realized
when chest impact results in sudden elevation in LV pressure leading to further increase in repolarization dispersion. Analogous to this hypothesis is the R on T phenomenon. In non-ischemic myocardium, premature ventricular depolarization during the T wave does not normally induce VF. Thus, continuous ventricular pacing (VOO) is generally safe. However, with the increase in repolarization dispersion in the setting of ischemia, the potential for inducing VF can be realized when a PVC falls on the vulnerable portion of the T wave [17
In addition, the experiments by Bode et al provide further insight into the electrical properties by which increase in repolarization dispersion might produce VF in CC [16
]. In their model, it was observed that the LV myocardium was not excited simultaneously by a global pressure pulse. 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. VF was induced when a sufficient electrical gradient was able to activate myocardium with early local recovery, but failed to activate myocardium that was refractory. Based on these findings, non-uniform excitation might thus form the basis for the initiation of reentry and the induction of VF in CC.
Although activation of the K+ATP
channel is shared by both CC and ischemic myocardium, the mechanism of activation is quite different. In our model, angiography performed immediately after impact in animals that developed VF did not reveal any evidence of stenosis or spasm in epicardial coronary arteries [1
]. Myocardial perfusion imaging with technetium 99m sestamibi performed after impact revealed only small mild apical defects in a minority (25%) of the animals tested. In addition, left ventriculograms and echocardiograms performed immediately after defibrillation revealed only mild apical or distal septal hypokinesis, regions distant from the area of precordial impact [1
]. On pathologic examination, structural cardiac damage has not been observed with impact velocities of less than 80 km/h (50 mph) [8