VF and nonsustained PMVT
In the combined end point of VF and nonsustained PMVT, the results were similar. There were no cases of nonsustained monomorphic ventricular tachycardia. Velocity of impact (P < 0.0001), impact distance from the center (P < 0.0001), peak LV pressure induced by the blow (P < 0.0001), and weight (P = 0.001) were univariate predictors. All remained multivariate predictors of VF and PMVT (peak LV pressure (P < 0.0001), velocity (P = 0.0002), distance from the center (P < 0.0001), and weight (P = 0.0059)).
Premature ventricular depolarizations
Premature ventricular depolarizations were observed in 499 of 624 impacts. The induction of VF or nonsustained PMVT necessarily included an initial ventricular beat, which for the purposes of this study was defined as a premature ventricular depolarization. Velocity of impact (P < 0.0001), baseball (P = 0.01), distance from the center (P < 0.0001), and peak LV pressure (P = 0.0002) were associated with PVC (Table 3). In a multivariate model controlling for repeated measures on the same animals, baseball was no longer significant. Velocity remained highly significant (P < 0.0001), as did distance from the center (P = 0.0004), and weight remained marginally significant (P = 0.058).
The end point of ST-segment elevation was assessed only in animals that did not have induction of VF and subsequent defibrillation. ST-segment elevation was observed in 163 of 446 impacts. Velocity (P < 0.0001), chest wall thickness (P = 0.0003), peak LV pressure induced by the blow (P < 0.0001), and weight (P < 0.0001) were all predictors of ST-segment elevation (Table 4). In a multivariate model controlling for repeated measures on the same animals, velocity and chest wall thickness were no longer independent predictors (P = 0.55 and P = 0.69, respectively); peak LV pressure and animal weight both remain highly significant (P < 0.0001 for both).
In animals without sustained VF and defibrillation, transient heart block occurred after impact in 16 of 446 blows and lasted from 1 to 200 beats. Heart block only occurred in animals weighing <34 kg and when observed in animals weighing <14 kg, typically the animal had severe structural myocardial damage. Velocity of impact (P < 0.0001), ball type (P < 0.0001), and animal weight (P = 0.0008) were associated with heart block. In a multivariate model including velocity and ball type, and also controlling for repeated measures on the same animals, all remain highly significant: velocity (P = 0.0003), baseball (P = 0.0008), and weight (P < 0.0001).
Bundle Branch Block
In animals without VF, velocity (P < 0.0001), baseball (P < 0.0001), peak LV pressure (P < 0.0001), and weight (P < 0.0001) all predicted for BBB induced by the blow. In a multivariate model including velocity, baseball, peak pressure, and weight, and also controlling for repeated measures on the same animals, all variables remained significant; however certain variables dropped slightly in significance, perhaps owing to the smaller sample size: velocity (P < 0.0001), baseball (P = 0.0044), peak pressure (P = 0.0011), and weight (P = 0.0001).
In these data from a commotio cordis experimental model, animal size (and by influence age) is now included as an important variable to the susceptibility of VF induction by chest wall impact. Notably, the susceptibility to chest impact induced VF is not linear. The 4 lower weight groups had a similar incidence of VF induction, whereas there was a significant decrease in vulnerability to VF induction in the largest animals (>44 kg). In the human commotio cordis registry, there is a marked reduction in commotio cordis events in individuals older than 20 yr (only 9% of cases occurred in those ≥25 yr of age) (6). It remains unclear whether this reduced incidence is due to biological variables or simply relates to a reduced exposure to chest wall blows in an age group with a lower rate of participation in sport. On the basis of our data, it would seem that biologic maturation plays a role in reducing the risk of commotio cordis. Biologic maturation could include increased precordial padding from increased muscle and other soft tissue mass, or from stiffer chest wall or rib cage, or possibly from changes in the myocardium itself. In the current study, a significantly thicker chest wall in the larger animals did not protect against VF in multivariate analysis. This finding suggests that the protective effects of aging are less likely related to increased precordial padding of muscle and fat, but perhaps to an increased stiffness of the chest. Although stiffness of the chest wall was not directly measured in this study, its effects can be indirectly assessed by the peak LV pressure produced by precordial impacts. In this study, balls thrown at similar velocity caused correspondingly reduced peak LV pressure in larger animals, a finding that may support increased stiffness of chest wall in these animals.
The current data may have implications for the design of chest wall protectors for the prevention of commotio cordis in sport. In a prior study from this laboratory, commercially available chest wall protectors composed predominantly of foams and plastics did not reduce the risk of commotio cordis (14). In the current experiment, wall thickness (significantly increased in larger animals) was not linked to susceptibility to VF, suggesting that increasing the thickness of energy absorbing foams in chest protectors to a degree that still maintains functionality for the athlete may be unlikely to protect from commotio cordis. To prevent chest blow–induced VF, an effective chest barrier may require a stiffer material to prohibit penetration of the ball into the chest cavity, thus reducing peak LV pressure.
We considered the possibility that the respiratory phase at the time of impact might also predict VF inducibility due to alterations in intrathoracic and intracardiac pressures. However, it would seem that such respiratory changes are small and overwhelmed by the marked increase in LV pressure caused by the chest blow. Although respiration alters the contour of the thorax in swine (similar to human anatomy), there is no lung tissue lying between the chest wall and the heart in our experimental animals. Thus, we would not expect the phase of respiration to have much effect on the transmission of force from the impact object to the underlying myocardium.
A previous experimental study showed the importance of site of chest impact for induction of VF in our commotio cordis animal model. In that study, impacts outside the cardiac silhouette did not produce VF, whereas blows at the LV base and apex were associated with lower risk for VF compared with impacts directed to the center of the LV (8). This present study confirms that prior finding and underscores that blows even small distances (1 cm) from the center of the heart will dramatically lower the risk of VF by up to 80%.
Animal body weight is an important determinant of commotio cordis, although not as a linear function. Only in the largest animals studied (≥44 kg) did the incidence of chest blow–induced VF decrease. Notably, greater chest wall thickness did not reduce the risk of commotio cordis. These data have implications for the design of protective chest wall barriers because increased foam thickness alone may not convey increased protection from VF.
The authors thank Stacey Supran for her assistance with the statistical analysis.
This study was supported by the National Operating Committee on Standards for Athletic Equipment, Overland Park, KS.
Mark S. Link has research support from the National Operating Committee on Standards for Athletic Equipment. No other author has any disclosures.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
The results of the study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation.
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Keywords:© 2018 American College of Sports Medicine
COMMOTIO CORDIS; VENTRICULAR FIBRILLATION; ATHLETES; SUDDEN CARDIAC DEATH