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Size as an Important Determinant of Chest Blow–induced Commotio Cordis

MADIAS, CHRISTOPHER1; MARON, BARRY J.1; DAU, NATHAN2; ESTES, NATHAN A. MARK III1; BIR, CYNTHIA3; LINK, MARK S.4

Medicine & Science in Sports & Exercise: September 2018 - Volume 50 - Issue 9 - p 1767–1771
doi: 10.1249/MSS.0000000000001630
BASIC SCIENCES
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Purpose Commotio cordis is sudden cardiac death caused by a relatively innocent blow to the left chest wall. Adolescents account for the majority of the cases; whether this is due to the higher frequency of adolescents playing ball sports or whether there is some maturational reduction of risk is not known.

Methods In a swine model of commotio cordis, the effect of body weight/size (directly related to age) to the susceptibility of chest impact–induced ventricular fibrillation (VF) is examined.

Methods Ball impacts were delivered at escalating velocities from 48.3 to 96.9 km·h−1 (30–60 mph) to 128 swine ranging in weight from 5 to 54 kg.

Results VF occurred in 29% of impacts to the smallest animals compared with 34% in the 14- to 239-kg group, 27% in the 24- to 33.9-kg group, 30% in 34- to 43-kg group, and 15% in the 44- to 54-kg animals. The highest-weight group was associated with a significantly lower incidence of VF compared with other weights (P = 0.002). In a multivariate logistic regression analysis, controlling for repeated measures, four variables predicted VF: body weight (P = 0.0008), velocity (P < 0.0001), distance from the center of the heart, (P < 0.0001), and peak left ventricular pressure induced by the blow (P = 0.0007).

Conclusions In this experimental model, animals weighing <44 kg seem to have a similar susceptibility to commotio cordis, whereas animals weighing ≥44 kg have a lower susceptibility. An increase in size of the individual, rather than reduced play of ball sports, is the likely reason for the decreased commotio cordis incidence in older individuals.

1Tufts Medical Center, Cardiac Arrhythmia Center, Boston, MA;

2Biomedical Engineering Center, Wayne State University, Detroit, MI;

3Keck School of Medicine, University of Southern California, Los Angeles, CA; and

4UTSouthwestern Medical Center, Dallas TX

Address for correspondence: Mark S. Link, M.D., UTSouthwestern Medical Center, 5939 Harry Hines Blvd, POB 1, Dallas, TX 75390; E-mail: mark.link@UTSouthwestern.edu.

Submitted for publication November 2017.

Accepted for publication March 2018.

Sudden cardiac death as a result of a seemingly innocent chest blow is defined as commotio cordis (1–4). Although once considered rare, commotio cordis is now increasingly reported as a cause of sudden cardiac death in young athletes (1,5–7). Typically, commotio cordis victims are male adolescents with a mean age of 15 yr in the US Registry (6), and it is rare for individuals older than 20 yr to experience such an event. Multiple factors may contribute to this age-dependent risk, including less frequent participation in sports by older individuals and the increased stiffness of the chest wall with biologic maturation. Experiments with a juvenile swine model have demonstrated that chest blow–induced ventricular fibrillation (VF) is the mechanism by which commotio cordis occurs (2). This model has also been used to evaluate variables important in the generation of VF including timing in the cardiac cycle (2), impact location (8), impact object velocity (9), stiffness (2,10), and shape (11), as well as individual susceptibility (12). The current study analyzes the effect of animal size on the incidence of VF with chest impact in the commotio cordis model.

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METHODS

Male swine were sedated with 12 mg·kg−1 intramuscular ketamine and then anesthetized with inhaled isoflurane (2). The animals were intubated and placed on a respirator, with general anesthesia maintained throughout the experiment with 2% isoflurane gas in 100% oxygen gas. Millar Mikrotip® (Houston, TX) pressure catheters were placed into the left ventricle (LV) via the femoral artery. A Piezo Respiratory Belt Transducer (AD Instruments, Colorado Springs, CO) was placed around the chest. The animals were then placed prone in a sling and continuous six-lead ECG were recorded on an AD instruments PowerLab data acquisition system using LabChartPro software (Mountain View, CA). This study was approved by the Institutional Animal Care and Use Committee of Tufts Medical Center (Boston, MA) in conformity with the regulations of the Association for Assessment and Accreditation of Laboratory Animal Care.

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Protocol

In the current protocol, animals weighing ≥24 kg were investigated. These included 15 animals of weights from 24.0 to 33.9 kg, 12 animals of weights from 34.0 to 43.9 kg, and 9 animals of weights from 44.0 to 54 kg (Table 1). Impacts were given with a baseball or lacrosse ball in free flight aimed at the center of the heart (guided by transthoracic echocardiogram) during the vulnerable time of the cardiac cycle 40 to 10 ms before the T-wave peak. If VF occurred, animals were immediately defibrillated and then blood pressure, ECG, and LV function (by echocardiogram) were observed. Impact location relative to the center of the cardiac silhouette was assessed by the individual aiming the projectile. The protocol consisted of three successive impacts at increasing projectile velocities: 48.3 km·h−1 (30 mph), 64.4 km·h−1 (40 mph), 80.5 km·h−1 (50 mph), and 96.6 km·h−1 (60 mph). If after an impact or defibrillation the LV function did not return to normal, no further impacts were given. At the end of each study the animal was euthanized with a saturated solution of potassium chloride while remaining under general anesthesia.

Smaller animals from previous protocols were also included in the analysis (32 animals of weights from 4.0 to 13.9 kg, 60 animals of weights from 14.0 to 23.9 kg). Data from these animals have been previously published from studies on sites of impact (8), energy limits of commotio cordis (9), stretch-activated channels in commotio (13), and chest protectors (14). Impacts from these animals were included if they met the following criteria: appropriately timed impact over the cardiac silhouette with no pharmacologic administration other than anesthetic agents. In these animals, only the first three impacts at each impact velocity were included for analysis. In some of these protocols, a baseball was used as the impact object, whereas in others, it was a lacrosse ball.

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Analysis

The primary end point of the current investigation is to evaluate whether larger animals exhibit reduced susceptibility to chest blow–induced VF compared with smaller animals. Secondary end points included the combined end point of VF and nonsustained polymorphic ventricular tachycardia (PMVT), premature ventricular contractions (PVC), ST-segment elevation, induction of heart block, and bundle branch block (BBB). Besides weight, other variables included in the analysis were respiratory phase at impact (inspiratory vs expiratory), velocity of the ball, type of ball (baseball vs lacrosse), impact distance from the center of the LV, chest wall thickness, and peak LV pressure caused by the chest blow.

Impacts were analyzed based on animal size: <14, 14–23.9, 24–33.9, 34–43.9, and 44–54 kg. Statistical analysis was performed using SAS 9.1 (SAS Institute Inc., Cary, NC). Continuous data were analyzed using the Student’s t-test; categorical data were assessed using the chi-square or Fisher exact test. Univariate logistic regression was performed for the comparison of LV pressure and risk of VF. A P value of <0.05 was considered statistically significant. Data are presented as mean ± SD.

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RESULTS

VF induction

A total of 329 impacts were administered to 36 animals weighing ≥24 kg. In 92 smaller animals (<24 kg) from prior studies, 291 impacts were also analyzed. Baseline QTc was longest in the smallest animals (422 ± 41 ms) and was significantly different when compared with the 14- to 23.9-kg group (403 ± 43 ms; P = 0.04) and the 34- to 43.9-kg group (395 ± 16 ms; P = 0.024). There were no other significant differences in QTc between any animal groups (24–33.9 kg: QTc, 403 ± 43 ms; 44–54 kg: QTc, 398 ± 29 ms). When VF occurred, it was immediately after the chest blow—there were no delayed arrhythmias observed. Ventricular tachycardia was never observed. Overall, VF occurred in 29.2% of blows to the <14-kg group, 34.3% in 14- to 23.9-kg group, 26.9% in 24- to 33.9-kg group, 29.8% in 34- to 43.9-kg group. In the largest animals (44–54 kg), VF occurred in only 15.1% in the 44- to 54-kg animals. The highest weight group was associated with a significantly lower incidence of VF compared with the other groups (P = 0.002). There was no difference in the incidence of VF among the lower four weight groups. The largest animals were less vulnerable to VF induction across all impact velocities (Table 1, Fig. 1). In univariate analyses, velocity of the impact object (P < 0.0001), distance from the center of the LV (P < 0.0001), weight of the animal (P = 0.010), and peak LV peak pressure induced by the blow (P < 0.0001) were predictors of VF (Table 2, Fig. 2). Chest wall thickness, ball type, and respiratory phase were not significant predictors of VF. In multivariate analysis, controlling for repeated measures on the same animal, size is even more significant (P = 0.0008) and velocity (P < 0.0001), distance from the center (P < 0.0001), and peak pressure (P = 0.0007) maintain significance.

FIGURE 1

FIGURE 1

FIGURE 2

FIGURE 2

TABLE 1

TABLE 1

TABLE 2

TABLE 2

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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)).

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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).

TABLE 3

TABLE 3

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ST-segment elevation

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).

TABLE 4

TABLE 4

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Heart block

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).

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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).

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DISCUSSION

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%.

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CONCLUSIONS

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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REFERENCES

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Keywords:

COMMOTIO CORDIS; VENTRICULAR FIBRILLATION; ATHLETES; SUDDEN CARDIAC DEATH

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