Pediatrics-2006-Weinstock-e656-62 Failure of Commercially Available Chest Wall

DOI: 10.1542/peds.2005-1270; originally published online March 1, 2006; 2006;117;e656Pediatrics

Estes III and Mark S. LinkJonathan Weinstock, Barry J. Maron, Christopher Song, Paresh P. Mane, N.A. Mark

Commotio CordisCardiac Death Induced by Chest Wall Blows in an Experimental Model of

Failure of Commercially Available Chest Wall Protectors to Prevent Sudden

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ARTICLE

Failure of Commercially Available Chest WallProtectors to Prevent Sudden Cardiac Death Inducedby Chest Wall Blows in an Experimental Model ofCommotio CordisJonathanWeinstock, MDa, Barry J. Maron, MDb, Christopher Song, BAa, Paresh P. Mane, MDa, N.A. Mark Estes, III, MDa, Mark S. Link, MDa

aCardiac Arrhythmia Center, Division of Cardiology, Department of Medicine, Tufts University School of Medicine, Tufts-New England Medical Center, Boston,Massachusetts; bMinneapolis Heart Institute Foundation, Minneapolis, Minnesota

The authors have indicated they have no nancial relationships relevant to this article to disclose.

ABSTRACT

OBJECTIVE. Sudden cardiac death that results from chest wall blows (commotio cor-dis) the second leading cause of death in young athletes. Most events are causedby blows from projectiles, such as baseballs or lacrosse balls, with a substantialproportion occurring despite the use of a chest protector. In the present experi-ment, we tested the effectiveness of commercially available chest protectors inpreventing ventricular fibrillation (VF) that results from chest wall strikes withbaseballs and lacrosse balls.

METHODS. Twelve different baseball or lacrosse chest protectors were evaluated injuvenile swines that were subjected to 40-mph baseball or lacrosse ball blows tothe precordium during the vulnerable period of repolarization for VF and werecompared with control impacts without chest protectors. Seven baseball chestprotectors were hit by regulation baseballs, and 5 lacrosse chest protectors weretested by blows with standard lacrosse balls. Each animal received 2 chest blows foreach protector and 2 control impacts without a chest protector, with the sequenceof impacts assigned randomly.

RESULTS.VF was elicited by 12 (32%) of 37 strikes in control animals withoutbaseball chest protectors. None of the baseball chest wall protectors tested wereshown to decrease significantly the occurrence of VF when compared with con-trols. VF was elicited by 11 (46%) of 24 strikes in control animals without lacrossechest protectors. None of the lacrosse chest wall protectors tested decreasedsignificantly the occurrence of VF when compared with controls.

CONCLUSION. In our experimental animal model of commotio cordis, commerciallyavailable baseball and lacrosse chest wall protectors were ineffective in protectingagainst VF that was triggered by chest blows and, by inference, sudden cardiacdeath. Improvements in materials and design of chest wall barriers are necessary

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doi:10.1542/peds.2005-1270

The opinions expressed herein are theopinion of the authors and do notnecessarily represent the opinions of thefunding organizations.

KeyWordsdeath, sudden cardiac, arrhythmia,ventricular brillation, pediatrics,commotio cordis, athletes

AbbreviationsVFventricular brillationECGelectrocardiogramLVleft ventricularBBBbundle branch block

Accepted for publication Nov 11, 2005

Address correspondence to Mark S. Link, MD,Tufts-New England Medical Center, Box 197,750 Washington St, Boston, MA 02111. E-mail:[email protected]

PEDIATRICS (ISSN Numbers: Print, 0031-4005;Online, 1098-4275). Copyright 2006 by theAmerican Academy of Pediatrics

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to reduce the occurrence of these tragic events and makethe athletic field safer for youths.

SUDDEN DEATH THAT results from chest wall blows(commotio cordis) has been recognized with in-creasing frequency as a devastating risk of sports andother activities.114 Currently, commotio cordis is thesecond leading cause of death in youth athletics,4 occur-ring most frequently between 7 and 16 years of age inbaseball but increasingly also in lacrosse. Most cases thathave been reported to date involved a projectile such asbaseballs, lacrosse balls, and hockey pucks. In a recentreport from the US Commotio Cordis Registry,125% ofthe fatal events that occurred during organized compet-itive sports involved athletes who were wearing com-mercially available chest protectors that were intendedto prevent adverse consequences of chest wall blows.

We have developed an experimental animal model ofcommotio cordis in which baseballs that hit the chestwall during the vulnerable period of the cardiac cycle(1030 ms before the T-peak) produced ventricular fi-brillation (VF).1518 This model has been particularly use-ful in defining the determinants of commotio cordis,including the importance of precordial location,18 veloc-ity of impact (optimal at 40 mph),16 and direct relation-ship of projectile hardness to the susceptibility for VF.19

Commercially available chest barriers for both base-ball and lacrosse are marketed with implied or directclaims of protecting sports participants from harm thatresults from trauma to the chest wall. Using our estab-lished swine model of commotio cordis, we sought totest the effectiveness of a variety of such chest barriers inpreventing VF that results from strikes with baseballsand lacrosse balls.

METHODS

Experimental Animal ModelSix to 8-week-old domesticated juvenile swine thatweighed 11 to 18 kg were used in this study. The pro-tocol was approved by the Animal Research Committeeof the Tufts-New England Medical Center in conformitywith the standards of the Association for Assessment andAccreditation of Laboratory Animal Care. Animals weresedated with 12 mg/kg intramuscular ketamine, intu-bated, and then anesthetized using inhaled 1% to 2%isoflurane mixed with oxygen and nitrous oxide, whichmaintained sedation during the experiment. During theexperiment, surface electrocardiogram (ECG) was re-corded continuously, and left ventricular (LV) pressuredata were measured by a Millar catheter (Millar Mik-rotip, Houston, TX) that was positioned in the left ven-tricle via the femoral approach. A Power Lab (AD In-struments, Anaheim, CA) device converted signals fromanalog to digital, which then were displayed and stored

on a personal computer (Macintosh G3; Apple Com-puter Inc, Cupertino, CA).

Animals were placed prone in a sling to approximatephysiologic blood flow and cardiac hemodynamics. Thevelocity,16 location,18 and timing15 of chest wall blowswere designed to maximize the chance of producing VF.Chest wall impact was achieved by propelling a baseballor a lacrosse ball (depending on the protector beingtested), mounted on a 20-g aluminum shaft, at 40 mphtoward the center of the cardiac silhouette under echo-cardiographic guidance. Impact was gated to the portionof the cardiac cycle that is vulnerable for VF, 0 to 40msec before the peak of the T wave and by use of acommercially available cardiac stimulator (EP-2; EPMedical Inc, Budd Lake, NJ), triggered by surface ECGinput from the animal. Chest impacts that occurred out-side this time window were excluded from the analysis.Impact velocity was measured by a chronographic in-strument (Oehler Research, Austin, TX).

Chest Protectors TestedThe chest protectors that were chosen for this experi-ment are in common usage and are largely representa-tive of commercially available products in both designand composition. Seven commercially available baseballchest protectors and 5 lacrosse chest protectors (Fig 1)were tested in this series of experiments. All of the chestbarriers tested had a soft compliant layer that was com-posed of foam of varying density and thickness, andmost (Brine GBP [Brine Inc, Milford, MA], WarriorGoalie Guard 5000 [Warrior Inc, Warren, MI], RawlingsBatters Chest Protector 550 [BCP550; Rawlings Sport-ing Goods Company Inc, St Louis, MO], Heart-Gard[S&M Human Performance Products, Inc, Denver, CO],Louisville TPX Youth CBP [TPX-CBP; Hillerich &Bradsby Co, Louisville, KY], and Provest [Provest, LakeBluff, IL]) had a harder plastic layer either on the exter-nal surface or embedded within the foam layer(s). TheBrine Pro lacrosse protector had a unique soft layer thatwas composed of sleeves of expanded polypropylenebeads, whereas the soft layer in all other protectors wascomposed of closed cell foam (Figs 2 and 3).

Because of their design, 1 of the baseball protectors(Provest) and 2 of the lacrosse protectors (Brine GBP andWarrior) had the potential to have 2 different barriermaterials overlying an athletes precordium. The Provestprotector has an optional and removable plastic outershell; therefore, it was tested with (ProvestPlastic) andwithout (Provest) the shell. In the case of the Brine GBPand Warrior protectors, different barrier materials couldpotentially overlie the precordium, depending on theposition of the athlete and body motion; therefore, eachof these materials was tested separately (designatedBrine GBP Side and Brine GBP Center; Warrior Side andWarrior Center). Thus, a total of 15 different chest pro-tector materials, from 12 products, were tested. Baseball

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and lacrosse protectors were tested in 2 independentexperiments with different sets of animals.

Baseball chest protectors were hit by regulation base-balls (Rawlings Little League baseball [LLB-1]), and la-crosse chest protectors were tested by blows with stan-dard lacrosse balls (Brine Inc).

ProtocolA 4 4-in portion of each of the chest protectors wasremoved from that portion of the protector that wasdesigned to cover an athletes precordium. Before eachstrike, an echocardiogram was performed to identify thecenter of the LV silhouette.18 With this guidance, thedetached portion of each chest protector then was placedon the chest wall and secured by use of elastic straps that

were fastened around the chest of the animal. The base-ball or the lacrosse ball then was directed toward and hitthe previously identified target area on the chest wall.Measures were taken to ensure identical speed, timing,and location of the chest wall blows. In addition, eachchest protector material was affixed in an identical man-ner, and any migration of the protector between chestwall blows was corrected by realignment with echocar-diographic imaging before each strike.

The order in which chest protectors were applied toeach animal was randomized, after which blows weredelivered once to each chest protector and once to thesame animal when no protector was present (whichserved as a control). After this initial series, a secondrandomization was performed and the same animal un-

FIGURE 1Baseball and lacrosse chest protectors that were testedagainst chest blowinduced VF. Baseball protectors in-cluded products marketed for use by catchers (CooperBP-40, Cooper Pro BPX, Rawlings Youth LBP-1, and Lou-isville TPX Youth CBP) and those that are targeted formore general use (Heart-Gard, Provest, and Rawlings Bat-ters Chest Protector 550). All of the lacrosse protectorstested are designed and marketed for use by lacrossegoalies: Brine BP Pro, deBeer Icon Chest Guard, Brine GBP,STX Aegis, and Warrior Goalie Guard 5000.

FIGURE 2Baseball chest protector design tested in this experiment. In the protector with layeredidentical components (BP-40), black lines are placed between layers. The portion of theprotector at thickness 0 rests against the chest wall.

FIGURE 3Lacrosse chest protector design tested in this experiment. In protectors with layeredidentical components (Warrior Side, Brine GBP Side, Warrior Center, and Brine GBP Cen-ter), black lines are placedbetween layers. Theportionof theprotector at thickness 0 restsagainst the chest wall.


derwent another series of strikes in a different sequence.Thus, each animal received 2 impacts to each of the chestprotectors tested and also 2 blows directly to the unpro-tected precordium. When VF did not result from a givenchest blow, the subsequent impact was delivered with aninterval of no less than 3 minutes. When VF was trig-gered, prompt defibrillation was performed, after whichblood pressure, LV systolic function, and ECG patternwere assessed during an observation period of 5 min-utes; when these parameters returned to normal, addi-tional impacts were performed. When the animal re-mained unstable, no additional chest blows weredelivered, data from that incomplete series of impactswere excluded from the analysis, and the animal waseuthanized. Autopsy examination limited to the thoraxwas performed after completion of the protocol in eachanimal.

In the baseball protocol, 20 animals received a total of365 chest impacts, and in the lacrosse experiment, 12animals had 193 chest blows. Of these 558 blows, 33occurred either outside the 0- to 40-msec interval ofvulnerability for VF or after hemodynamic deteriorationand, as prospectively determined, therefore were ex-cluded from analysis. Consequently, a total of 333 base-ball impacts and 192 lacrosse impacts compose thepresent data set.

Statistical AnalysisThe primary endpoint of this study was the occurrenceof VF. Data first were analyzed using a 2 test to comparethe response to each protector versus controls (no pro-tector). Second, the McNemars test was used to controlfor possible confounding variables among the animals,such as body weight, and chest wall characteristics, suchas different rib structure and compliance.

Assuming an incidence of VF in control strikes of50%, using a 2-sided test with an level of .05 and apower level of 80%, detection of a reduction in VF from50% to 10% would require 20 impacts per chest protec-tor. In this experiment, each baseball protector under-went 40 chest wall blows, and each lacrosse protectorwas exposed to 24 chest wall blows.

Secondary endpoints include peak intracavitary LVpressure measured at chest impact, as well as ST segmentelevation and the presence of bundle branch block (BBB;defined as 100% increase in QRS duration). Peak LVpressure was measured from the digitally recorded pres-sure from the LV catheter and compared with controlimpacts with a paired t test. ST segment elevation andBBB were assessed only in strikes that did not result inVF. The degree of ST elevation was measured from thedigitally recorded surface ECG, 80 ms after the J point ofthe first technically satisfactory beat immediately afterchest impact. Differences in the incidence of BBB be-tween animals with chest protectors and controls were

assessed using McNemars test. For all analyses, P .05was considered statistically significant.

RESULTS

Baseball Chest Protectors

VFVF was elicited by 12 (32%) of 37 strikes as a result ofcontrol impacts in animals without baseball chest pro-tectors. None of the baseball chest wall protectors testedsignificantly decreased the occurrence of VF when com-pared with controls (Fig 4). With chest protectors, VFoccurred in the range of 22% to 49% of chest blows:Provest, 18 (49%) of 37 (P .16); Provest with plastic,8 (22%) of 37 (P .30); BCP550, 15 (41%) of 37 (P .47); Heart-Gard, 15 (41%) of 37 (P .47); Cooper ProBPX (BPX; Bauer Inc, Toronto, Ontario, Canada), 10(27%) of 37 (P .61); TPX-CPB (Bauer Inc), 14 (38%)of 37 (P .63); Cooper BP-40 (BP-40; Bauer Inc), 13(35%) of 37 (P .81); and LBP-1, 13 (35%) of 37 (P .81).

Secondary EndpointsThe peak LV pressure that was produced by the blowcorrelated linearly with the probability of VF. Mean peakLV pressure in controls was 709 114 mm Hg. Threechest protectors showed significantly lower mean LVpressures than controls: BCP550 (676 mm Hg; P .014),BPX (648 mm Hg; P .012), and TPX-CBP (675 mm Hg;P .027).

Mean ST segment elevation in control strikes that didnot result in VF was 214.7 132.3 v. Two chestprotectors were associated with significantly less ST seg-ment elevation compared with controls: BPX (150.9 v;P .025) and Provest with plastic (120.1 v; P .001).

FIGURE 4Incidence of VF with baseball chest wall blows for each of 8 baseball chest protectormaterials and for controls. Numbers above bars are P values calculated for chest protec-tors versus controls. Corresponding P values using McNemars test are as follows:ProvestPlastic, 0.35; BPX, 0.95; LBP-1, 1.00; BP-40, 1.00; TPX-CPB, 0.75; BCP550, 0.45;Heart-Gard, 0.45; and Provest, 0.18.


Among controls, BBB was observed in 16 (64%) of 25strikes. No significant reduction in the occurrence ofBBB was attributable to any of the baseball chest pro-tectors.

Lacrosse Chest Protectors

VFVF was elicited by 11 (46%) of 24 strikes as a result ofcontrol impacts in animals without lacrosse chest pro-tectors. None of the lacrosse chest wall protectors testedsignificantly decreased the occurrence of VF when com-pared with controls (Fig 5). With chest protectors, VFoccurred in the range of 21% to 50% of chest blows:Brine GBP Center, 8 (33%) of 24 (P .37); WarriorCenter, 8 (33%) of 24 (P .37); deBeer Icon (deBeerInc, Albany, NY), 9 (38%) of 24 (P .55); Brine GBPSide, 12 (50%) of 24 (P .77); STX Aegis (STX, Balti-more, MD), 12 (50%) of 24 (P .77); and Warrior Side,12 (50%) of 24 (P .77). The Brine Pro demonstrated atrend toward lower probability of VF when comparedwith control strikes (21% vs 49%; P .07).

Secondary EndpointsIn this protocol, the peak LV pressure that was producedby the chest blow also correlated linearly with the prob-ability of VF. Mean peak LV pressure that was producedby chest wall blows in controls was 641 116 mm Hg.Significantly lower mean maximum LV pressure wasobserved during lacrosse ball impacts with 3 protectors:the Brine Pro (598 mm Hg; P .007), Brine GBP Center(597 mm Hg; P .006), and Brine GBP Side (611 mmHg; P .040).

Mean ST segment elevation with chest impact in con-trols was 63.2 30.3 v. Three chest protectors showedsignificantly less ST elevation when compared with con-

trol chest wall blows: the Brine Pro (19.8 v; P .001),deBeer Icon (35.5 v; P .016), and the Brine GBPCenter (19.6 v; P .001).

Among controls without lacrosse chest protectors,BBB was observed after all 13 (100%) strikes. Whencompared with controls, 6 of the 7 materials tested hadsignificantly lower frequency of BBB: Brine Pro (42%; P .016), deBeer Icon (46%; P .031), Brine GBP Center(18%; P .004), Brine GBP Side (40%; P .031),Warrior Center (46%; P .031), and Warrior Side(30%; P .016).

DISCUSSIONCommotio cordis is an increasingly recognized cause ofsudden death on the athletic field during organized,competitive sports17 and of mounting concern amongthe general public and those who are involved in youthsports.6,7 Previous efforts to reduce the risk for theseevents have focused on the use of softer-than-normal(safety) baseballs that have been shown to reduce (inour experimental model)15,19 but not abolish the likeli-hood of VF during play.1

In our experimental animal model of commotio cor-dis, commercially available baseball and lacrosse chestwall protectors failed to protect against VF that wastriggered by chest blows. These findings are consistentwith the clinical observation that commotio cordis notinfrequently occurs despite the use of chest wall barriersthat are believed to be protective. Indeed, in a recentreport from the US Commotio Cordis Registry (Minne-apolis, MN), almost 30% of fatal commotio cordis eventsoccurred in athletes who were nevertheless affordedsome form of chest protection.1 In some cases, the lack ofprotection by the chest barriers was apparently attribut-able to migration of the equipment during physical ac-tivity, exposing the precordium to direct impact. In othercases, however, projectiles were known to strike directlyon the chest protector, including several lacrosse goaliesand baseball catchers.1 Indeed, in the present animalmodel, with a representative portion of the chest pro-tector material securely affixed directly over the heart,VF nevertheless occurred frequently with each of thebarriers tested and no less frequently than in controlswithout chest protectors.

The velocity, location, and timing of chest wall im-pacts in our model were designed to maximize the like-lihood of VF. Although chest wall impacts during athletictraining and competition do not always share these char-acteristics, testing protectors under laboratory circum-stances allows for assessment of their ability to protectagainst a worst-case scenario, the standard against whichprotector design should be measured.

All but 1 of the chest protectors evaluated in thisexperiment were composed of a compliant layer(s) ofclosed cell foam of varying thickness and density, whichis intended to dissipate the energy of an impact, and did

FIGURE 5Incidence of VF with lacrosse ball chest wall blows for each of 7 lacrosse chest protectormaterials and for controls. Numbers above bars are P values calculated for chest protec-tors versus controls. Corresponding P values using McNemars test are as follows: BrinePro, 0.07; Brine GBP Center, 0.45; Warrior Center, 0.45; deBeer Icon, 0.69; Brine GBP Side,1.00; STX, 1.00; and Warrior Side, 1.00.


or did not have a harder plastic shell material eithercovering or embedded within the foam, which is in-tended to diffuse the force of impact over a greatersurface area. Given the presence of such soft, presum-ably energy-absorbing material, we intuitively expectedthese chest barriers to afford a large measure of protec-tion against commotio cordis; however, this did not oc-cur under our experimental conditions. Furthermore,there is no evidence that the presence of a hard plasticshell acted to reduce significantly the occurrence of VF.Only the Brine Pro protector exhibited a trend towardprotection from VF as induced by chest impacts withlacrosse balls. Of note, this particular chest barrier(which does not have a hard plastic shell) is composed ofa layer that contains sleeves of expanded polypropylenebeads, a unique material composition that is not foundin other available products.

Only 1 previous study has assessed the protectiveeffect of chest barriers against baseball impacts.20 Theseinvestigators used a nonbiological 3-rib structure to as-sess responses to a baseball projected at speeds thatranged from 40 to 70 mph. Four of the 5 chest protectorstested reduced the viscous response, which is a measureof deformation and compression of the experimentalmodel over the duration of the impact. However, such anonbiological model does not test or produce VF or mimicthe complex phenomenon of commotio cordis15,17; there-fore, its relevance to this clinical problem may be limited.

Our animal model of commotio cordis, out of neces-sity, is not identical to the human condition. For exam-ple, swine chest walls are more ovoid than humans;however, at the site of impact in both swine and hu-mans, the precordial strike occurs perpendicular to thechest wall, minimizing the differences in the chest wallanatomy. Our experimental design used a 4 4-inmaterial that was cut from the commercially availablechest protector that was affixed over the swine precor-dium, thereby also minimizing the potential effects ofdifferent chest contours in humans and swine.

Chest wall protectors have been widely marketed andpromoted as providing protection against injury in bothbaseball and lacrosse, particularly in organized youthsports, for catchers and goalies. Manufacturers havebeen (and may continue to be) unaware of commotiocordis and its consequences and therefore have designedchest barriers to protect athletes primarily against softtissue and bone injury but not against VF, potentially amore lethal potential outcome of chest wall trauma.When commotio cordis occurs despite the use of a chestprotector, the event is especially troubling, given thefalse sense of security that is conveyed unintentionallyby wearing such a commercially available barrier.

The present experimental data, showing that none ofthe commercial chest barriers tested in our swine modelprovided significant protection against commotio cordis,has stimulated our laboratory to undertake a systematic

effort to determine, under experimental conditions withthe swine model, the most optimal chest barrier materialcomposition and design with the potential ultimately tooffer virtually absolute protection against chest blowinduced VF. Novel materials and design that are effectivein dissipating impact energy in time and space differentlyfrom barriers that are designed to protect against tissueinjury may be necessary to achieve this goal. The find-ings of this experiment provide a starting point for ef-fective chest protector design by exposing the ineffec-tiveness of the available protectors, as well as thepotential implied by a unique material such as expandedpolypropylene beads in contrast to the more standard(closed cell foam) materials.

Some of the chest protectors tested here seemed toblunt some of the previously reported facets of commo-tio cordis, such as ST segment elevation, BBB, and LVsystolic pressure. This may be evidence that the chestwall barriers that we tested do, in fact, mitigate in somerespect the commotio cordis phenomenon. However,the failure of chest barriers to abolish VF in our experi-ment represents the most clinically relevant evidence oftheir ineffectiveness in preventing commotio cordis andemphasizes the inadequacy of the materials that cur-rently are in use. It is our expectation that by using thepresent experimental data, improved chest barriers thatultimately will prevent this increasingly recognizedcause of sudden cardiac death during sports activities canbe designed and produced.

ACKNOWLEDGMENTSThis study was supported by grants from Kiwanis Pedi-atric Trauma Institute, Tufts-New England Medical Cen-ter (Boston, MA), National Operating Committee onStandards for Athletic Equipment (Overland Park, KS),and Louis J. Acompora Foundation (Northport, NY).

We are indebted to Stacey E. Supran, Division ofClinical Care Research, New EnglandMedical Center, forassistance with statistical analysis.

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DOI: 10.1542/peds.2005-1270; originally published online March 1, 2006; 2006;117;e656Pediatrics

Estes III and Mark S. LinkJonathan Weinstock, Barry J. Maron, Christopher Song, Paresh P. Mane, N.A. Mark

Commotio CordisCardiac Death Induced by Chest Wall Blows in an Experimental Model of

Failure of Commercially Available Chest Wall Protectors to Prevent Sudden

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