INTRODUCTION:Cardiac arrest due to chest wall blows (commotio cordis) has been reported with increasing frequency in children, and only about 15% of victims survive. Automated external defibrillators (AEDs) have been shown to be life saving in adults with cardiac arrest, but data on their use in children are limited. In a swine model of commotio cordis designed to be most relevant to young children, we assessed the efficacy of a commercially available AED for recognition and termination of ventricular fibrillation.METHODS AND RESULTS:Ventricular fibrillation was produced in anesthetized juvenile swine by precordial impact from a baseball under controlled conditions. Animals were randomized to defibrillation after 1, 2, 4, or 6 minutes of ventricular fibrillation. Twenty-six swine underwent 50 ventricular fibrillation inductions. Sensitivity of the AED for recognition of ventricular fibrillation was 98%, and specificity for nonshockable episodes was 100%. All episodes of ventricular fibrillation were successfully terminated by the AED.CONCLUSION:In this experimental model of commotio cordis, the AED proved to be highly sensitive and specific for recognition of ventricular fibrillation and effective in terminating the arrhythmia and restoring sinus rhythm. These findings suggest that early defibrillation with the AED could save young lives on the athletic field.

OBJECTIVES:In an animal model of commotio cordis, sudden death with chest-wall impact, we sought to systematically evaluate the importance of impact velocity in the generation of ventricular fibrillation (VF) with baseball chest-wall impact. BACKGROUND:Sudden cardiac death can occur with chest-wall blows in recreational and competitive sports (commotio cordis). Analyses of clinical events suggest that the energy of impact is often not of unusual force, although this has been difficult to quantify. METHODS:Juvenile swine (8 to 25 kg) were anesthetized, placed prone in a sling to receive chest-wall strikes during the vulnerable time window during repolarization for initiation of VF with a baseball propelled at 20 to 70 mph. RESULTS:Impacts at 20 mph did not induce VF; incidence of VF increased incrementally from 7% with 25 mph impacts, to 68% with chest impact at 40 mph, and then diminished at >/=50 mph (p < 0.0001). Peak left ventricular pressure generated by the chest blow was related to the incidence of VF in a similar Gaussian relationship (p < 0.0001). CONCLUSIONS:The energy of impact is an important variable in the generation of VF with chest-wall impacts. Impacts at 40 mph were more likely to produce VF than impacts with greater or lesser velocities, suggesting that the predilection for commotio cordis is related in a complex manner to the precise velocity of chest-wall impact.

OBJECTIVES In an experimental model of sudden death from baseball chest wall impact (commotio cordis), we sought to determine if sudden death by baseball impact could be reduced with safety baseballs. BACKGROUND Sudden cardiac death can occur after chest wall impact with a baseball (commotio cordis). Whether softer-than-standard (safety) baseballs reduce the risk of sudden death is unresolved from the available human data. In a juvenile swine model, ventricular fibrillation (VF) has been shown to be induced reproducibly by precordial impact with a 30-mph baseball 10 to 30 ms before the T-wave peak, and this likelihood was reduced with the softest safety baseballs (T-balls). To further test whether safety baseballs would reduce the risk of sudden death at velocities more relevant to youth sports competition, we used our swine model of commotio cordis to test baseballs propelled at the 40-mph velocity commonly attained in that sport. METHODS Forty animals received up to 3 chest wall impacts at 40 mph during the vulnerable period of repolarization for VF with 1 of 3 different safety baseballs of varying hardness, and also by a standard baseball. RESULTS Safety baseballs propelled at 40 mph significantly reduced the risk for VF. The softest safety baseballs triggered VF in only 11% of impacts, compared with 19% and 22% with safety baseballs of intermediate hardness, and 69% with standard baseballs. CONCLUSION In this experimental model of low-energy chest wall impact, safety baseballs reduced (but did not abolish) the risk of sudden cardiac death. More universal use of these safety baseballs may decrease the risk of sudden death on the playing field for young athletes.

OBJECTIVES In an experimental model of sudden death from chest wall impact (commotio cordis), we sought to define the chest wall areas important in the initiation of ventricular fibrillation (VF).BACKGROUND Sudden death can result from an innocent chest blow by a baseball or other projectile. Observations in humans suggest that these lethal blows occur over the precordium. However, the precise location of impact relative to the risk of sudden death is unknown.METHODS Fifteen swine received 178 chest impacts with a regulation baseball delivered at 30 mph at three sites over the cardiac silhouette (i.e., directly over the center, base or apex of the left ventricle [LV]) and four noncardiac sites on the left and right chest wall. Chest blows were gated to the vulnerable portion of the cardiac cycle for the induction of VF.RESULTS Only chest impacts directly over the heart triggered VF (12 of 78: 15% vs. 0 of 100 for noncardiac sites: p < 0.0001). Blows over the center of the heart (7 of 23; 30%) were more likely to initiate VF than impacts at other precordial sites (5 of 55; 9%, p = 0.02). Peak LV pressures generated instantaneously by the chest impact were directly related to the risk of VF (p < 0.0006).CONCLUSIONS For nonpenetrating, low-energy chest blows to cause sudden death, impact must occur directly over the heart. Initiation of VF may be mediated by an abrupt and substantial increase in intracardiac pressure. Prevention of sudden death from chest blows during sports requires that protective equipment be designed to cover all portions of the chest wall that overlie the heart, even during body movements and positional changes that may occur with athletic activities. (C) 2001 by the American College of Cardiology.

Introduction: Previous electrophysiologic investigations have described AV conduction disturbances in connexin40 (Cx40)-deficient mice. Because expression of Cx40 occurs predominantly in the atria and His-Purkinje system of the mouse heart, the AV conduction disturbances were thought to be secondary to disruption in His-Purkinje function. However, the lack of a His-bundle electrogram recording in the mouse has limited further investigation of the importance of Cx40. Using a novel technique to record His-bundle recordings in Cx40-deficient mice, we define the physiologic importance of deficiencies in Cx40.Methods and Results: Ten Cx40(-/-) mice and 11 Cx40(+/+) controls underwent a blinded, in vivo, closed chest electrophysiology study at 9 to 12 weeks of age. In the Cx40(-/-) mice, the PR interval was significantly longer compared with Cx40(+/+) mice (44.6 +/- 6.4 msec vs 36.0 +/- 4.1 msec, P = 0.002). Not only the HV interval (14.0 +/- 3.0 msec vs 10.4 +/- 1.2 msec, P = 0.003) but also the AH interval (33.2 +/- 4.8 msec vs 27.1 +/- 3.7 msec, P = 0.006), AV Wenckebach cycle lengths, and AV nodal effective and functional refractory periods were prolonged in Cx40(-/-) compared with Cx40(+/+) mice.Conclusion: Cx40-deficient mice exhibit significant delay not only in infra-Hisian conduction, as would be expected from the expression of Cx40 in the His-Purkinje system but also in the electrophysiologic parameters that reflect AV nodal conduction. Our data suggest a significant role of Cx40 in atrionodal conduction and/or in proximal His-bundle conduction.

Microwave Ablation with Spiral Antenna Design. Introduction: Theoretical studies have suggested that microwave energy can increase the depth of heating compared with radiofrequency energy. A spiral microwave antenna design may have advantages over previous designs using smaller designs because the resulting power deposition pattern is considerably larger than the catheter diameter. We tested the efficacy of a spiral antenna using microwave energy in a porcine thigh muscle preparation. Methods and Results: In five anesthetized pigs, the thigh muscle was exposed and bathed in heparinized bovine blood (36° to 37°C). A helical microwave catheter with a fiberoptic thermometer attached to the distal end was positioned perpendicular to the thigh muscle. The antenna‐tissue interface and tissue temperatures at depths of 3.0 and 6.0 mm were measured. A 915‐MHz microwave generator delivered energy at one of three power outputs (50, 100, or 150 W) for 60 seconds. Seventy lesions were created: 50 W (n = 23), 100 W (n = 24), and 150 W (n = 23). The mean depths at 50, 100, and 150 W were 4.3 ± 1.8 mm, 7.2 ± 1.7 mm, and 9.4 ± 0.9 mm, respectively. Lesion depth (R = 0.96, P = 0.05), maximum surface dimension (R = 0.99, P = 0.06), and volume (R = 0.99, P = 0.04) were closely correlated to the power applied. Conclusion: Power is an important determinant of lesion size using a spiral microwave antenna. A novel, spiral microwave antenna design can create lesions of significant depth that may be applicable for the ablative therapy of ventricular tachycardia.

A new type of catheter-based microwave antenna cardiac ablation applicator has been developed, Unlike previously developed ablation catheters, this device forms a wide aperture that produces a large heating pattern, The antenna consists of the center conductor of a coaxial line, shaped into a spiral and insulated from blood and tissue by a nonconductive fluid-filled balloon, The antenna will be stretched straight inside a catheter for transluminal guiding, Once in place at the cardiac target, the balloon will be inflated, and the coiled spiral antenna will be ejected into the inflated balloon. The wide aperture antenna generates a ring-shaped power pattern. The heat generated from this deposited power is conducted through a volume larger than the spiral diameter, ablating diseased tissue. The resultant lesion profile is both wider and deeper than that of either conventionally used RF catheter-based ablation electrodes or that of other recently reported microwave applicators, and may offer greater heating accuracy and controllability, The new antenna design is tested by measuring S-11- and S-21-parameters, and by comparing power deposition patterns to conventional monopole antenna in a tissue-equivalent phantom, Heating experiments on in vitro organ tissue and on live pigs using 50, 100, and 150 W of 915-MHz microwave power have been performed to test the efficacy of the wide-aperture antenna design, These studies confirm the hypotheses that the wide-aperture microwave antenna can create lesions of significant depth that may be applicable for the ablative therapy of ventricular tachycardia.

Heart Block in a Mouse Model of Myotonic Dystrophy. Introduction: A mouse strain lacking functional myotonic dystrophy protein kinase (DMPK) has recently been developed. DMPK-/- mice exhibit muscular and conduction abnormalities consistent with the disease; however, the site of abnormal cardiac conduction is unknown.Methods and Results: Nine homozygous DMPK-/- mice and seven age matched wild-type (WT) controls underwent in vivo electrophysiologic studies using an endocardial 2-French catheter. Baseline intervals as well as Wenckebach and 2:1 cycle lengths were measured to assess AV and ventriculoatrial (VA) conduction. Effective refractory periods (ERP) and functional refractory periods were determined during atrial and ventricular premature stimulation. His-bundle recordings were obtained on all the studied animals (16/16). DMPK-/- mice had significantly prolonged PR (48.1 +/- 5.5 vs 40.9 +/- 3.9 msec, P = 0.010) and AH (36.7 +/- 4.0 vs 31.6 +/- 4.8 msec, P = 0.037) intervals compared to WT controls. HV intervals were very significantly prolonged as well (14.7 +/- 2.0 vs 10.3 +/- 0.8 msec; P < 0.0001). Three of 9 DMPK-/- and 1 of 7 WT mice exhibited VA block. Atrial ERP was reached before AV node ERP in 2 (22%) of 9 of the knockout mice and 5 (71%) of 7 of the controls (P = 0.06). Only one mouse (DMPK-/-) exhibited infra-Hisian block on premature atrial stimulation.Conclusion: In this mouse model of myotonic dystrophy, AV conduction abnormalities were localized to the supra-Hisian and infra-Hisian conduction tissues, with a higher predilection to the latter, a finding similar to the human form of the disease.

To investigate the delivery of microwave energy by a catheter positioned inside the heart for ablating small abnormal regions producing cardiac arrhythmias, a 2 1/4-turn spiral catheter-based microwave antenna applicator has been developed. The antenna consists of the center conductor with continuous insulating material extending from the coaxial feed cable formed into a spiral antenna. The insulator completely isolates the center conductor from tissue. Phantom experiments were performed on homogeneous tissue equivalent medium. The reflection coefficient of the antenna at different frequencies and for different spiral lengths, the time course and temperature profile of an ablation, and the dosimetry of power versus temperature, all indicate that the high-power heating patterns from this antenna are both wider and deeper than with the other microwave antenna systems and radio frequency electrodes.

BACKGROUNDSudden death due to relatively innocent chest-wall impact has been described in young individuals (commotio cordis). In our previously reported swine model of commotio cordis, ventricular fibrillation (with T-wave strikes) and ST-segment elevation (with QRS strikes) were produced by 30-mph baseball impacts to the precordium. Because activation of the K(+)(ATP) channel has been implicated in the pathogenesis of ST elevation and ventricular fibrillation in myocardial ischemia, we hypothesized that this channel could be responsible for the electrophysiologic findings in our experimental model and in victims of commotio cordis.METHODS AND RESULTSIn the initial experiment, 6 juvenile swine were given 0.5 mg/kg IV glibenclamide, a selective inhibitor of the K(+)(ATP) channel, and chest impact was given on the QRS. The results of these strikes were compared with animals in which no glibenclamide was given. In the second phase, 20 swine were randomized to receive glibenclamide or a control vehicle (in a double-blind fashion), with chest impact delivered just before the T-wave peak. With QRS impacts, the maximal ST elevation was significantly less in those animals given glibenclamide (0.16+/-0.10 mV) than in controls (0.35+/-0.20 mV; P=0.004). With T-wave impacts, the animals that received glibenclamide had significantly fewer occurrences of ventricular fibrillation (1 episode in 27 impacts; 4%) than controls (6 episodes in 18 impacts; 33%; P=0.01).CONCLUSIONSIn this experimental model of commotio cordis, blockade of the K(+)(ATP) channel reduced the incidence of ventricular fibrillation and the magnitude of ST-segment elevation. Therefore, selective K(+)(ATP) channel activation may be a pivotal mechanism in sudden death resulting from low-energy chest-wall trauma in young people during sporting activities.

BACKGROUND:The syndrome of sudden death due to low-energy trauma to the chest wall (commotio cordis) has been described in young sports participants, but the mechanism is unknown.METHODS:We developed a swine model of commotio cordis in which a low-energy impact to the chest wall was produced by a wooden object the size and weight of a regulation baseball. This projectile was thrust at a velocity of 30 miles per hour and was timed to the cardiac cycle.RESULTS:We first studied 18 young pigs, 6 subjected to multiple chest impacts and 12 to single impacts. Of the 10 impacts occurring within the window from 30 to 15 msec before the peak of the T wave on the electrocardiogram, 9 produced ventricular fibrillation. Ventricular fibrillation was not produced by impacts at any other time during the cardiac cycle. Of the 10 impacts sustained during the QRS complex, 4 resulted in transient complete heart block. We also studied whether the use of safety baseballs, which are softer than standard ones, would reduce the risk of arrhythmia. A total of 48 additional animals sustained up to three impacts during the T-wave window of vulnerability to ventricular fibrillation with a regulation baseball and safety baseballs of three degrees of hardness. We found that the likelihood of ventricular fibrillation was proportional to the hardness of the ball, with the softest balls associated with the lowest risk (two instances of ventricular fibrillation after 26 impacts, as compared with eight instances after 23 impacts with regulation baseballs).CONCLUSIONS:This experimental model of commotio cordis closely resembles the clinical profile of this catastrophic event. Whether ventricular fibrillation occurred depended on the precise timing of the impact. Safety baseballs, as compared with regulation balls, may reduce the risk of commotio cordis.