Role of streptomycin-sensitive stretch-activated channel in chest wall impact induced sudden death (commotio cordis)

Arthur R. Garan, Barry J. Maron, Paul J. Wang, N. A.Mark Estes, Mark S. Link

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Introduction: Deaths secondary to low-energy impacts to the precordium in young individuals (commotio cordis) have been reported with increasing frequency. In a swine model, baseball impacts induce ventricular fibrillation when directed at the center of the left ventricle during the vulnerable portion of repolarization just prior to the T-wave peak. It has been hypothesized that activation of stretch-sensitive channels could be crucial for this electrophysiological phenomenon. In this study, a nonselective stretch-activated cation channel was pharmacologically blocked prior to chest blows to determine whether this channel represents a possible pathway by which commotio cordis events occur. Methods: In a randomized and blinded experiment, 12 swine (mean 17.1 ± 2.5 kg) received either 2-g streptomycin intramuscularly (mean serum concentration 115 ± 18 μM) or sterile water prior to chest impact. Each animal received six precordial impacts with a baseball propelled at 40 mph. Results: There was no significant difference in the frequency of induced VF in the animals administered streptomycin (10 of 19 impacts: 53%) compared to those control animals receiving only sterile water (10 of 31: 32%) (P = 0.15). However, the magnitude of ST segment elevation was less in the streptomycin-treated animals (19 ± 19 mV) versus controls (61 ± 46 mV) (P = 0.015). Conclusion: Streptomycin did not alter the frequency of ventricular fibrillation in our commotio cordis model, indicating that the stretch-activated channel is not implicated in the genesis of chest blow-induced cardiac arrest. However, streptomycin did reduce ST elevation following impact suggesting that the stretch-activated channel may play a role in ST segment elevation following chest wall blows.

Original languageEnglish (US)
Pages (from-to)433-438
Number of pages6
JournalJournal of Cardiovascular Electrophysiology
Volume16
Issue number4
DOIs
StatePublished - Apr 1 2005

Fingerprint

Commotio Cordis
Thoracic Wall
Streptomycin
Sudden Death
Baseball
Thorax
Ventricular Fibrillation
Electrophysiological Phenomena
Swine
Induced Heart Arrest
Water
Heart Ventricles
Cations
Serum

Keywords

  • Arrhythmia (mechanisms)
  • Calcium channel
  • Commotio cordis
  • Stretch/mechanical electrical coupling
  • Sudden death
  • Ventricular arrhythmia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Role of streptomycin-sensitive stretch-activated channel in chest wall impact induced sudden death (commotio cordis). / Garan, Arthur R.; Maron, Barry J.; Wang, Paul J.; Estes, N. A.Mark; Link, Mark S.

In: Journal of Cardiovascular Electrophysiology, Vol. 16, No. 4, 01.04.2005, p. 433-438.

Research output: Contribution to journalArticle

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abstract = "Introduction: Deaths secondary to low-energy impacts to the precordium in young individuals (commotio cordis) have been reported with increasing frequency. In a swine model, baseball impacts induce ventricular fibrillation when directed at the center of the left ventricle during the vulnerable portion of repolarization just prior to the T-wave peak. It has been hypothesized that activation of stretch-sensitive channels could be crucial for this electrophysiological phenomenon. In this study, a nonselective stretch-activated cation channel was pharmacologically blocked prior to chest blows to determine whether this channel represents a possible pathway by which commotio cordis events occur. Methods: In a randomized and blinded experiment, 12 swine (mean 17.1 ± 2.5 kg) received either 2-g streptomycin intramuscularly (mean serum concentration 115 ± 18 μM) or sterile water prior to chest impact. Each animal received six precordial impacts with a baseball propelled at 40 mph. Results: There was no significant difference in the frequency of induced VF in the animals administered streptomycin (10 of 19 impacts: 53{\%}) compared to those control animals receiving only sterile water (10 of 31: 32{\%}) (P = 0.15). However, the magnitude of ST segment elevation was less in the streptomycin-treated animals (19 ± 19 mV) versus controls (61 ± 46 mV) (P = 0.015). Conclusion: Streptomycin did not alter the frequency of ventricular fibrillation in our commotio cordis model, indicating that the stretch-activated channel is not implicated in the genesis of chest blow-induced cardiac arrest. However, streptomycin did reduce ST elevation following impact suggesting that the stretch-activated channel may play a role in ST segment elevation following chest wall blows.",
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N2 - Introduction: Deaths secondary to low-energy impacts to the precordium in young individuals (commotio cordis) have been reported with increasing frequency. In a swine model, baseball impacts induce ventricular fibrillation when directed at the center of the left ventricle during the vulnerable portion of repolarization just prior to the T-wave peak. It has been hypothesized that activation of stretch-sensitive channels could be crucial for this electrophysiological phenomenon. In this study, a nonselective stretch-activated cation channel was pharmacologically blocked prior to chest blows to determine whether this channel represents a possible pathway by which commotio cordis events occur. Methods: In a randomized and blinded experiment, 12 swine (mean 17.1 ± 2.5 kg) received either 2-g streptomycin intramuscularly (mean serum concentration 115 ± 18 μM) or sterile water prior to chest impact. Each animal received six precordial impacts with a baseball propelled at 40 mph. Results: There was no significant difference in the frequency of induced VF in the animals administered streptomycin (10 of 19 impacts: 53%) compared to those control animals receiving only sterile water (10 of 31: 32%) (P = 0.15). However, the magnitude of ST segment elevation was less in the streptomycin-treated animals (19 ± 19 mV) versus controls (61 ± 46 mV) (P = 0.015). Conclusion: Streptomycin did not alter the frequency of ventricular fibrillation in our commotio cordis model, indicating that the stretch-activated channel is not implicated in the genesis of chest blow-induced cardiac arrest. However, streptomycin did reduce ST elevation following impact suggesting that the stretch-activated channel may play a role in ST segment elevation following chest wall blows.

AB - Introduction: Deaths secondary to low-energy impacts to the precordium in young individuals (commotio cordis) have been reported with increasing frequency. In a swine model, baseball impacts induce ventricular fibrillation when directed at the center of the left ventricle during the vulnerable portion of repolarization just prior to the T-wave peak. It has been hypothesized that activation of stretch-sensitive channels could be crucial for this electrophysiological phenomenon. In this study, a nonselective stretch-activated cation channel was pharmacologically blocked prior to chest blows to determine whether this channel represents a possible pathway by which commotio cordis events occur. Methods: In a randomized and blinded experiment, 12 swine (mean 17.1 ± 2.5 kg) received either 2-g streptomycin intramuscularly (mean serum concentration 115 ± 18 μM) or sterile water prior to chest impact. Each animal received six precordial impacts with a baseball propelled at 40 mph. Results: There was no significant difference in the frequency of induced VF in the animals administered streptomycin (10 of 19 impacts: 53%) compared to those control animals receiving only sterile water (10 of 31: 32%) (P = 0.15). However, the magnitude of ST segment elevation was less in the streptomycin-treated animals (19 ± 19 mV) versus controls (61 ± 46 mV) (P = 0.015). Conclusion: Streptomycin did not alter the frequency of ventricular fibrillation in our commotio cordis model, indicating that the stretch-activated channel is not implicated in the genesis of chest blow-induced cardiac arrest. However, streptomycin did reduce ST elevation following impact suggesting that the stretch-activated channel may play a role in ST segment elevation following chest wall blows.

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