Commotio Cordis. Agitation of the Heart

Transcription

1 Commotio Cordis Agitation of the Heart Man Young Lee, MD. Division of Cardiology, Dept. of Int. Med. Yeouido St. Mary s Hospital The Catholic University of Korea

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3 Commotio Cordis A form of Ventricular Fibrillation (V-Fib) - as a result of a chest wall strike (blow) to the area directly over the heart at a critical time during the cycle of a heart beat - not mechanical damage to the heart muscle or surrounding organs, and not the result of heart disease

4 Commotio Cordis Usually during sports. most often during baseball (; caused by a projectile object) Common cause of SCD in athletes - second leading cause of death (next to hypertrophic cardiomyopathy) Occurs mostly in boys and young men yrs(average age 15)

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7 Commotio cordis registry 60 cases of commotio cordis outside US Male predominance Frequency of survival - 25% (vs 26% in US) Soccer/Cricket/Hockey(47% of events); non US Heart Rhythm 2011;8:1969

8 Tufts Medical Center Model 8-12 kg pigs 30 mile/hr NEJM 1998;338:

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12 Variables Critical to the induction of Ventricular Fibrillation Impact occurring within a specific ms portion of Ascending Phase of the T wave (40 ms before the peak of T wave) : The small window of vulnerability explains why it is a rare event. Direction of Impact over the Precordium - perpendicular to the chest wall : never in glancing blow center of LV 30% Relative exercise-induced hypoxia and acceleration of the excito-conductive system of the heart make it more susceptible to stretch-induced ventricular fibrillation

13 Variables Critical to the induction of Ventricular Fibrillation Impact Eenergies at least 50 J. up to 130 joules ; hockey pucks and lacrosse balls 450 joules in karate punches 1028 joules in boxer Rocky Marciano's punch. The 50-joule threshold, however, can be considerably lowered when the victim's heart is under ischemic conditions, such as in coronary artery insufficiency. Velocity of the impact object - Critical. (40 mph for 20-kg pig) Never with velocities of < 20 mph At velocities of > 50 to 70 mph, the occurrence of VFIB dropped and the incidence of cardiac rupture and major trauma increased. : contusio cordis (from Latin for bruising of the heart).

14 Variables Critical to the induction of Ventricular Fibrillation Velocity Hardness Shape Impact object location 150 g wooden objects Flat round Spherical 72mm 72mm/ 42 mm Individual susceptability

15 Mechanism of Commotio Cordis : Altered Repolarization & Trigger

16 Ventricular Fibrillation Induced by Stretch Pulse: Implications for Sudden Death Due to Commotio Cordis FRANK BODE, M.D., MICHAEL R. FRANZ, M.D., PH.D., IRIS WILKE, M.D., HENDRIK BONNEMEIER, M.D., HERIBERT SCHUNKERT, M.D., and UWE K.H. WIEGAND, M.D. From the Medical University Luebeck, Luebeck, Germany; and VAMC and Georgetown University, Washington, DC, USA VF may result from sudden stretch during a vulnerable window, which is determined by Repolarization Inhomogeneity Examined action potential morphologies and VF inducibility in response to sudden myocardial stretch in the left ventricle (LV). - In six, Langendorff perfused rabbit hearts, the LV was instrumented with a fluid-filled balloon. - Increasing volume and pressure pulses were applied at different times of the cardiac cycle. Monophasic action potentials (MAPs) were recorded simultaneously from five LV epicardial sites. Inter-site dispersion of repolarization was calculated in the time and voltage domains. J Cardiovasc Electrophysiol, 2006;17:

17 Induction of Ventricular Fibrillation by a stretch-pulse

18 10 episode of VF coupling interval of msec after QRS onset pressure amplitude mmhg

19 Dispersion of Repolarization in time domain

20 Dispersion of Repolarization in voltage domain Vulnerable window for ventricular fibrillation induction corresponded with the time of intrinsic increase in dispersion of repolarization between sites

21 The Minimum Rise of LV pressure necessary to induce VFIB mmhg optimal pr. 400 to 500 mm Hg >600 mm Hg structural damage : myocardial rupture, acute mitral valve insufficiency, cardiac contusion

22 Cellular Mechanism of Commotio Cordis Coupling between electrical and mechanical events - probably related to the activation of mechano-sensitive proteins (; ion channels.) - although still poorly understood The most important mechano-electric coupling - Sarcolemmal channels - a variety of ionic channels activated by cell stretch - Stretch-Activated Channels (SACs) important contributors to the proarrhythmic substrate The nonuniform distribution of positive myofiber strain (stretching) during mechanical contraction under a variety of pathologic conditions could produce, via SAC, a proarrhythmic dispersion in electrophysiologic properties.

23 Selective Activation of the K1 ATP Channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (Commotio Cordis) Mark S. Link, MD; Paul J. Wang, MD; Brian A. VanderBrink, BA; Erick Avelar, MD; Natesa G. Pandian, MD; Barry J. Maron, MD; N.A. Mark Estes III, MD Stretch Activated Channels involved in commtio cordis calcium stretch activated channel, the K ATP channel, certain other known potassium and sodium channels, and possibly even some unknown channels. The First candidate channel - the K ATP channel. because of the similarities of ventricular fibrillation and ST-segment elevation between our experimental model and acute ischemia. In addition, this channel is known to be activated by stretch. To block K ATP channel 20 swine - randomized to glibenclamide or a control vehicle, & with T-wave impacts, Circulation. 1999;100:

24 Circulation. 1999;100:

25 Selective Activation of the K1 ATP Channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (Commotio Cordis) Mark S. Link, MD; Paul J. Wang, MD; Brian A. VanderBrink, BA; Erick Avelar, MD; Natesa G. Pandian, MD; Barry J. Maron, MD; N.A. Mark Estes III, MD blocking the KATP channel with glibenclamide nearly eliminated ventricular fibrillation Circulation. 1999;100:

26 Models of Stretch-activated Ventricular Arrhythmias :Cellular Mechanism of VFIB in Commotio Cordis Natalia A. Trayanova, PhD, Jason Constantino, BS, Viatcheslav Gurev, PhD Department of Biomedical Engineering and Institute for Computational Medicine, Johns Hopkins University, Baltimore, MD Elucidation of mechanism of Commotio cordis hampered by the lack of experimental methodologies that can record the 3-D electromechanical activity simultaneously at high spatiotemporal resolution. Computer modeling Journal of electrocardiology, 2010;43:

27 Models of Stretch-activated Ventricular Arrhythmias :Cellular Mechanism of VFIB in Commotio Cordis Natalia A. Trayanova, PhD, Jason Constantino, BS, Viatcheslav Gurev, PhD Department of Biomedical Engineering and Institute for Computational Medicine, Johns Hopkins University, Baltimore, MD Stretch-Activated Channels(SAC) Recruitment of SAC during different phases of the APD resulted in different responses depending on the timing of the stretch and its magnitude - If stretch was applied during the plateau phase, it changed the time course of repolarization, resulting in either shortening or lengthening of APD. - If SAC were activated when the cell is already repolarized, it resulted in a new activation if the magnitude of the SAC current was above threshold. Journal of electrocardiology 2010;43:

28 Three Different types of Responses can be induced within the region of impact.

29 Electrophysiologic model, in which mechanical impact was assumed to open SACs : a case of mechanically induced sustained reentry within the vulnerable window

30 Treatment and Outcome leading cause of fatalities in youth baseball in the US, with 2 to 3 deaths per year Most cases are fatal; AED - increase the survival rate to 60%

31 Prevention The risk would probably be reduced by improved coaching techniques, Teaching young batters to turn away from the ball to avoid errant pitches Defensive players in lacrosse and hockey are now taught to avoid using their chest to block the ball or puck. Adequate chest protectors and vests are designed to reduce trauma from blunt bodily injury, but this does not offer protection from commotio cordis and may offer a false sense of security. Almost 20% of the victims in competitive football, baseball, lacrosse and hockey were wearing protectors.

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33 Legal Issues Several people have been convicted of involuntary manslaughter - in cases involving insufficient and slow medical help - as well as in cases of intentional delivery of contusive blows. Blunt chest blows, often innocent in appearance, may nevertheless trigger ventricular fibrillation (commotio cordis)

34 Conclusions Commotio cordis is a significant cause of morbidity and mortality on the playing field. The epidemiology of commotio cordis has been well established to include young male athletes participating in sports with a solid small ball. Experimental models point to the importance of timing, location, velocity, and shape and hardness of the object as determinants of ventricular fibrillation Biological characteristics such as sex, pliability of the chest wall, and genetic susceptibility also play a role. The mechanism of ventricular fibrillation in commotio cordis is likely a combination of impact-initiated heterogeneity of repolarization and a premature ventricular depolarization trigger A reduction in the risk of commotio cordis & Resuscitation are possible