N. A. Mark Estes, III, MD University of Pittsburgh

1. Sudden Cardiac Death by Chest Wall Impact
Commotio Cordis
N. A. Mark Estes III M.D.
Professor of Medicine
University of Pittsburgh School of Medicine
Professor of Medicine
9th Annual Duke Sports Cardiology Symposium
Friday April 12, 2024

2. Definitions and Background
Commotio Cordis
 Concussion of the heart
 Commotio cordis-disturbed or agitated heart
motion (Latin)
 Chinese Martial Art Dim Mak (death touch)
precordial blow results in sudden death in
one’s opponent
 Sudden death from chest wall impact
 At autopsy, no pathologic abnormalities

3. Case Report
 14 year old healthy boy.
 During football he is hit in anterior chest.
 Patient immediately states that he is dizzy and
then loses consciousness.
 CPR begins within 1 minute, and EMS arrives
at 6 minutes.
Link, et al, Chest, 1998

4. Initial Electrocardiogram

5. Definitions and Background
Commotio Cordis
 Concussion of the heart.
 Sudden death from chest wall
impact during sports.
 At autopsy, no pathologic
abnormalities are found.

6. Maron B Estes N N Engl J Med 2010;362:917-27.

7. Commotio Cordis
Maron B Estes N N Engl J Med 2010;362:917-27.

8. Collapse and Arrhythmias
 Instantaneous collapse in one half
 In the others a brief period of
consciousness with lightheadedness
 Initial rhythms are generally
ventricular fibrillation.
 Post resuscitation ECGs show ST
elevations

9. Animal Studies-Our Protocol
 Juvenile
anesthetized male
swine placed prone
in a sling.
 Baseball propelled
at 30 mph.
 Release of the
object was timed so
that the impact
could be adjusted
according to the
cardiac cycle.
II pa t
Lo c a tio n
Inha le d
Ane s th e s ia
im ul
t E le c tro c a rdio g ra m
R e le a s e
P ro je c tile
S ling
X
Impact location
Electrocardiogram
Stimulator

10. T-wave Impact

11. QRS Impact

12. Possible Variables Important in Commotio
Cordis
 Timing (examined)
 Energy of impact (examined)
 Location of impact (examined)
 Hardness of impact object (examined)
 LVP in commotio (examined)
 Role of ANS (examined)
 Role of KATP Channel (examined)
 Efficacy of chest protectors (examined)
 Effective chest wall protector (2016)
 Efficacy of defibrillation (examined)

13. Vulnerable Time Window
of Chest Impact in
Commotio Cordis
Vulnerable Window for
the Electrical Induction
of VF
Hou, et al, Circ. 1995; 92: 2558

14. Chest Impact Sites
Maron,
NEJM, 1995

15. Site of Impact
 Chest impacts with a
regulation baseball thrown
at 30 mph and striking
during the vulnerable
period for ventricular
fibrillation.
 Impacts randomly given to
5 sites on the left chest
wall and 2 sites on the
right chest wall.
 Left ventricular pressures
measured with Millar®
mikro-tip catheters.

16. Sites of Impact-Results
0
5%
10%
15%
20%
25%
30%
Incidence of VF
Center
of LV
Base
of LV
Apex
of LV
L lat
chest
Lpost
chest
R lat
chest
R post
chest

17. Importance of the Velocity of Impact
(Energy)
 Animals were subjected to impacts at velocities
ranging from 20 mph to 70 mph.
 All impacts were given during the vulnerable
portion of the cardiac cycle for ventricular
fibrillation.
 All impacts were given over the center of the
left ventricle.
 Experiment performed in both small (8-12 kg)
and larger (18-25kg) swine.

18. Results: Velocities/Energy
20 25 30 40 50 60 70
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
Incidence
of
Ventricular
Fibrillation
Baseball velocity in mph
8-12 kg animals 18-25 kg animals

19. Left Ventricular Pressure In
Commotio Model

20. Protocol-Object Hardness
 Animals given impacts during vulnerable time
period for ventricular fibrillation with 1 of 4
different baseballs that differed by hardness.
 RIF 1 (Reduced injury factor, Worth®); marketed
for youths aged 3 to 7
 RIF 5; marketed for youths age 8 to 10
 RIF 10; youths 11-13 years
 Regulation baseball
 Experiment performed with both 30 and 40
mph baseball.

21. Results-Safety Baseballs
RIF 1 RIF 5 RIF 10 STANDARD
0
10
20
30
40
50
60
70
Incidence
of
Ventricular
Fibrillation
Hardness of Baseball
30 mph 40 mph

22. Mechanisms of VF In Commotio Cordis?
 Hypervagotonia/Hypersympathetic state
 Coronary vasospasm
 Conversion of mechanical to electrical energy
 Myocardial disarray produced by contusion
 Activation of myocardial ionic channels
 Trauma related conformational changes in cell
membrane
 Pressure related changes
 Myocardial stretch

23. Autonomic Nervous System
 Protocol: Animals given autonomic blockade
(atropine 0.04 mg/kg and propanolol 0.2
mg/kg) or control solution prior to impact.
 Personnel blinded to which agent given.
 Impacts with a 30 mph baseball directly over
the center of the LV during vulnerable time
window for VF.

24. ANS-Results
Control ANS Blockade
0
0.05
0.1
0.15
0.2
0.25
0.3
0.35
0.4
Incidence
of
Ventricular
Fibrillation
Animal Group

25. Coronary vasospasm
 In our initial studies, acute coronary
angiography did not show obstructive lesions.
 Furthermore, in acutely ischemic myocardial
tissue VF does not occur until at least 1
minute has transpired.
 Since the VF produced by chest wall impact
in our experimental model and in clinical
cases of VF is immediate, myocardial
ischemia cannot be the etiology.

26. KATP Channels-Commotio Cordis
 Since the electrocardiographic changes seen in commotio
cordis (ST segment elevation and VF) mimic those in ischemia
we hypothesized that the KATP channel may be activated by
chest wall impact.
 We evaluated this hypothesis by infusing a agent known to
block the activation of KATP channels (glibenclamide) or a
control agent.
 In the first series of animals, impacts were given during the
QRS segment.
 In the second series of animals, impacts given during the
upslope of the T-wave.

27. QRS
Impact
Link,
Circulation,
1999

28. T-wave
Impact
Link,
Circulation,
1999

29. K+
ATP Channel
Link,
Circ,
1999

30. Lacrosse Chest Wall Protection
Brine Ventilator Pro
Brine GBP
DeBeer Icon
STX
Warrior

31. Development of a Chest Wall Protector Effective in
Preventing Sudden Cardiac Death by Chest Wall Impact
(Commotio Cordis)
Kumar et al Clin J Sport Med 2016;0:1–5

32. Commotio AEDs
Link et al
JACC 2002

33. Commotio AEDs
Link et al
JCE 2002

34. Commotio AEDs
Link et al
JCE 2002

35. Eligibility and Disqualification Recommendations for
Competitive Athletes With Cardiovascular Abnormalities:
Task Force 13: Commotio Cordis
by Mark S. Link, N.A. Mark Estes, and Barry J. Maron
Circulation
Volume 132(22):e339-e342
December 1, 2015

36. Commotio Cordis

37. Commotio Cordis Conclusions
 In humans, the clinical scenario is produced by
low energy chest wall impact in an area
overlying the heart
 Young males are the most susceptible to
commotio cordis
 The initial rhythm, when documented, is most
often ventricular fibrillation
 Survivors have had ST elevation on EKGs

38. Commotio Cordis Conclusions
 Low energy trauma during a 30 ms window on the
upslope of the T-wave causes ventricular fibrillation
in juvenile swine
 The VF produced is immediate and not preceded by
PVC’s, ST elevations or other EKG abnormalities
 The site of impact must directly overlie the cardiac
silhouette
 Changes in LV pressure may mediate VF

39.  Activation of the K+
ATP channel may be the cause of
the ventricular fibrillation seen with chest wall
impact
 Softer than standard baseballs (safety balls)
decrease the incidence of commotio cordis
 Most currently available chest wall protectors are
inadequate to protect against sudden death
 Immediate defibrillation can result in improved
survival
 Further research is needed to identify methods of
reducing the risk of death from commotio cordis
Commotio Cordis Conclusions

40. Emergency Action Plan
Written Emergency Action Plan for SCA
Emergency communication system
Trained responders in CPR/AED
AED locations – all staff awareness
Access to early defibrillation (<3-5 min
collapse to shock)
Practice and review of the response plan at
least annually
Integrate AEDS into local EMS system
 10 seconds: “I don’t like how he went down.” “All-call. All-call.” “We need an airway doctor,
everybody. Bring the cot with the medics.”
 60 seconds: CPR initiated

41. Sudden Cardiac Death by Chest Wall Impact
Commotio Cordis
N. A. Mark Estes III M.D.
Professor of Medicine
University of Pittsburgh School of Medicine
Professor of Medicine
9th Annual Duke Sports Cardiology Symposium
Friday April 12, 2024