Description of a rare cardiology disorder associated with sporting events

1. JOURNAL REVIEW
COMMOTIO CORDIS
Review article
NJEM Vol 362:917-927 March 11,2010

2. INTRODUCTION
• Ventricular fibrillation & sudden death from a
blunt,non penetrating blow to the chest.
• No damage to ribs,sternum,heart
• No underlying cardiovascular disease
• “Commotio cordis” latin for agitation of heart
• First described in 19th century

3. • Occurs in children,adolescents,young adults
• Often in the setting of
recreational,competitive sports
• This review focuses on clinical
profile,proposed mechanisms, prevention and
treatment of commotio cordis

4. INCIDENCE
• Unknown
• Third most frequent cause of sudden death in
young athletes after hypertrophic
cardiomyopathy and congenital coronary
artery anomalies

5. EPIDEMIOLOGY
• From episodic case studies and the
Minneapolis registry- 224 documented cases
over 15 yrs
• Children & adolescents: mean age 15+_ 9
years
• 26% < 10 yrs
• 9% > 25yrs
• 20% of victims remain physically active
seconds after the blow

6. EPIDEMIOLOGY
According to National commotio cordis Registry
in Minneapolis-
Rarely in blacks or females
• Competitive sports
• Recreational sports
• Others- (25% of cases) horse kicks,playground
swings

9. OUTCOME
• Usually but not invariably fatal
• 25% of cases did CPR or defibrillation result
in survival
• Survival rates have increased over time.
35% in last 10yrs,compared with 15% in
preceding 10yrs
Between 2006-2009 no of successful
resuscitations>no of deaths by 20%

10. • This improvement is due to increased public
awareness,increased availability of AEDS,early
activation of chain of
survival(911,CPR,Defibrillation,)
• Some commotio cordis events abort
spontaneously

11. MECHANISM
• Mechanical energy of the blow alters electrical
activity of heart resulting in ventricular
fibrillation
• Theoretical explanations such as excessive
vagal reflex, coronary arterial vasospasm have
since been abandoned

12. DETERMINANTS & TRIGGERS
• 1.location of blow- directly over heart , at
centre of cardiac silhouette
• 2.Timing of blow- 10-20ms on upstroke of T
wave
• 3.Velocity of projectile- impact velocity of
64km/hr
• 4. Object characteristics- hard,small sphere
shaped objects
5. Thorax- thin,undeveloped ribcage

14. CELLULAR MECHANISMS
• Mechanical force causes Left ventricular
pressure to rise to 250-450mmHg
• Cell membranes stretch ,activating ion
channels(ATP sensitive potassium channels),
increased transmembrane current flow.

15. PREVENTION
• Public education-
• Improved coaching techniques
• Improved sports equipment- soft balls, air
filled balls rarely implicated .
• Chest protectors & vests

17. SECONDARY PREVENTION
• AEDs(Automated External Defibrillators)-
Has been effective in terminating life
threatening ventricular tachyarrthmias and
restoring sinus rhythm
May also fail to restore normal rhythm even
under optimal conditions
• Precordial thumps not Shown to be effective

18. SUMMARY
• Increasing public awareness of commotio cordis
as a cause of sudden death
• Commotio cordis occurs in otherwise healthy
active young people during recreational and
competitive sports
• Fatal cardiac events can occur secondary to even
innocent precordial blows delivered at a
particular moment in cardiac cycle
• Further efforts are needed in increased
education, better athletic equipment, more AEDs
at athletic events

23. Differentials of exercise related sudden
death
• 1.Hypertrophic cardiomyopathy
Dominant cause of ESD
Greater prevalence in blacks
Abnormal hypertrophy of LV walls,spatial disarray
of fibres at molecular level
• 2.Congenital coronary artery anomalies
-Left main artery from sinus of valsava
-intramural course of coronary artery(“malignant “
myocardial bridge)

25. • 3.Arrythmogenic Right ventricular
cardiomyopathy
Leading cause in Italy,Europe
ECG- QRS widening with epsilon wave
4.Myocarditis- asymptomatic or suble
symptoms- exercise intolerance,resting
tachycardia,palpitations
• 5.Wolff-Parkinson-white

27. • 6.Primitive electric heart diseases
(Channelopathies)
-Long , Short QT syndrome
-Brugada syndrome
-Polymorphic catecholamine ventricular tachycardia
• 7.Pharmacologic treatment & doping
-sympathomimetics-ephedrine,epinephrine,cocaine
-Erythropoietin
Anabolic steroids

28. THANK YOU IMMENSELY