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

Commotio cordis

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Page 1: Commotio cordis

JOURNAL REVIEW

COMMOTIO CORDIS

Review article

NJEM Vol 362:917-927 March 11,2010

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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

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• 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

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INCIDENCE

• Unknown

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

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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

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EPIDEMIOLOGY

According to National commotio cordis Registry in Minneapolis-

Rarely in blacks or females

• Competitive sports

• Recreational sports

• Others- (25% of cases) horse kicks,playgroundswings

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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%

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• This improvement is due to increased public awareness,increased availability of AEDS,earlyactivation of chain of survival(911,CPR,Defibrillation,)

• Some commotio cordis events abort spontaneously

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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

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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

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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.

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PREVENTION

• Public education-

• Improved coaching techniques

• Improved sports equipment- soft balls, air filled balls rarely implicated .

• Chest protectors & vests

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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

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SUMMARY

• Increasing public awareness of commotio cordisas 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

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Differentials of exercise related sudden death

• 1.Hypertrophic cardiomyopathyDominant cause of ESDGreater prevalence in blacksAbnormal 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)

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• 3.Arrythmogenic Right ventricular cardiomyopathy

Leading cause in Italy,Europe

ECG- QRS widening with epsilon wave

4.Myocarditis- asymptomatic or sublesymptoms- exercise intolerance,restingtachycardia,palpitations

• 5.Wolff-Parkinson-white

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• 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

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THANK YOU IMMENSELY