assessing and managing the health of a young athlete

Assessing and Managing the Health of a Young Athlete Predisposed to

Myoneural Dysfunction

Professor Sanjay Sharma

St George’s University of London

sasharma@sgul.ac.uk

@SSharmacardio

Sudden Cardiac Death in Athletes

POPULATION AGE DURATION INCIDENCE

Organised high school1 13-17 12 years 0.5/100,000 and college athletes

Competitive athletes2 14-35 25 years 2/100,000/yr

Marathon (London)3 Mean 42 26 years 2.2/100,000 runs

Rhode island jogger4 30-65 7 years 13/100,000/yr

Incidence of Sudden Cardiac Death

1. Roberts WO. JACC. 2013; 62: 1298 2. Corrado D. JAMA. 2006; 296: 19533. Tunstall-Pedoe D. Sports Med. 2007; 37: 4484. Thompson P. JAMA. 1982; 12: 247

Sudden Death In Young Athletes

• Incidence is approximately 1/50,000

• Mean age at death in athletes 23 years-old

• 40% deaths in athletes aged < 18 years old

• Males > females (9:1)

• Black athletes > white athletes

• 90% deaths during or immediately after exertion

Sudden Cardiac Death in Young AthletesHarmon. Heart. 2014; 15: 1185-1192

Sudden Cardiac Death in Sport

Hypertrophic Arrhythmogenic right

Cardiomyopathy ventricular cardiomyopathy

Coronary arteries and aorta

LQTS

Brugada

WPW

Electrical DisordersSudden Cardiac Death with a Normal Heart

Causes of Sudden Cardiac Death in SportFinnochiaro G, Sharma JACC 2016

357 consecutive athletes. Mean age 29 ±11 years old.

92% Male. 69% competitive.

Cardinal Symptoms of Cardiac Disease

Chest tightness on exertion or emotional stress

Breathlessness

Palpitation

Syncope

Cardinal Symptoms of Cardiac Disease

Chest tightness on exertion or emotional stress

Breathlessness

Palpitation

Syncope

Syncope

Transient loss of consciousness and loss of postural tone.

Rapid onset. Spontaneous recovery.

Due to global cerebral hypoperfusion.

Usually benign.

May be indicative of a life threatening disorder or may precede cardiac arrest.

Syncope after Exercise

SyncopeCardiac

Neurological

Neurocardiogenic

Orthostatic

Metabolic

London Marathon Experience

3% of contacts presenting to the medical team during the

London Marathon.

Mostly benign. Usually due to physiological factors

Volume depletion

Vasodilation

Heat ADPAcidosis

Reduced Activity from Muscle Pump

Empty LV

Increased Mechano-

receptor activity

Altered Neuro-cardiogenic

reflexes

? Potentiated by sudden

withdrawal of sympathetic tone

Cerebral Hypoperfusion/Syncope

DehydrationAdrenergic

surges

Electrolyte

imbalanceAcid/base

disturbance

Syncope after Exercise May be Serious

Assessment

Aim is to exclude a potentially sinister cause

History (helpful to have witness account)

Examination (vitals, cardiovascular and neurological)

(Blood glucose)

ECG

Vasovagal Syncope

Loss of vasomotor tone cardio-inhibition

Transient loss of consciousness

Always upright

More common in a hot environment

Transient drowsiness but complete recovery

No cardiac history

Hypotension with relatively low heart rate (< 100 bpm)

4Ps

Posture (patient is usually

upright) at time of onset.

Provoking factors (fatigue,

dehydration, pain)

Prodrome; unwell, dizzy,

diminution of vision, nausea

and vomiting.

Pallor

Red Flags

Age > 45 years old

Syncope whilst (1) lying supine (2) syncope without warning and (3) syncope during exertion

Chest pain, palpitation, headache, transient seizure like activity.

New or unexplained breathlessness

Known history of cardiovascular disease

Family history of premature sudden cardiac death

Cardiac murmur/Focal neurology

Abnormal ECG

Red Flags

Age > 45 years old

Syncope whilst (1) lying supine (2) syncope without warning and (3) syncope during exertion

Chest pain, palpitation, headache, transient seizure like activity.

New or unexplained breathlessness

Known history of cardiovascular disease

Family history of premature sudden cardiac death

Cardiac murmur/Focal neurology

Abnormal ECG

Colvocci et al. EHJ 2004; 15: 1749

Long QT

VT

Complete Heart Block

Ischaemia

AF

Pre-excitation

Multiple VEs

Brugada syndrome

Brugada ECG pattern

Abnormal repolarisation

Role of the ECG

Management

A Airway

B Breathing

C Circulation

(D) Determine blood glucose, core temp and plasma sodium (if slow to recover/disorientated and confused 5 minutes afterwards)

E Elevate legs (ECG monitoring)

12-lead ECG in all

F Fluids/fuel (orally)

May need to proceed to cardiac arrest protocol

Management of Post Exercise Syncope

Fluid redistribution/replacement to improve cerebral and core organ circulation

Elevation of legs and buttocks

Oral fluids in the majority

Carbohydrate fuel

(Treat temperature abnormalities)

Indicators of Transfer to Hospital from a Field Hospital Environment

Cardiac symptoms

Previous history of cardiac disease.

Focal neurology/disorientation or drowsiness despite normal blood glucose, core temp and plasma sodium.

Cardiac arrhythmia.

Systolic BP persistently below 90 mm Hg despite fluids

ECG suggestive of a serious cardiac disease.

Cardiac Investigations

History, Examination and ECG

Possible Cardiac Cause Simple Faint

Echocardiogram and Exercise Stress Test

At least 48 hour ECG MonitoringZiopatch

REVEAL device

Case 1

• 33 year old male completed his first marathon

in 3 h 20 min.

• Collapsed and was unconscious for

approximately 30 secs.

• His friends reported that he was pale prior to

collapse.

• The paramedics arrived at the scene within 1

minute. By this time the patient was conscious

and was complaining of nausea.

Case 1

• On examination he appeared pale and was

slightly disorientated. No evidence of central

cyanosis.

• HR 90/min and regular. BP 80 mm Hg systolic.

RR 15/min

• Normal heart sounds. Chest clear.

• No focal neurology.

• Core temp 38oC. Blood glucose 8 mmol/l

What would you do next?

A Start IV fluids

B Elevate legs/oral fluids

C High concentration oxygen

D Cool patient aggressively

E Give glucogel

Case 1

• Patient improved after his legs were elevated. He did not

have any chest pain prior to collapse but recalls

dizziness, nausea and diminution of vision prior to

losing consciousness.

• Similar history 2 years ago after running a half marathon

at high temperatures.

Which investigation is required next?

A Plasma sodium concentration

B ECG

C Echocardiography

D Cardiac troponin

E Serum BNP level

Next step

• ECG was normal.

What would you do next?

A Arrange out-patient 24 hour ECG

monitoring

B Echocardiography

C Coronary angiography

D Discharge; no further investigations

necessary

E Organise CT scan of the brain.

Case 2

• 39 year old male completed his second

marathon and collapsed shortly afterwards.

• Witnesses reported brief tonic-clonic

movements whilst he was on the ground.

• Rousable after 1 minute.

• No warning before collapse apart from

fatigue.

• No obvious FH of note. No DH.

Case 2

• On examination he appeared pale and was

slightly disorientated for a few minutes. No

evidence of central cyanosis.

• HR 100/min and regular. BP 108 mm Hg

systolic. RR 15/min

• Normal heart sounds. Chest clear.

• No focal neurology.

• Core temp 39.2oC

• Blood glucose 9.4 mmol/l

• Oxygen sat 94%

Case 2

What would you do next?

A Arrange out-patient 24 hour ECG

monitoring.

B Transfer to hospital for further assessment

and monitoring.

C Discharge; no further investigations

necessary

Electrocardiogram demonstrating the right precordial leads V1-V3ST-segment changes prior, at peak and during the recovery phase of the exercise stress test

V1

V2

V3

Case 3

• 53 year old man collapsed suddenly just before

the finish line after a half marathon. Transient

seizure activity.

• Head and facial lacerations.

• No pulse felt by paramedics with immediate

bystander CPR commenced for a minute and

prompt return of spontaneous circulation.

• Confused for over 20 minutes afterwards

Case 3

Case 3

• Blood tests normal with exception of a mild rise

in cardiac troponin.

• Echocardiogram- normal biventricular function

with no valve pathology

ETT performed few days later- 15 minutes 34 seconds

(18 METS). No ECG features of ischaemia.

Screening Strategies for Detecting Athletes with Potentially Serious Cardiac

Disease

Screening Athletes

Condition History Examn ECG Echo

HCM Pos/Neg Pos in 25% Positive Pos

ARVC Pos/Neg Negative Positive Neg/Pos

WPW Pos/Neg Negative Positive Neg

LQTS Pos/Neg Negative Positive Neg

Marfan Pos/Neg Positive Negative Pos

CAA Pos/Neg Negative Negative Neg

Myocarditis Pos/Neg Pos/Neg Pos/Neg Pos

INCREASING COST

HCM ARVC95% 40-50%

ECG in Patients with Cardiomyopathy

Inferior and/or lateral TWIST segment depressionPathological q waves

Anterior TWI (V2-V3/V4) with isoelectric J pointEpsilon waveVentricular extra-systoles

22 athletes diagnosed with HCM

3 identified on basis of family Hx

16 identified by abnormal ECG

2 identified on basis of murmur

(14%) (9%)

73%

NEJM, 1998; 339(6):364-369

33,735 competitive athletes were screened

Does Cardiac Screening Save Lives?

TIME-TREND OF SUDDEN CARDIAC DEATH INCIDENCE IN ATHLETES VS NON-ATHLETES

Veneto Region of Italy 1979-2002

Corrado. JAMA 2006; 296:1593-1601

Low incidence of sudden cardiac death

High number of false positives

Concerns relating to false negatives

Cost

Other issues

Concerns Relating to ECG Screening

Prevalence of Young Athletes with Conditions Predisposing to SCD

Reference Population Prevalence

AHA (2007) Competitive athletes (U.S.) 0.3%

Fuller (1997) 5,617 high school athletes (U.S) 0.4%

Corrado (2006) 42,386 athletes age 12-35 (Italy) 0.2%

Wilson (2008) 2,720 athletes /children age 10-17 0.3%

Bessem (2009) 428 athletes age 12-35 (Netherlands) 0.7%

Baggish (2010) 510 collegiate athletes 0.6%

Sheikh (2015) 5000 British elite athletes 0.3%

Low incidence of sudden cardiac death

High number of false positives

Concerns relating to false negatives

Cost

Other issues

Concerns Relating to ECG Screening

ECG Interpretation in an Athlete

TWI in a Black Athletes

12.4%

53%

6%

Differences from the ESC 2010

Following included in the normal category:

• T wave inversion in V1-V4 in black athletes.

• T wave inversions in V1-V2 in all athletes.

• QTc < 470 M and < 480 F.

• Criteria for RVH also include RAD

Evidence Based ECG Interpretation: 2004-2014

Sensitivity for all conditions 60%Sensitivity for serious conditions 100%Specificity 94% in Caucasians

84% in Black athletes

The “Athlete’s Heart”- Overlap with Cardiomyopathy

Electrical

Structural

• Sinus bradycardia

•Voltage for chamber enlargement

• Repolarisation anomalies

•Increased cavity size

•Increased wall .thickness

• Increase in stroke vol.

FunctionalPhysiology Pathologyvs.

Overlap with cardiomyopathy. Differentiation between

the 2 entities is crucial.

T-Wave Inversion

Juvenile EKG pattern

Long standing endurance

athlete

Anabolic drug abuse

Black athletes

Cardiomyopathy

Overlap With Disease

Low incidence of sudden cardiac death

High number of false positives

Cost

Concerns relating to false negatives

Concerns

Further investigations following positive screen

Prospective follow-upWorkload and cost

implicationsContemporary criteria applied

retrospectively

Screening protocol

H+P (12-point AHA)

(1.6%)

12-lead ECG (2010 recommendations)

(21.8%)

4,925 athletes (age 14-35 years)

Mandatory requirement Previously un-screened83% Male 85% White

26 Sporting disciplines

4,925 athletes

Screened cohort Impact of Refined criteria

No compromise in sensitivity

↓>50% in positive screens

↓ 50% ↓ 8%

↓ 12% ↓ 18%

Dhutia et al. JACC. 2016

Potential use of savings

Purchase an additional 95 AEDs

Screen an additional 2,120 athletes

2010 ESC recommendations

Cost per athlete: $110Cost per diagnosis: $35,993

Dhutia et al. JACC. 2016

21% cost reduction

Seattle criteria

Cost per athlete: $92Cost per diagnosis: $30,251

Refined criteria

Cost per athlete: $87Cost per diagnosis: $28,510

Low incidence of sudden cardiac death

High number of false positives

Cost

Concerns relating to false negatives

Concerns

Deaths Despite Screening with ECG

Alternative Strategies

Exercise related cardiac arrestIncidence in the general population France (2005 – 2010)

Mean age 46.1 ± 15.8. 93% Male.

Survival 15%

Exercise related cardiac arrestIncidence in the general population Netherlands (2006 – 2009)

Mean age 58.8 ± 13.6. 95% Male.

Survival 45%

Exercise related cardiac arrest

Country Netherlands France

Age, years 58.8 ± 13.6 46.1 ± 15.8

Men 93% 95%

Success rate 45% 15%

Bystander witnessed arrest 89% 94%

Bystander CPR 87% 31%

AED use 36% 1%

Shockable initial rhythm 80% 47%

Time to first shock (min) 9.8 (6.4 – 12.5) 12.5 (10.5 – 15.5)

10.9 million runs

59 deaths. 29 % survival death rate

FACTOR ODDS RATIO

By stander CPR 3.73 CI 2.19-6.39

Time of collapse to CPR 1.32 CI 1.08-1.61

Initial use of AED 3.71 CI 2.07-6.64

Kim et al NEJM 2012

Report of 1710 US high schools with an on-site AED program.

Survey relating to sudden cardiac arrest (SCA) between Jan 2006-July 2007

36 cases of SCA

14 (high school) 22 older non studentsMean age 16 Mean age 57

64% survived to hospital discharge in each groupHigher survival rates may have been to the onsite AED (79%) and smaller

number of cases of hypertrophic cardiomyopathy (21%)

Prompt CPR 94%

AED shock 83%

Drezner 2009

Delay Intervals

• Mean time from collapse to CPR

1.5 Minutes

• Mean time from SCA to first shock

3.6 Minutes

PersonnelCommunication

system

Location of the AED

Practice and review

of emergency

response plan

Emergency response plan

The Emergency Response Plan

7264

9097

41

65

26

0

20

40

60

80

100

120

%

Premier League March 2012

Key Messages

• Sudden cardiac death (SCD) in young athletes is rare.

• Exercise is a trigger for SCD in predisposed athletes.

• Syncope is relatively common in athletes. Most cases are benign but may represent serious cardiac disease. The history (including witness reports) is an important discriminator.

• Pre-participation screening with ECG identifies athletes with electrical disease and cardiomyopathy.

• The ECG cannot identify all athletes at risk of SCD.

• Early CPR and AEDs save lives in sport.

Assessing and Managing the Health of a Young Athlete Predisposed to

Myoneural Dysfunction

Professor Sanjay Sharma

St George’s University of London

sasharma@sgul.ac.uk

@SSharmacardio