The document discusses sudden cardiac death (SCD) in various populations. It notes that SCD accounts for 12-15% of natural deaths and almost 90% have cardiac causes. The peak ages for SCD are within the first year of life and between 45-75 years. The most common causes of SCD in children are congenital heart defects while in those over 35 it is coronary heart disease. Rare causes like hypertrophic cardiomyopathy also contribute to SCD in young adults. Exercise-related SCD is often due to congenital anomalies or premature heart disease in young and older athletes respectively.

2. HISTORY

3. HANK GATHERS
1967 - 1990

7. DEFINITION

8. INCIDENCE

10. INCIDENCE
• Retrospective death certificate studies have demonstrated
• that a temporal definition of sudden death of less than 2 hours
• after the onset of symptoms results in 12% to 15% of all natural
• deaths being defined as “sudden” and almost 90% of all natural
• sudden deaths having cardiac causes.
• In contrast, application of a
• 24-hour definition of sudden death increases the fraction of all
natural
• deaths falling into the sudden category to more than 30% but
reduces
• the proportion of all sudden natural deaths resulting from cardiac
• causes to 75%.

11. • Approximately
• 50% of all SCDs are unexpected first
expressions of a cardiac disorder,
• often striking during the victim’s productive
years.

12. HYPERTROPHIC CARDIOMYOPATHY
• Affects 1 in 500 individuals
• Genetically determined
• Sporadic or inherited
• At least 11 genes, 1400 mutations
• Accounts for 35 – 40% of athletic deaths
• Can be symptomatic/detectable before SCA
• Increased risk with age
• Ventricular arrhythmia is primary cause of death

13. • CAUSES

14. • Approximately 25% of cases of SCDs in children occur
• in those who have undergone previous surgery for congenital
cardiac
• disease. Of the remaining 75%, more than half occur in children
who
• have one of four lesions: congenital aortic stenosis, Eisenmenger
• syndrome, pulmonary stenosis or atresia, or obstructive
hypertrophic
• cardiomyopathy (see Chapter 62). Other common causes included
• myocarditis, hypertrophic and dilated cardiomyopathy, congenital
• heart disease, and aortic dissection.

16. • only 19% of sudden natural deaths in children
• between 1 and 13 years of age have cardiac causes; the proportion
• increases to 30% in the 14- to 21-year age group.
• In the transition age range between adolescence and young adulthood
• (to the age of 25 years) and in the middle and older ages (beginning
• at 35 years of age), coronary heart disease emerges to its position
• as the dominant cause of SCD. However, rare disorders, such as
• hypertrophic cardiomyopathy, Brugada syndrome, long-QT syndrome,
• and right ventricular dysplasia, are significant contributors to the
distribution
• of causes of SCD in this age group. In one study, myocardial
• fibrosis of unknown etiology was a significant cause in this age
• group.

18. YOUNG ATHLETE: Less than 35 years
old
ADULT ATHLETE: Greater than 35
years old

19. Sudden cardiac arrest symptoms are immediate and drastic.
•Sudden collapse.
•No pulse.
•No breathing.
•Loss of consciousness.

20. PATHOGENESIS

22. Gangasani, S. R. et al. Chest 2000;118:249-252
Physiologic alterations accompanying acute exercise and
recovery, and their possible sequelae

23. EXERCISE INTENSITY
• Light
• Daily activities, gentle walk
• < 3 METs
• Moderate
• Brisk walk, easy jog or bike
• < 6 METs
• Vigorous/Intense
• Running, Biking, High Intensity Interval, “Boot Camp”
• RPE 7 – 10, METs > 6

24. THE YOUNG ATHLETE
A SAMPLING OF THE CAUSES
 Structural Heart Disease
• Hypertrophic Cardiomyopathy
• Anomalous Origin of the Coronary Arteries
• Arrhythmogenic Right Ventricular Cardiomyopathy
• Myocarditis/Cardiomyopathy
• Valvular Disease
 The “Channelopathies”
 Drugs

25. DIAGNOSTIC CRITERIA

26. Diagnosis
History Familial disease by histology
EKG Epsilon waves or QRS 110 ms+ in V1-V3
Biopsy Endomyocardial biopsy with fibrofatty replacement
Severe isolated RV dilatation & dysfunction
Severe segmental dilatation of RV
Localized RV aneurysm (DK)
History Family history of SCD
LBBB VT
Late potentials on SAECG
TWI in V2 & V3 (no rbbb)
Mild isolated global RV dilatation and/or dysfunction
Mild segmental dilatation of RV
Regional RV HK
Echo/MRI
MINOR
Criteria for the Diagnosis of ARVD
MAJOR
Echo/MRI
EKG
2major or 1major + 2minor or 4minor

27. Diagnosis
• ECHO

28. Arrhythmogenic Right Ventricular Dysplasia
• Defective Desmosome
• Fibrofatty replacement of the RV myocardium
• 1:1000
• AD vs AR

30. Diagnosis: Schwartz score

31. PRIMARY PREVENTION
① Identifying individuals at high risk of SCD:-
▪Combination of factors more useful
▪Most imp parameter-LVEF
▪EP testing, ambulatory ECG, SAECG, HRV, T WAVE
Alternans have been used
②Pharmacological agents-
▪Beta blockers, ACEI, Amiodarone
▪Revascularisation
▪ ICD/CRT

34. Defibrillation: Electrode Placement

35. Zio Patch
• It is a recording device that provides continuous
single-lead ECG data for up to 14 days.
• The Zio Patch uses a patch that is placed on the left
pectoral region.
• The patch does not require patient activation.
• However, a button on the patch can be pressed by
the patient to mark a symptomatic episode.
• At the end of the recording period, the patient mails
back the recorder to a central monitoring station
Mittal et al, 2011

36. REAL-TIME CONTINUOUS CARDIAC
MONITORING SYSTEMS
• They combine the benefits and overcome the
limitations of Holter monitors and standard
ELRs.
• They are worn continuously and are similar in
size to the standard ELR.
• They automatically record and transmit
arrhythmic event data from ambulatory
patients to an attended monitoring station.

37. DIFFERENCES

38. Successful resuscitation following cardiac arrest
requires an integrated set of coordinated actions
represented by the links in the Chain of Survival

39. SUDDEN CARDIAC ARREST
• When the mechanism is pulseless VT, the
outcome is best
• VF is the next most successful
• Asystole and PEA generate dismal outcome
statistics

41.  Prior Episode of V.TACH
 Low LVEF.
 Previous Myocardial Infarction.
 Coronary Artery Disease
 Family History of SCD.
 Cardiomyopathy
 Congestive Heart Failure
 Long QT Syndrome.
 Right Ventricular Dysplasia.
Risk Factors of Sudden Cardiac Death (SCD)

42. Take Home Messages
– The commonest diseases associated with life
threatening arrhythmias in the young are HOCM and
congenital coronary anomalies.
– The commonest disease associated with life
threatening arrhythmias in the older athletes is
premature ischemic heart disease.
– Screening of persons going into competitive games
is difficult but essential.

43. Take Home Messages
– Arrhythmias are very common in athletes.
– Those associated with structurally normal hearts are
benign and should not cause disqualification.
– Those with heart disease can cause serious or
catastrophic effects.

44. Take Home Messages
• EVERYBODY SHOULD EXERCISE
• EXERCISE CARRIES A SMALL RISK OF A CARDIAC
EVENT THAT IS “AGE” SPECIFIC
• GET APPROPRIATE “SCREENING”
• DON’T IGNORE SYMPTOMS. THERE IS NO
LIFETIME WARRANTY FROM A SINGLE SCREENING

45. SCREENING GOAL
• To identify those at risk
• Prevent injury and lethal events
TO ASSIST YOUNG ATHLETES AND THEIR FAMILIES
IN MAKING
RATIONAL DECISIONS REGARDING THE RISK OF
ATHLETIC PARTICIPATION

46. OTHER POTENTIAL LETHAL CARDIAC
DISEASE AND EXERCISE
VALVULAR HEART DISEASE
• Aortic stenosis
• Aortic insufficiency
• Mitral Valve Prolapse

47. THE CHANNELOPATHIES AND SUDDEN
CARDIAC ARREST
• Long QT Syndrome
• Brugada Syndrome
• Catecholaminergic Polymorphic Ventricular
Tachycardia
• Short QT syndrome

48. 50

50. Fabrice Muamba
1988-2012

51. RISK FACTORS

52. • Emerging Markers of Risk for Sudden Cardiac Death
• Additional risk markers with independent or added predictive power
• are being studied for risk profiling. Among these are techniques such
• as microvolt T wave alternans,57 contrast-enhanced magnetic resonance
• imaging of the postinfarction border,58 measures of QT
• variability,59 derivatives of heart rate variability methods,60,61 124I-
miodobenzylguanidine
• (MIBG) imaging,62 and studies of familial
• clustering of SCD as an expression of coronary heart disease35-38 and
• for the potential of genetic risk profiling.2 With the possible exception
• of the predictive accuracy of a negative T wave alternans study,63
• these techniques are all in their infancy in terms of clinical
• application.

53. • Exercise-induced PVCs and short runs of
nonsustained VT
• indicate some level of risk for SCD, even in the
absence of recognizable
• structural heart disease

56. GENETICS

59. • Most of the mutations
• are at loci that encode elements in the contractile protein complex,
• the most common being beta-myosin heavy chain and cardiac
troponin
• T, which together account for more than half of identified
abnormalities.
• In the beta-myosin heavy chain form, there is a relationship
• between the severity of left ventricular hypertrophy and risk for
SCD;
• in the troponin T form, left ventricular hypertrophy may be less
severe
• despite risk for SCD.

60. SCREENING

61.  Ephedrine and its analogues
 Anabolic steroids
 Gama hydroxybutyrate
 Cocain
Illicit Drugs Used By Athletes During
Competitive Sports

62. Therapy
NEJM 2008; 358:169-175

67. • Prodromes, occurring weeks or months before an
event, are not
• sensitive or specific predictors of an impending
event, but premonitory
• signs and symptoms, which can occur during the
days or weeks
• before cardiac arrest, may be more specific for
imminent cardiac
• arrest when they begin abruptly.

68. • Substrate-based risk
• refers to prediction of the evolution or identification
• of vascular or myocardial substrates that
• establish risk for SCD (i.e., atherogenesis, scar
• patterns, remodeling) and to quantification of
• these risks. It should not be perceived as limited
• to anatomic features because molecular variants
• may also provide risk substrates.
• In contrast,expression-based risk refers to the identification
• of mechanisms and pathways that contribute to the clinical manifestation of
the risk established by the substrate. This category includes plaque
• transition and acute coronary syndromes (plaque
• disruption and thrombogenesis) and their potential
• for specific expression as an arrhythmic event
• in susceptible individuals. The arrhythmogenic
• category of risk can also be viewed to include modifiers of molecularbased
• risk that drive individual expression

69. Prospective studies have demonstrated that approximately 50% of
all deaths caused by coronary heart disease are sudden and unexpected
and occur shortly (instantaneous to 1 hour) after the onset of
symptoms. Because coronary heart disease is the dominant cause of
both sudden and nonsudden cardiac deaths in the United States, the
fraction of total cardiac deaths that are sudden is similar to the fraction
of deaths from coronary heart disease that are sudden, although there
does appear to be geographic variation in the fraction of coronary
deaths that are sudden.

70. • In the transition age range between adolescence and young
adulthood
• (to the age of 25 years) and in the middle and older ages (beginning
• at 35 years of age), coronary heart disease emerges to its position
• as the dominant cause of SCD. However, rare disorders, such as
• hypertrophic cardiomyopathy, Brugada syndrome, long-QT
syndrome,
• and right ventricular dysplasia, are significant contributors to the
distribution
• of causes of SCD in this age group. In one study, myocardial
• fibrosis of unknown etiology was a significant cause in this age
• group

71. • The incidence of sudden death has two
• peak ages: within the first year of life
(including
• sudden infant death syndrome [SIDS]; see
• Chapter 62) and between 45 and 75 years of
• age. Among the general populations of infants
• younger than 1 year and middle-aged or older
• adults, the incidence is surprisingly similar

72. • The incidence of sudden death has two
• peak ages: within the first year of life
(including
• sudden infant death syndrome [SIDS]; see
• Chapter 62) and between 45 and 75 years of
• age. Among the general populations of infants
• younger than 1 year and middle-aged or older
• adults, the incidence is surprisingly similar

73. • However, the most recent studies demonstrate a higher risk for cardiac
• arrest and SCD in blacks than in whites (see Fig. 39-5B and Chapter
• 2).25 SCD rates in Hispanic populations were lower. These differences
• were observed across all age groups.
• Sex.
• SCD syndrome has a large preponderance in men relative to
• women during the young adult and early middle-age years because
• of the protection that women enjoy from coronary atherosclerosis
• before menopause (see Fig. 39-5B)
• . Various population studies have
• demonstrated a fourfold to sevenfold greater incidence of SCD in men
• than in women before 65 years of age, at which point the difference
• decreases to 2:1 or less, and continues to decrease with advancing
• age. As risk for coronary events increases in postmenopausal women,
• risk for SCD increases proportionately, with similar rates in men and
• women. Even though the overall risk for SCD is much lower in younger
• women, coronary artery disease is the most common cause of SCD in
• women older than 40 years, and the classic coronary risk factors,
• including cigarette smoking, diabetes, use of oral contraceptives, and
• hyperlipidemia, all influence risk in women (see Chapter 77).26 Data
• from the Nurses’ Health Study suggest that a healthy lifestyle, defined
• as no cigarette smoking, a low body mass index, regular exercise, and
• a healthy diet, reduces the risk for SCD in women by as much as 46%
• to more than 90%, depending on the number of low-risk markers
• present.27 Women are 50% less likely to have severe left ventricular
• dysfunction and 66% less likely to have known coronary heart disease
• before SCD28 and are therefore less likely to be profiled as high risk
• and more likely to have SCD as a first cardiac event

74. • https://www.clinicalkey.com/#!/content/playC
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75. • http://www.ncbi.nlm.nih.gov/pubmed/22405
969
• Scd and tuberculosis
• http://www.tuberculosisjournal.com/article/S
1472-9792(12)00027-3/abstract

76. • Sudden Death Associated With Anomalous
Coronary Origin and Obstructive Coronary
Disease in the Young