2. Definition
• Sudden and unexpected death
• Occurring within 1 hour of symptom onset
Or
• In patients found dead within 24 hours of
being asymptomatic
• Presumably due to:
– Cardiac arrhythmia
– Haemodynamic catastrophe
Natural, Rapid and Unexpected
3. Incidence of SCD
• Almost 50% of all CV deaths
• At least 25% -first symptomatic event
• M>F
• 70%- out-of-hospital*
• Out-of-hospital SR- 6%
• In-hospital SR-24%
• Rapid emergency response, public knowledge
• Prognosis better in shockable > PEA/asystole
4. Incidence of SCD
• India- >7,00,000 deaths/year and approx 10.3% of mortality (Rao et
al.)
• Peak age – 45 to 75 yrs, M>F (3:1)
• SR <1%
• Vital data esp. from rural areas – unaccounted for
• Rural-urban gradient in CAD (7.6-12% v 3.1-7.4%) - different risk
factors
• Urban India and Western SCD trends similar- Gupta et al. (2007)
• Prevailing RFs- HTN, DM, smoking
5. Four temporal elements
1. Prodrome- Predictors of an impending
cardiac event
2. Onset of terminal event- from onset of
1st symptom to SCA
3. Cardiac arrest
4. Biologic death- upto 1 hour from
terminal event
7. Etiology of SCD
Structural HD Cardiomyopathy
HCM, NIDCM, ARVC
Myocardial scarring and fibrosis
Inherited Arrhythmia syndromes BrS, LQTS, WPW, CPVT
Channelopathies
Ischaemic Heart Disease** - X 2.8-5.3 risk (Framingham)
LVEF < 30-35% *
Valvular HD AS, MVP, Prosthetic valve dysfunction
Mechanical pathologies Acute cardiac tamponade, Massive PE, Acute
intracardiac thrombus, Commotio cordis
Congenital HD Congenital AS, PS, VSD+Eisenmenger
physiology, Anomalous origin of coronary
arteries, post-TOF repair
SIDS- Sudden infant death syndrome - <0.5/1000 live births, M>F infants
8. Contributory Risk factors
1. Hypertension
2. Type 2 DM
3. Dyslipidaemia
4. CKD
5. Obesity
6. OSA
7. Seizures
8. Smoking
9. Type A personality
10. Nutritional deficiencies
9. Risk analysis
1. Age
– 2 peaks- <1 year (SIDS) and 45-75 yrs
– Strong predictor, non-linear, >35 yrs, 1 in 1000/yr
– Risk decreases in later years >75 yrs, Framingham
– Steep increase- adolescent to middle-age (IHD)
– HCM, BrS, LQTS, ARVC- important considerations
2. IHD
– MC substrate a/w SCD
– Transition from mid-20s to mid-30s (>40% of cases)
14. Risk analysis
7. LVEF
– <30%- single most powerful independent predictor of SCD
– MR rate changes the most btw 30-40%
– Infarct size, fibrosis- better predictor of cardiac events
– LV dysfunction- modulates risk in Post-MI pts with VPCs
8. Ventricular arrhythmias
– Benign- most VPCs, NSVT (short runs)- in absence of structural HD
– If present during TMT (peak/recovery)- higher risk
– VPCs in Post-ACS pts- increased risk (>10/hour)
– Polymorphic NSVT- drug/electrolyte/functional
15. Mechanisms of SCD
1. Automaticity
– Enhanced normal
– Abnormal
2. Afterdepolarisations Triggered activity
– Early
– Late
3. Re-entry phenomenon
16. Automaticity
• Phase 4- spontaneous depolarisation of
transmembrane AP
• In MI/ischaemia:↑ EC K+ causes partial
depolarisation of RMP
• Injury currents develop btw healthy and
infarcted/ischaemic myocardium
• This initiates spontaneous activity
• Purkinje fibres and Ventricular myocytes
17. Triggered Activity
• AP prolongation may occur due to
– ↑ inward currents (Na+/Ca2+/Na+-Ca2+ exchange)
– ↓ repolarising K curents
• Early afterdepolarisations- late phase 3/early
phase 3 of AP
• TdP VT associated with QT-Prolongation
(medications/hereditary)
• Delayed afterdepolarisations- after complete
membrane repolarisation, due to Ca2+ overload
• CPVT, Digoxin toxicity, idiopathic outflow tract VA
18. Re-entry phenomenon
• Most sustained VA in the presence of
structural HD
• Ischaemia, Brugada syndrome
• Re-entry requires a trigger to initiate the
arrhythmia and a substrate to sustain it
• Trigger- VPC (automaticity)
• Substrate-
1. Fixed anatomical obstacle- patchy fibrosis, scar
(post-MI or post-surgery, CM, hypertrophy)
2. Functional block- functional re-entry. Rotor vs.
Multiple wavelet re-entry