Transcript sudden cardiac death (SCD)

Sudden Cardiac Death
(Evaluation of the survivor of SCD)
Division of Cardiology
R4
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Introduction
Sudden cardiac arrest (SCA) & sudden cardiac death (SCD)
 Sudden cessation of cardiac activity with hemodynamic
collapse
 If intervention(defibrillation)/spontaneous reversion restore
circulation → SCA (Aborted SCD)
if the Pts dies → SCD
 Typically d/t sustained VT / VF
 Mostly occur in Pts with structural heart disease
 Usually no premonitory Sx or nonspecific Sx
 Unconscious within seconds to min as a result of insufficient
cerebral blood blow
Definitions
Difficulties in deriving a specific definition
① Events are witnessed in only 2/3 of cases (Dx ??)
② It’s not possible to restrict the definition of SCA (documented cases of
VF) : cardiac rhythm at clinical presentation is unknown
③ duration of Sx prior to SCA generally defines the suddenness of
death (However, It is unknown in 1/3 of cases)
SCD is defined as unexpected natural death because of
circulatory collapse within 1h of the onset of acute
symptoms in a person who leads an uneventful life.
Hinkle et al. Circulation 1982;65:457-464
Goldstein S. Am Heart J 1982;103:156-9
Epidemiology
13% of all natural deaths & 50% of the mortality from CAD
The Framingham study. Am Heart J 1987;113:799-804
SCD in US in 1999 : 450,000
MMWR Morb Mortal Wkly Rep 2002;51:123
SCD was implicated in 5.6% of annual mortality
Chugh et al. JACC 2004;44:1268-75
Etiology
Previously silent coronary artery disease is likely to be the predominant
disease condition contributing to sudden cardiac death in the general population.
Sumeet S. et al. Prog Cardiovasc Dis 2008;51:213-228
Etiology (Korea)
• A report of the 51 year experience of autopsies
conducted between 1946 and 1996 in Korea
(10% of deaths were intrinsic sudden death)
Underlying disease of SCD
23%
50%
14%
13%
CVD
CNS system
Pulmonary
others
Lee YS. J Korean Med Ass 1998;3:661-671
Etiology
♣Major causes of SCD
Ischemic heart disease (65~70%)
CAD with MI for angina
Coronary artery embolism
Nonatherogenic CAD (arteritis, dissection, congenital anomaly..)
Coronary artery spasm
Nonischemic heart diseases (10%)
Hypertropic cardiomyopathy
Dilated cardiomyopathy
Valvular heart disease
Congenital heart disease
Arrhythmogenic right ventricular dysplasia
Myocarditis
Acute pericardial tamponade
Acute myocardial rupture
Aortic dissection
Etiology
♣Major causes of SCD (continue)
No Structural heart disease (5~10%)
Primary electrical disease (idiopathic ventricular fibrillation)
Brugada syndrome (RBBB & ST seg. Elevation in V1~3)
Long QT syndrome
Preexicitation syndrome
Complete heart block
Familial SCD
Chest wall trauma (commotio cordis)
Noncardiac disease (15~35%)
Pulmonary embolism
Drug-induced
Intracranial hemorrhage
Central airway obstruction
Drowning
Sudden infant death syndrome
Pickwickian syndrome
Evaluation
“complete cardiac evaluation”
I.
Identification and treatment of acute reversible causes
II. Evaluation for structural heart disease
III. In patients without obvious arrhythmic triggers or cardiac
structural abnormalities, an evaluation for primary electrical
diseases
IV. Neurologic and psychologic assessment
V. In selected patients with a suspected or confirmed
heritable syndrome, evaluation of family members
Diagnostic algorithm for the testing approach to the cardiac arrest survivor
Initial testing
Routine testing
Discretionary
testing
ECG
Rule out CAD
Echo
Assess LV function
Detect Cardiomyopathy
CAG
Rule out CAD
Exercise test
Assess for CPVT, LQTS
SAECG
Detect late potentials
From Cardiomyopathy
Cardiac MRI
Detect Cardiomyopathy
Provocative drug
Detect CPVT, Brugada, LQTS
EPS
Induce VT
Voltage map for Scar/ARVC
Evaluation
I. Identification and treatment of acute reversible causes
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Acute cardiac ischemia & MI
Antiarrhythmic drugs
Medication (eg, QT prolonging drugs), toxin, illicit drugs ingestion
Electrolyte abnormality
II. Evaluation for structural heart disease
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ECG
Cardiac catheterization with coronary angiography
Echocardiography
Cardiac MR
Myocardial biopsy
Evaluation
III. Primary electrical disease
 Electrophysiologic study
 Exercise testing
(long QT syndrome, catecholamindergic polymorphic VT…)
 Ambulatory monitoring
 Pharmacologic challenge
(epinephrine : Catechol. PMVT / procainamide : Brugada synd.)
 Myocardial biopsy
IV. Neurologic and psychologic assessment
 Complete neurologic examination
 PTSD
Primary prevention
I.
II.
III.
IV.
general population.
Patients surviving an AMI
Patients with HF and cardiomyopathy.
Patients with one of the congenital disorders associated
with an increased risk of SCA (eg, Brugada syndrome,
congenital long QT syndrome, WPW)
Primary prevention
Post MI patients
: increased risk of SCA
① standard medical Tx (beta blockers & ACEi) → incidence of SCD ↓
② Risk stratification to identify those pts at the highest risk of SCA
③ ICD >>>> Antiarrhythmic agents
④ ICD implantation in selected patients (Class I)
- LVEF <35% / at least 40d post-MI & NYHA Class II or III
- LVEF <30% / at least 40d post-MI & NYHA Class I
- LVEF <40% / nonsustained VT d/t prior MI or sustained VT at EPS
ACC/AHA/HRS 2008 guidelines
♣ at least 40d post-MI & medication (우리나라 보험인정기준)
- EF < 30% & NYHA Class II or III
- EF < 35% & nonsustained VT or sustained VT at EPS
Primary prevention
Non-ischemic HF & Cardiomyopathy
① HF & LV systolic dysfunction (regardless etiology) → SCA ↑
② ICD in selected pts & standard medical Tx → SCA ↓
③ ICD Ix
- LVEF < 35% & NYHA Class II or III (Class I & B)
- significant LV dysFx & nonischemic DCM + unexplained syncope
(Class IIa & C)
ACC/AHA/HRS 2008 guidelines
- 보험인정기준
:1년 이상의 여명, 3개월 이상의 약물치료, EF <30%, NYHA II or III
: EF<35% & nonsustained VT or sustained VT at EPS
Primary prevention
Long QT syndrome
① Beta blockers, Pace maker, Lt cervicothoracic sympathectomy
② ICD : recurrent syncope despite drug Tx, sustained VT, SCA
ACC/AHA/HRS 2008 guidelines
Hypertrophic CMP
① Major risk factor
- prior cardiac arrest, spontaneous sustained/nonsustained VT,
FHx of SCD, syncope, LV thickness >30mm,
abnormal BP response to exercise
② ICD
- syncope and/or VT while beta blockers (IIa & B)
- risk factors for SCD (IIb & B)
ACC/AHA/HRS 2008 guidelines
Secondary prevention
ICD therapy
- preferred therapeutic modality in most survivors of SCA
- not prevent the recurrence….but effectively terminates…
Antiarrhythmic drugs
- less effective
- in pts who do not want or are not candidates for an ICD
End
예비파일
Epidemiology
The magnitude of the influence of underlying cardiac dis. on
the risk of SCA
① ↑ SCA risk
six- to ten-fold in clinically recognized heart disease.
two- to four-fold in the presence of CHD risk foactors
② SCD is the mechanism of death in over 60% of pts with known CHD
(SCA is the initial clinical manifestation of CHD in 15%)
Ambulatory ECG monitoring findings in 157cases of SCD
Etiology
Percent
Ventricular tachyarrhythmia
83.4
VF/VT
62.4
Primary VF
8.3
Torsade polymorphic VT
12.7
Bradycardia
16.5
Electrocardiographic abnormalities
Finding or frequency
Increase in VPBs
75 to 90 %
Increase in complex VPBs
70%
R on T VPBs
15%
Monomorphic VT duration before VF
167sec
Polymorphic VT duration before VF
34sec
Heart rate before VT or VF
Accelerated
VT cycle length before VF
Accelerated
Ischemic ST segments change
13%
QTc
Unchanged
Bayes. et al. Am Heart J 1989:117;151-9
Albert CM. et al. Circulation 1999;100:994-50
Risk Factor
Most risk factors for CHD are also risk factors for SCA
(Dyslipidemia, HTN, cigarette smoking, physical activity, obesity, DM,
and a family Hx of premature CHD or MI)
Exercise
 During & up to 30min after strenuous exercise : transient ↑
 Actual risk during any one episode of vigorous exercise : very low
 Regular exercise : resting HR ↓, HR variability ↑…
→ reduction in the risk of SCD at other time >> small transient risk ↑
Family Hx of SCA
 Alone or with MI → 1.5~1.8-fold risk ↑
 Potential gene-environment interactions
 Interactions of mutations or polymorphism in specific gene
+ environmental factors
Risk Factor
Serum CRP
: elevated serum CRP a/w an increased risk of SCD
Excess alcohol intake
: moderate alcohol intake may decrease the risk of SCD
Psychosocial factors
- possible relation between acutely stressful situation & SCD risk
- major disaster (earthquakes and war) : rapid transient ↑
Caffeine
- potential risk factor VS no significant association
Fatty acid
- free fatty acid ⇔ ventricular arrhythmia & SCD after MI
- higher intake / level of long-chain n-3 polyunsaturated fatty acids
Primary prevention
General population
① screening & risk stratification to identify individuals who benefit from
specific intervention (eg, stress test, screening ECG)
: according to standard guideline
- Screening for risk factors for Cardiovascular disease
- Screening for CHD
- routine additional testing for the purpose of SCA risk stratification
→ not recommended
② Risk factor reduction
- Effective treatment of hypercholesterolemia & HTN
- Adoption of a heart-healthy diet, regular exercise,
- Smoking cessation, Moderation of alcohol consumption,
- Effective treatment of diabetes
Priori. et al. Eur Heart J 2001;22:1374-1450
Long QT syndrome