SUDDEN CARDIAC DEATH.pptx

A BRIEF INSIGHT ON -
SUDDEN CARDIAC DEATH
Dr VARSHITH K
DrNB CARDIOLOGY RESIDENT
ASTER MIMS, KOZHIKODE

CONTENTS
• DEFNITION
• EPIDEMIOLOGICAL OVERVIEW
• RISK FACTORS
• ETIOLOGIES
• CLINICAL FEATURES
• MANAGEMENT
• PREVENTION

Sudden cardiac death is natural death from cardiac
causes heralded by abrupt loss of consciousness
within 1 hour of the onset of an acute change in
cardiovascular status.
Pre-existing heart disease may or may not have been known
to be present, but the time and mode of death are
unexpected.

Term Cardiovascular collapse Cardiacarrest Sudden
cardiac
death
Definition Sudden loss of effective blood
flow due to cardiac and/or
peripheral vascular factors that
may reverse spontaneously
(e.g.syncope) or require
interventions(e.g., cardiac arrest)
Abrupt cessation of cardiac
mechanical function, which may be
reversible byaprompt intervention
but will lead to death in itsabsence
Sudden,
irreversible
cessation of
all biological
functions
Qualifiers Nonspecific term:includes
cardiacarrest and its
consequences and transient
events that characteristically
revert spontaneously
Rare spontaneousreversions;
likelihood of successful
intervention relates to mechanism
of arrest, clinical setting, and
prompt return of circulation
none
Mechanisms Same as "Cardiac Arrest," plus
vasodepressorsyncope or other
causes of transient loss of blood
flow
VT
, VF
,Asystole ,Bradycardia,
pulseless electricalactivity

EPIDEMIOLOGY
• SCD, constitute major public health problems, accounting for approximately 50% of all
cardiovascular deaths and with at least 25% being first symptomatic cardiac events
• In USA when the etiologic definition is limited to coronary heart disease the incidence of SCD is
250,000 annually and when all causes are included incidence is 460,000 per annum.
• Annually about 7-lakh SCD cases occur in India.
• The incidence of sudden death has bimodal distribution within the first year of life (including
sudden infant death syndrome [SIDS] and between 45 and 75 years of age.
• Men remain at higher risk than women across the entire age spectrum.

AGE RELATED RISK OF SCD
• Increasing age is a strong
predictor of risk for SCA, but
it is not linear.
• The population of children
and adolescents has an
overall annual risk of 1 per
100,000, and there is
somewhat a higher risk of
SCD at the younger end of
that age range.
• Risk in the general
population, over time,
beginning at 35 years of age
has been estimated at 1 per
1000 population per year

PARADOX !
The highest risk categories identify the smallest number of total annual events, and the
lowest risk category accounts for the largest number of events per year

Anatomy
 autopsy -acute changes in coronary plaque morphology,
such asthrombus,
plaque disruption, orboth,
in 50% of cases of sudden coronary death,
in hearts with myocardial scars and no acute infarction-
active coronary lesions 46% of cases.
 because mechanisms responsible for sudden cardiac death depend in part on
anatomic substrate, which naturally varies from one individualto another,
 the usefulness of risk assessment modalities varies from one patient and
particular type of anatomic substrate to another.

Activity
 Vigorous exercise -trigger sudden cardiac death and acute myocardial infarction
(possibly by increasing platelet adhesiveness and aggregability)
 Moderate exercise-may bebeneficial
Evidences
 Annual incidenceof SCD during exercise -1per 200 000 to 250 000 healthy young
 Very rare in athletes -only 20 to 25 annually in the U.S.(despite the publicity)
 Cardiac rehabilitation programs- cardiac arrests occur at a rate of 1in 12000
 During stress testing -cardiac arrest occurs at a rate of 1per 2000
 Experimentally- regular exercise in dogs prevents ischemia induced VF and death by
increasing vagalactivity
`
 Thus, regular exercise decreasescardiovascularmorbidity andmortality, whereas
vigorous exercise, particularly in untrained individuals, may have an adverse effect.

Other riskfactors
 Smokingis an important risk factor.
In the Framingham study, the annual incidence increased from 13per 1000 in
nonsmokers to almost 2.5times of that for people who smoked 20 cigarettes
per day.
Stopping smoking promptly reduced this risk.
 Elevated serum cholesterol appears to predispose patients to rupture of vulnerable
plaques( whereas cigarette smoking predisposes patients to acute thrombosis)
 Emotional stresscan be animportant trigger for sudden cardiac death, as shown by
the Northridge earthquake that struck the Los Angeles area at 4:31AM January 17,
1994.

 Depressionin a patient in the hospital after myocardial infarction is asignificant predictor of
the 18-month post–myocardial infarction cardiac mortality, and the risk associated with
depression was greatest among patients with frequent premature ventricular complexes.
 Socioeconomicfactors are also important; sudden cardiac death after myocardial infarction
increases 3-fold in men with low levels of education and complex ventricular ectopy
compared with better educated men who have the same arrhythmias.

Impaired left ventricularfunction
 Left ventricular dysfunction is amajor independent predictor of total and sudden cardiac
mortality in patients with ischemic and non-ischemic cardiomyopathy.
 For example, in survivors of cardiac arrest who have a LVEF <30%,
the risk of sudden cardiac death exceeds 30% over 1to 3 years( if the patients
do not have inducible ventricular tachycardia)
 whereas it ranges between 15%and 50% in those who have inducible ventricular
tachyarrhythmias despite therapy with drugs that suppress the inducible arrhythmias or
with empiricalamiodarone.

Relationship between left ventricular ejection fraction (EF) and ventricular premature
depolarizations (VPD) and survival during 3 years of follow-up after myocardial infarction.
Copyright © American Heart Association

 ECGabnormalities can help identifypatients at increased risk for sudden
cardiac death.
 These include the presence of AV block or
intraventricular conduction defectsand
QT prolongation,
 an increase in resting heart rate to 90 bpm, and increased QT dispersion in survivors
of out-of hospital cardiac arrest.
 A recent study failed to support the usefulnessof QTdispersionin predicting risk in
patients after myocardialinfarction.
 The presence of complex ventricular arrhythmias, such as nonsustained ventricular
tachycardia,is also a marker.

 History can provide clues to the high-risk patient.
 For example, in patients with ventricular tachycardia after myocardialinfarction,
on the basis of clinical history, the following 4 variables identify patients at
increasedrisk of suddencardiacdeath:
 (1)syncope at the time of the first documented episode of arrhythmia,
 (2) NYHA class III or IV
,
 (3) ventricular tachycardia/fibrillationoccurring early after myocardial infarction (3
days to 2months), and
 (4) history of previous myocardial infarctions.
 In some patients, family history can be important.

PATHOPHYSIOLOGY

Transient RiskFactors
 Unfortunately, most of these more stable risk factors lack sufficient sensitivity,
specificity, and predictive accuracy to pinpoint the patient at risk with a degree of
accuracy that would permit using a specific therapeutic intervention before an
actual event.
 This probably relates, at least in part, to the transient nature of manyrisk factors,
such as myocardial ischemia andreperfusion;
hemodynamic dysfunction;
electrolytes( hypokalemia and hypomagnesemia )
changes in pH or PO2;
influence of central and peripheralneurophysiological actions;
transient effects of toxins (drugs or alcohol)
 Structural cardiacabnormalities of the myocardium, coronary arteries, or cardiac
nerves provide the substrate on which a transient risk factor operates.
 Myocardial hypertrophy, congestive heart failure, and cardiac dilation as well as
regional autonomic dysfunction all may be important.

 Thus, if structural factors for the most part only create a substrate on which the
transient factors operate to initiate a ventricular tachyarrhythmia, risk
identification requires finding those subjects whose inherent physiological
characteristicsmake the initiation of electrophysiologicalinstability more likely
when these conditions are met.
 This requires clinicallyidentifiable,
genetically based oracquired,
individualdifferences in the responses of membrane channels,
receptors,
exchangers, and
pumps in thesusceptible
individual,
 a formidable challenge at present.
 Patients with the congenital long-QT syndrome serve as the prototypic example
of the interaction between a molecular myocardial abnormality, an “ionopathy,”
and an inciting event, eg, exercise in LQT1and sleep/rest in LQT3.

DRUGS
 Antiarrhythmic drugs have long been known to be capable of provoking ventricular
tachyarrhythmias and sudden cardiac death.
 Non-antiarrhythmic drugs that prolong repolarization along with class IA
antiarrhythmic agents, can cause torsade de pointes.
 Class IC drugs in the CAST study
• An antiarrhythmic drug cancreate the abnormality on which a transient risk
event, such as ischemia,interacts to provoke a lethal arrhythmia.
• For example, in the CAST experience, despite the increased risk of sudden cardiac
death established by the presence of complex forms of ventricular ectopy,
particularly in older age groups and in patients post myocardial infarction,
• suppression of those ventricular arrhythmias with encainide and flecainide
conferred anincreasedrisk of death and/or no improvement in survival with
moricizine.

 The results of CAST taught us at least 3 important lessons:
(1)that mechanisms responsible for premature ventricular complexes, which were
suppressed, were different from mechanismsthat causedsuddencardiacdeath,
presumably from a ventricular tachyarrhythmia, which was increased;
(2)that proarrhythmia from an antiarrhythmic agent couldoccurmonthsafter drug
initiation and was not always an early event; and
(3) that antiarrhythmic drugscouldbecomearisk factor when the myocardial
substrate changed, presumably when ischemia developed.
 Drug-drug interactions during poly-pharmacycan be dangerous, even with
apparently innocuous medications.
 Phosphodiesterase inhibitors and other positive inotropic agents that increase
intracellular calciumloading have also been demonstrated to exert proarrhythmic
actions and increase the risk of sudden cardiac death.

ELECTROL
YTES
 Hypokalemia (in some instances provoked by potassium-wasting diuretics),
hypomagnesemia, and increased intracellular calcium concentration may be
important as primary or triggeringevents.
 It is sometimes difficultto determine whether a patient resuscitated from
ventricular fibrillation had the arrhythmia provoked byhypokalemia,
 because in the postresuscitation period,serum concentrationsof potassiummaybe
reduced becauseof the effects of catecholaminerelease after the cardiac arrest.
 Thus, unless there is a history of electrolyte imbalance, drugs known to deplete
potassium, special diets such as the liquid protein diet,or documented electrolyte
abnormalities when the patient is in a steady state, the diagnosis of hypokalemia
may be indoubt.
 And search for other cause or precipitator should also be made

Autonomic NervousSystem
 Abnormalities of the autonomic nervous system appear to be involved in the
genesis of sudden cardiac death.
 Myocardial infarction, for example, produces regional cardiac sympathetic and
parasympathetic dysfunction not only in the infarcted area but alsoin regions
apical to the infarct, presumably because of interruption of afferent and efferent
nerve fibers traversing the infarct .
 Denervated regions show supersensitivity to catecholamine infusion, with
disproporti-onate shortening of refractoriness that creates autonomic
heterogeneity, resulting in dispersion of refractoriness and/orconduction, which
can be conducive to development of ventricular arrhythmias.
 Any process that creates electrical heterogeneity favors the development of
ventricular fibrillation.
 Recent data indicatethat sympathetically denervated ventricular myocardium
demonstrates abnormal oxygen utilization, which could also affect
arrhythmogenesis (G.D. Hutchins, PhD, unpublished observations, 1998).

ETIOLOGIES OF SCD
Coronary artery abnormalities Hypertrophy of the ventricular
myocardium
Myocardial diseases and
dysfunction
A. Coronary atherosclerosis
B. Congenital abnormalities of
coronary arteries
C. Coronary artery embolism
D. Coronary arteritis
A. Hypertensive heart disease
B. Hypertrophic
cardiomyopathy
C. Primary or secondary
pulmonary hypertension
A. Chronic congestive heart
failure
B. Myocarditis, acute or
fulminant
C. Takotsubo syndrome
D. Acute alcoholic cardiac
dysfunction
Diseases of the cardiac valves Infiltrative, neoplastic, and
degenerative processes
Congenital heart disease
A. Valvular aortic
stenosis/insufficiency
B. Mitral valve prolapse
C. Prosthetic valve
dysfunction
A. Sarcoidosis
B. Amyloidosis
C. Chagas disease
D. Idiopathic giant cell
myocarditis
A. Congenital aortic or
pulmonic valve stenosis
B. Eisenmenger physiology
C. Late after surgical repair of
congenital lesions

Electrophysiologic
abnormalities
Electrical instability related to
neurohumoral influences
Miscellaneous
A. Congenital long–QT
interval syndrome
B. Congenital short–QT
interval syndrome
C. Brugada syndrome
D. ERS
A. Catecholaminergic
polymorphic ventricular
tachycardia
B. Psychic stress, emotional
extremes (takotsubo
syndrome)
A. Commotio cordis—
blunt chest trauma
B. Mechanical
interference with
venous return
C. Dissecting aneurysm of the
aorta

Causes of sudden cardiac death in competitive athletes.

CORONARY ARTERYDISEASE
Atherosclerotic changes–
 At least 80% of patients have as the underlying anatomic substrate
 Autopsy -recent occlusive coronary thrombus in 15%to 64% of victims
with many hearts showing plaque fissuring, hemorrhage, and thrombosis.
no specificpattern of distribution of coronary artery lesions
 Interestingly, chronicischemiamayexert a protective effect by causing the
development ofcoronary collaterals
 So,an acute occlusion of a minimally stenosed coronary artery can result in a more
disastrousoutcome
Nonatherosclerotic abnormalities
 Important in only a very small number of SCD
 Include coronary arteritis, embolism,dissection, and
anomalousorigin of aleft coronaryartery from the pulmonary artery or of
a left coronary artery from the right or noncoronary aortic sinus of Valsalva, passing
between the aortic and pulmonary artery roots.

CARDIOMYOPATHY
 Represent the secondlargest group of patients who experience sudden cardiac
death.
Hypertrophic cardiomyopathy
 prevalence -2in 1000 youngadults
 incidence of SCD- 2%to 4% per year in adults
 risk factors -ahistory ofSCA
sustained VT
,
familyhistory of SCD,
a diverse genotype,
recurrent syncope,
multiple episodes of non-sustained VT
,and
massive LVH
 mechanisms -arrhythmias, abrupt hemodynamic deterioration,and/orischemia.
Idiopathic dilated cardiomyopathy
 substrate for 10%of SCD in the adult population.
 high risk of suddendeath -nonsustainedventricular tachycardia
Syncope in heart failure patients
 mechanisms –arrhythmias (ventricular tachycardia ,asystole or electromechanical
dissociation)

Hypertrophic Cardiomyopathy
Defect in the myocardial contractile proteins
HCM isa familial disease
hallmark :myocardial hypertrophy that is
inappropriate, often asymmetrical, and occurs in
the absence of an obvious inciting hypertrophy
stimulus.

SCD
DOE
Syncope
Heart failure
Chest Pain
Palpitation
Asymptomatic
Systolic Crescendo-decrescendo murmur
LLSB/apex
Decreases w/ squatting, handdrip
Increase w/ standing
Bifid pulses
EKG-LVH

Arrhythmogenic right ventriculardysplasia
 gene defect recently localizedto chromosomes 1and 14
 autosomal dominantinheritance.
 familialdisorder in '30% of cases
 responsible for sudden death in young individuals and adults,
 Exercise can precipitate ventricular tachycardia in these patients,
 with an annual incidenceof sudden death estimated to be '2%.
 pathological patterns- fattyand
fibrofatty myocardialinfiltration
ECG during sinus rhythm often exhibits T-wave inversion in V1to V3 or complete or
incomplete right bundle-branch block, and the ventricular tachycardia has a left bundle-
branch blockcontour

Asymptomatic
Palpitation, syncope, atypical chestpain,
dyspnea
Arrhythmias SCD
Exercise associated

Criteria for the Diagnosis of ARVD
MAJOR
History Familial disease by histology
EKG Epsilon waves or QRS 110 ms+ in V1-V3
Biopsy Endomyocardial biopsy with fibrofatty replacement
Echo/MRI
Severe isolated RV dilatation & dysfunction
Severe segmental dilatation of RV
Localized RV aneurysm (DK)
MINOR
History Family history of SCD
EKG
LBBB VT
Late potentials on SAECG
TWI in V2 & V3 (no rbbb)
Echo/MRI
Mild isolated global RV dilatation and/or dysfunction
Mild segmental dilatation of RV
Regional RV HK
2majoror1major+ 2minor or4minor

Primary electrophysiological abnormalities
Represent a group in whom mechanical function of the myocardium isnormal and an
electrophysiological derangement represents the primary cardiac problem.
This includes patients with the
1.long-QT syndrome,
2.Wolff-Parkinson-White syndrome,
3.idiopathic ventricularfibrillation
4.Brugada’ssyndrome
5.completeAV block

Long QTSyndrome
Autosomal Dominate- Romano-Ward
Autosomal Recessive- Jervell and Lange-Nielsen
Acquired
1/10,000

Palpitations, Presyncope, Syncope, Seizures,or
Cardiac arrest
Asymptomatic prolonged QTc
Referred by familymembers
Has a predilection for younger patient

Brugada Syndrome
Autosomal dominate defect in cardiac Na
channels- variable expression
0.4%USpopulation
Male predominance
Average ageof Dx=41

• Funny looking ECG
• SCD/Syncope
• Triggers
• Fever
• Sleep
• Glucose/insulin
• Cocaine/ETOH
• Electrolytes

Wolff-Parkinson-Whitesyndrome
WPW syndrome is a recognized but rare cause of sudden death.
 In a study by Klein et al of 31patients with VF and WPW syndrome, a history of atrial
fibrillation or reciprocating tachycardia was an important predisposing factor.
 Thepresenceof multipleaccessorypathways,
posteroseptal accessory pathways,and
a pre-excited R-R interval of less than 220 ms
during atrialfibrillation areassociated with higher riskfor SCD.
 Symptomatic patients should be treated by
antiarrhythmic medications (eg,procainamide),
catheter ablation of the accessory pathway, or
electrical cardioversion
depending on the severity and frequency of symptoms.
 Asymptomatic patients may be observed without treatment.
 Medications such as digoxin, adenosine, and verapamil that block the A
Vnodeare
contraindicated in patients with WPW and atrial fibrillation because they may
accelerate conduction through the accessory pathway, potentially causing VF and
SCD.

The existence of an atrio-ventricular accessory pathway in this
syndrome results in ventricular pre-excitation, which appears
with short PR interval, wide QRS complex, and delta wave on
ECG.

CommotioCordis
SCD due to low-impact precordial trauma
Male predominance, youngage
High mortality
Probability related to speed, time, hardness of
object and location of impact

Congenital CoronaryArtery Anomalies
Variation in the take off the Coronary Arteries
Incidence 5.6 0.17%
Deaths related toexertion
Compression betweenthe pulmonary artery and
aorta
Acute angletake off
Myocardial necrosis
Angina
Atypical chestpain
Syncope
Palpitation
Dizziness
SCD

Prodromal symptoms :SCD may be presaged by increasing angina,
dyspnea, palpitations,easy fatigability, and other nonspecific complaints.
 generally predictiveof any major cardiac event
 not specificfor predicting SCD.
Theonset of the clinical transition: leading to cardiac arrest, is defined as an
acute change in cardiovascular status preceding cardiac arrest by up to 1h.
Continuous electrocardiographic (ECG) recordings :
demonstrate changes in cardiac electrical activity (over minutes or hours)
 tendency for the heart rate to increase and
 advanced grades of PVCs
 begin with a run of nonsustained or sustained VT
,
 which then degenerates into VF
.

Progression to biologic death is a function of the mechanism of cardiac arrest
and the length of the delay before interventions.
VF or asystole without CPR within the first 4–6 min has a poor outcome even if
defibrillation is successful because of superimposed brain damage; there are few
survivors among patients who had no life support activities for the first 8 min after
onset.

MANAGEMENT
The response to cardiac arrest is driven by two principles: (1) maintaining continuous cardiopulmonary
support until ROSC has been achieved and (2) achieving ROSC as quickly as possible.
Post CA
care
ACLS
Early D-
Fib
BLS
Initial
assessme
nt

Measures to ReduceSuddenDeath inPatients Knownto Have CardiacDisease
Correctingischemia Revascularization beta-Blockingagent
Preventing plaquerupture
Statin
ACE inhibitor Aspirin
Stabilizing autonomicbalance
beta-Blockingagents ACE inhibitor
Improving pumpfunction
ACE inhibitor
beta-Blocking agent
Prevention ofarrhythmias beta-Blocking agent Amiodarone

Treatment algorithm for patient resuscitated from cardiac arrest.

Prevention of cardiac arrest and SCD
Primary prevention
High risk patients of advanced heart disease with
low EF and other high risk markers
Less advanced common or uncommon structural
heart diseases
Structurally normal hearts, subtle or minor structural
abnormalities, or genetically based molecular
disorders that establish risk for ventricular
arrhythmias
General population
Secondary prevention
Prevention of recurrent events in survivors of cardiac
arrest or pulseless VT or other symptomatic
tachycardias considered life-threatening

STRATEGIES TO REDUCE SCD
• Anti arrhythmic Drugs
• Therapy Guided by Programmed Electrical Stimulation
• Surgical Intervention Strategies
• Catheter Ablation Therapy
• Implantable Defibrillators

Anti-arrhythmic drug therapy
• Historically, ambient arrhythmia suppression by AAD therapy enjoyed a short period
of popularity as a strategy for reduction of SCD.
• Currently, with the exception of beta blockers there is no evidence from RCTs that
antiarrhythmic medications improve survival when given for the primary or secondary
prevention of SCD.
• However the use of these medications may be considered in some patients to
control arrhythmias and improve symptoms.
Medications With Prominent Sodium Channel Blockade:
• Intravenous lidocaine for patients with refractory VT/ cardiac arrest.
• Oral mexiletine for congenital long QT syndrome
• Quinidine for patients with Brugada syndrome
• Flecainide for patients with catecholaminergic polymorphic
ventricular tachycardia
• In ICD patients with drug- and ablation-refractory VT.

Anti-arrhythmic drug therapy
Beta Blockers:
• Excellent safety profile and effective in treating VA and reducing the risk of SCD.
• Their antiarrhythmic efficacy is related to the effects of adrenergic-receptor
blockade on sympathetically mediated triggering mechanisms
• Reduce all-cause mortality and SCD in patients with HF with reduced EF (HFrEF)
• Reduce mortality after MI
• First-line therapy for some cardiac channelopathies (e.g., long QT syndrome,
catecholaminergic polymorphic ventricular tachycardia).
Class III anti arrythmic agents:
• For primary prevention, in some studies, amiodarone was found to reduce
the risk of SCD and all-cause mortality, but the quality of the supporting
evidence was very low.
• For secondary prevention of SCD, the same systematic review identified
neither risk nor benefit with amiodarone.

The use of programmed electrical stimulation to identify
benefit on the basis of suppression of inducibility by an anti
arrhythmic drug gained popularity for evaluation of long-term
therapy among survivors of out-of-hospital cardiac arrest.
Nonetheless, most studies have demonstrated limitations
based on observations that a relatively small fraction of cardiac
arrest survivors had inducible arrhythmias.
Drug suppression of inducibility during electrophysiologic
testing as an endpoint for secondary prevention of SCD/
primary prevention in high-risk post–myocardial infarction
patients has yielded to the benefits of ICD therapy in most
subgroups

Intraoperative map-guided cryoablation may
be used for patients who have –
inducible, hemodynamically stable sustained
monomorphic VT during electrophysiologic
testing
and have suitable ventricular and coronary
artery anatomy amenable to catheter ablation.
It can be used as adjunctive therapy for ICD
recipients whose arrhythmia burden requires
frequent shocks.

Catheter ablation techniques to treat VT most
successful for the benign focal tachycardias
that originate in the right ventricle or left side
of the IVS
VT caused by bundle branch reentrant
mechanisms, ablation of the right bundle
branch to interrupt the reentrant cycle
catheter ablation techniques are not used for
the treatment of higher risk ventricular
tachyarrhythmias or for definitive therapy

ICDs
The first generation of defibrillators required a
thoracotomy to place the sensing and defibrillator
leads epicardially, and the generator size mandated
implantation of the device in an abdominal pocket
Current-generation ICD integrate pacing, sensing,
and high-voltage defibrillation abilities
have the additional ability to deliver low-energy
cardioversion, ATP for VT, and anti bradycardia pacing
Given the excellent safety and good profile of
current ICD, implantation is not a major challenge
Identification of patient populations most appropriate for
this potentially lifesaving therapy

Randomised Trials of ICD Therapy
“Primary prevention” - patients who
have not yet had VT or VF, but are
thought to be at high risk

5 10 20 30
CABG-Patch
MUSTT
MADIT I
ns VT
High risk
no VA MADIT II
DEFINITE
SCD-HeFT
DINAMIT
CAT
LV-EF (%)
ICD Trials - Primary
prophylaxis

ICD10 Prevention Trial Results
CABG-Patch
MUSTT
MADIT I
MADIT II
DINAMIT
SCD-HeFT
DEFINITE
AMIOVIRT
CAT
0 2 2.5
CAD, MI
NICM
CAD,
NICM
Hazard Ratio
0.5 1 1.5
ICD better No ICD better

Overview of Primary Prevention
Trials Results
MADIT 54% reduction in mortality with ICD
MUSTT
MADIT II
55-60% reduction in mortality with
ICD
31% reduction in mortality with ICD
DEFINITE Mortality benefit 5.7% at 2 years
with ICD
SCDHeFT 23% reduction in mortality with ICD

ICD
Class I
VT/VF survivors with irreversible etiology
sustained VT with structural heart disease
syncope + VT/VF at EPS
NYHA II-III, LV EF<35%
NYHA I, post-MI, LV EF<30%
NSVT, post-MI, LV EF<40%, VT/VF at EPS

ICD
Class IIa
syncope, LV dysfunction, non-ischemic
DCM
Sustained VT
HCM with major risk factors
ARVD with major risk factors
LQTS with syncope while on BB therapy
transplant bridge
Brugada syndrome with syncope or VT
Catecholaminergic polymorphic VT with
syncope

ICD
Class IIb
NYHA I, LV EF<35%
LQTS and SCD risk factors
idiopathic syncope and advanced SHD
familial CMP
LV noncompaction

ICD
Class III
Expected survival less than 1 year (other
cause)
Incessant VT/VF
Significant psychiatric illness
NYHA IV without transplant or CRT indication
Idiopathic syncope with no inducible VT/VF
and SHD
VT/VF amenable with ablation
VT/VF with reversible cause

Why not to consider ICD for all high risk
patients?......ICD Cost effectiveness
• The cost-effectiveness ratio becomes rapidly
unfavorable as the extension in survival time falls below
1 year, particularly below 0.5 year.
• This inverse relation strongly suggests that the value
provided by an ICD will be highest when the risk of
arrhythmic death due to VT/VF is relatively high and the
risk of nonarrhythmic death (either cardiac or
noncardiac) is relatively low.
• Thus, appropriate patient selection is fundamental to
high value care in using the ICD to prevent SCD.

In Summary
SCD is not common
About half of all cardiovascular deaths
Approx. 50% of all SCDs are unexpected
first expressions of a cardiac disorder
High-risk people usually identified by
symptoms or family history – priority for
evaluation
Cure not possible, but correct management
can prevent complications

1. Sudden cardiac death (SCD) is an important public health issue and warrants further study to better quantify its occurrence, its impact on society,
and the opportunities for improving outcomes through public education and provision of automated external defibrillators and cardiopulmonary
resuscitation (CPR) training.
2. For survivors of sudden cardiac arrest (SCA), victims of sudden unexplained death (SUD), and their relatives, a multidisciplinary team is central to
thorough investigation, so as to maximize the opportunity to make a diagnosis. Where there has been an SCD or resuscitated SCA and a genetic
cause is suspected, genetic testing and counseling is essential for families, to ensure that risks, benefits, results, and the clinical significance of
genetic testing can be discussed.
3. The psychological care of families affected by SUD and survivors of SCA (and their families) should run in parallel with the investigation process.
Assessment by professionals trained in psychological care should be offered, as well as grief counseling and peer support, where appropriate.
4. For the investigation of SUD, a detailed personal and family history is essential, with attention to sentinel symptoms during life such as syncope or
seizures, witness accounts, premorbid investigations, and inspection of any cardiac rhythm monitoring around the time of death.
5. A comprehensive autopsy is an essential part of the investigation of SUD and should include collection and storage of tissue suitable for genetic
analysis. When the autopsy suggests a possible genetic cause, or no cause and the heart is normal, referral to a multidisciplinary team for further
investigation is indicated.

6. For victims of SCD or survivors of cardiac arrest where the phenotype is known, genetic testing of the proband focused on likely candidate genes, along
with clinical evaluation of family members, aids in identifying family members with, or at risk of developing, the same condition.
7. For victims of SCD or survivors of cardiac arrest where the phenotype is not known, arrhythmia syndrome–focused genetic testing may help
arrive at a secure diagnosis, whereas wider testing without careful consideration of the implications of indeterminate results by experienced
clinicians may only serve to add uncertainty and lead to misinterpretation of results.
8. For the investigation of SCA survivors, essential inquiry includes detailed personal and family history, witness accounts, physical examination,
multiple ECGs, and cardiac imaging. Ambulatory monitoring and/or provocative testing (exercise, pharmacological, and invasive
electrophysiological) may provide additional useful information. A sample suitable for future DNA testing should be taken early in the patient’s
course and stored.
9. Genetic investigation of SCA survivors is best undertaken at a center with multidisciplinary care infrastructure and should focus on likely
candidate genes known to be causally related to the suspected phenotype. In some cases, genetic evaluation without a suspected phenotype
may be undertaken with appropriate genetic counseling, although genetic evaluation of patients with a known nongenetic cause of cardiac arrest
is discouraged.
10. The investigation of the families of victims of SUD and survivors of SCA should include clinical and, if known, genetic cascade testing. If the cause of
SUD (or rarely, SCA) is unknown, then clinical investigation of first-degree relatives may include physical examination, ECGs, cardiac imaging,
ambulatory monitoring, and provocative testing (exercise, pharmacological, and rarely invasive electrophysiological) with multidisciplinary team
supervision. Follow-up and periodic re-evaluation are important and are directed by initial findings.

ICD is most cost-effective when used for patients at
high-risk of arrhythmic death and low-risk of other causes
of death.
Specific patient populations are now recognized for whom the
benefit of ICD therapy outweighs any risks
Categorizing patients on the basis of only LVEF and NYHA
Functional Class can aid in identification of patients who
have highest benefit from primary preventions

SUDDEN CARDIAC DEATH.pptx

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