Sudden Cardiac Death

1
Sudden Cardiac Death

• Suhail Allaqaband, MD
• University of Wisconsin-Milwaukee Clinical Campus
• Sinai Samaritan Medical center

2

• Sudden cardiac death (SCD) is a syndrome defined
  by its clinical presentation rather than by a
  discrete pathophysiology
• The World Health Organization definition has been
  widely accepted sudden collapse occurring within
  one hour of symptoms
• However, as the name implies, SCD is
  instantaneous and most individuals become
  unconscious within seconds to minutes as a result
  of insufficient cerebral blood
• Underlying heart disease is present the vast
  majority of patients with SCD

3
Sudden Cardiac Death

• Incidence
• 400,000 - 500,000/year in U.S.
• Only 2 - 15 reach the hospital
• Half of these die before discharge
• High recurrence rate

4
Underlying Arrhythmia of Sudden Death
Primary VF 8
Torsades de Pointes 13
VT 62
Bradycardia 17
5
ARRHYTHMIC MECHANISM OF SUDDEN CARDIAC DEATH

• In approximately 80 percent of cases, a sustained
  ventricular arrhythmia is preceded by an increase
  in ventricular ectopy
• These spontaneous arrhythmias are present for a
  variable period of time prior to the development
  of a sustained ventricular tachyarrhythmia
• In about one-third of cases, the tachyarrhythmia
  is initiated by an early R on T ventricular
  premature beat in the remaining two-thirds, the
  arrhythmia is initiated by a late cycle VPB

6
ARRHYTHMIC MECHANISM OF SUDDEN CARDIAC DEATH

• A bradyarrhythmia or asystole is an important but
  less common cause of SCD, being observed in only
  about 10 percent of cases
• A bradyarrhythmia is more often associated with a
  nonischemic cardiomyopathy

7
ETIOLOGY OF SUDDEN CARDIAC DEATH

• There are many cardiac and noncardiac causes for
  a sustained ventricular tachyarrhythmia that can
  result in SCD
• In one study of 809 patients with a cardiac
  arrest, 34 percent had a noncardiac origin, most
  commonly due to trauma, nontraumatic bleeding,
  intoxication, near drowning, or pulmonary
  embolism

8
Causes of Sudden Cardiac Death

• Nonischemic Heart Disease (cont)
• myocarditis
• acute pericardial tamponade
• acute myocardial rupture
• Noncardiac Disease
• sudden infant death syndrome
• drowning
• Pickwickian syndrome
• pulmonary embolism
• drug-induced
• airway obstruction
• no structural heart disease - primary electrical
  disease, chest wall trauma (commotio cordis),
  Brugadas syndrome (right bundle branch block
  and ST segment elevation V1 to V3)

• Ischemic Heart Disease
• CAD with MI or angina
• coronary artery embolism
• nonathogenic coronary artery disease
• coronary artery spasm
• Nonischemic heart disease
• CAD without MI or angina
• cardiomyopathy - obstructive, nonobstructive,
  nonischemic
• valvular heart disease
• congenital heart disease
• prolonged QT syndrome
• preexcitation syndrome
• complete heart block
• arrhythmogenic RV dysplasia

9
ETIOLOGY OF SUDDEN CARDIAC DEATH

• Most patients who experience SCD have an
  underlying cardiac abnormality, particularly
  coronary heart disease
• The incidence of SCD increases with age in both
  men and women
• However, at any level of multivariate risk, women
  are less vulnerable to sudden death than men and
  a higher fraction of SCDs in women occur in the
  absence of prior overt coronary heart disease

10
Incidence of Sudden Death Increases with Age
During a 38 years follow-up of subjects in the
Framingham Heart Study, the annual incidence of
sudden death increased with age in both men and
women.However, at each age, the incidence of
sudden death is higher in men than women. (Am
Heart J 1998 136205)
11
ETIOLOGY OF SUDDEN CARDIAC DEATH

• Symptoms of an acute ischemic episode are
  generally absent, and the collapse is typically
  instantaneous, without any warning
• Approximately 75 to 80 percent of patients have
  no ECG changes or enzyme abnormalities after
  resuscitation that are suggestive of an acute
  myocardial infarction as a precipitating factor

12
Clinical Substrates Associated with VF Arrest

• Myocardial ischemia and infarction
• Acute myocardial infarction is associated with an
  approximate 15 risk of VF within the first 24 to
  48 hours, with the incidence falling to only 3
  percent over the next several days
• When VF is provoked by an AMI, symptoms of the
  infarction are present for minutes to hours
  before sudden death occurs over 80 percent of VF
  episodes occur within the first 6 hours

13
Clinical Substrates Associated with VF Arrest

• Congestive heart failure
• The presence of CHF increases overall mortality
  and the incidence of SCD in both men and women

14
CHF Predict Increased Sudden Death and Overall
Mortality
During a 38 years follow-up of subjects in the
Framingham Heart Study, the presence of CHF
significantly increased sudden death and overall
mortality in both men and women. P lt0.001.
15
Risk of Sudden Death Data from GISSI-2 Trial
1.00
1.00
0.98
0.98
p log-rank 0.002
0.96
0.96
0.94
0.94
Survival
Survival
0.92
0.92
p log-rank 0.0001
0.90
0.90
0.88
0.88
A
B
0.86
0.86
0
30
60
90
120
150
180
0
30
60
90
120
150
180
Days
Days

• Patients withoutLV Dysfunction

Patients withLV Dysfunction
No PVBs1-10 PVBs/hgt 10 PVBs/h
16
Clinical Substrates Associated with VF Arrest

• Left ventricular hypertrophy
• Hypertension with LVH appears to increase the
  risk of SCD
• In one study, patients with hypertension and LVH
  who died suddenly had less extensive coronary
  disease than normotensives who had SCD
• These findings suggest that the hypertrophied
  myocardium is more susceptible than normal
  myocardium to the the effects of ischemia

17
Clinical Substrates Associated with VF Arrest

• Absence of structural heart disease (primary
  electrical disease)
• Rarely, SCD occurs in patients younger than 40
  years of age who have no evidence of structural
  heart disease
• However, in approximately 90 percent of these
  cases autopsy reveals evidence of underlying
  heart disease that was unrecognized, including
  myocarditis, hypertrophic cardiomyopathy,
  arrhythmogenic RV dysplasia, sarcoidosis, or
  asymptomatic coronary heart disease
• The remaining 10 percent of patients have
  idiopathic ventricular fibrillation ("primary
  electrical disease)

18
Clinical Substrates Associated with VF Arrest

• Brugada's syndrome
• One interesting subgroup are patients with
  Brugada's syndrome who have a peculiar ECG
  pattern consisting of a RBBB and ST segment
  elevation in V1 to V3
• One study reported data on 63 such patients, 41
  of whom were diagnosed after an episode of SCD
• During a 34 month follow-up, a recurrent
  arrhythmic event occurred in 34 percent of
  symptomatic patients and in 27 percent of
  asymptomatic patients

19
Clinical Substrates Associated with VF Arrest

• Commotio cordis
• Sudden death has been described in young athletes
  who have been struck in the precordium with a
  projectile object such as a baseball, hockey
  puck, or fist
• One study described an animal model in which
  low-energy blows to the chest wall delivered
  during repolarization, just before the peak of
  the T wave, produced ventricular fibrillation

20
Clinical Substrates Associated with VF Arrest

• Family history
• A family history of myocardial infarction or SCD
  is associated with an increased risk for SCD
• Genetic abnormality
• A defect located on chromosome 1p1-1q1, has been
  associated with sudden death
• Affected individuals have progressive cardiac
  conduction abnormalities and symptomatic sinus
  bradycardia, requiring pacemaker therapy
• Sudden death generally occurs beyond the age of
  30 and is not prevented by pacemaker therapy

21
OUTCOME OF RESUSCITATION

• When the initial rhythm is asystole, the
  likelihood of successful resuscitation is low
  and, when performed out of hospital, less than 10
  percent survive to hospitalization
• The outcome is much better when the initial
  rhythm is a sustained VT (65 to 70 survival)
• Approximately 25 percent of patients with VF
  survive to be discharged in the majority of
  these patients an acute myocardial infarction is
  the underlying mechanism
• Patients who have SCD due to PEA also have a poor
  outcome

22
FACTORS RELATED TO THE OUTCOME OF RESUSCITATION

• The only effective way to reestablish organized
  electrical activity and myocardial contraction is
  prompt electrical defibrillation
• It has been estimated that organ damage becomes
  irreversible after approximately 4 minutes of VF
• As a result, the longer the duration of the
  cardiac arrest, the lower the likelihood of
  resuscitation or survival even if initial
  resuscitation is successful

23
FACTORS RELATED TO THE OUTCOME OF RESUSCITATION

• The Seattle Heart Watch program has reported on
  the outcome of patients resuscitated at the scene
  by a bystander trained in CPR compared with CPR
  initiated by emergency medical personnel
• There was no difference in the percentage of
  patients resuscitated at the scene and admitted
  alive to the hospital (67 versus 61 percent)
• However, the percentage discharged alive was
  significantly higher among those with
  bystander-initiated CPR (43 versus 22 percent, plt
  0.001)

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Bystander-initiated CPR Improves Outcome
25
Causes of in-hospital mortality

• The cause of death in hospital is most often
  noncardiac, usually being due to anoxic
  encephalopathy or to respiratory complications
  from long-term respirator dependence
• Only about 10 percent of patients die from
  recurrent arrhythmia, while approximately 30
  percent die from a low cardiac output or
  cardiogenic shock

26
FACTORS RELATED TO THE OUTCOME OF RESUSCITATION

• In addition to later onset of CPR, there are a
  number of other factors that are associated with
  a poor outcome with CPR

• Cancer or Alzheimer's disease
• History of gt2 chronic diseases
• A history of cardiac disease

• Absence of any vital signs
• Sepsis
• An initial rhythm of asystole or PEA
• CPR lasting gt5 minutes
• CVA with severe neurologic deficit

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ACUTE THERAPY FOR THE SCD VICTIM

• The only effective approach for terminating VF is
  defibrillation using 200 to 400 J of energy
  delivered transthoracically in a nonsynchronized
  fashion
• The initial success of defibrillation depends
  upon the duration of the arrhythmia and
  promptness of defibrillation
• When VF has been present for seconds to a few
  minutes, the success rate is high

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ACUTE THERAPY FOR THE SCD VICTIM

• Intravenous amiodarone
• The ARREST trial (Amiodarone in the
  Out-of-hospital Resuscitation of Refractory
  Sustained Ventricular Tachyarrhythmias)
  randomized 504 patients with a cardiac arrest due
  to VF or pulseless VT who were not resuscitated
  after at least three defibrillation shocks to
  intravenous amiodarone (300 mg) or placebo
• Survival to hospitalization was greater in the
  amiodarone group (44 versus 35 percent)
• Time to therapy with the study drug was an
  independent predictor of survival to hospital
  faster treatment was associated with a better
  outcome
• More than 50 percent of patients who survived to
  discharge had no neurological impairment

29
Evaluation of the survivor of SCD

• The evaluation begins immediately after
  resuscitation
• The first concern is to establish any obvious
  provoking factors that may have led to the event
  and which need to be corrected so as to prevent
  an immediate recurrence
• The patient or/and family should be questioned
  about previous diagnoses of heart disease the
  use of any medication, especially antiarrhythmic
  agents, diuretics, or digoxin and antecedent
  symptoms

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PROVOKING FACTORS

• Electrolyte disturbances
• Any reversible metabolic abnormalities should be
  identified and corrected, particularly
  hypokalemia and hypomagnesemia which may
  predispose to ventricular tachyarrhythmias
• Antiarrhythmic drugs
• Whenever possible, antiarrhythmic drugs should be
  discontinued prior to any diagnostic studies

31
PROVOKING FACTORS

• Use of an illicit drug such as cocaine can
  directly cause arrhythmia or produce coronary
  artery vasospasm and ischemia
• A prolonged QT interval which may be acquired
  (due, for example, to a drug or electrolyte
  disturbance) or inherited

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CARDIAC EVALUATION

• It is essential that the patient undergo a
  complete cardiac examination to establish the
  nature and extent of underlying heart disease
• The LV function and coronary anatomy should be
  assessed utilizing physical examination, echo,
  cardiac catheterization, and, if warranted,
  myocardial biopsy
• Since global LV dysfunction due to myocardial
  stunning may be present as a result of the
  cardiac arrest, baseline evaluation of left
  ventricular function should be performed at least
  48 hours after resuscitation

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ARRHYTHMIA EVALUATION

• There are different approaches (termed
  conservative and aggressive) to the evaluation
  and treatment of SCD
• Ongoing controlled trials may in the future
  provide information as to which of these
  approaches is associated with the best outcome

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Conservative approach

• The conservative approach involves a complete
  arrhythmia evaluation to establish at baseline
  the type, frequency, and reproducibility of
  spontaneous ventricular ectopy, and the
  inducibility of a ventricular tachyarrhythmia
• This involves the use of noninvasive ambulatory
  monitoring for 48 hours, an exercise test, and an
  invasive electrophysiologic study

35
Conservative approach

• For patients with SCD, in whom sustained
  monomorphic VT is induced at baseline, the use of
  antiarrhythmic agents to prevent the induction of
  sustained VT may be an adequate and effective
  first approach
• For those patients who have recurrent arrhythmia,
  the ICD could be considered as an additional or
  alternative therapy

36
Aggressive approach

• The aggressive approach uses the ICD in all
  victims of SCD whose chance of recurrence with
  therapy cannot be accurately predicted
• High, medium and low risk are all objective,
  since recurrence of ventricular fibrillation is
  often lethal

37
Aggressive approach

• When using an aggressive approach, the value of
  diagnostic testing is to find conditions that do
  not require ICD insertion, like episodic
  prolonged sinus arrest, severe AV nodal or
  infranodal disease causing intermittent third
  degree AV block, and preexcitation with AF
  leading to VF
• These and some other arrhythmias should be
  treated with pacemaker, radiofrequency ablation
  or therapies other than ICD

38
Nonpharmacologic therapy in survivors of sudden
cardiac death

• RADIOFREQUENCY ABLATION
• There are a small number of sudden death
  survivors in whom sustained monomorphic VT
  appears to be the primary arrhythmia and in whom
  a single, discrete arrhythmogenic focus can be
  localized by electrophysiologic mapping
• In such patients radiofrequency ablation is an
  option for destroying the fixed anatomic lesion
  responsible for the arrhythmia

39
IMPLANTABLE CARDIOVERTER DEFIBRILLATOR

• The ICD is a well-established and highly
  effective therapy for patients who have
  experienced SCD
• While a device does not prevent the arrhythmia,
  it reverses it automatically and promptly when it
  occurs
• There are many reports showing an impressive
  improvement in expected arrhythmia mortality
  (ranging from one to five percent per year) in
  patients who have received an ICD
• However, there is still a substantial cardiac
  mortality (approximately 5 to 10 percent per
  year) as a result of progressive CHF

40
IMPLANTABLE CARDIOVERTER DEFIBRILLATOR

• The ICD would not be expected to reduce death
  from heart failure or non-cardiac causes what it
  may do is shift the cause of death from sudden to
  non-sudden cardiac death
• As a result, the only appropriate endpoint is
  total mortality which has now been reported in
  three trials, CASH, CIDS, and AVID

41
The Cardiac Arrest Survival in Hamburg (CASH
trial )

• German prospective randomized trial of ICD versus
  antiarrhythmic drugs
• In this study, patients were randomized to
  receive an ICD, metoprolol, propafenone, or
  amiodarone
• In an interim two year analysis, the SCD rate was
  lower with the defibrillator than with amiodarone
  or metoprolol (0 versus 8 percent)
• However there was no difference in total
  mortality with the defibrillator, metoprolol, or
  amiodarone (12 percent)

42
The Canadian ICD Study (CIDS)

• 659 patients with VT, VF, or syncope deemed to be
  secondary to arrhythmia were randomized to
  amiodarone or an ICD
• After a five-year follow up, the total mortality
  with the ICD was reduced compared to amiodarone
  (25 versus 30 percent, p0.072)

43
The Antiarrhythmic Drug Versus Defibrillator
(AVID) trial

• Enrolled patients with a history of VT,VF, or
  syncope judged to be secondary to arrhythmia
• Survival benefit was noted in the 507 patients
  receiving the ICD compared to the 509 patients
  receiving sotalol or amiodarone
• The unadjusted survivals for the ICD versus drug
  groups were 89 versus 82 percent at one year, 82
  versus 75 percent at two years and 75 versus 65
  percent at three years
• The total cost for the ICD was 27,500 more than
  for drug therapy and the cost for additional year
  of survival was 127,000

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