Sudden cardiac death by malj

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									                             Sudden cardiac death
                   - Electrophysiological aspect -

                                                                       서울대학병원 소아과학 교실
                                                                                           배 은 정
________________________________________________________________________________________


1) Introduction
    Sudden cardiac death is very common mechanism for cardiac mortality in adult population in all
  developed countries.      But identification of individuals at increased risk for sudden death and
  effective prevention remains elusive. Although the exact incidence of sudden cardiac death in
  South Korea is unknown, there are 300,000 such deaths in each year in United States. Among
  older adults, sudden deaths are often due to atherosclerotic coronary artery disease and terminal
  ventricular fibrillation. Sudden cardiac deaths in the young people are few but have numerous
  causes. The lists of underling disease are in Table 1.      According to the study of 469 sudden
  death in the young people (1-30 years old) the rate of SD (sudden death) was 1.3-8.5/100000
  patient.year. There also was male predominance, 2/3 had cardiac causes. Before 1 year of age
  ductus dependent congenital heart anomaly was dominant etiology. Thereafter long QT syndrome,
  aortic stenosis, tetralogy of Fallot, pulmonary vascular obstructive disease, cardiomyopathy and
  myocarditis were important causes.      The patients of SD with postoperative cardiac anomaly had
  poor NYHA functional class (III-IV) in 3/4, cardiomegaly in 87%, pulmonary hypertension in 43%
  and arrhythmia in 53%.     50 % of them had preceding symptom such as syncope and chest pain.
  About 1/3 of sudden cardiac death (SCD) has apparently normal heart. The pathologic study of
  SCD in the young people with apparently normal heart (n=76) revealed that 79% of them had
  abnormality such as focal myocarditis, histologic arrhythmogenic right ventricular cardiomyopathy,
  and conduction system abnormality.
     For many years the focus of the SCD research in adult has concentrated on averting those
  conditions that are its primary antecedents, such as coronary artery disease and heart failure.
  Recently however, major advances have occurred in understanding molecular and cellular events
  that contribute to SCD.




2) Mechanism of ventricular fibrillation and sudden cardiac death
    The speculated and documented factors for mechanism of VF/SCD are as follows
        1. transient myocardial ischemia
        2. autonomic nervous system dysfunction; increased sympathetic tone, decresed
           baroreceptor sensitivity, changed heart rate variability
        3. platelet activation
        4. released cardiac toxin
        5. abnormal gene expression
        6. ion channel or gap junction alteration
        7. sarcoplasmic reticulm dysfuction
        8. altered calcium ion influx
        9. shift in wavefront propagation


3) Myocardial ischemia and ventricular fibrillation/ sudden death
      Myocardial infartion often developes in adults with coronary artery disease and ventricular
   arrhythmias commonly complicate management and outcome in these patients. The report on
   ventricular tachycardia or fibrillation on postinfarction course in pediatric population is few.
   Johnsrude reviewed 96 infartion chilren, 28% had ventricular tachycardia /fibrillation in early
   period ( by 2 days after diagnosis)    and they had higher mortality( approximately 80% ). The 61
   postinfarction survivors were monitored for an average of 4.9 years, and none had significant
   reccurent ventricular arrhythmia or late sudden death.     According to the adult study 40-75 % of
   SCD victims had healed myocardial infarction. Acute coronary artery thrombosis or distal
   microembolization from ruptured atheromatous plaque may lead SCD. However the question if
   myocardial ischemia induce directly ventricular fibrillation requires further evaluation. Although
   there can be subclinical or microscopic ischemia, ST changes preceding ventricular fibrillations
   are uncommon among SCD victims in clinical setting.
      Experimentally acute ischemia is marked by alterations in cell metabolism, cell signaling,
   intercellular   communication         and   electrical   impulse    propagation.    Among     the
   electrophysiologically relevent changes that occur rapidly after the onset of ischemia are
   reduction of tissue pH, increses in interstitial K+ and intracellular Ca2+ concenturations ,all of
   which alter exitability and refractoriness, promote electrical uncoupling and generate
   spontaneous electrical activity. Altered connexin expression (Cx43) at ischemic mouse heart
   showed altered intercellular coupling, which was related ventricular fibrillation induction. Such
   changes are heterogeneous at different parts of myocardium like midmyocardium and
   subepicardium, which lead gross abnormalities of ventricular repolarization.
   Prolongation of QT interval and QT dispersion are considered to increase SCD in the patients
    with ischemia. Sympathetic nerve sprouting after myocardial infarction coupled with electrical
    remodelly remodeled myocardium results in VT, VF and SCD.


4) Mechanoelectrical contribution to sudden cardiac death
       The most important predictor of SCD after myocardial infarct is LV ejection fraction.    EF less
than 40% has 68%sensitivity 69% specificity of SCD. EF less than 30m % has 3.5 fold risk for SCD.
Furthermore according to SCD study of postoperative TOF, the more dilated RV or longer QRS
duration the higher risk of SCD or ventricular tachycardia.
       The acute and chronic stretch were associated with prolongation of action potential and
electrophysiological heterogeneity/ dispersion and after depolarization.
Several investigations have demonstrated that mechanical alterations alter Ca ion during diastole
as well as systole. Sustained increase in Ca ion oscillations that are conductive to membrane
oscillations and thus result in generating premature beats and arrhythmias. The cytoskeleton could
be an important modulator of stretch activated Ca transients.


5) Predilection , clinical evaluation and prevention of sudden cardiac death
        Cardiac failure has been noted to be an important predisposing factors in              SCD as
previously discussed. LV EF is a consistent predictor of SD in heart failure.     A strong relationship
has been demonstrated between prevalence of premature ventricular beats and the degree of left
ventricular dilation in heart failure and dilated cardiomyopathy.    However the predictive value of
SCD is low.    Moreover their suppression by antiarrhythmic drugs does not prevent SCD, so the
value of Holter monitoring is limited.   Electrophysiological induction study also has limitation to
predict SCD because of the problems of significance of inducible VT, low incidence of inducibility ,
lack of utility of antiarrhythmic drugs, reproducibility, and few prospective randomized clinical trial.
Signal average ECG and baroreceptor sensitivity and HR variability may be helpful.
     For therapeutic options to prevent SCD after initial cardiac arrest survival, ICD is the best.
According to AVID trial, with ICD 2 years survival was 81.6%, higher than that ( 74.7%)of
antiarrhythmis drug( amiodarone, sotalol).        ClassIc drug is not recommended due to its
proarrhythmic effect. Among antiarrhythmis drug class III drug , especially amiodarone is effective.
CASCADE trial documented that higher 2 year survival rate free of death, VF with
amiodarone( 82%) than with class I drug(69%).
  If the SCD survival has obstuctive coronary heart disease with normal LV function , coronary
bypass surgery is recommended . 1 year and 5 year survival rates were 92% and 82 % in the
bypass group for sudden cardiac arrest survival, which were higher than that of medical treatment
group. (80%, 50%).
  Radiofrequency ablation for this particular situation of SCD/ ventricular fibrillation has limited
effect.




     Table 1, Gross pathologic findings in 273 SCD victims
                                               n                  %
  Abnormal hearts                              197                72
  Obstructive coronary disease                 54                 27
  Valve disease                                31                 16
  Non atherosclerotic coronary disease         28                 14
  Arrhythmogenic RV dysplasia                  27                 13
  Hypertrophic cardiomyopathy                  18                 9
  Aortic rupture                               13                 7
  Dilated cardiomyopathy                       12                 6
  Postoperative congenital heart disease       5                  2.5
  Pulmonary thromboembolism                    4                  2
  Other                                        5                  2.5


  Apparently normal heart                      76                 28

								
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