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					  VULNERABLE
     PATIENT
   SYMPOSIUM
 SCA Risk Factors:
What are the triggers?
            SOBERING STATS
• 30-50% SCD that are due to CAD occur as first
  cardiac event
• 1/3 SCD occur in pts with known CAD or risk
  markers but power insufficient to be useful marker
• Only a small % have well established risk markers
  (ICD trials)
• Therefore, >2/3 unable to predict




 Zipes and Wellens Circ 1998; 98:2334; Myerburg JCE 2002; 13:709;
     PROBLEMS WITH RISK
          FACTORS
• LACK OF SPECIFICITY, SENSITIVITY,
  PREDICTIVE ACCURACY
• ABLE TO IDENTIFY POPULATIONS AT RISK
  BUT NOT INDIVIDUAL
• Present risk factors identify risk of developing SHD
  rather than proximate precipitator
• Need individual-specific predisposition: single
  patient probabilities, not population predictions
• Lack insight into mechanisms of SCD

  Zipes and Wellens Circ 1998; 98:2334; Myerburg JCE 2002; 13:709;
              Risk Factors for SCA
1.   Previous Sudden Cardiac Arrest Event   10   Fatty acid metabolism:
     or Prior Episode of Ventricular             mitochondrial defects
     Tachyarrhythmia (VT)
                                            11   Serum biomarkers:
2.   Decreased LVEF and heart failure
                                                 cytokines, other proteins
3.   Previous Myocardial Infarction
     (MI)/Coronary Artery Disease (CAD)     12   Inflammation: (CRP),
4.   Ventricular Ectopy in Chronic
                                                 troponin
     Ischemic Heart Disease; PVCs during    13   Molecular markers: beta
     recovery from TME                           receptor subtypes
5.   EP/ECG parameters: QTc. QRSd,          14   Genetics: control of
     HRV, BRS, EPS, TWA, SAECG, QT               substrate, thrombosis
     dispersion                                  precipitators, inherited
6.   Atrial fibrillation                         arrhythmias
7.   Smoking                                15   Single nucleotide
8.   Obesity, DM                                 polymorphisms (SNPs): ion
9.   Inactivity                                  channels, other
                                      16         Temperature
     STANDARD                     NEW 17         Perfusion patterns: MRI
                                      18         Heart rate turbulence
  Time Dependence of Mortality Risk
         Post-MI: MADIT-II
                             Conv
                       30    ICD                                       26.7
                       25
                                                         22.1
                       20
                            15.6          15.8                                16.9
         % Mortality




                                                                15.3
                       15          13.8
                                                 9.8
                       10

                        5

                        0
                            1-17 mo       18-50 mo       51-121 mo     > 121 mo
                                                 Time from MI
                           (n = 296)       (n = 284)       (n = 290)    (n = 289)
              Hazard Ratio    1.08            0.56           0.56          0.56
                           (p = 0.81)     (p < 0.001)     (p< 0.001)   (p < 0.001)

David J. Wilber MD, NASPE 2003. Abstract ID. 100865
           Time Dependence of Mortality
                  Risk Post-MI
        Maastricht Circulatory Arrest Registry:
             – In 224 SCA victims, only 4% were
               due to an acute MI.

             – The median time from MI to SCA
               was 9 years in 92 patients
               (41% of total).


Gorgels PMA. European Heart Journal. 2003;24:1204-1209.
WHAT TRIGGERS SUDDEN
     CARDIAC DEATH?
“Why Did He Die On Tuesday
 and Not On Monday? Or On
        Wednesday?”
  Adapted from an editorial (Zipes
 DP Less heart is more. Circulation
   107:2531, 2003) for a paper on
 ventricular remodeling by Pfeffer
          and Braunwald
                       ANATOMIC/FUNCTIONAL                     TRANSIENT INITIATING
                           SUBSTRATE                                 EVENTS

                          Coronary artery disease                     Neuro/endocrine
                          Cardiomyopathy                              Drugs
                                Dilated                               Electrolytes, pH, pO2
                                Hypertrophic                          Ischemia/reperfusion
                          Right ventricular dysplasia
                          Valvular                                    Hemodynamic
                          Congenital                                  Stretch
                          Primary electrophysiological EMD            Arising/Stress/Sleep
                          Neurohumeral                  Asystole      ALCOHOL
                          Developmental                     VT
                          Inflammatory, infiltrative,       VF
                            neoplastic, degenerative, toxic




                                             Reentry
                                             Automaticity
                                             Triggered activity
                                             Block/cell-to-cell uncoupling


Zipes, Wellens
Sudden Cardiac Death
Circulation 1998 Circ 1998; 98:2334
  Zipes and Wellens                     ARRHYTHMIA MECHANISMS
              40 yo man developed incessant SVT after
              second MI and development of RBBB


          Rate 74 bpm                        Rate 81 bpm




                                                   Spontaneous onset SVT




Prystowsky, Heger, Jackman, Naccarelli and Zipes AHJ 103:426-30, 1982
Atrial pre-excitation when His is refractory established
presence of a concealed       accessory pathway




                                   Early A


     AHJ 103:426-30, 1982
                       HV interval 50 ms: AP refractory

                                 REMODELING                REMODELING
                                                           THAT ALTERS
                                                           CONDUCTION
                             74 bpm               81 bpm   BY A FEW MSEC
                                                           CAN PRECIPITATE
                                                           TACHYCARDIA
                                                           IN A SUBSTRATE
                                                           PRESENT BUT
                                                           DORMANT FOR
                                                           YEARS
                       HV interval 90 ms post RBBB:
AHJ 103:426-30, 1982
                       AP conducts and SVT is initiated.
WHY DO SOME PVCs INDUCE VT
     BUT OTHERS DO NOT?
EPICARDIUM IS MORE SENSITIVE
 TO THE EFFECTS OF ISCHEMIA
 THAN IS THE ENDOCARDIUM.

  Transmural Reentry Triggered by Epicardial
  Stimulation during Acute Ischemia in Canine
               Ventricular Muscle
                  Wu J, Zipes DP
            American Journal of Physiology
                283: H2004-11, 2002
       OPTICAL MAPPING

Di-4-Anepps and cytochalasin D
Asymmetrical conduction initiated by epi- & endocardial
         stimulation during acute ischemia
        “WINDOWS OF
     OPPORTUNITY DURING
          ISCHEMIA”
TIMING IS CRITICAL FOR DEVELOPMENT
      OF REENTRANT VT v. NONE
  EPICARDIAL v. ENDOCARDIAL PVCS

Heterogeneity precludes safe and
 effective pharmacotherapy but
    supports benefits of ICDs
    Optical Mapping of the
 Functional Reentrant Circuit of
Ventricular Tachycardia in Acute
     Myocardial Infarction
            Jianyi Wu, MD
       Tamana Takahashi, MD
      Pascal van Dessel, MD, PhD
          William Groh, MD
           John Miller, MD
         Douglas P. Zipes, MD



       SUBMITTED FOR PUBLICATION
Therefore, timing and activation
sequence determine whether or
not VT/VF will occur after MI.

But, can ischemia predispose to
VT/VF via other mechanisms?
     Prior ischemia enhances
  arrhythmogenicity in isolated
canine ventricular wedge model of
            Long QT 3
    Norihiro Ueda, Douglas P. Zipes, Jiashin Wu
Krannert Institute of Cardiology, Indiana Univ. Sch. of
                       Medicine

                 IN PRESS
         CARDIOVASCULAR RESEARCH
              Conclusions
A prior episode of acute ischemia, even
after apparent electrophysiologic
recovery, enhances the arrhythmogenicity of
ATX II (LQT3 model) through the
development of EADs and reentry.
CAN ISCHEMA “SENSITIZE” PATIENTS
WITH LQTS, OR OTHER DISEASE
STATES, TO DEVELOPING SCD?
           TRIGGERS
• MYOCARDIAL EP PROCESSES
  PROBABLY DETERMINE ONSET/LACK
  OF VT/VF/SCD
• DIFFICULT TO MEASURE CLINICALLY;
  INDIRECT EP SURROGATES
• MUST CONTINUE TO RELY ON OTHER
  INDIRECT RISK FACTORS FOR NOW
• BUT MUST HAVE AED DEPLOYMENT
  FOR IMMEDIATE RESPONSE TO SAVE
  LIVES IN THE FORSEEABLE FUTURE

				
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posted:3/31/2011
language:English
pages:20