Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Vulnerable patient mar 04


Published on

SHAPE Society

Published in: Health & Medicine
  • Don't forget another good way of simplifying your writing is using external resources (such as ⇒ ⇐ ). This will definitely make your life more easier
    Are you sure you want to  Yes  No
    Your message goes here
  • I was overwhelmed by all the love and support really. It's such a powerful program and the fact that you make it so personal and affordable is incredible. You are doing a beautiful thing Shaye. It makes me tear up just thinking about the love you are pouring out over this community. ➤➤
    Are you sure you want to  Yes  No
    Your message goes here
  • Be the first to like this

Vulnerable patient mar 04

  1. 1. VULNERABLE PATIENT SYMPOSIUM SCA Risk Factors: What are the triggers?
  2. 2. 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;
  3. 3. 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;
  4. 4. Risk Factors for SCA 1. Previous Sudden Cardiac Arrest Event or Prior Episode of Ventricular Tachyarrhythmia (VT) 2. Decreased LVEF and heart failure 3. Previous Myocardial Infarction (MI)/Coronary Artery Disease (CAD) 4. Ventricular Ectopy in Chronic Ischemic Heart Disease; PVCs during recovery from TME 5. EP/ECG parameters: QTc. QRSd, HRV, BRS, EPS, TWA, SAECG, QT dispersion 6. Atrial fibrillation 7. Smoking 8. Obesity, DM 9. Inactivity 10 Fatty acid metabolism: mitochondrial defects 11 Serum biomarkers: cytokines, other proteins 12 Inflammation: (CRP), troponin 13 Molecular markers: beta receptor subtypes 14 Genetics: control of substrate, thrombosis precipitators, inherited arrhythmias 15 Single nucleotide polymorphisms (SNPs): ion channels, other 16 Temperature 17 Perfusion patterns: MRI 18 Heart rate turbulence STANDARD NEW
  5. 5. 26.7 22.1 15.815.6 16.9 15.3 9.8 13.8 0 5 10 15 20 25 30 1-17 mo 18-50 mo 51-121 mo > 121 mo Conv ICD (n = 296) (n = 284) (n = 290) (n = 289) Hazard Ratio 1.08 (p = 0.81) 0.56 (p < 0.001) 0.56 (p< 0.001) 0.56 (p < 0.001) David J. Wilber MD, NASPE 2003. Abstract ID. 100865 Time Dependence of Mortality Risk Post-MI: MADIT-II Time from MI %Mortality
  6. 6. 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.
  7. 7. 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
  8. 8. ANATOMIC/FUNCTIONALANATOMIC/FUNCTIONAL SUBSTRATESUBSTRATE TRANSIENT INITIATINGTRANSIENT INITIATING EVENTSEVENTS ARRHYTHMIA MECHANISMSARRHYTHMIA MECHANISMS Coronary artery diseaseCoronary artery disease CardiomyopathyCardiomyopathy DilatedDilated HypertrophicHypertrophic Right ventricular dysplasiaRight ventricular dysplasia ValvularValvular CongenitalCongenital Primary electrophysiologicalPrimary electrophysiological NeurohumeralNeurohumeral DevelopmentalDevelopmental Inflammatory, infiltrative,Inflammatory, infiltrative, neoplastic, degenerative, toxicneoplastic, degenerative, toxic Neuro/endocrineNeuro/endocrine DrugsDrugs Electrolytes, pH, pO2Electrolytes, pH, pO2 Ischemia/reperfusionIschemia/reperfusion HemodynamicHemodynamic StretchStretch Arising/Stress/SleepArising/Stress/Sleep ALCOHOLALCOHOL EMDEMD AsystoleAsystole VTVT VFVF ReentryReentry AutomaticityAutomaticity Triggered activityTriggered activity Block/cell-to-cell uncouplingBlock/cell-to-cell uncoupling Zipes and Wellens Circ 1998; 98:2334 Zipes, Wellens Sudden Cardiac Death Circulation 1998
  9. 9. 40 yo man developed incessant SVT after second MI and development of RBBB Prystowsky, Heger, Jackman, Naccarelli and Zipes AHJ 103:426-30, 1982 Spontaneous onset SVT Rate 74 bpm Rate 81 bpm
  10. 10. Atrial pre-excitation when His is refractory established presence of a concealed accessory pathway Early A AHJ 103:426-30, 1982
  11. 11. HV interval 50 ms: AP refractory HV interval 90 ms post RBBB: AP conducts and SVT is initiated. AHJ 103:426-30, 1982 81 bpm74 bpm REMODELING REMODELING THAT ALTERS CONDUCTION BY A FEW MSEC CAN PRECIPITATE TACHYCARDIA IN A SUBSTRATE PRESENT BUT DORMANT FOR YEARS
  12. 12. 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
  13. 13. OPTICAL MAPPING Di-4-Anepps and cytochalasin D
  14. 14. Asymmetrical conduction initiated by epi- & endocardial stimulation during acute ischemia
  15. 15. “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
  16. 16. 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
  17. 17. 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?
  18. 18. 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
  19. 19. 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?