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Electrical Storm in Coronary Artery Disease Saeed Oraii MD, - PowerPoint PPT Presentation

Electrical Storm in Coronary Artery Disease Saeed Oraii MD, Cardiologist Interventional Electrophysiologist Tehran Arrhythmia Clinic July 2016 48 yrs. Old diabetic with ACS 48 yrs. Old diabetic with ACS 48 yrs. Old diabetic with ACS 48


  1. Electrical Storm in Coronary Artery Disease Saeed Oraii MD, Cardiologist Interventional Electrophysiologist Tehran Arrhythmia Clinic July 2016

  2. 48 yrs. Old diabetic with ACS

  3. 48 yrs. Old diabetic with ACS

  4. 48 yrs. Old diabetic with ACS

  5. 48 yrs. Old diabetic with ACS

  6. 48 yrs. Old diabetic with ACS

  7. Prevalence • Ventricular arrhythmias are common complications of acute coronary syndrome. • They occur in almost all patients, even before monitoring is possible. • They are related to the formation of re-entrant circuits at the confluence of the necrotic and viable myocardium, as well as to irritable ischemic myocardium.

  8. Prevalence • Premature ventricular contractions occur in approximately 90% of patients with ACS. • At the other end of the spectrum, the incidence of VF is reported as approximately 2% to 4%. • The incidence of VF in patients with ACS seen in CCUs over the past three decades appears to have declined.

  9. Reperfusion Arrhythmias • Ventricular arrhythmias happens more commonly in reperfused patients. • Among patients who underwent fibrinolytic therapy in the GUSTO-I study, approximately 10% experienced VT/VF. • In the APEX-AMI study, which included patients treated with primary PCI, sustained VT/VF developed in 5.7%. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries Assessment of Pexelizumab in Acute Myocardial Infarction

  10. Warning Arrhythmias • Frequent ventricular premature complexes (PVCs) of more than five per minute, PVCs with a multiform configuration, early coupling (the “R -on- T” phenomenon), and repetitive patterns in the form of couplets or salvos were thought to precede VF. • The previous practice of prophylactic suppression of PVCs with antiarrhythmic drugs is not indicated and may actually increase the risk for fatal bradycardic and asystolic events.

  11. AIVR • An accelerated idioventricular rhythm (AIVR) typically occurs during the first 2 days, with about equal frequency in anterior and inferior infarctions. • Most episodes are of short duration.

  12. AIVR • Accelerated idioventricular rhythm is often observed shortly after successful reperfusion has been established with fibrinolytic therapy. • In contrast to rapid VT, accelerated idioventricular rhythm is thought not to affect prognosis, and does not need to be treated routinely except in rare occasions when it is associated with hemodynamic deterioration.

  13. Prognosis • Clinical outcomes are worse in patients with VT/VF than in those without. – Additionally, mortality rates are worse in those with early versus late VT/VF; specifically, when compared with patients without VT/VF. • The risk for mortality at 90 days increases twofold in patients with both early and late VT/VF, respectively. Mehta RH et al: Incidence of and outcomes associated with ventricular tachycardia or fibrillation in patients undergoing primary percutaneous coronary intervention. JAMA 301:1779, 2009.

  14. Anti-arrhythmic drugs • Routine prophylaxis with anti-arrhythmic drugs is not recommended and may worsen the clinical course. • Early administration of an intravenous beta blocker effectively reduces the incidence of VF in cases of evolving MI. Mehta RH et al: Incidence of and outcomes associated with ventricular tachycardia or fibrillation in patients undergoing primary percutaneous coronary intervention. JAMA 301:1779, 2009.

  15. Acute Treatment • Successful interruption of unstable ventricular arrhythmias or prevention of refractory recurrent episodes can be facilitated by the intravenous administration of amiodarone. • Bicarbonate injections to correct acidosis are not usually necessary because of the high osmotic load that they impose and because hyperventilation of the patient is probably a more suitable means of clearing the acidosis.

  16. Correction of Underlying Causes • After reversion to sinus rhythm, every effort should be made to correct any underlying abnormalities such as hypoxia, hypotension, acid-base or electrolyte disturbances, and digitalis excess. • Urgent attempts at revascularization are warranted if ventricular arrhythmias are ongoing and caused by ischemia.

  17. Electrical Storm • Definition: – Three or more episodes of ICD therapies in 24 hours – No ICD: >2 unstable events in 24hrs – Incessant VT lasting for hours • Highly lethal • Frequent in VT, rare in VF • Rare during ACS • 10-20% of ICD recipients

  18. Timing of Events • 10-28% over 1-3yr follow up • AVID 20% – avg 9.2 months • • MADIT II 4% – avg 11 months 83% episodes < 1 hour apart Time Between Ventricular Arrhythmias, Wood et al. J Cardiovasc Electrophysiol 2005

  19. Shocks & Electrical Storm are bad! N Engl J Med. 2008 Sep 4;359(10):1009-17.

  20. Shocks & Electrical Storm are bad! Sesselberg et al. Heart rhythm 2007;4 1395-1402

  21. Shocks & Electrical Storm are bad! Gatzoulis et al. Europace 2005: 7: 184-192 • AVID death RR 2.4 • MADIT II death RR 7.4

  22. Predictors • VT or VF as indication for ICD • EF < 25% • Chronic renal failure • QRS >120 msec • Absence beta blocker therapy • Use of digoxin • Absence of revascularization after index arrhythmia • CAD Exner et al. Circ 2001, Brigadeau et al. EHJ 2005, Arya et al. AJC 2006, Verma et al. JCE 2004

  23. VT Morphologies • Monomorphic VT 86-97% Think Reentry • Polymorphic Ventricular Tachycardia 2-8% • Ventricular Fibrillation 1-21% Think metabolic, drugs, ischemia, brady

  24. Always look for treatable cause... • Ischemia • Electrolyte disturbance • Decompensated heart failure • Drugs, proarrhythmia • Pacing induced, Biventricular pacing • “Pseudo -Storm ” - inappropriate therapies • Unknown – approximately 66% cases

  25. Bradycardia & Torsade

  26. CHB & VF

  27. Brugada Syndrome • Isoproterenol • Normalizes ECG • Prevents VF induction • The recommended treatment in electrical storms

  28. Isoproterenol in Brugada Syndrome

  29. Drug Therapy • Amiodarone • Beta blockers • Lidocaine • Mexiletine • Quinidine • Procainamide

  30. Drug therapy • Amiodarone – 18% stopped • Sotalol – 24% stopped • Carvedilol, Bisoprolol – 5% stopped

  31. Device Programming may help • Avoid shocks • 3 zones • Longer detection • ATP for faster VT • ATP only in slower zones/tolerated VT Heart Rhythm, Volume 7, Issue 3, March 2010, Pages 353-360

  32. Adjunctive Measures • Sedation or General anesthesia – Propofol • Left stellate ganglion denervation

  33. What about Defibrillators • ICD implantation is virtually contraindicated during a VT storm.

  34. When other options don’t work....

  35. Emergent Catheter Ablation • A promising therapy for electrical storm

  36. VT Mechanisms • The majority of sustained monomorphic VTs in patients with structural heart disease are due to reentry (scar related reentry). Isthmus Exit site Bystander site Outer loop

  37. Concealed Entrainment Presystolic Potentials

  38. Termination with Burn

  39. Multiple VT Morphologies

  40. Mapping the Unmappable • 3 dimensional Voltage maps are created with High- density electroanatomic mapping of electrogram amplitude. Low-voltage regions (1.5 mV in bipolar recordings) identify areas of scar. • A potential isthmus or channel within low-voltage regions can also be identified during sinus rhythm, suggested by local abnormal ventricular activities (LAVA) during sinus rhythm or ventricular pacing, low-amplitude isolated potentials and late potentials inscribed after the end of the QRS complex. • During sinus rhythm the exit can often be located by pace mapping along the scar border.

  41. Changing Voltage Scales 0.5-1.5 mV 0.1-0.5 mV

  42. LAVA in Substrate Ablation of VT

  43. LAVA & Presystolic Potentials

  44. Polymorphic VT/VF Ablating the Triggers • Mapping PVCs may be used as a “surrogate” for mapping during VT to identify critical areas in scar-related VT. • This approach assumes that frequent PVCs occur via the same reentrant pathway as VT in patients with scar related VT. • Hence, identification of the site of origin of the PVC should identify the exit site of the VT.

  45. Surrogate PVCs Bogun F, et al. Relationship of frequent post-infarction premature ventricular complexes to the reentry circuit of scar-related ventricular tachycardia. Heart Rhythm 2008;5:367 – 374.

  46. Repeated VT

  47. Targeting PVCs Purkinje related?

  48. Burn

  49. Triggers for Initiation of VT/VF Szumowski L, et al. JACC 2004

  50. Purkinje Fiber-Mediated VT Post Infarction • A relatively narrow QRS duration during VT • Verapamil sensitivity • Presystolic or diastolic Purkinje potentials during VT • VT termination by a single or a few RF energy applications to that site. Bogun F, et al. Role of Purkinje fibers in post-infarction ventricular tachycardia. J Am Coll Cardiol 2006; 48:2500 – 2507.

  51. Purkinje-related Triggers • Purkinje potentials precede the ventricular activation during both sinus and PVCs. Szumowski L, et al. JACC 2004

  52. Purkinje-related VT/VF

  53. Purkinje-related Triggers

  54. Purkinje-related Triggers, Pace Map

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