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Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp
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  • 1. Dr Ranjith MP Senior Resident Department of CardiologyGovernment Medical college Kozhikode
  • 2. Mechanisms of VTVT arises distal to the bifurcation of the His bundle in the specialized conduction system, ventricular muscle, or combinations of bothDisorders of impulse formation  Enhanced automaticity  Triggered activity Disorders of impulse conduction  Re-entry (circus movements)
  • 3. Mechanisms of VT Disorders of impulse formationEnhanced automaticity  Can occur in virtually all cardiac tissues  Occurs due to increasing the rate of diastolic depolarization or changing the threshold potential  Can arise from cells that have reduced maximum diastolic potentials, often at membrane potentials positive to −50 mV
  • 4. Mechanisms of VT Disorders of impulse formationAutomatic ventricular arrhythmias  Premature ventricular complexes  Ventricular tachycardia associated with:  Acute myocardial infarction or ischemia  Electrolyte and acid-base disturbances, hypoxemia  Increased sympathetic tone
  • 5. Mechanisms of VT Disorders of impulse formationTriggered activityPause-dependent triggered activity  Early afterdepolarization (phase 3)  Polymorphic ventricular tachycardiaCatechol-dependent triggered activity  Late afterdepolarizations (phase 4)  Idiopathic right ventricular tachycardia
  • 6. Mechanisms of VT Disorders of impulse formationTriggered activity Figure A :- Early afterdepolarizations in phase 3 of the AP Figure B :- Late afterdepolarizations seen in late phase 3 or phase 4 of the AP
  • 7. Mechanisms of VT Disorders of impulse conductionRe-entry (circus movements) Electrical Impulse Cardiac Conduction Tissue Fast Conduction Path Slow Conduction Path Slow Recovery Fast Recovery  Two distinct pathways that come together at beginning and end to form a loop  A unidirectional block in one of those pathways  Slow conduction in the unblocked pathway
  • 8. Mechanisms of VT Disorders of impulse conduction Premature Beat Impulse CardiacRepolarizing Tissue (long Conductionrefractory period)) TissueFast Conduction Path Slow Conduction PathSlow Recovery Fast Recovery An arrhythmia is triggered by a premature beat The fast conducting pathway is blocked because of its longrefractory period so the beat can only go down the slowconducting pathway
  • 9. Mechanisms of VT Disorders of impulse conductionRe-entry (circus movements) Cardiac Conduction Tissue Fast Conduction Path Slow Conduction Path Slow Recovery Fast Recovery The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway
  • 10. Mechanisms of VT Disorders of impulse conductionRe-entry (circus movements) Cardiac Conduction Tissue Fast Conduction Path Slow Conduction Path Slow Recovery Fast Recovery  On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit
  • 11. Mechanisms of VT Disorders of impulse conductionReentrant ventricular arrhythmias  Premature ventricular complexes  Idiopathic left ventricular tachycardia  Bundle branch reentry  Ventricular tachycardia and fibrillation when associated with chronic heart disease:  Previous myocardial infarction  Cardiomyopathy
  • 12. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 13. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 14. Healed MI is the most frequent clinical setting for the development of sustained VTThe first episode of VT can occur years after infarct healingClinical presentation- tolerated sustained VT to SCDIncidence reduced from 3% to 1%
  • 15. Focal activation by abnormal automaticity in the ischemic border zonea/c ischemia activates KATP channels causing an increase in extracellular K along with acidosis and hypoxia in the cardiac muscleMinor increases in extracellular K depolarize the myocardiocyte’s RMP , which can increase tissue excitability in early phases of ischemia
  • 16. Focal discharge by Ca overload & triggered activity in the form of delayed or early after-depolarizations - not been proven experimentally
  • 17. Reentry is the mechanism underlying the VT associated with healed or healing MI (>95%)  The ability to reproducibly initiate and terminate VT with programmed ventricular extrastimuli- the sine qua non of reentry  Induction of VT in coronary disease is stimulation site specific  An inverse relationship of the extrastimulus coupling interval to the onset of the first tachycardia beat is observed in many VTs
  • 18. Important determinants of arrhythmia risk after MI  The extent of myocardial necrosis  Presence of septal involvement  Degree of left ventricular dysfunctionAnatomic substrate – extensive scarVT consistently arises from surviving myocytes within extensive areas of infarction Conduction is slow & discontinuous, owing to fibrosis and abnormalities in gap junction distribution & function
  • 19. Electrophysiologic substrate for VT develops in the first 2 weeks after MI - remain indefinitelyTriggers – Acute ischemia – Surges in the autonomic tone – Heart failureOnce sustained monomorphic VT occurs, risk continues indefinitely, even if acute ischemia & heart failure are adequately controlled Josep Brugada et al JACC Vol. 37, No. 2, 2001:529–33
  • 20. Reentry – macro/ micro reentryRepolarization of individual myocardial cells not homogenous. Some cells excitable, some refractory
  • 21. Sinus rhythm mapping in a patient with VT in the setting of extensive healed anteriorinfarction. The map is color-coded to represent bipolar electrogram voltage: red (representingdense scar) denotes = 0.5 mV, purple = 1.5 mV, and the intervening colors represent voltagevalues in between. Multiple inducible VTs of varied morphology were localized tocircuits within the scar
  • 22. In the setting of an old MI, the ECG during VT is affected by  The size of infarction  The region of infarction  The region within the scar where the circuit is located  The proximity to the His-Purkinje system  The influence of concomitant pharmacological agents
  • 23. Presence of Q waves (qR, QR or Qr) in related leads Notched or wide QRS complexes Low QRS voltage Multiple ventricular tachycardia morphologies Paroxysmal sustained episodes
  • 24. Surface ECG tends to locate the reentry circuit exit rather than the VT originLocation should be defined in 3 axes:  septal vs lateral walls  superior vs inferior walls  apical vs basal regionsBundle branch block patterns -sequence of ventricular activation
  • 25. Lateral wall VT  RBBB pattern  Wider QRS complexesSeptal VT  LBBB pattern  Narrower QRS complexes
  • 26. The QRS axis in inferior leads indicates the sequence of activation between the superior and inferior walls Inferior MI  Superior axis (80%)Anterior MI  Superior axis (55% )  Inferior axis (45%)
  • 27. Predominant polarity of QRS complexes in precordial leads can help discriminate between VTs from the basal or the apical regionsVT from the apex  Negative concordant R progressionVT from the basal  Positive concordant R progression
  • 28. The key determinant of hemodynamic tolerance  Tachycardia rate  Left ventricular function  Development of ischemia, and mitral insufficiencyHemodynamic collapse – cardioversionIntravenous procainamide, sotalol, and amiodarone have been demonstrated to have superior efficacy
  • 29. Goal of long-term therapy- prevention of SCD & recurrence of symptomsAsymptomatic NSVT with NLVEF- no treatmentSymptomatic NSVT in pts with NLVEF- betablockersCardiac arrest survivors / SUS VT in ↓LVEF- ICDPrimary pvt - ICD > Amiod- pvt of SCD
  • 30. subendocardial resection of arrhythmogenic focusCryoablationLaser vaporizationPhotocoagulation
  • 31. Patients resuscitated from VF when coronaryrevascularization is not possible, and there is evidence ofprior MI and significant LV dysfunction I IIa I IIa IIbIIb III III LV dysfunction due to MI who present withhemodynamically unstable VT I IIa I IIa IIb IIb III IIIPrimary prevention - LV dysfunction due to prior MI whoare at least 40 days post-MI and have an LVEF 30%-40% &NYHA II or III I I IIa IIa IIb IIb III III
  • 32. Primary prevention ICD is reasonable in patients with LVdysfunction due to prior MI who are at least 40 days post-MI,and have an LVEF 30%-35% & NYHA I I IIa I IIa IIb IIb III III ICD implantation is reasonable in patients with post-MIwith normal LV function and recurrent VT I I IIa IIa IIb IIb III III
  • 33. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 34. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 35. DCM has a propensity to the development of ventricular arrhythmias and sudden deathIncidence of DCM - 4 to 8 cases per 100,000 populationIncidence of VT – 50-60% DCM, resp for 8-50% deathsGenetics - Relationship between individual genotypes and arrhythmogenicity is poorly understood
  • 36. Multiple factors responsible for VT in DCM
  • 37. Myocardial fibrosis/scar - may act as sites for reentry  At autopsy, extensive subendocardial scarring in the LV in 33% & multiple patchy areas of replacement fibrosis in 57%Sustained stretch-induced shortening of refractory period and AP duration, predisposing to reentryShort, pulsatile, stretch-induced after depolarizations
  • 38. Diastolic Ca overload caused by decreased sacrcoplasmic reticulum Ca2+–adenosine triphosphatase pumpAfterdepolarizations induced by increased Na+-Ca2+ exchanger activityHypokalemia, hypomagnesemia (often related to diuretic use)Increased circulating catecholamines
  • 39. Increased sympathetic tonePurkinje system conduction delay Increased endocardial surface area in dilated atrium or ventricle Drugs (antiarrhythmics, digoxin, sympathomimetic)
  • 40. Macro reentry - dominant mechanismBundle branch reentry ventricular tachycardia (BBRVT) is the most characteristicBBRVT - Responsible for VT in up to 41% of DCMMacro-reentrant circuit involving the His-Purkinje system, usually with antegrade conduction over the RBB and retrograde conduction over the LBB
  • 41. Severity of LV dysfunction - most powerful predictorSCD is significantly greater in patients with syncope Laboratory values - low serum sodium and increased plasma norepinephrine, renin, and ANP,BNPLBBB & of first- and second-degree AV block has been associated with poor outcome
  • 42.  Vesnarinone Trial (VEST) showed a significant association between the degree of QRS prolongation and mortality Gottipaty V, et al. J Am Coll Cardiol 33:145A, 1999
  • 43. ACEI – reduction in SCD due to VT (37% vs 46%) new VT developed less frequent at 1,2 yrs in enalapril group (VHeFT-II trial)
  • 44. Amiodarone  Used only on specific arrhythmic indications  Reduces ICD shock frequency , without worsening heart failure (SCDHeFT)Implantable Cardioverter-Defibrillators  AMIOVIRT- No difference in mortality ( amio vs ICD)  SCD-HeFT - Significant reduction in total mortality in ICD groupCatheter ablation
  • 45. Biventricular pacing- severe drug refractory heart failure , in elderly  Improve systolic function by shortening the duration of mechanical systole and increasing dP/dt  Improve diastolic function by prolonging diastolic filling time  Reduce presystolic MR by earlier activation of the lateral papillary muscle without the adverse effect on the sympathetic nervous system seen with inotropic agents
  • 46. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 47. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 48. Commonly occurs in disease with severe LV dysfunction like DCM & conduction abnormalities in the HPSBBR VT may also be seen in:  Myotonic dystrophy  Hypertrophic cardiomyopathy  Ebstein anomaly  Following valvular surgery  Proarrhythmia due to Na channel blockers Presyncope, syncope or sudden death - VT with fast rates > 200 bpm
  • 49. Macro re-entrant circuit employing  His Bundle  Both bundle branches  Ramifications of left bundle  Transeptal myocardium
  • 50. May present with LBBB or RBBB morphology depending on the antegrade conductionLBBB morphology is common BBR –LBBB: - antegrade direction -RB & reterograde LB BBR –RBBB:- antegrade direction-LB & reterograde RB
  • 51. VT QRS Activation Morphology SequenceLBBB LB-H-RB-VRBBB RB- H-LB-V
  • 52. Surface ECG in sinus rhythm - non-specific or typical bundle branch block patterns with prolonged QRS durationTotal interruption of conduction in one of the BB would theoretically prevent occurrence of reentryCan occur in patients with relatively narrow QRS complex - functional conduction delay
  • 53. Electrophysiologic features During tachy QRS morphology is commonly LBBB type His electrograms precede each V HV interval during tachycardia > HV in baseline Changes in V–V interval follow the changes in H–H Delay in HPS conduction facilitates induction
  • 54. Electrophysiologic features
  • 55. Electrophysiologic featuresBlock in Bundle branches or HPS will terminate the tachy Ablation of RB renders tachycardia noninducibleVT of myocardial origin mimics BBR-LB pattern VT – can be differentiated by the presence of rapid intrinsicoid deflection due to initial ventricular activation through the HPS in the later
  • 56. The reentrant circuit involves superior and inferior division of the left bundleRBBB and anterior or posterior fascicular block is present during sinus rhythmusually has RBBB morphologyAntegrade - LAF & retro – LPF –RADAntegrade- LPF & retro – LAF- LAD
  • 57. HV interval shorter than sinus rhythmLB potential before HIS deflections
  • 58. High recurrence rate after drugsRFA - first line therapy Treatment of choice for BBR VT is ablation of the RBA PPI should be implanted if the post-ablation HV interval is 100 ms or longerICD implant should be considered if myocardial VT occur spontaneously or are inducible or if EF < 35%
  • 59. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 60. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 61. Most frequent – ARVDExtensive myocardial fibrosis - substrate for reentry RV outflow tract RV apex RV inflow segments Marcus fi et al.Circulation 1982; 65:384–398
  • 62. ECG in sinus rhythm1. Prolonged QRS duration ≥ 110 ms in V1-V3 (Sens-55%, Spec-100%)2. T wave inversion in right precordial leads (Seen in 60%)3. Epsilon wave (Seen in 30%)4. Low-voltage QRS amplitude (Indicate severe cases)
  • 63. Ventricular arrhythmias are usually exercise-relatedSensitive to catecholaminesMost Common- LBBB morphology VTUp to 12 VT morphologies have been reported in a single patientRBBB VT - LV involvement or a left septal breakthrough site
  • 64. VT in ARVD may be confused with RVOT VT O’Donnell D ET et al. Eur Heart J. 2003;24:801-810, 2003.
  • 65. High Risk FeaturesYounger patientsRecurrent syncopeHistory of cardiac arrest or sustained VTClinical signs of RV failure or LV involvementPatients with or having a family member with the high risk ARVD gene (ARVD2)Increase in QRS dispersion ≥ 40 msec  QRS dispersion = max measured QRS minus min measured QRS
  • 66. Documented VT/VF on c/c OMT, have reasonable expectation of survival- ICD to prevent SCD I I IIa IIa IIa IIb IIb III III BSevere disease LV inv, FH of SCD, undiagnosed syncope, on c/c OMT I I IIa IIa IIa IIb IIb III III CAmiodarone or sotalol effective , when ICD not feasible I I IIa IIa IIa IIb IIb III III CAblation can be adjunctive I I IIa IIa IIa IIb IIb III III CEP testing might be useful for risk assessment I I IIa IIa IIa IIb IIb III III C
  • 67. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 68. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 69. SCD in adults with asymptomatic HCM- 1% NSVT – 8%On 24-hr Holter -90% have ventricular arrhythmias Prevalence of ventricular and supraventricular arrhythmias on 24-hour Holter recording in 178 patients from a community-based population of patients with hypertrophic cardiomyopathy J Am Coll Cardiol 45:697-704, 2005
  • 70. In LVH action potential prolongation is due to a decrease in Ito. This results in nonhomogeneous repolarization and propensity for EAD Hypertrophied myocytes may produce DAD due to an increase in Ca loadAbnormal pacemaker current (If) has been reported in LVH. Intensity of this current increases with beta adrenergic stimulationIn LVH the density of Ito is reduced. The density of ICaL and IK is unchanged and density of If is increased
  • 71. Pharmacologic Treatment  Beta-blockers, verapamil, amiodarone  Long term prophylactic pharmacologic therapy now not recommended in high-risk populationICD implantation is reasonable for patients who have 1 or more major risk factor for SCD. (Level of Evidence: C)
  • 72. 1. Family history of premature HCM-related death2. Unexplained syncope, particularly in young patients, or if demonstrated to be arrhythmia-based3. Frequent, multiple, or prolonged episodes of NSVT4. Hypotensive or attenuated BP response to exercise5. Extreme LVH with maximum wall thickness ≥ 30 mmPresence or magnitude of LVOT obstruction has not proved to be aconsistently strong independent risk factor for SCD in HCM and thereforedoes not constitute a sole justification for prophylactic ICD implantation
  • 73. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 74. Coronary Artery DiseaseDilated CardiomyopathyBundle Branch Re-entry Ventricular TachycardiaArrhythmogenic Right Ventricular CardiomyopathiesHypertrophic CardiomyopathyAfter Surgery for Congenital Heart Disease
  • 75. Ventricular Tachycardia in Patients after Surgery for Congenital Heart DiseaseMost information concerning patients with VT and congenital heart disease pertains to TOFVT in these patients are due to the effect of  Years of chronic cyanosis  Presence of a ventriculotomy  Elevation of RV pressures  Severe pulmonic regurgitation with RV dysfunctionThese factors lead to myocardial fibrosis, resulting reentrant circuits
  • 76. Ventricular Tachycardia in Patients after Surgery for Congenital Heart DiseaseMechanism of VT is reentry involving the RVOT, either at the site of anterior rt. ventriculotomy or at VSD patchThe incidence of VT significantly higher in patients with RVSP >60 mm Hg and RVEDP > 8 mm HgZeltser et al showed RV volume overload is the most important predictor of inducible ventricular arrhythmias J Thorac Cardiovasc Surg 130:1542-1548, 2005
  • 77. Ventricular Tachycardia in Patients after Surgery for Congenital Heart DiseaseThe risk of VT can be assessed by QRS duration Syncope & VT- squares Sudden death- triangles Syncope with Afl- star Gatzoulis MA et al. Circulation 95:401-404, 1997
  • 78. Ventricular Tachycardia in Patients after Surgery for Congenital Heart Disease TreatmentAntiarrhythmics medicationRadiofrequency catheter ablationSurgical CryoablationICD implantationA combined approach of correcting significant structural abnormalities with intra-operative EP-guided ablation may reduce the potential risk of deterioration in ventricular function
  • 79. References- Journal1. Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease. John M. et al. Circulation 77, No. 4, 759-766, 1988.2. Coronary Artery Revascularization in Patients With Sustained Ventricular Arrhythmias in the Chronic Phase of a Myocardial Infarction: Effects on the Electrophysiologic Substrate and Outcome. Josep Brugada et al JACC Vol. 37, No. 2, 2001:529–333. Ventricular Tachycardia in Coronary Artery Disease . B. Benito, M.E. Josephson / Rev Esp Cardiol. 2012;xx(x):xxx–xxx4. Role of Ablation Therapy in Ventricular Arrhythmias. Mithilesh K. Das et al. Cardiol Clin 26 (2008) 459–4795. Ventricular Arrhythmias in Heart Failure Patients Ronald Lo, Henry H. Hsia. Cardiol Clin 26 (2008) 381–403
  • 80. References- Journal5. A Comprehensive Approach to Management of Ventricular Arrhythmias, Fred Kusumoto. Cardiol Clin 26 (2008) 481–4966. Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease, J M Miller et al. Circulation. 1988;77:759-7667. Arrhythmogenic right ventricular cardiomyopathy: A cause of sudden death in young people, A. Thomas mcrae et al, Cleveland clinic journal of medicine volume 68 ,No.5, 2001:459-4678. Ventricular arrhythmias in idiopathic dilated cardiomyopathy K Von Olshausen et al. Br Heart J 1984; 51: 195-2019. Non-Sustained Ventricular Tachycardia in Hypertrophic Cardiomyopathy: An Independent Marker of Sudden Death Risk in Young Patients. Lorenzo Monserrat et al, Vol. 42, No. 5, 2003:873–910. Sustained Ventricular Tachycardia in Adult Patients Late After Repair of Tetralogy of Fallot. David A. Harrison et al. JACC Vol. 30, No. 5,November 1, 1997:1368–73
  • 81. References – Text Books1. Zipes 5th ed. Cardiac Electrophysiology From Cell to Bedside2. Basic Cardiac Electrophysiology for the Clinician .2nd ed. José Jalife, MD3. Clinical arrhythmology and electrophysiology: a companion to Braunwald’s heart disease 8th ed.4. Handbook of Cardiac Electrophysiology. Andrea Natale MD.5. Management of Cardiac Arrhythmias, edited by Leonard I. Ganz, MD, 2002
  • 82. THANK YOU
  • 83. MCQ-1True statement regarding AVRDA. Ventricular arrhythmias are usually exercise-relatedB. Sensitive to catecholaminesC. Most Common- LBBB morphology VTD. All are true
  • 84. MCQ-1True statement regarding AVRDA. Ventricular arrhythmias are usually exercise-relatedB. Sensitive to catecholaminesC. Most Common- LBBB morphology VTD. All are true
  • 85. MCQ-212 lead ECG of BBR-VT is given below. The antegrade conduction through------------A. Right bundle branchB. Left bundle branchC. Left posterior fascicleD. Left anterior fascicle
  • 86. MCQ-212 lead ECG of BBR-VT is given below. The antegrade conduction through------------A. Right bundle branchB. Left bundle branchC. Left posterior fascicleD. Left anterior fascicle
  • 87. MCQ-3 Exists site of the VT circuit given below is ?A. LV lateral wallB. SeptumC. Right ventricleD. Both B & C
  • 88. MCQ-3 Exists site of the VT circuit given below is ?A. LV lateral wallB. SeptumC. Right ventricleD. Both B & C
  • 89. MCQ-4A 45yr old smoker with past history of hospitalization for chest pain presented to causality with palpitation and hypotension. Patient was stabilized with DC cardio version and taken to echo lab. His presentation ECG shown below. Echo likely to show?A. LV apical aneurysmB. RWMA anterior wallC. RWMA Inferior wallD. RV outflow aneurysm
  • 90. MCQ-4A 45yr old smoker with past history of hospitalization for chest pain presented to causality with palpitation and hypotension. Patient was stabilized with DC cardio version and taken to echo lab. His presentation ECG shown below. Echo likely to show?A. LV apical aneurysmB. RWMA anterior wallC. RWMA Inferior wallD. RV outflow aneurysm
  • 91. MCQ-5A 39 yr old smoker with hypotension in ED was stabilized with DC cardio version and his echo is shown below(Left side) . His presentation ECG is most likely to be ? B A C D
  • 92. MCQ-5A 39 yr old smoker with hypotension in ED was stabilized with DC cardio version and his echo is shown below(Left side) . His presentation ECG is most likely to be ? B A C D
  • 93. MCQ-6All are true about BBR- VT except?A. High recurrence rate after drugsB. Treatment of choice for BBR VT is ablation of the RBC. Usually has LBBB morphologyD. V precede each his electrograms
  • 94. MCQ-6All are true about BBR- VT except?A. High recurrence rate after drugsB. Treatment of choice for BBR VT is ablation of the RBC. Usually has LBBB morphologyD. V precede each his electrograms
  • 95. MCQ-7VT in post TOF repair patients are due to the effect of all except? A. Years of chronic cyanosis B. Presence of a ventriculotomy C. Elevation of RV pressures D. Severe pulmonic regurgitation with RV dysfunction E. None
  • 96. MCQ-7VT in post TOF repair patients are due to the effect of all except? A. Years of chronic cyanosis B. Presence of a ventriculotomy C. Elevation of RV pressures D. Severe pulmonic regurgitation with RV dysfunction E. None
  • 97. MCQ-8 Sudden death risk factors in HCM are all except?A. Family history of premature HCM-related deathB. Unexplained syncope, particularly in young patients, or if demonstrated to be arrhythmia-basedC. Hypotensive or attenuated BP response to exerciseD. Presence or magnitude of LVOT obstruction
  • 98. MCQ-8 Sudden death risk factors in HCM are all except?A. Family history of premature HCM-related deathB. Unexplained syncope, particularly in young patients, or if demonstrated to be arrhythmia-basedC. Hypotensive or attenuated BP response to exerciseD. Presence or magnitude of LVOT obstruction

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