Ventricular tachycardia in abnormal heart Dolly mathew

VT after MI Sustained monomorphic VT- 3% extensive MI LV dysfunction LV aneurysm septal involvement Successful revascularization - <1%

pathophysiology Anatomic substrate – extensive scar Arises from surviving myocytes Healthy & damaged myocardium interlaced with the fibrous scar at border zone of scar Conduction is slow & discontinuous due to fibrosis & abnormalities in gap junctions gradually develops in the first 2 weeks after myocardial infarction remain indefinitely

Triggers – a/c ischemia - surges in the autonomic tone - heart failure Once sustained monomorphic VT occurs, risk continues indefinitely, even if a/c ischemia & heart failure adequately controlled

Substrate modified by ischemic insults late ventricular remodelling worsening pump function Neurohormonal activation progressive LV dilatation increase in wall tension

Mechanism of ischemic VT Reentry – macro/ micro reentry Repolarization of individual myocardial cells not homogenous Some cells excitable, some refractory

MI Scar-Related Sustained Monomorphic VT Circuit

Sinus rhythm mapping in a patient with VT in the setting of extensive healed AWMI red ( dense scar) = 0.5 mV purple = 1.5 Mv intervening colors represent voltage values in between

In MI Mostly from LV / septum VT - LV apex – RBBB - rt superior axis VT - upper half of septum - LBBB - rt inf axis anterosupr LV – RBBB – Rt inf axis post inf LV – RBBB – Lt supr axis

QRS morphology The more rapid the initial forces, the more likely VT arising from normal myocardium (Josephson & Callans;heart rhythm2004) Slurring of the initial forces – scarring low amplitude VT – diseased myocardium Notching of the QRS – scar qRr, qr, QR complexes – s/o infarct Septal VT less wide QRS

ECG features 12 lead ECGs of 297 LBBB monomorphic VT recorded during catheter ablation ; 95 scar VT, 23 idiopathic Diagnosis of scar based on SR ECG, cardiovascular imaging, & catheter mapping Precordial transition beyond v4, notching of S downstroke in v1/v2, onset of QRS- S nadir v1 >90 ms, were independent predictors of scar related VT scar VT if any of the above criteria met Idiopathic if none In prospective validation,this algorithm was highly sensitive (96%) & specific (83%) for scar LBBB VTs (Adrianus P, Wijnmaalen et al,Circulation may 2011)

Sustained Ventricular Tachycardia:Role of the 12-lead Electrocardiogram in Localizing Site of Origin MARK E. JOSEPHSON, M.D., LEONARD N. HOROWITZ, CIRCULATION 1981 QRS morphology of 41 morphologically distinct VT was correlated with their site of origin as determined by catheter and intraoperative mapping. 12-lead ECG could not precisely identify the site of origin in patients with CAD Could differentiate anterior from posterobasal regions, particularly in VT -LBBB. ECG was less useful in localizing VT-RBBB because of overlapping patterns General QRS patterns were useful in differentiating anterior from posterior regions of origin

LOCUSFINDINGS APICALQ in L 1, V2 &V6(all Three Leads) BASALR in L1,V2 & V6 POSTEROBASALPOSITIVE PRECORDIAL CONCORDANCE SUPERIORINFERIOR AXIS (NL OR RIGHT) INFERIORSUPERIOR AXIS (LEFT OR NORTHWEST)

ECG pattern less likely to predict site of origin in AWMI than with IWMI (37% vs 74% ; p< 0.001) VT-LBBB  on or adjacent to septum VT-RBBB  septal/ free wall location ( 73 vs 31% ; p< 0.001) Relationship between the 12-lead ECG during VT and endocardial site of origin in patients with coronary artery disease; JM Miller ;Circulation 1988;,

The QRS morphology in post-MI VT, study of 100 tracings compared with 70 cases of idiopathic VT ( P. COUMEl, J. F. LECLERCQ, P. ATTUEL and P. MAISONBLANCHE) The two groups of tracings differed in terms of QRS axis, most often normal in idiopathic VT (75%) and abnormal in MIVT (74%) The sum of QRS amplitude in unipolar limb leads was greater in idiopathic VT (4.3±1.3 mv, mean±S.D.) than in MIVT (2.6±0.8 mv, P>0.001) The QRS width was also different: 135±11 ms in idiopathic VT vs. 171±32 ms in MIVT (P>0.001) The QRS morphology in MIVT- QR pattern in leads other than aVR, or a QS pattern in V 5 –V 6 These two aspects were constantly absent in idiopathic VT & present in 89%of MIVT ECG signs of MI observed in the same leads during sinus rhythm and during VT, In only 38 MIVT tracings In 51 MIVT tracings the location of the MI indicated by the VT tracing differed from that displayed in sinus rhythm

Clinical presentation & mgt Determinants of hemodynamic stability- rate, LV fn, ischemia, MR Sedation, i/v medicines, DC cardioversion

Long term mgt Goal of longterm therapy-a) pvt of SCD b) Rec of symp VT Asymptomatic NSVT in pts 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 SECONDARY PVT - Class lll > l - ICD > amio in LVEF<35% CAD-NL LVEF + SUST VT - amio, icd + amio, RFA

subendocardial resection of arrhythmogenic focus Cryoablation Laser vaporization Photocoagulation

Ventricular arrhythmias in the setting of coronary artery disease all available antiarrhythmics except Amiodarone, l-Sotalol and Dofetilide increase mortality in the post MI population

Secondary Prevention of SCD survivors of card arrest or sustained VT- ICD provides the lowest mortality.

Primary Prevention of SCD in Ventricular Arrhythmias a prior MI, dec EF and NSVT -ICD provides the lowest mortality. a prior MI, dec EF and NSVT -ICD provides the lowest mortality.

Primary Prevention of SCD in absence of Ventricular Arrhythmias patients with significant LV dysfunction - best survival with ICD patients with significant LV dysfunction - best survival with ICD

Indication for ICDclassSupporting study Structural heart disease, sustained VT Class IAVID, CASH, CIDS Syncope of undetermined origin, inducible VT or VF at EPS Class ICIDS LVEF < 35% due to prior MI, at least 40 days post-MI, NYHA Class II or III Class ISCD-HeFT LVEF ≤35%, NYHA Class II or III Class ISCD-HeFT LVEF ≤30% due to prior MI, at least 40 days post-MI Class IMADIT II LVEF < 40% due to prior MI, inducible VT or VF at EPS Class IMADIT, MUSTT Unexplained syncope, significant LV dysfunction, nonischemic CM Class IiaExpert opinion Sustained VT, normal or near-normal ventricular function Class IiaExpert opinion

Hypertrophic CM with 1 or more major risk factors Class IiaExpert opinion ARVD/C with 1 or more risk factors for SCD Class IiaExpert opinion Cardiac sarcoidosis, giant cell myocarditis, or Chagas diseas Class iiaExpert opinion

VT in non ischemic cardiomyopathy DCM Asymptomatic VT common Incidence – 50-60% DCM, resp for 8-50% deaths Factors contributing- -myocardial fibrosis, scar -increased circulating catecholamines -increased sympathetic tone -stretch induced afterdepolarizations -Sustained stress induced shortening of refractory period  reentry

Pathophysiology - subendocardial scarring 30% (autopsy), 57% (histology) - Patchy fibrosis intermingled with viable myocardium – substrate for reentry - Basal & mid myocardial LV mechanism - Macro reentry dominant mechanism - BBRVT- most characteristic - 6% vt in all patients, 41% in DCM

Severity of LV dysfunction most impt predictor of mortality Association between QRS prolongation & mortality ( vesnarinone trial ) ACEI – reduction in SCD due to VT, less frequent at 3 months (37% vs 46%); new VT less, at 1,2 yrs in enalapril group (VHeFT-II trial)

Beta blocker therapy trialInclusiondrugTDSDCHFD Carvedilol HFSG:1094/ 570 NYHAII-IV EF<35% Carvedilol mg 65%55%79% CIBIS:2647/ 317 NYHA III-IV EF<35% Bisoprolol mg 34%44%26% MERIT- HF:3991/13 85 NYHA II-IV EF<40% Metoprolol mg/d 34%41%49% relative risk reduction

Amiodarone - Used only on specific arrhythmic indications - Reduces ICD shock frequency, without worsening heart failure (SCDHeFT) Biventricular pacing- severe drug refractory heart failure, in elderly ICD- arrhythmic mortality reduction greater in classiii>ii ( DFINITE TRIAL) -No difference in mortality ( amio vs ICD) - Significant reduction in total mortality in icd group(SCDHeF) LV assist devices – some pts tolerate ventricular arrhythmias well Catheter ablation- failure due to mid myocardial source, critical isthmus, difficult epicardial access

VT in HOCM SCD in adults with HCM- 1% NSVT – 8% Amiodarone improve survival, young pts ( retrospective non randomized trials) ICD implantation is reasonable for patients who have 1 or more major risk factor for SCD. (Level of Evidence: C)

No randomized trials regarding ICD therapy Recom for life threatening VT/VF Pts who have either one of the preceding life threatening arrhythmias or 1 or more other risk factors for SCD -NSVT,FH of premature SCD, unexplained syncope, LV thickness >30mm, abn exercise BP

Macro re-entrant circuit employing – HPS – Both bundle branches – Ramifications of the left bundle – Transeptal myocardium Hallmark: His-Purkinje system disease – functional or structural very fast conduction velocity and a long refractory period Bundle Branch Re-Entry Ventricular Tachycardia

BBR -LBBB -antegrade direction -RB & reterograde LB BBR –RBBB- antegrade direction-LB & reterograde RB

LB Catheter RB Catheter V Catheter His Catheter VT QRS Morphology Activation Sequence LBBBH-RB-V-LB RBBBH-LB-V-RB

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

presyncope, syncope or sudden death - VT with fast rates > 200 bpm LBBB pattern-mc VT morphology VT of myocardial origin vs BBR-LB pattern – rapid intrinsicoid deflection initial ventricular activation through the HPS

BBRVT 1) Sinus rhythm – prolonged HV- prerequisite 2) Every ventricular depolarisation preceeded by His deflections 3) HV interval during tachy ≥ HV interval of the spontaneous normally conducted QRS complexes 4) Documentation of H- RB – V – LB – VT LBBB H- LB –V – RB – VT RBBB

BBR VT

VT

INTERFASCICULAR REENTRY TACHYCARDIA usually has RBBB morphology Antegrade - LAF & retro – LPF –RAD Antegrade- LPF & retro – LAF- LAD

INTERFAS VT Vs RBBB RE ENTRY HV interval shorter than sinus rhythm LB potential before HIS deflections

High recurrence rate after drugs RFA - first line therapy choice is ablation of the RB

VT ARVD Ventricular arrhythmias are usually exercise-related sensitive to catecholamines. right axis deviation, Supr axis,LBBB morph in v1 Multiple morphologies of ventricular tachycardia multiple foci or pathways.

RVOT VT in ARVD

Arrhythmogenic Right Ventricular Cardiomyopathy - ARVC

ARVC 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

ACC/AHA/ESC 2006 guidelines for mgt of vent arrhythmias in ARVD Documented VT/VF on c/c OMT, have reasonable expectation of survival- ICD to prevent SCD – class 1,level of evidence B Severe disease LV inv,FH of SCD,undiagnosed syncope, on c/c OMT-class iia, level of evidence C Amiodarone or sotalol effective, when ICD not feasible – class iia, level of evidence C Ablation can be adjunctive classiia, level of evidence C EP testing might be useful for risk assessment – class iib, level of evidence C

VT with CHD Post op DORV, TOF, TGA Monomorphic, macro reentrant VT Originates from RVOT, conal septum Myocardial fibrosis due to c/c pressure or vol overload- substrate LBBB morphology

VT in cardiac sarcoidosis Mech – reentry Class IIa recommendation for ICD VT in chagas cardiomyopathy rec monomorphic VT mech – reentry ablation ICD – class IIa