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 Electrocardiogramin 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

LOCUS FINDINGS

APICAL Q in L 1, V2 &V6(all Three Leads)

BASAL R in L1,V2 & V6

POSTEROBASAL POSITIVE PRECORDIAL CONCORDANCE

SUPERIOR INFERIOR AXIS (NL OR RIGHT)

INFERIOR SUPERIOR 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 V5–V6

• 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.

Primary Prevention of SCD in absence of Ventricular Arrhythmias

patients with significant LV dysfunction - best survival with ICD

Indication for ICD class Supporting studyStructural heart disease, sustained VT

Class I AVID, CASH, CIDS

Syncope of undetermined origin, inducible VT or VF at EPS

Class I CIDS

LVEF < 35% due to prior MI, at least 40 days post-MI, NYHA Class II or III

Class I SCD-HeFT

LVEF ≤35%, NYHA Class II or III

Class I SCD-HeFT

LVEF ≤30% due to prior MI, at least 40 days post-MI

Class I MADIT II

LVEF < 40% due to prior MI, inducible VT or VF at EPS

Class I MADIT, MUSTT

Unexplained syncope, significant LV dysfunction, nonischemic CM

Class Iia Expert opinion

Sustained VT, normal or near-normal ventricular function

Class Iia Expert opinion

Hypertrophic CM with 1 or more major risk factors

Class Iia Expert opinion

ARVD/C with 1 or more risk factors for SCD

Class Iia Expert opinion

Cardiac sarcoidosis, giant cell myocarditis, or Chagas diseas

Class iia Expert opinion

VT in non ischemic cardiomyopathyDCM

• 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

trial Inclusion drug TD SD CHFD

Carvedilol HFSG:1094/570

NYHAII-IVEF<35%

Carvedilol 3.125-50mg

65% 55% 79%

CIBIS:2647/317

NYHA III-IVEF<35%

Bisoprolol1.25-10mg

34% 44% 26%

MERIT-HF:3991/1385

NYHA II-IVEF<40%

Metoprolol12.5-25mg/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 CatheterRB Catheter

V Catheter

His Catheter

VT QRS Morphology

Activation Sequence

LBBB H-RB-V-LB

RBBB H-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

Thank you