Ventricular tachycardia in abnormal heart

Ventricular tachycardia in abnormal heart
Dr Ranjith MP Senior Resident Department of Cardiology Government Medical college Kozhikode

Ventricular tachycardia in abnormal heart OUTLINE
Coronary Artery Disease Dilated Cardiomyopathy Bundle Branch Re-entry Ventricular Tachycardia Arrhythmogenic Right Ventricular Cardiomyopathies Hypertrophic Cardiomyopathy After Surgery for Congenital Heart Disease

VT in Patients with CAD 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%

VT in Patients with CAD Mechanism of VT in a/c ischemia
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

VT in Patients with CAD Mechanism of VT in a/c ischemia
Focal discharge by Ca overload & triggered activity in the form of delayed or early after-depolarizations - not been proven experimentally

VT in Patients with CAD Mechanism
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

VT in Patients with CAD Pathophysiologic Substrate
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

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

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

VT in Patients with CAD Sustained Monomorphic VT Circuit

Sinus rhythm mapping in a patient with VT in the setting of extensive healed anterior infarction. The map is color-coded to represent bipolar electrogram voltage: red (representing dense scar) denotes = 0.5 mV, purple = 1.5 mV, and the intervening colors represent voltage values in between. Multiple inducible VTs of varied morphology were localized to circuits within the scar

VT in Patients with CAD ECG findings
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

VT in Patients with CAD ECG evidence of MI
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

VT in Patients with CAD Identifying the VT origin
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

Lateral wall VT RBBB pattern Wider QRS complexes Septal VT LBBB pattern Narrower QRS complexes

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%)

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

VT in Patients with CAD Clinical Presentation & Management
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

VT in Patients with CAD Long-Term Management
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

subendocardial resection of arrhythmogenic focus Cryoablation Laser vaporization Photocoagulation

Major ICD trials in patients with CAD

Primary Prevention of SCD in absence of Ventricular Arrhythmias

Current recommendations for ICD implantation in the setting of CAD
Patients resuscitated from VF when coronary revascularization is not possible, and there is evidence of prior MI and significant LV dysfunction LV dysfunction due to MI who present with hemodynamically unstable VT Primary prevention - LV dysfunction due to prior MI who are at least 40 days post-MI and have an LVEF 30%-40% & NYHA II or III I IIa IIb III A I IIa IIb III A I IIa IIb III A

Current recommendations for ICD implantation in the setting of CAD
Primary prevention ICD is reasonable in patients with LV dysfunction due to prior MI who are at least 40 days post-MI, and have an LVEF 30%-35% & NYHA I ICD implantation is reasonable in patients with post-MI with normal LV function and recurrent VT I IIa IIb III B I IIa IIb III \ C

VT in Patients with DCM 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

VT in Patients with DCM Arrhythmogenesis
Multiple factors responsible for VT in DCM

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

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

Increased sympathetic tone Purkinje system conduction delay Increased endocardial surface area in dilated atrium or ventricle Drugs (antiarrhythmics, digoxin, sympathomimetic)

VT in Patients with DCM Mechanisms
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

VT in Patients with DCM Predictors of Mortality &Ventricular Arrhythmias
Severity of LV dysfunction - most powerful predictor ISCD 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

VT in Patients with DCM Predictors of Mortality &Ventricular Arrhythmias
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

VT in Patients with DCM Treatment
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)

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

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

Bundle Branch Re-entry VT
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

Bundle Branch Re-entry VT Mechanisms
Macro re-entrant circuit employing His Bundle Both bundle branches Ramifications of left bundle Transeptal myocardium

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

VT QRS Morphology Activation Sequence LBBB LB-H-RB-V RBBB RB- H-LB-V

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

Bundle Branch Re-entry VT 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

Block in Bundle branches or HPS will terminate the tachy Ablation of RB renders tachycardia noninducible VT of myocardial origin vs BBR-LB pattern – rapid intrinsicoid deflection initial ventricular activation through the HPS

Interfascicular VT 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

Interfascicular VT vs BB Re-entry VT
HV interval shorter than sinus rhythm LB potential before HIS deflections

Bundle Branch Re-entry VT Treatment
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%

Arrhythmogenic Right Ventricular Cardiomyopathies
Most frequent – ARVD Extensive myocardial fibrosis - substrate for reentry Triangle of dysplasia RV outflow tract RV apex RV inflow segments Marcus fi et al.Circulation 1982; 65:384–398

ARVD - ECG in sinus rhythm
Prolonged QRS duration ≥ 110 ms in V1-V3 (Sens-55%, Spec-100%) T wave inversion in right precordial leads (Seen in 60%) Epsilon wave (Seen in 30%) Low-voltage QRS amplitude (Indicate severe cases)

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

VT in ARVD may be confused with RVOT VT O’Donnell D ET et al. Eur Heart J. 2003;24: , 2003.

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 Severe disease LV inv, FH of SCD, undiagnosed syncope, on c/c OMT Amiodarone or sotalol effective , when ICD not feasible Ablation can be adjunctive EP testing might be useful for risk assessment I IIa IIb III B I IIa IIb III C I IIa IIb III C I IIa IIb III C I IIa IIb III C

VT in Patients with HCM 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: , 2005

VT in Patients with HCM Mechanisms
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

VT in Patients with HCM Prevention of Sudden Death
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)

VT in Patients with HCM Sudden death risk factors
Family history of premature HCM-related death Unexplained syncope, particularly in young patients, or if demonstrated to be arrhythmia-based Frequent, multiple, or prolonged episodes of NSVT Hypotensive or attenuated BP response to exercise Extreme LVH with maximum wall thickness ≥ 30 mm Presence or magnitude of LVOT obstruction has not proved to be a consistently strong independent risk factor for SCD in HCM and therefore does not constitute a sole justification for prophylactic ICD implantation

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

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: , 2005

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: , 1997

Antiarrhythmics medication Radiofrequency catheter ablation
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

References- Journal 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, , 1988. 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, 2001:529–33 Ventricular Tachycardia in Coronary Artery Disease . B. Benito, M.E. Josephson / Rev Esp Cardiol. 2012;xx(x):xxx–xxx Role of Ablation Therapy in Ventricular Arrhythmias. Mithilesh K. Das et al. Cardiol Clin 26 (2008) 459–479 Ventricular Arrhythmias in Heart Failure Patients Ronald Lo, Henry H. Hsia. Cardiol Clin 26 (2008) 381–403

References- Journal A Comprehensive Approach to Management of Ventricular Arrhythmias, Fred Kusumoto. Cardiol Clin 26 (2008) 481–496 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: 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: Ventricular arrhythmias in idiopathic dilated cardiomyopathy K Von Olshausen et al. Br Heart J 1984; 51: 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, 2003:873–9 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

References – Text Books
Zipes 5th ed. Cardiac Electrophysiology From Cell to Bedside Basic Cardiac Electrophysiology for the Clinician .2nd ed. José Jalife, MD Clinical arrhythmology and electrophysiology: a companion to Braunwald’s heart disease 8th ed. Handbook of Cardiac Electrophysiology. Andrea Natale MD. Management of Cardiac Arrhythmias, edited by Leonard I. Ganz, MD, 2002

THANK YOU

MCQ-1 True statement regarding AVRD
Ventricular arrhythmias are usually exercise-related Sensitive to catecholamines Most Common- LBBB morphology VT All are true

MCQ-2 12 lead ECG of BBR-VT is given below. The antegrade conduction through Right bundle branch Left bundle branch Left posterior fascicle Left anterior fascicle

MCQ-3 Exists site of the VT circuit given below is ? LV lateral wall
Septum Right ventricle Both B & C

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? LV apical aneurysm RWMA anterior wall RWMA Inferior wall RV outflow aneurysm

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

MCQ-6 All are true about BBR- VT except?
High recurrence rate after drugs Treatment of choice for BBR VT is ablation of the RB Usually has LBBB morphology V precede each his electrograms

MCQ-7 VT in post TOF repair patients are due to the effect of all except? Years of chronic cyanosis Presence of a ventriculotomy Elevation of RV pressures Severe pulmonic regurgitation with RV dysfunction None

MCQ-8 Sudden death risk factors in HCM are all except?
Family history of premature HCM-related death Unexplained syncope, particularly in young patients, or if demonstrated to be arrhythmia-based Hypotensive or attenuated BP response to exercise Presence or magnitude of LVOT obstruction