Transcript VT IN NORMAL AND ABNORMAL HEARTS

VT IN NORMAL AND ABNORMAL
HEARTS
Ventricular Tachycardia
Ventricular Tachycardia is Defined as Three or more
consecutive PVC’s
•
rate is usually Between 100-200 BPM
• Sustained VT
– Episodes last at least 30 seconds/ req intervention
for termination
• Non-sustained VT
– Episodes last at least 6 beats but < 30 seconds
VENTRICULAR TACHYCARDIA
• CLASSIFICATION
ECG MORPHOLOGY
DURATION
MECHANISM
ETIOLOGY
Mechanisms of VT
• Reentrant
Reentry circuit (fast and slow pathway) is
confined to the ventricles and/or bundle
branches
• Automatic
– Automatic focus occurs within the ventricles
• Triggered activity
– Early afterdepolarizations (phase 3)
– Delayed afterdepolarizations (phase 4)
MECHANISM
ARRHYTHMIA
AUTOMATICITY-ENHANCED ST , IDIOPATHIC VT
NORMAL
EFFECT ON
PHASE 4 DEPOLARISATION
(↓)
ABNORMAL
AUTOMATICITY
AIVR
TRIGGERED ACTIVITY
EAD:-
TORSADES de POINTES
↓ AP DURATION
DIGITALIS INDUCED
RVOT VT
Ca ⁺⁺ overload
DAD:RE-ENTRY
Na⁺ channel dept
Sustained monomorphic
VT,BB R VT, VF
Ca⁺⁺ channel dept
Verapamil sensitive VT
“
VT IN NORMAL HEART
• 10% with VT - no apparent SHD
• Idiopathic ventricular tachycardia (VT)-SUBTYPES
1) QRS morphology
2) ventricular origin, and
3) response to pharmacologic agents
• management and prognosis
• DEF:-implies a structurally nl heart in young & middle aged
subjects & a nl QT interval, although biopsy & MRI may detect
subtle micro / macroscopic abnormalities
• Synd of idiopathic VT refers specifically to
monomorphic VTs.
• Polymorphic VTs and VF -structurally normal hearts
differ from idiopathic VT
-mechanistically and prognostically
• Commonly- subgrouped as
1)outflow tract tachycardias,
2)idiopathic left VTs (ILVTs), and
3)automatic VTs.
Outflow tract tachycardia
• outflow tract region
- RV region between the pulm and tricuspid valves,
- Basal left ventricle- outflow tract under the AoV, the
aortic cusps, and the basal LV epicardium.
•
A)repetitive monomorphic VT
B)paroxysmal sustained VT
Classification by symptoms
REPETITIVE MONOMORPHIC VT
repetitve runs of NSVT-LBBB+ N/R axis
PAROXYSMAL SUSTAINED
MONOMORPHIC VT
Episodes > spread out in time
Asymptomatic- incidental detection
> sustained
Suppressed with exercise
Inducible with PES, facilitated by
isoproterenol
Outfow tracts of RV/LV
Triggered activity
Automatic mechanism
Prognosis -excellent
• delayed afterdepolarization(DAD)-mediated triggered
activity - mechanism
• DAD- mediated by intracellular calcium overload
• Freq precip by catecholaminergic stimulation,↑ in
intracellular cAMP and ca
• rapid stimulation- isoproterenol infusion.
• dependence on cAMP- sensitivity to β-blockade, CCB
and adenosine
• RVOT VTs -75%
- LBBB+ INF AXIS
-QRS transition from V₃\V₄ (late)
•
Jadonath RL et al, localizing the origin of right ventricular outflow tract tachycardia. Am
Heart J 1995
RVOT - 9 regions and used QRS morphology in leads I and aVL + R wave transition to diff ant
from post RVOT sites
• Anterior sites- Q wave (Q or qR) in lead I and a QS in lead aVL.
• Posterior site- R wave in lead I and an early precordial
transition( R to S) in V3
• Septal- taller, narrower monophasic R-inferior leads
• Free wall RVOT VTs-notchi inf leads and later transition (>V3)
• RVOT VT-Posterior- +ve in V1, ant- -ve in V1
RVOT VT
• VT arising from the LVOT
(1)a) RBBB + inf axis
b) dominant R wave in V1
c) lack of precordial transition
d)+_a late appearing S wave in V6 and V2
(2) a) LBBB+ inferior axis+
b)early precordial R wave transition (<V₂)
• Aortic cusps
Dep on the s/o origin from the R/L cor cusp- RBBB or
LBBB
VT- LCC or aortomitral cont- terminal S wave in lead I
Precordial transition-earlier in cusp VT (< V3)
R duration & the R/S ratio V1 & V2 were > in cuspVT
Lcc VT
• 9%–13% of idiopathic VT- originate from epicardial
locations
R amplitude was signif > inferior leads
lead I had an S wave ( rS or QS pattern)
Q wave ampli was >in aVL vs aVR (ratio >1.4)
• LV epicardial grp1)R wave in V1 with a > amplitude than in the RV
endocardial group
2)signif S waves in V1 (>1.2 mV) and V2
SITE
FEATURES
-Ant septal side of RVOT
- R/L cc of Ao
-Pul artery
LBBB
LV- mitral annulus
-epicardium at outflow tract
RBBB
VT with LBBB morph from LV
Early R progression( R in V1,V2,transition by V3),
Dominant R across precordium
VT with LBBB –RVOT/ PUL art
Late R progression ( V3 or V4)
Posterior septal RVOT VT
> Leftward axis
Free wall RVOT VT
Lower QRS amplitude, QRS notched in inf leads
Late R wave transition V4 ,V5
Epicardial VT s
Loss of R in V1 V2 with broad R from V3- V6
• Outflow tract VT - good prognosis- benign course
• Polymorphic VT- unusually short–coupled RVOT
VPCs- respond well to successful VPC ablation
• Management of outflow tract VTs
medical therapy or catheter ablation.
• adenosine, verapamil, b-blockers, and carotid sinus
massage-acutely
• b-blockers and CCBs-c/c supp therapy (efficacy 67%
typical RVOT VT)
• Pats- breakthrough tachy on b-blocker or CCB, class I
or class III antiarrhythmic therapy
• Catheter ablation - high success rate (>80%) in
treating these arrhythmias
• Long-term cure rates after a successful initial
ablation are high
• overall recurrence rate is approximately 10%
Idiopathic left ventricular tachycardia
• MC-ILVT is verapamil-sensitive tachycardia
• 1st -Zipes and colleagues in1979
• Belhassen – demon verapamil sensitivity of the
tachycardia
(Response of recurrent sustained ventricular tachycardia to verapami , Br Heart J ;1981)
triad:
(1) induction with atrial pacing
(2) RBBB morphology+ left axis deviation
(3)no structural heart disease
• 15- 40 years old.
• Typical symptoms
palpitations, fatigue, and presyncope.
Syncope and SCD are rare but described
Incessant- tachycardia-induced cardiomyopathy
Most episodes occur at rest( making exercise
testing unreliable in assessment)
• Anatomic basis for ILVT is unclear
• earliest site of activation -inferoposterior LV septum
• originates from a false tendon - extending from the
posteroinferior LV to the basal septum
• localized reentry as the pred mech in verapamilsensitive ILVT.
Fascicular VT - Circuit
Fascicular VT – Anatomy and Physiology
• Relatively narrow WCT
• 90% originate from left
posterior fascicle
• Anatomic substrate: LV “false
tendon” or postero-inferior
fibromuscular band to basal
septum
• Diagnostically – may require
isoprenaline to facilitate
induction
Purkinje Tissue running in false tendon
• baseline 12-lead ECG is normal in most patients.
•
ILVT-RBBB, left sup axis + rel narrow QRS duration(≤140 ms),
RS int <80 ms
-exit site near the area of the left posterior fascicle
• ILVT-RB+ RAD –exit site near anterior fasicle
Three Subtypes
Anatomic Origin
LAHB
LPHB
Upper Left
Septal
QRS
Morphology
RBBB
RBBB
Narrow
QRS Axis
Rightward
Leftward
Normal
L post fascicle-RBBB+R SUP AXIS
Fascicular VT – Rare mimics
1. Inter-fascicular VT
•
•
RBBB and right or leftward axis
Structurally abnormal heart: Previous
anterior infracts and LAFB or LPFB
•
A subtype of BBR VT
2. Idiopathic mitral annular VT
•
•
•
RBBB and rightward axis
Variable verapamil-sensitivity
Ill-defined
• Long term prognosis good
• A/c-iv verapamil, c/c-oral verapamil
• RFA- severe symptoms, resistant or intolerant to med
tpy
• Long-term success after catheter ablation is >than
90%
Automatic ventricular tachycardia
• adrenergic or propranolol sensitive VT
• automaticity from within the Purkinje fibers
mediated by I f
• result from adrenergically mediated automaticity
• <50 yrs, ppt by exercise
• Mc sites-mitral annulus,pappilary mus, RV in flo
• ECG - RBBB or LBBB morph and may present as
monomorphic or polymorphic VT
• sensitive to b-blockers
• unresponsive to CCBs
• cannot be initiated with programmed stimulation
VT IN ABNORMAL HEART
CAD
•
Incidence of sustained, monomorphic VT after infarction -3%.
• Modern therapy- > smaller infarcts and less aneurysm
formation ---↓ incidence of VT to <1 %
• electrophysiologic substrate - develops in the first 2 weeks
• once established- remain indefinitely
• Once sustained VT occurs, the risk for arrhythmia continues
indefinitely
• inducible VT signifies the presence of an anatomic VT
substrate
PATHOPHYSIOLOGY
•
In post MI -re-entry
• Areas of slow conduction -substrate for re-entry
• conduction is slow and discontinuous
-abnormalities in gap junction distribution and function
• anatomic characteristics - islands of relatively viable
muscle alternating with areas of necrosis and later
fibrosis
• result in fragmentation of the propagating electromotive
forces
MI Scar-Related Sustained Monomorphic
VT Circuit
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
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)
RBBB &
LBBB VTANTERIOR
RBBB & LBBB
VT -POSTERIOR
q wave in lead 1 and/or V6
- RBBB –
anteriorly
RBBB-FROM
ANTEROLATERAL
LEFT VENTRCLE
R in leads L1 and V1 through
V6, in RBBB
specific for a posterior origin
Electrocardiograrm During Ventricular Tachycardia with Left Bundle Branch
Morphology
LBBB pattern+
Q waves in leads I
and V6 -anterior
superior and
leftward axis inferior aspect of
septum.
LBBB+
q in L1 ,V6-ant
inferior & rightward axis
- superior septum
LBBB-POSTEROBASAL
LV
-R in L1 ,V2,V3& V6
JM Miller ;Circulation 1988;,
Relationship between the 12-lead ECG during VT and endocardial site
of origin in patients with coronary artery disease
• Endocardial mapping - 182 VTs in 108 patients with prior AW/IW MI
• Endocardial sites of origin -identified with use of catheter or
intraoperative activation mapping
• ECGs - 4 features a)location of infarction,b) BBB type c) axis d) precordial R
wave prog pattern
• specific combination- 4 features- particular endocardial origin in 87 VTs
(48% of total)
•
An asso (> 70% ppv)
1)left> right, BBB type (73% vs 31%)
2) VT related to inf > ant infarction ( 74% vs 37%).
ANTERIOR WALL MI
PRECORDIAL LEADS IN LOCATING VT
INFEROAPICAL SEPTAL
FOCUS
V1 NEGATIVE + LAD + NO LATE R PROGRESSION
ANTEROSUPERIOR
APICAL SEPTAL FOCUS
V1 NEGATIVE + INF AXIS (NL/R)
ANTEROAPICAL SEPTAL
FOCUS
V1 POSITIVE + RAD + ABRUPT LOSS OF PRECORDIAL
PROGRESSION
INFERIOR MI
INFEROBASAL SEPTAL
FOCUS
V1 NEGATIVE + LAD + GROWING R PROGRESSION
INFEROBASAL FREEWALL
FOCUS
V1 POSITIVE +SUP AXIS + REVERSE LATE R
PROGRESSION
MIDPOSTERIOR SEPTAL
FOCUS
V1 NEGATIVE + INF RIGHT AXIS + REVERSE
(early/late)R PROGRESSION
Regions are:
A, inferoapicalseptum;
B, anteroapical septum;
C, anteroapical free wall;
D, anterobasal free wall;
E, anterobasal and midseptum;
F, inferobasal septum;
G, inferomedial free wall;
H, inferolateral free wall;
I, midinferior
J, inferoapical free wall.
G + H =inferobasal
free wall.
• Algorithm developed with the above criteria was
applied prospectively to 110 VTs (all mapped) in 63
patients
• algorithm could correctly predict endocardial region
of origin for a mean of 60 of 65 (93%) VT
ANTERIOR INFARCTION-VT
INFERIOR INFARCTION -VT
INFARCTIO SITE OF
N
ORIGIN
VT TYPE
ANTERIOR
LBBB
INFEROAPICA
L
JOSEPHSON’S
q –L1, V6
MILLERS
Poor R Progression/ no
or late progression
SUP± LAD
ANTEROAPIC
AL
LBBB
q –L1 ,V6
Any precordial prog
INF AXIS
ANTEROAPIC
AL
RBBB
q –L1&/ V6
Dominant R / abrupt
loss
INF AXIS
INFERIOR
INFEROBASA
L
LBBB
R –L1,V2,V3&V6
Growing R pattern
SUP ± LAD
INFEROBASA
L
RBBB
R-L1,V2,V3&V6
Reverse R prog- late
/early
SUP ± LAD
INFEROLATER
AL
RBBB
R-L1,V2 ,V3,V6
INF AXIS
Late reverse R prog
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 SCD 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
• Goal of longterm therapy-a) pvt of SCD ,
b) Rec of symp VT
After MI
Asymptomatic NSVT in pats with NLVEF- no treatment
Symptomatic NSVT in pats with NLVEF- betablockers
NSVT in red LVEF-↑ SCD
PRIMARY PVT - ICD > AMIOD- pvt of SCD
SECONDARY PVT- Class lll > l
- emperical amio > than EP guided antiarry’s
- ICD > amio in LVEF<35%
SCD/SUS VT in ↓LVEF- ICD
CAD-NL LVEF + SUST VT-? , amio, icd + amio, RFA
Bundle Branch Re-Entry Ventricular
Tachycardia
• Macro re-entrant (→Ventricular flutter) circuit
employing…
– Both bundle branches
– Ramifications of the left bundle
• Hallmark: His-Purkinje system disease – functional or
structural
• Acquired heart disease or apparently normal hearts
• Ischemic (6%) vs. non-ischemic (40%) cardiac disease
His Catheter
RB Catheter
LB Catheter
V Catheter
VT QRS
Activation
Morphology Sequence
LBBB
H-RB-V-LB
RBBB
H-LB-V-RB
VT Due to Bundle
Branch Reentry
• VT incorporating both bundle branches into the reentry circuit
• usually in an acquired heart disease and significant
conduction system impairment
• Reentry within HPS in humans was first documented by
Akhtar et al 1974
• sustained bundle branch reentry can not be induced in
patients with normal HPS.
• Nl- very fast conduction velocity and a relatively long
refractory period which precludes formation of a stable
reentry circuit
• Persistent BBR as a mechanism of sustained VT has been
demonstrated in patients with conduction system impairment
• Dilated cardiomyopathy
-non-ischemic- 40% Vs ischemic - 6%
• Aortic or mitral valve surgery
Close anatomical proximity of the HPS to the valvular annuli
early postoperative period ( first 2 weeks)
preserved systolic left ventricular function
• Myotonic myocardial dystrophy
characterized by relatively selective and significant
conduction system impairment
• idiopathic isolated conduction system disease
• 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
• “complete” BBB -not an accurate marker of complete
conduction block
• Can occur in patients with relatively narrow QRS complex functional conduction delay
• presyncope, syncope or sudden death - VT with fast rates >
200 bpmleft
• LBBB pattern-mc VT morphology
• VT of myocardial origin vs BBR-LB pattern –
rapid intrinsicoid deflection - initial ventricular activation
through the HPS
• BBR -LBBB -antegrade direction -RB & reterograde LB
• BBR –RBBB- antegrade direction-LB & reterograde RB
• Prolonged H-V interval in sinus rhythm
• Fig 2
INTERFASCICULAR REENTRY TACHYCARDIA
• usually has RBBB morphology
• Antegrade - LAF & retro – LPF –RAD
• Antegrade- LPF & retro – LAF- LAD
• Fig 3
• Pharmacologic therapy- empiric and EP guided - ineffective
• RFA - first line therapy
• choice is ablation of the RB
ARVC
Ind JH et al. Indian Pacing Electrophys J. 2003:3:148
– Fibro-fatty replacement of
the myocardium
– Thin and enlarged RV wall.
– Trichrome stain
– Areas of mature fibrosis (F)
and adipose tissue (A) within
the epicardial (Epi) and midmyocardial zones
Arrhythmogenic Right Ventricular
Cardiomyopathy - ARVC
• Major Conduction abnormalities
– Epsilon waves in V1 - V3
– Localized prolongation (>110 ms) of QRS in V1 - V3
• MINOR
– Inverted T waves in V2 and V3 in an individual over 12
years old, in the absence RBBB
– Late potentials on SAECG
– Ventricular tachycardia with a LBBB morphology
– Frequent PVCs (> 1000 PVCs / 24 hours)
ARVD
• Ventricular arrhythmias are usually exerciserelated
• sensitive to catecholamines.
• right axis deviation ,LBBB
• Multiple morphologies of ventricular
tachycardia
• multiple foci or pathways.
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
• Naxos disease
• Sotalol
• Catheter ablation
–
–
–
–
–
treat intractable ventricular tachycardia
60-90% success
recurrence is common (60% recurrence rate)
drug-refractory VT
frequent recurrence of VT causing frequent discharges of the ICD.
VT
MONOMORPHIC
RBBB
STRUCTURALLY NL HEART
POLYMORPHIC
LBBB
STRUCTURALLY ABNORMAL HEART
RBBB
NORMAL HEART
Outflow tract VT
mitral annulus,
epicardium of out flow
Ao mitral cont
ILVT
- RAD- LAF
ABNORMAL HEART
POST MI
- septum/free wall- inf
- apex- sup + RAD
BBR VT
-ante LB -retro-RB
- LAD – LPF
AUTOMATIC / PROP SEN
FASCICULAR VT
- RAD –ante –LAF
- LAD – ante - LPF
LBBB
NORMAL HEART
OUTFLOW TRACT VT
- RVOT
- LV SITE OF THE SEPTUM
ABNORMAL HEART
POST MI
ARVD
UHL’S ANOMALY
POST SX –TO
AUTOMATIC / PROP SENS
DCM
- LV VT
-BBR VT
ante-RB.retro-LB