Transcript Ventricular tachycardia in abnormal heart

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
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anterosupr LV – RBBB – Rt inf axis
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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)
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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
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 stabilityrate, 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 study
Structural 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 Class iia
myocarditis, or Chagas diseas
Expert 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
relative risk reduction
trial
Inclusion
drug
TD
SD
CHFD
Carvedilol
HFSG:1094/
570
NYHAII-IV
EF<35%
Carvedilol
3.125-50mg
65%
55%
79%
CIBIS:2647/
317
NYHA III-IV
EF<35%
Bisoprolol
1.25-10mg
34%
44%
26%
MERITHF:3991/13
85
NYHA II-IV
EF<40%
Metoprolol
12.525mg/d
34%
41%
49%
• 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
Bundle Branch Re-Entry Ventricular
Tachycardia
• 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
BBR -LBBB -antegrade direction -RB &
reterograde LB
BBR –RBBB- antegrade direction-LB &
reterograde RB
His Catheter
RB Catheter
LB Catheter
V Catheter
VT QRS
Activation
Morphology 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
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choice is ablation of the RB
VT ARVD
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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
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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
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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