Download When CRT May Run Proarrhythmic Effect?

Alexandru I Costea, MD
Associate Professor of Medicine
Director of EP Services at WCMC
University of Cincinnati
• CRT improves exercise capacity, quality of life and functional class
in patients with severe drug refractory CHF form LV dysfunction
and electrical dyssynchrony
• Patients with CHF are at risk for SCD due to monomorphic
ventricular tachycardia and ventricular fibrillation
• It is generally accepted that ICD should be used in addition to CRT
therapy in patients with severe CHF due to LV dysfunction
• Since the beginning of the CRT there has been a concern that LV
stimulation in these patients may be proarrhythmic
Effective CRT decreases the potential for arrhythmias directly or
through positive remodeling:
•Reduced sympathetic activity
•Increased heart rate variability
•Suppresses the frequency of PVC’s
•Reduces the ventricular tachycardia events and the need for ICD
therapies
•Decreases inducibility of sustained ventricular tachycardia during
EPS
• Electrical heterogeneity of myocardium described first in 1991
• Significant differences in the EP properties between the
endocardial, epicardial and M cells
• M cells prolong the action potential out of proportion to that of
epicardium and endocardium in response to slowing of the
heart rate or agents that prolong the action potential
• The duration of action potential of the M cells determines the
QT interval while Epicardial cells determine QT peak interval
Sicouri S, Antzelevitch C. A subpopulation of cells with unique electrophysiological
properties: the M Cells. Circ Res 1991;68;1729-41)
• Trans-mural dispersion of repolarization is defined as the
difference between the longest and shortest repolarization
times across the LV wall
• CRT is based on pacing the LV from the epicardium,
reversing the normal endocardial to epicardial activation
vector
• Abnormal activation sequence accentuates the trans-mural
dispersion while amplifying the intrinsic heterogeneity
existent at baseline
Medina Ravell V, Kowey P. Effect of Epicardial or Biventricular pacing to prolong QT
interval and increase transmural dispersion of repolarization. Circulation 2003:107;
740-746
• The non-homogenous depolarization resulted from delayed
activation and repolarization of the M cells creates a
substrate for reentrant arrhythmias
• Reversed activation also prolongs the QT interval and the T
peak to T end interval; T peak to T end is a measure of
dispersion
• This leads to increased EAD induced extrasystole, R on T
phenomenon and Torsades de Pointes
Fish JM, Anzelevitch C. Epicardial activation of the left ventricular wall prolongs QT
interval and transmural dispersion of repolarization. Circulation 2004:109:2136 -42
• QT interval increased from 442.1 ± 6.7 to 464.7 ± 20.5 and T peak
to T end increased from 111 ± 15 to 138 ± 24
• Voltage sensitive dye used experimentally to measure
ventricular activation times and conduction patterns
• Ischemia was produced gradually during the experiment
• Several risk factors for conduction abnormalities leading to VF
were identified:
o High LV output pacing
o Long inter-ventricular delay
o LV apical pacing
Haissaguerre M. Optical mapping technique applied to BIV pacing: potential mechanisms
for ventricular arrhythmias occurrence. Pacing Clin Electrophysiol 2003; 26: 197 -205
• Scar–related VT induction is pacing site specific. Robertson
et al. reported that 10% of patients with VT require LV pacing
for induction.
• LV pacing during CRT may facilitate preferential input into
the LV reentrant circuit
• By penetrating the reentry circuit LV pacing could lead to VT
Robertson JE, Josephson ME. Anatomic and electrophysiologic correlates of VT
requiring ventricular stimulation. Am J Cardiol 1982;48: 263 -268
• Several cases of monomorphic ventricular tachycardia induced
or exacerbated by LV pacing were published starting with 2003
• Groh et al. reported a case of ischemic CMP patient with a
preexistent monomorphic VT that had an exacerbation of same
VT with LV pacing only
• VT was successfully controlled with ATP and Amiodarone
Guerra J, Groh W. Increase in VT frequency after biventricular ICD upgrade. J Cardiovasc.
Electrophysiol. 14: 1245 -1247; Nov 2003
• Report of a 75 y old male with ischemic cardiomyopathy
• Refractory CHF and LBBB with a QRS of 195 ms
• Developed drug resistant monomorphic VT that could be
terminated only transiently by ICD therapies
• Medical therapy was ineffective
• The only effective intervention was inactivation of LV pacing
Mykytsey A, Kehoe R. Ventricular Tachycardia Induced by BIV Pacing in Patient with Severe
Ischemic Cardiomyopathy. J Cardiovasc Electrophysiol, Vol 16, 655-658. 6. 2005
• QT, JT and TDR were measured in 29 patients with CHF during
RV, LV and BIV pacing
• Both LV and BIV pacing led to prolongation of all three
parameters
• 4/29 patients developed TDP with LV or BIV pacing
• Arrhythmia corrected by RV pacing alone
Medina Ravell V, Kowey P. Effect of Epicardial or Biventricular pacing to prolong QT interval
and increase transmural dispersion of repolarization. Circulation 2003:107; 740-746
• First large study group evaluated the incidence of CRT induced
arrhythmias on 145 patients
• 3.4% patients developed incessant ventricular arrhythmias
within 72 hours after implantation:
o 4 monomorphic VT in 3 ischemic and 1 non ischemic patients
o 1 VF in an ischemic patient
• Controlled with antiarrhythmic medication, VT catheter ablation
(2 p) and/or discontinuation of LV pacing (permanently in 1 p)
Shukla G, Haffajee C. Potential proarrhythmic effect of biventricular pacing: fact or myth?
Heart Rhythm 2005; 2: 951-956
• 191 patients with BIV ICD de novo or as upgrade enrolled.
VT/VF incidence, clinical characteristics and management reported
• Eight patients (4%) had recurrent sustained monomorphic VT
• All patients were men
• Seven had ischemic CMP, one had non ischemic CMP
Nayal H, Marchlinski F. Ventricular tachycardia storm after initiation of BIV pacing. J
Cardiovasc Electrophysiol, Vol19, 708-715. July 2008
•All the patients had a history of monomorphic VT prior to the BIV
ICD implant (spontaneous or induced during EPS)
•No other differences with the rest of the patients
•VT occurred at a mean of 16± 12.5 days after BIV pacing was
initiated
•Medical therapy with amiodarone or lidocaine was ineffective long
term although acutely successful
Nayal H, Marchlinski F. Ventricular tachycardia storm after initiation of BIV pacing. J
Cardiovasc Electrophysiol, Vol19, 708-715. July 2008
•All the patients had a history of monomorphic VT prior to the BIV
ICD implant
•VT occurred at a mean of 16± 12.5 days after BIV pacing was
initiated
Nayal H, Marchlinski F. Ventricular tachycardia storm after initiation of BIV pacing. J
Cardiovasc Electrophysiol, Vol19, 708-715. July 2008
• Four patients agreed to an EP study and had a successful
ablation of a reentrant VT
• Two patients were managed by turning the LV pacing off
• One patient had 2 LV leads in place. Alternate LV pacing
corrected the arrhythmias
• One patient was managed by decreasing the LV pacing output
• Despite management of the VT, all 8 patients developed severe
CHF; 3 expired and one received OHT
Nayal H, Marchlinski F. Ventricular tachycardia storm after initiation of BIV pacing. J
Cardiovasc Electrophysiol, Vol19, 708-715. July 2008
RV Pacing: non clinical VT
LV Pacing: clinical VT
Yamada T, Kay N. Successful catheter ablation of epicardial VT worsened by CRT.
Online published ahead publication. Europace. 16 Dec 2009
Ablation Map and Fluoroscopy
VT Entrainment and EGMs
LV lead entrainment can help diagnosis and localize reentry
LV lead entrainment can help diagnosis and localize reentry
• Following 332 patients with BIV ICD implants
• LV pacing had to be discontinued in 3 patients:
 Symptomatic PVC count affecting % BIV pacing
 Worsening CHF in a patient with narrow QRS at baseline
 VT salvoes and VF in NICMP – successfully ablated
• Severe cardiac failure
• Prolonged QT at baseline either disease or medication induced
• Electrolyte abnormalities
• High output LV pacing
• Ischemic CMP and location of the LV pacing lead relative to scar
• Sustained VT documented prior to BIV implant
ICMP patients usually develop VT, while NICMP usually have VF
• Discontinuation of LV Pacing is always effective
• Alternate sites of LV pacing can be considered
• Minimizing the LV output can be useful
• Antiarrhythmics rarely work, but can be used in conjunction
with other therapies
• VT ablation, usually with epicardial access is necessary
• COMPANION trial demonstrated that BIV pacing has a
beneficial effect on survival; it included both BIV ICD and
BIV pacemakers – both groups were compared to a control
group but not each other
• CARE HF trial showed significant long term benefits of CRT
pacing alone with respect to survival as a single end point
 Does CRT ICD provide better survival benefits than CRT P?
 Is it safe to implant a CRT P only device without an ICD
backup?