(Circulation. 2000;101:1288.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Linear Ablation Lesions for Control of Unmappable Ventricular Tachycardia in Patients With Ischemic and Nonischemic Cardiomyopathy
From Allegheny University Hospitals–Medical College of Pennsylvania Division and the University of Pennsylvania Health System, Philadelphia, Pa.
Correspondence to Francis E. Marchlinski, MD, Hospital of the University of Pennsylvania, 9th Floor Founders—Cardiology, 3400 Spruce Street, Philadelphia, Pa 19104. E-mail: fmphilapa{at}home.com
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—Conventional activation mapping is difficult without inducible, stable ventricular tachycardia (VT).
Methods and Results—We evaluated 16 patients with drug refractory, unimorphic, unmappable VT. Nine patients had ischemic and 7 had nonischemic cardiomyopathy. All patients had implantable defibrillators and had experienced 6 to 55 VT episodes during the month before treatment. Patients underwent bipolar catheter mapping during baseline rhythm. The amount of endocardium with an abnormal electrogram amplitude was estimated using fluoroscopy in 3 patients and a magnetic mapping system (CARTO) in 13 patients. For the magnetic mapping, normal endocardium was defined by an amplitude >1.5 mV; this measurement was based on sinus rhythm maps in 6 patients who did not have structural heart disease. Radiofrequency point lesions extended linearly from the "dense scar," which had a voltage amplitude <0.5 mV, to anatomic boundaries or normal endocardium. To limit radiofrequency applications, 12-lead ECG during VT and pacemapping guided placement of linear lesions. No new antiarrhythmic drug therapy was added. The amount of endocardium demonstrating an abnormal electrogram amplitude ranged from 25 to 127 cm2. A total of 8 to 87 radiofrequency lesions (mean, 55) produced a median of 4 linear lesions that had an average length of 3.9 cm (range, 1.4 to 9.4 cm). Twelve patients (75%) have been free of VT during 3 to 36 months of follow-up (median, 8 months); 4 patients had VT episodes at 1, 3, 9, and 13 months, respectively. Only one of these patient had frequent VT.
Conclusions—Radiofrequency linear endocardial lesions extending from the dense scar to the normal myocardium or anatomic boundary seem effective in controlling unmappable VT.
Key Words: tachycardia • ablation • defibrillators, implantable
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The presence of multiple morphologies, hemodynamic intolerance, and noninducibile ventricular tachycardia (VT) have limited the widespread applicability of catheter ablative therapy.1 2 3 An anatomically based approach deployed in sinus rhythm might eliminate the requirement for mapping all ventricular arrhythmias and extend the applicability of ablative therapy.
On the basis of prior experience with sinus rhythm electrogram mapping and surgical ablative therapy, we hypothesized that in patients with unmappable, unimorphic VT, (1) the abnormal endocardium can be defined using detailed sinus rhythm voltage mapping, and (2) linear ablation lesions that repeatedly and/or selectively interrupt the border zone of abnormal endocardium could control VT.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Patient Population
This study included 12 men and 4 women who had recurrent VT that induced shocks from their implantable defibrillator. Nine patients had coronary disease and a prior infarction, and 7 patients had nonischemic cardiomyopathy. Four of the 7 patients had primarily right ventricular (RV) involvement, with marked RV dilatation and marginally depressed left ventricular (LV) systolic function (Table 1
). Two patients had idiopathic
cardiomyopathy, with dilatation of both ventricles.
The last patient with nonischemic
cardiomyopathy had biventricular
involvement in the setting of rheumatic valvular disease.
Despite drug therapy, all patients had frequent VT, which was
documented by electrograms stored in the implantable defibrillator
(Table 1). Thirteen of the 16 patients had received long-term
(>2 months) therapy with amiodarone, and 6 had prior ablation
attempts. Most patients had evidence of multiple VT morphologies, as
based on 12-lead ECG or stored electrograms. All documented,
spontaneous VT was unimorphic. The 16 patients came from a pool of 48
patients who were referred to our hospital for catheter ablation.
|
The study patients were evaluated after informed consent
was obtained. All procedures were done following the institutional
guidelines of the Allegheny University of the Health Sciences. A total
of 15 patients were also treated with antiarrhythmic agents during the
study (Table 1
). Antiarrhythmic agents were not withdrawn
because (1) 14 patients were being treated with amiodarone and
(2) all patients were experiencing recurrent VT. All patients underwent
programmed stimulation through triple extrastimuli at 2 RV sites to
document the mode of induction, the cycle length, and the configuration
of the induced VT (Table 1). At the time of evaluation, VT was
not mappable because of hemodynamic collapse with VT,
changes in QRS morphology with attempted mapping, or the inability to
induce sustained VT (Table 1).
Sinus Rhythm Mapping
Detailed endocardial mapping was performed during
supraventricular rhythm (14 patients) or, if the patients
were pacemaker-dependent, paced rhythm (2 patients). A total of 72 to
430 sites were recorded per chamber. Only the LV was mapped in
patients with coronary disease. In patients with
nonischemic cardiomyopathy, both ventricles
were mapped. Access to the LV was via a retrograde aortic approach in
14 patients and a transseptal approach in 2 patients. During all
LV mapping and ablation, heparin was administered to achieve and
maintain an activated coagulation time >250 s.
Reference Values for Sinus Rhythm Bipolar Electrogram
Mapping
In the first 3 patients, all mapping and ablation was performed
using a 7-F extended-curve thermistor catheter (SteeroCath-T,
Electrophysiology Technologies, Inc) that had a 4-mm tip electrode. The
catheter provided temperature and impedance monitoring during energy
delivery, as well as bidirectional steerability. All recordings
were bipolar, with an interelectrode distance of 2 mm. Signals
were filtered at 30 to 500 Hz and were displayed at 100 to 200
mm/s on a physiological recording system
(Prucka, Inc). Electrogram amplitudes were measured with electronic
calipers. Sites with an electrogram amplitude <3.0 V were considered
abnormal.4
In the next 13 patients, we used the CARTO (Biosense, Inc) magnetic mapping system with the Navistar catheter.5 6 Navistar catheters were 7 or 8 Fr, unidirectionally deflectable, and provided impedance but not temperature monitoring. The Navistar bipole consists of a 4 mm-tip electrode and a 2 mm-ring electrode separated by 1 mm of spacing. Electrograms were filtered at 10 to 400 Hz and displayed at 100 mm/s; peak-to-peak amplitude was measured automatically.
Reference values for distinguishing normal and abnormal electrograms with this system were established by mapping the RV (4 patients) and/or LV (4 patients) in 6 patients who did not have structural heart disease. A total of 71 to 168 sites were recorded per normal ventricle. None of these subjects was taking cardioactive drugs. Five of these subjects were men, and their mean age was 37±12 years.
Reference Values of Magnetic Mapping System
The mean bipolar electrogram amplitude recorded from the
normal RV was 3.7±1.7 mV (range, 0.4 to 11.5 mV). Of note, 95% of all
bipolar electrogram signals recorded from the RV were >1.44 mV.
The mean bipolar electrogram amplitude recorded from the LV was
4.8±3.1 mV (range, 0.6 to 20.5 mV). Of note, 95% of all LV
electrograms were >1.55 mV. Using these data, we defined normal
endocardium using the CARTO-Biosense system as that demonstrating a
bipolar electrogram of >1.5 mV. On the basis of our previous
experience with catheter and intraoperative mapping, we then
arbitrarily designated a value of <0.5 mV as consistent with
"densely scarred" endocardium.7 8
Voltage Map Color Display and Technique for Estimating Extent of
Abnormal Endocardium
The magnetic mapping system includes a magnetic sensor in the
catheter tip that can be localized in 3D space using the ultralow
magnetic field generators placed under the fluoroscopic table. The
electrogram amplitude recorded from the catheter at different
endocardial locations can be shown on a computer display as a voltage
map. The color display for illustrating abnormal myocardium
was set with a color range of 0.5 to 1.5 mV to highlight the border
zone (Figures 1 through 6).
The CARTO system can also calculate the anatomic distance between any 2
designated points.5 6 Thus, by assuming a rectangular or
trapezoidal shape of any abnormal segment, the extent of the
endocardium demonstrating abnormal (<1.5 mV) and densely scarred
(<0.5 mV) voltage amplitudes could be estimated (Tables 2 and 3).
|
0.5 mV); and range
between purple and red, border zone (signal amplitudes between 0.5 and
1.5 mV). Top, RV map from patient without heart disease is
represented almost entirely by color purple. Bottom, RV map
from patient with VT and RV cardiomyopathy with
abnormal endocardium over superior RV free wall and septum. Linear
ablation lesions, identified by contiguous dark circles, extend from
dense scar to normal endocardium. APEX indicates location of RV
apex.
|
|
|
|
|
|
|
Ablation Technique and Location of Linear Lesions
Linear lesions were placed using 3 guiding principles. (1)
Lesions would extend across the borders of the endocardium that
demonstrated abnormal bipolar electrogram voltage. (2) Lesions would
typically extend from the areas demonstrating the lowest amplitude
signals (<0.5 mV) to areas demonstrating a distinctly normal signal
(>3 mV for the first 3 patients and >1.5 to 2.0 mV for the last 13
patients) or to a valve continuity. (3) Lesions would cross through the
border zones at sites where mapping approximated the QRS morphology of
VT. Twelve-lead ECG recordings of spontaneous and induced VT
were analyzed to regionalize the site of origin of the VT using
standard criteria.9 10 The mapping catheter was then
placed along the appropriate border of the scar, and pacemapping
was performed to create a 12-lead ECG that approximated the VT (Figures 3 and 4). This modification to a purely anatomic ablation
approach was essential because (1) the extent of electrogram
abnormalities was large (Tables 2 and 3) and (2) the size
and 3D character of the VT circuit was not established. In 5 of the 16
patients, the electrograms stored in the defibrillator did not match
the electrograms of induced VT, and 12-lead ECGs of spontaneous VT were
unavailable. In these patients, linear lesions were created at 3- to
5-cm intervals along all aspects of the border zone. (Figure 5).
Sequential point lesions created the linear lesions. For each
point lesion, radiofrequency energy was applied for 90 to 120 s
using a power output to achieve a targeted temperature of 60°C
(SteeroCath-T catheter) or a targeted impedance drop of 6 to 10 ohms
(Navistar catheter). Power output started at 5 W and was titrated over
30 s to a maximum output of 50 W or until the targeted temperature
or impedance was achieved. To avoid an impedance rise, output was
decreased manually whenever the impedance drop exceeded 10 ohms or
temperature exceeded 60°C to 65°C. For the first 3 patients, the
linear lesion location and size were estimated using fluoroscopy. This
process was facilitated using 3D magnetic mapping (CARTO-Biosense) in
the last 13 patients.5 6 Radiofrequency energy
applications were "tagged" for display, and the length of the
linear lesion was documented (Tables 2 and 3).
In 8 of the 16 patients, programmed stimulation was repeated after making linear lesions on one end of the endocardium that demonstrated abnormal electrograms to assess the inducibility of specific, targeted tachycardia morphologies. In all but one of the 16 patients, stimulation that resulted in VT in the baseline state (and that included triple extrastimuli) was performed after creating all linear lesions. In the one patient in whom this was not done, prolonged periods of hemodynamic instability followed the prior episodes of VT.
Follow-Up
VT recurrence was identified via device interrogation
and a report of clinical symptoms. No new antiarrhythmic drug therapy
was added (Table 4). In addition, we
assessed the effects of the linear lesions on the LV by using gated
nuclear blood pool scanning in 6 patients with ischemic
cardiomyopathy. A policy regarding anticoagulation
after the procedure was established after the first 2 left-sided
ablation procedures. Coumadin was prescribed for 3 months to achieve an
international normalized ratio >2.0.
|
Statistical Analysis
Results are presented as mean±SD unless otherwise
indicated. Comparisons of total procedure and fluoroscopy time between
patients with coronary disease and those with
nonischemic cardiomyopathy were made using
an unpaired Student’s t test. A comparison of LV ejection
fraction before and after the ablation procedure was made using a
paired Student’s t test. P<0.05 was considered
significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Endocardial Voltage Maps in Patients With Coronary Disease
The extent of LV endocardium subtended by contiguous bipolar recordings demonstrating abnormal electrograms in patients with coronary artery disease was 65±24 cm2 and ranged from 51 to 110 cm2 (Table 2
and
Figures 2, 5, and 6). The dense scar (<0.5
mV) ranged from 5 to 44 cm2 (Table 2).
Endocardial Voltage Maps in Patients With Dilated
Cardiomyopathy
In all patients with dilated cardiomyopathy,
abnormal endocardial electrograms were recorded from the RV septum
and free wall (Figures 1 and 6). In contrast, abnormal
electrograms were recorded from the LV in only 3 patients. Only one
of these patients had extensive LV septal and free wall abnormalities
(Table 3).
The extent of the RV endocardium subtended by contiguous bipolar
recordings demonstrating abnormal electrograms was 60±36
cm2 and ranged from 25 to 127
cm2 (Table 3). The abnormal endocardium in
the single patient with extensive LV involvement measured 45
cm2. Dense scar (<0.5 mV) was also identifiable
in all patients with nonischemic
cardiomyopathy. The estimated size of the dense
scar ranged from 8 to 50 cm2 (Table 3).
Linear Radiofrequency Ablation Lesions
A total of 8 to 87 (median, 55) radiofrequency lesions were
applied per patient. Point lesions created 1 to 9 linear lesions
(median, 4). The average length of the linear lesion was 3.9 cm, and
the range was 1.4 to 9.4 cm (Tables 2 and 3).
Programmed Stimulation After Ablation
In 6 of the 8 patients in whom programmed stimulation was repeated
after making lesions on one end of the scar, only VT morphologies
consistent with an origin from the opposite end of the scar
were induced (Table 4). In response to stimulation at the
completion of all ablation lines, 7 of the 15 patients had no inducible
VT. Of the 8 patients with persistent inducible VT, 5 had rapid VTs
inducible with double (2 patients) or triple (3 patients) extrastimuli.
These VTs did not match the cycle length or morphology of the
spontaneous arrhythmias. In the remaining 3 patients, a slower
tachycardia was still inducible. In 1 of these 3 patients,
the induced VT did not match spontaneous VT. In the second patient, the
VT matched a clinical VT morphology but was slower in rate. In the last
patient, no ECG information was available for the spontaneous VT.
Duration of Procedure and Fluoroscopy Exposure and
Complications
The total procedure time ranged from 6.0 to 13.5 hours (mean,
8.8±1.9 hours). The total fluoroscopy time ranged from 60 to 196
minutes (mean, 121±38 minutes). The total procedure time (10.8±2.1
versus 8.1±2.1 hours; P<0.05) and the total fluoroscopy
time (156±32 versus 90±27 minutes; P<0.01) were greater
for patients with VT who had nonischemic rather than
ischemic cardiomyopathy.
None of the 6 patients with LV ejection fraction measurements before (mean, 24±6%) and after (mean, 23±9%) ablation demonstrated a deterioration (>5%). One patient experienced a cerebral vascular accident with right-sided hemiparesis at the end of the procedure. Residual arm weakness persisted at 6 months. In this patient, an impedance rise occurred during radiofrequency energy application. When the ablation catheter was removed through a transseptal sheath, residual coagulum was noted.
Follow-Up
All patients have been followed for 
3 months (range, 3 to 36
months; median, 8 months; Table 4). Three patients died at 3, 4,
and 8 months after the ablation procedure from refractory heart failure
(baseline LV ejection fraction was 18%, with associated severe mitral
regurgitation), pneumonia, and complications of
abdominal surgery. Fifteen patients were free of VT during the initial
follow-up month (Figure 7), and 12
patients (75%) have been free of any recurrence of VT during
the entire duration of follow-up. Only 1 of the 4 patients with VT
during follow-up had frequent recurrences. Recurrent VT in this
patient has been slow and amenable to pacing therapy.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The current study describes a new approach for the ablation of unmappable, unimorphic VT associated with ischemic and nonischemic cardiomyopathy. The study documents that (1) the extent and voltage characteristics of the abnormal endocardium can be defined using sinus rhythm, bipolar electrogram, voltage mapping, and (2) catheter-based ablative therapy that creates linear lesions targeting the border zone can control recurrent VT.
Electroanatomic Substrate for VT
The magnetic mapping system (CARTO) provided a tool for
creating a 3D bipolar electrogram voltage map.5 6 In
patients with both ischemic and nonischemic
cardiomyopathy, the extent of abnormal electrogram
recordings was large, averaging >50 cm2
(Tables 2 and 3). Cassidy and colleagues7
noted a comparable degree of endocardial electrogram abnormalities in
patients with monomorphic VT in the setting of ischemic and
nonischemic cardiomyopathy. Of note,
sampling was typically limited to <20 sites in that study. By sampling
from hundreds of sites, we could characterize the electroanatomic
substrate in more detail. Almost uniformly, contiguous areas of very
abnormal signals with an amplitude <0.5 mV were identified in patients
with ischemic and nonischemic
cardiomyopathy. This dense scar was typically
surrounded by large "border zone" areas with signal amplitudes
between 0.5 and 1.5 mV, which transitioned into normal
myocardium (Figures 1 through 6).
Linear Lesion Deployment Based on Surgical Experience
Subendocardial resection guided by the presence of the endocardial
scar is associated with a 70% to 80% arrhythmia cure
rate.11 12 Such surgical therapy is performed when
uniform, sustained VT can not be initiated at the time of
surgery. This extensive surgical experience served as the basis
for creating linear lesions that connected the dense scar area to the
normal endocardium; we used electrogram recordings during sinus
rhythm as a guide. The magnetic electroanatomic mapping system assisted
in creating contiguous lesions through the defined border zone by
documenting the location of the catheter tip and its relationship to
the endocardial anatomy.
Use of 12-Lead ECG During VT and Pacemapping to Guide Placement of
Linear Lesions
Eliminating all of the border zone endocardium using current
catheter-based ablative techniques would be impractical and possibly
unsafe. The placement of linear lesions was guided by an interpretation
of the 12-lead ECG during VT and pacemapping in the border
zone.9 10 Linear lesions were created in regions that
crossed the border zone and intersected the best pacemap site. We
hypothesized that the best pacemap site approximated the exit site of
the VT circuit and that the described endocardial linear lesion would
likely interrupt a portion of a reentrant circuit (Figure 8). This described modification to a
purely anatomic approach allowed us to target specific regions of the
border zone in most patients.
|
Limitations
Because of the variability in the frequency of VT, it is
difficult to ascertain whether a good clinical response is causally
related to any ablation procedure. We validated the assumption of
causality by (1) documenting the frequency of VT in the month before
ablation, (2) using diagnostic information from the
implantable defibrillator to document VT recurrence, (3) not
adding new antiarrhythmic drug therapy, and (4) including only patients
followed for 3 months. Because of these strict criteria, we are
confident that arrhythmia control after ablation occurred in
most patients.
Although linear lesions were created using repeated point radiofrequency applications, we do not wish to imply that we created conduction block. Our technique is descriptive, and the mechanism of efficacy is speculative.
Each patient had unimorphic tachycardia that was documented. We do not know whether a similar ablation technique would be effective in patients with polymorphic VT. In addition, given the average duration of the procedure and the duration of fluoroscopic exposure, the technique as described might not be practically applied in many institutions.
Finally, although we think that we have validated the efficacy of the described technique, we cannot be as certain about its safety. Indeed, we found no evidence of deterioration in LV function with repeat radionuclide scans. Nevertheless, a cerebral vascular accident occurred in one of our patients. The use of magnetic mapping catheters with temperature-monitoring capabilities may decrease the risk of thromboembolic phenomena.
Received May 6, 1999; revision received September 21, 1999; accepted October 7, 1999.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-
Morady F, Harvey M, Kalbfleisch SJ, El-Atassi R,
Calkins H, Langberg JL. Radiofrequency catheter ablation of VT in
patients with coronary artery disease.
Circulation. 1993;87:363–372.
[Abstract/Free Full Text]
-
Stevenson WG, Khan H, Sager P, Saxton LA,
Middlekauff HR, Natterson PD, Weiner I. Identification of reentry
circuit sites during catheter mapping and radiofrequency ablation of VT
late after myocardial infarction. Circulation. 1993;88:I647–I670.
-
Callans DJ, Zado E, Sarter BH, Schwartzman D,
Gottlieb CD, Marchlinski FE. Efficacy of radiofrequency ablation for VT
in healed myocardial infarction. Am J Cardiol. 1998;82:429–432.[Medline]
[Order article via Infotrieve]
-
Cassidy DM, Vassallo JA, Marchlinski FE, Buxton
AE, Unterecker WJ, Josephson ME. Endocardial mapping in humans in sinus
rhythm with normal LVs: activation patterns and characteristics of
electrograms. Circulation. 1984;70:37–42.
[Abstract/Free Full Text]
-
Shpun S, Gepstein L, Hayam G, Ben-Haim SA.
Guidance of radiofrequency endocardial ablation with real-time
three-dimensional magnetic navigation system. Circulation. 1997;96:2016–2021.
[Abstract/Free Full Text]
-
Gepstein L, Hayam G, Ben-Haim SA. A novel method
for nonfluoroscopic catheter-based electroanatomical mapping of the
heart: in vitro and in vivo accuracy results. Circulation. 1997;95:1611–1622.
[Abstract/Free Full Text]
-
Cassidy DM, Vassallo JA, Miller JM, Poll DS, Buxton
AE, Marchlinski FE, Josephson ME. Endocardial catheter mapping during
sinus rhythm: relation of underlying heart disease and
ventricular arrhythmia. Circulation. 1986;73:645–652.
[Abstract/Free Full Text]
-
Kienzle MG, Miller J, Falcone FA, Harken A,
Josephson ME. Intraoperative endocardial mapping during sinus rhythm:
relationship to site of origin of VT. Circulation. 1984;70:957–965.
[Abstract/Free Full Text]
-
Miller JM, Marchlinski FE, Buxton AE, Josephson
ME. Relationship between the 12-lead electrocardiogram
during VT and endocardial site of origin inpatients with
coronary artery disease. Circulation. 1988;77:759–766.
[Abstract/Free Full Text]
-
Josephson ME, Waxman HL, Cain ME, Gardner MJ,
Buxton AE. Ventricular activation during
ventricular endocardial pacing, II: role of pace-mapping to
localize the origin of VT. Am J Cardiol. 1982;50:11–22.[Medline]
[Order article via Infotrieve]
-
Moran JM, Kehoe RH, Loeb JM, Lichtenthal PR,
Sanders JH, Michaelis LL. Extended endocardial resection for the
treatment of VT and ventricular fibrillation. Ann
Thorac Surg. 1982;34:538–552.[Abstract]
-
Horowitz LN, Harken AH, Kastor JA, Josephson ME.
Ventricular resection guided by epicardial and endocardial
mapping for treatment of recurrent VT. N Engl J
Med. 1980;302:589–593.[Abstract]
This article has been cited by other articles:
 |
|
 |
|
  T. Sasano, M. R. Abraham, K.-C. Chang, H. Ashikaga, K. J. Mills, D. P. Holt, J. Hilton, S. G. Nekolla, J. Dong, A. C. Lardo, et al. Abnormal sympathetic innervation of viable myocardium and the substrate of ventricular tachycardia after myocardial infarction. J. Am. Coll. Cardiol., June 10, 2008; 51(23): 2266 - 2275. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Corrado, C. Basso, L. Leoni, B. Tokajuk, P. Turrini, B. Bauce, F. Migliore, A. Pavei, G. Tarantini, M. Napodano, et al. Three-Dimensional Electroanatomical Voltage Mapping and Histologic Evaluation of Myocardial Substrate in Right Ventricular Outflow Tract Tachycardia. J. Am. Coll. Cardiol., February 19, 2008; 51(7): 731 - 739. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Carbucicchio, M. Santamaria, N. Trevisi, G. Maccabelli, F. Giraldi, G. Fassini, S. Riva, M. Moltrasio, M. Cireddu, F. Veglia, et al. Catheter Ablation for the Treatment of Electrical Storm in Patients With Implantable Cardioverter-Defibrillators: Short- and Long-Term Outcomes in a Prospective Single-Center Study Circulation, January 29, 2008; 117(4): 462 - 469. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Dickfeld, P. Lei, V. Dilsizian, J. Jeudy, J. Dong, A. Voudouris, R. Peters, M. Saba, R. Shekhar, and S. Shorofsky Integration of Three-Dimensional Scar Maps for Ventricular Tachycardia Ablation With Positron Emission Tomography-Computed Tomography J. Am. Coll. Cardiol. Img., January 1, 2008; 1(1): 73 - 82. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Y. Reddy, M. R. Reynolds, P. Neuzil, A. W. Richardson, M. Taborsky, K. Jongnarangsin, S. Kralovec, L. Sediva, J. N. Ruskin, and M. E. Josephson Prophylactic Catheter Ablation for the Prevention of Defibrillator Therapy N. Engl. J. Med., December 27, 2007; 357(26): 2657 - 2665. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N.A. M. Estes III Ablation after ICD Implantation -- Bridging the Gap between Promise and Practice N. Engl. J. Med., December 27, 2007; 357(26): 2717 - 2719. [Full Text] [PDF]
|
|
|
|
 |
|
 C. Wolpert, H. Pitschner, and M. Borggrefe Evolution of ablation techniques: from WPW to complex arrhythmias Eur. Heart J. Suppl., December 1, 2007; 9(suppl_I): I116 - I121. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Zeppenfeld, M. J. Schalij, M. M. Bartelings, U. B. Tedrow, B. A. Koplan, K. Soejima, and W. G. Stevenson Catheter Ablation of Ventricular Tachycardia After Repair of Congenital Heart Disease: Electroanatomic Identification of the Critical Right Ventricular Isthmus Circulation, November 13, 2007; 116(20): 2241 - 2252. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. E. Eckart, T. W. Hruczkowski, U. B. Tedrow, B. A. Koplan, L. M. Epstein, and W. G. Stevenson Sustained Ventricular Tachycardia Associated With Corrective Valve Surgery Circulation, October 30, 2007; 116(18): 2005 - 2011. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Ashikaga, T. Sasano, J. Dong, M. M. Zviman, R. Evers, B. Hopenfeld, V. Castro, R. H. Helm, T. Dickfeld, S. Nazarian, et al. Magnetic Resonance Based Anatomical Analysis of Scar-Related Ventricular Tachycardia: Implications for Catheter Ablation Circ. Res., October 26, 2007; 101(9): 939 - 947. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Almendral and M. E. Josephson All Patients With Hemodynamically Tolerated Postinfarction Ventricular Tachycardia Do Not Require an Implantable Cardioverter-Defibrillator Circulation, September 4, 2007; 116(10): 1204 - 1212. [Full Text] [PDF]
|
|
|
|
|
|
D. Dalal, R. Jain, H. Tandri, J. Dong, S. M. Eid, K. Prakasa, C. Tichnell, C. James, T. Abraham, S. D. Russell, et al. Long-Term Efficacy of Catheter Ablation of Ventricular Tachycardia in Patients With Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy J. Am. Coll. Cardiol., July 31, 2007; 50(5): 432 - 440. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. G. Stevenson and K. Soejima Catheter Ablation for Ventricular Tachycardia Circulation, May 29, 2007; 115(21): 2750 - 2760. [Full Text] [PDF]
|
|
|
|
|
|
H. U. Klemm, R. Ventura, D. Steven, C. Johnsen, T. Rostock, B. Lutomsky, T. Risius, T. Meinertz, and S. Willems Catheter Ablation of Multiple Ventricular Tachycardias After Myocardial Infarction Guided by Combined Contact and Noncontact Mapping Circulation, May 29, 2007; 115(21): 2697 - 2704. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Aryana, A. d'Avila, E. K. Heist, T. Mela, J. P. Singh, J. N. Ruskin, and V. Y. Reddy Remote Magnetic Navigation to Guide Endocardial and Epicardial Catheter Mapping of Scar-Related Ventricular Tachycardia Circulation, March 13, 2007; 115(10): 1191 - 1200. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Volkmer, F. Ouyang, F. Deger, S. Ernst, M. Goya, D. Bansch, K. Berodt, K.-H. Kuck, and M. Antz Substrate mapping vs. tachycardia mapping using CARTO in patients with coronary artery disease and ventricular tachycardia: impact on outcome of catheter ablation. Europace, November 1, 2006; 8(11): 968 - 976. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Developed in Collaboration With the European Heart, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) J. Am. Coll. Cardiol., September 5, 2006; 48(5): e247 - e346. [Full Text] [PDF]
|
|
|
|
|
|
Writing Committee Members, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Europace, September 1, 2006; 8(9): 746 - 837. [Full Text] [PDF]
|
|
|
|
|
|
B. K. Kantharia, J. A. Patel, B. S. Nagra, and G. S. Ledley Electrical storm of monomorphic ventricular tachycardia after a cardiac-resynchronization-therapy-defibrillator upgrade Europace, August 1, 2006; 8(8): 625 - 628. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Bogun, E. Good, S. Reich, D. Elmouchi, P. Igic, K. Lemola, D. Tschopp, K. Jongnarangsin, H. Oral, A. Chugh, et al. Isolated Potentials During Sinus Rhythm and Pace-Mapping Within Scars as Guides for Ablation of Post-Infarction Ventricular Tachycardia J. Am. Coll. Cardiol., May 16, 2006; 47(10): 2013 - 2019. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Dickfeld, R. Kato, M. Zviman, S. Lai, G. Meininger, A. C. Lardo, A. Roguin, D. Blumke, R. Berger, H. Calkins, et al. Characterization of Radiofrequency Ablation Lesions With Gadolinium-Enhanced Cardiovascular Magnetic Resonance Imaging J. Am. Coll. Cardiol., January 17, 2006; 47(2): 370 - 378. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Dong, H. Calkins, S. B. Solomon, S. Lai, D. Dalal, A. Lardo, E. Brem, A. Preiss, R. D. Berger, H. Halperin, et al. Integrated Electroanatomic Mapping With Three-Dimensional Computed Tomographic Images for Real-Time Guided Ablations Circulation, January 17, 2006; 113(2): 186 - 194. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Schumacher, F. H. Gietzen, H. Neuser, J. Schummelfeder, M. Schneider, S. Kerber, R. Schimpf, C. Wolpert, and M. Borggrefe Electrophysiological Characteristics of Septal Hypertrophy in Patients With Hypertrophic Obstructive Cardiomyopathy and Moderate to Severe Symptoms Circulation, October 4, 2005; 112(14): 2096 - 2101. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. U. Klein and S. Reek "The Older the Broader": Electrogram Characteristics Help Identify the Critical Isthmus During Catheter Ablation of Postinfarct Ventricular Tachycardia J. Am. Coll. Cardiol., August 16, 2005; 46(4): 675 - 677. [Full Text] [PDF]
|
|
|
|
|
|
A. Verma, F. Kilicaslan, E. Pisano, N. F. Marrouche, R. Fanelli, J. Brachmann, J. Geunther, D. Potenza, D. O. Martin, J. Cummings, et al. Response of Atrial Fibrillation to Pulmonary Vein Antrum Isolation Is Directly Related to Resumption and Delay of Pulmonary Vein Conduction Circulation, August 2, 2005; 112(5): 627 - 635. [Abstrac |