World Journal of Cardiovascular Diseases, 2013, 3, 529-535 WJCD
http://dx.doi.org/10.4236/wjcd.2013.39084 Published Online December 2013 (http://www.scirp.org/journal/wjcd/)
Improvement of left ventricular function in patients with
persistent atrial tachyarrhythmia induced cardiomyopathy
undergoing radiofrequency ablation
Xiangmin Shi, Zhaoliang Shan, Hongyang Guo, Yutang Wang
Department of Cardiology, PLA General Hospital, Beijing, China
Received 25 September 2013; revised 29 October 2013; accepted 15 November 2013
Copyright © 2013 Xiangmin Shi et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. In accor-
dance of the Creative Commons Attribution License all Copyrights © 2013 are reserved for SCIRP and the owner of the intellectual
property Xiangmin Shi et al. All Copyright © 2013 are guarded by law and by SCIRP as a guardian.
ABSTRACT
Purpose: To investigate the alteration of left ven-
tricular function in subjects with persistent atrial
tachyarrhythmia induced cardiomyopathy (TIC) un-
dergoing radiofrequency ablation, and to study the
pathogenesis and effective treatment of TIC. Methods:
A total of 25 cases with persistent atrial tachyarrhy-
thmia and impaired left ventricular systolic function
were studied (16 men and 9 women, aged 53.3 ± 15.2
years), and all subjects underwent electrophysiological
study and radiofrequency ablation of atrial tachyar-
rhythmia under the guidance of CARTO system dur-
ing 2006.9-2011.8. Indexes related to cardia c functio n,
including left ventricular end diastolic diameter
(LVEDD), left ventricular ejection fraction (LVEF),
New York Heart Association functional classification
(NYHA class), 6 minutes walking test (6MWT), N-
terminal pro-brain natriuretic peptide (BNP) and 24
hours average heart rate (AHR), were analyzed at the
time point of 7 days, 3 and 6 months after the proce-
dure as well as 1 day before ablation. Results: No re-
fractory atrial arrhythmia recurred in all cases after
ablation, compared with LVEDD (51.7 ± 4.5 mm),
LVEF (39.0% ± 4.3%), number of patients with
NYHA class IV and III (n = 17), 6MWT (212 ± 56 m),
BNP (3622 ± 1860 ng/L) and AHR (112.5 ± 23.2 bpm)
before ablation, the index of LVEDD (45.2 ± 3.3 mm;
41.7 ± 2.5 mm; 40.5 ± 3.1 m), BNP (2429 ± 1355 ng/L;
1530 ± 866 ng/L; 1300 ± 520 ng/L), total number of
patients of NYHA class IV and III (n = 11; 3; 2) and
AHR (73.3 ± 15.3 bpm; 68.7 ± 13.5 bpm; 66.3 ± 13.6
bpm) significantly decreased (P < 0.05 ), LVEF (45.6 ±
3.5%; 51.5 ± 2.7%; 53.5 ± 3.1%) and 6MWT (262 ±
47 m; 305 ± 37 m; 313 ± 41 m) greatly increased (P <
0.05）in 7 days, 3 and 6 months after ablation respec-
tively. There was a statistical difference between 7 days
and 3 or 6 months after ablation in above-mentioned
indexes (P < 0.05) except AHR (P > 0.05), no signifi-
cant difference existed between 3 and 6 months in all
indexes (P > 0.05). Conclusion: long-lasting atrial ar-
rhythmia with rapid ventricular response could im-
pair left ventricle function, which could be reversed
within weeks after successful ablation and restoration
of sinus rhythm.
Keywords: Tachyarrhythmia-Induced Cardiomyopathy;
Radiofrequency Ablation; Left Ventricular Dysfunction;
Sinus Rhythm
1. INTRODUCTION
Atrial tachyarrhythmia is one of the most common en-
countered problems in clinical practice, long lasting of
which could result in tachycardia-induced cardiomyopa-
thy (TIC) [1], presenting cardiac enlargement and im-
paired left ventricular systolic function, similar to that of
idiopathic dilated cardiomyopathy (IDC) [2]. Meanwhile,
patients with IDC are susceptible to develop atrial ar-
rhythmia due to increased intra-atrium pressure [3],
which in turn further deteriorate the cardiac function and
cause refractory heart failure [4]. The aim of this study
was to investigate the impact of atrial tachyarrhythmia
on left ventricular function and its alteration after elimi-
nation of atrial arrhythmia by means of radiofrequency
ablation in 25 patients who already received optimized
medication for heart failure, and to study the role of ab-
lation in the treatment of TIC.
2. METHODS
2.1. Study Population
This study included 25 patients with persistent atrial ar-

X. M. Shi et al. / World Journal of Cardiovascular Diseases 3 (2013) 529-535 530
rhythmia with rapid ventricular response (16 men and 9
women, aged, 53.3 ± 15.2 years) referred for radiofre-
quency ablation during 2006.9-2011.8, number of sub-
jects with atrial fibrillation (AF), atrial flutter and atrial
tachycardia were 15, 7 and 3 respectively. All patients
had documented atrial tachyarrhythmia refractory to at
least 2 kinds of anti-arrhythmic drugs, of whom 4 sub-
jects suffered IDC prior to the development of arrhyth-
mia, the rest 21 cases were not detected underlying
structural heart disease at the first clinical visit and
gradually manifested symptoms of heart failure with the
prolongation of arrhythmia. Patients with hyperthyroid-
ism, old myocardial infarction, rheumatic valve disease,
chronic obstructive pulmonary disease (COPD) were not
recruited in this study. Most of patients were treated with
optimal medication of heart failure, including diuretics,
digoxin, β receptor antagonist, angiotension convert en-
zyme inhibitor (ACEI) or angiotension II receptor an-
tagonist (ARB) and vasodilators. Informed consent was
obtained from all subjects prior to procedure. Baseline
characteristics of patients undergoing radiofrequency
ablation are shown in Table 1.
2.2. Electrophysiological Study of Atrial
Fibrillation
Patients with persistent AF were kept on oral anticoagu-
lation with warfarin 1 month prior to procedure, warfarin
was withdrawn 3 days before ablation, all anti-arrhyth-
mic drugs were discontinued at least five half-lives. Eve-
ry patient after giving informed consent underwent an
electrophysiological study in a fasting and conscious-
sedated state. One decapolar mapping catheter (Biosense
Table 1. Baseline characteristics of patients undergoing radiof-
requency ablation.
Characteristics Values
Age (years)
Men (%)
LVEDD (mm)
LVEF (%)
Average heart rate (bpm)
Duration of arrhythmia (years)
Comorbidities
Hypertension (n)
Coronary artery disease requiring PCI
(n)
53.3 ± 15.2
16 (64%)
51.7 ± 4.5
39.0 ± 4.3
112.5 ± 23.2
2.8 ± 1.4
8 (32%)
5 (20%)
OSAHS (n) 5 (20%)
Diabetes mellitus (n) 6 (24%)
Idiopathic dilated cardiomyopathy (n)4 (16%)
Treatment
Diuretics (n) 21 (84%)
Inotropes (n) 20 (80%)
Beta blockers (n) 23 (92%)
ACEI or ARB (n) 23 (92%)
Vasodilators (n) 25 (100%)
Webster, Diamond Bar, CA) was positioned in the coro-
nary sinus (CS) through the right jugular vein access,
using the standard Brockenbrough technique [5], atrial
transseptal puncture was performed under fluoroscopic
guidance and two L1-type Swartz sheathes (St Jude Me-
dical, Minneapolis, MN) were transseptally introduced
into LA via right femoral vein. Intravenous heparin
5000U was administered immediately after atrial trans-
septal puncture and followed 1000U/h to maintain an
activated clotting time (ACT) of 300 - 350 s, the ACT
level was monitored every 30 min. In addition, heap-
rinized saline solution was continuously infused through
the transseptal sheath (3 mL/min) to avoid formation of
thrombi or air emboli. Selective PV venography was
performed to identify all PV ostia. One decapolar circu-
lar mapping catheter (Lasso, Biosense Webster) was
placed at the ostium of each PV to record PV potentials.
2.3. Circumferential Pulmonary Vein Isolation
(Cpvi)
The procedure of CPVI was performed under the guid-
ance of CARTO system (Biosense Webster), a 3.5 mm
saline-irrigated catheter (Navi-star, Thermocool, Bio-
sense Webster) was transseptally advanced into LA via
Swartz sheathe, LA geometry was reconstructed and
each PV ostium was tagged on it. Pulmonary vein isola-
tion was performed 5 to 10 mm outside of the PV ostia.
Ipsilateral pair of left and right PVs were isolated in one
circumferential lesion. Radiofrequency (RF) current was
delivered point by point at a target temperature 43˚C,
maximum power of 35 W, and an infusion rate of 17
mL/min. If AF could not terminate after the procedure of
CPVI, direct current cardioversion was performed to
restore sinus rhythm. The end point of CPVI was electri-
cal isolation of PV potentials, which was confirmed by
Lasso catheter mapping during sinus rhythm or isopro-
terenol infusion after 30 min. The end point was bidirec-
tional conduction block between LA and PVs. If AF was
not terminated by above-mentioned ablation, additional
ablation lines were created, including a bottom line con-
necting both inferior PVs and/or a mitral isthmus line.
Linear ablation at cavotricuspid isthmus was created in
patients with documented or inducible cavotricuspid
isthmus dependent atrial flutter, until bidirectional isth-
mus block was achieved.
2.4. Electrophysiological Study and Ablation of
Atrial Flutter and Atrial Tachycardia
For patients with atrial flutter, two quadripolar catheters
(2-5-2 mm, DAIG, St Jude Medical Inc, St Paul, MN,
USA) were positioned at the his bundle and right atrium
via the left femoral vein access, One decapolar mapping
catheter (Biosense Webster, Diamond Bar, CA) was po-

X. M. Shi et al. / World Journal of Cardiovascular Diseases 3 (2013) 529-535 531
sitioned in the coronary sinus (CS) through the right
jugular vein access. Activation sequence of atrial flutter
entrapment mapping was assessed by a 20-pole electrode
halo catheter (Biosense Webster, Diamond Bar, CA). The
electrophysiological definition of isthmus dependent
atrial flutter was demonstrated by the standard criteria
for entrainment mapping, a deflectable 5mm tipped qua-
dripolar catheter was used as the ablation catheter. RF
ablation started at the ventricular side of inferolateral
tricuspid annulus (TA) and end point was bidirectional
block of isthmus conduction. Energy was delivered at 50
W targeting 60˚C, this was followed by a series of dis-
crete applications along a line between the TA and IVC
orifice. A bidirectional isthmus block was demonstrated
by pacing technique which was performed at coronary
ostium and the low lateral right atrium. The line of block
was reevaluated 30 min after the catheter ablation. For
patients with atrial tachycardia (AT), we used CARTO
system to obtain three-dimensional mapping during AT
and ablated at the earliest activation sites or within supe-
rior vena cava (SVC) (Figure 1), a temperature-controll-
ed, 4-mm-tip ablating catheter (maximal temperature,
60˚C; maximal power, 30 W) with titration of power and
temperature was used for ablation. When a left-sided ori-
gin was suspected, access to the left atrium for mapping
and ablation was obtained transseptally using a Brocken-
brough needle. Acute procedural success was defined by
the absence of tachycardia or dissociation of SVC poten-
tials with right atrial activities in arrhythmia with SVC
origin (Figure 2) 30 min after ablation despite infusion
of isoproterenol and burst atrial pacing.
Figure 1. Successful ablation site in CARTO mapping system
(LAO projection), atrial tachycardia was converted into sinus
rhythm just after the ablation of target site located in the free
wall of SVC. LAO: left anterior oblique SVC: superior vena
cava.
Figure 2. ECG and intracardiac mapping after successful abla-
tion: SR was restored in surface ECG after ablation, irregular
rapid firing (arrow indicated) was recorded by the distal circu-
lar catheter in SVC, meanwhile, SR recorded by the proximal
circular catheter in HRA, indicating SVC-HRA exit block. (SR:
sinus rhythm; Lasso: circular catheter; CS: coronary sinus; RVa:
right ventricular apex; HRA: high right atrium; ABL: ablation
catheter).
2.5. Postoperative Care and Follow-Up
After the procedure, oral anticoagulation with warfarin
was resumed and the normalized ratio (INRs) was main-
tained in the therapeutic range for subjects with AF,
meanwhile, oral aspirin (75 - 100 mg/day) recommended
for 1 month to prevent thromboembolic complications
for patients with atrial flutter and atrial tachycardia. Fol-
low up was at 7 days, 3 and 6 months, all medication for
heart failure continued during the period of follow up.
Indexes related to cardiac function, including left ven-
tricular end diastolic diameter (LVEDD), left ventricular
ejection fraction (LVEF), New York Heart Association
functional classification(NYHA class), 6 minutes walk-
ing test (6MWT), and N-terminal pro-brain natriuretic
peptide (BNP), were obtained 1 day before ablation and
at 7 days, 3 and 6 months after the procedure.
2.6. Statistical Analysis
Continuous variables were expressed as mean±SD and
categorical variables as proportions (%). Data were ana-
lyzed with unpaired t-test, categorical variables were
compared with χ2 tests. A value of <0.05 was considered
statistically significant. All analyses were performed us-
ing SPSS 12.0.
3. RESULTS
3.1. Acute Procedure Result
CPVI was performed in all 15 AF subjects, of which 5

X. M. Shi et al. / World Journal of Cardiovascular Diseases 3 (2013) 529-535 532
AF converted into sinus rhythm spontaneously during the
process of CPVI and the other 10 cases required direct
current cardioversion to restore SR, bottom line and ca-
votricuspid line were created in 4 and 3 cases respec-
tively. 7 atrial flutter patients underwent right atrial ca-
votricuspid isthmus linear ablation, of which 6 were
counter clockwise (CCW) and 1 was clockwise (CW)
isthmus-dependent activation. For patients with atrial
tachycardia, 2 cases originated from crista terminalis (CT)
and the other one arising from superior vena cava (SVC).
SVC isolation (SVCI) was achieved under the guidance
of CARTO system (Figure 1) and Persistent rapid foci
firing within SVC still remained in the presence of sinus
rhythm restored after SVCI (Figure 2). No major com-
plication occurred except mild pericardial effusion in 2
patients receiving CPVI and transient phrenic nerve pal-
sies in 1 AT case undergoing ablation within SVC (Table
2). In the follow up, 3 AF and 1 AT subjects presented
recurrence of paroxysmal atrial tachyarrhythmia within 1
month after procedure, which were controlled by intra-
venous administration of amiodarone.
3.2. Alteration of Heart Function in the
Follow-Up
All subjects with tachycardia induced cardiomyopathy
(TIC) continued unchanged medication during the 6
months follow-up, compared with indexes of heart func-
tion one day before procedure, LVEDD, NYHA class,
BNP, 6MWT and LVEF significantly improved one week
after ablation, and demonstrated further improvement in
the follow-up, although there was no statistical difference
between 3 and 6 months (Table 3), the trend of im-
provement could be found.
4. DISCUSSION
Tachycardia-induced cardiomyopathy (TIC) is deterio-
rating in ventricular function secondary to sustained ta-
chycardia, which can lead to dilated cardiomyopathy and
Table 2. Comparison of different atrial tachyarrhythmia abla-
tion.
Procedure
time (min)
Fluoroscopic time
(min)
Complication
(n)
AF (n = 15) 156 ± 43 63 ± 17 Pericardial effusion(2)
Af (n = 7)
CCW (n = 6) 52 ± 18 28 ± 11 0
CW (n = 1) 48 25 0
AT (n = 3)
CT (n = 2) 68 ± 14 36 ± 13 0
SVC (n = 1) 29 13
transient phrenic
nerve palsies (1)
AF: atrial fibrillation; Af: atrial flutter; AT: atrial tachycardia; CCW:
counter clockwise isthmus-dependent; CW: clockwise isthmus-dependent;
CT: crista terminalis; SVC: superior vena cava.
Table 3. Comparison of heart function before and after abla-
tion.
−1 day 7 days 3 months 6 months
LVEDD (mm)51.7 ± 4.545.2 ± 3.3a 41.7 ± 2.5abc 40.5 ± 3.1ab
LVEF (%)39.0 ± 4.345.6 ± 3.5a 51.5 ± 2.7abc 53.5 ± 3.1ab
6-MWT (m)212 ± 56 262 ± 47a 305 ± 37 abc 313 ± 41ab
BNP (ng/L)3622 ± 18602429 ± 1355a 1530 ± 866abc 1300 ± 520ab
AHR (bpm)112.5 ± 23.273.3 ± 15.3 a 68.7 ± 13.5aec 66.3 ± 13.6 ae
NYHA
IV+ III (n)17(68%) 11(44%) a 3(12%)abc 2(8%)ab
II (n) 8(32%) 14(56%) d 14(56%)aec 13(52%)ae
I (n) 0(0%) 0(0%) d 8(32%)abc 10(40%)ab
aP < 0.05 compared with −1 day; bP < 0.05 compared with 7 days; cP > 0.05
compared with 6 months; dP > 0.05 compared with −1 day; eP > 0.05
compared with 7 days; −1 day: one day before procedure; AHR: average
heart rate.
symptom of heart failure [6]. Some studies proved that
TIC was partially or completely reversible after nor-
malization of the heart rate [7]. In patients with previous
underlying IDC, persistent tachyarrhythmia plays a key
role in the deterioration of cardiac function [8], therefore,
in the management of refractory heart failure, much at-
tention should be paid to heart rate. For patients without
structural heart disease, prolonged tachyarrhythmia could
result in development of left ventricular (LV) dysfunc-
tion [9], and a high suspicion of TIC is needed in the
evaluation of a patient with new onset heart failure in the
presence of atrial tachyarrhythmia. The diagnosis of TIC
can be made when an improvement in function is seen
after correction of arrhythmia [10]. The mechanism re-
sponsible for TIC has not been elucidated, and a number
of theories have been proposed to explain the etiology of
TIC, including depletion of high-energy phosphates, ab-
normal cellular remodeling and calcium handling [11,12].
It has also been proposed that chronic rapid heart rates
could result in ischemia, which subsequently leads to
reversible LV dysfunction due to myocardial shock or
stunning [13].
In this study, 21 patients exhibited structural normal
heart at first visit due to arrhythmia, and gradually de-
veloped symptoms of heart failure (HF) secondary to
sustainted atrial tachyarrhythmia, only 4 patients previ-
ously suffered from IDC prior to occurrence of arrhyth-
mia which consequently further aggravated HF. All sub-
jects manifested remarkable improvement of LV func-
tion after resolution of atrial tachyarrhythmia, which
supported the diagnosis of TIC because other forms of
cardiomyopathy with poor LV function rarely demon-
strated significant reverse of progression of disease within
a short period of time [14]. It was reported that AF was
the commonest cause of TIC, moreover, greater than
50% patients with AF and LV dysfunction who have
some degree of TIC [15]. In our research AF accounted

X. M. Shi et al. / World Journal of Cardiovascular Diseases 3 (2013) 529-535 533
for 60% of all subjects with TIC.
In terms of treatment for HF patients with AF, AF-
FIRM study [16] demonstrated that pharmacological
management for rhythm control was not superior to rate
control in reducing mortality, hospitalization and NYHA
functional class. However, rhythm control group was
associated with increased hospitalization due to side ef-
fects of antiarrhythmic drugs. Catheter-based therapy for
refractory AF in HF subjects has been an effective
therapeutic option over the past decade, which exhibited
better outcome than pharmacological therapy. Major
procedures include atrio-ventricular node (AVN) abla-
tion plus pacemaker implant and catheter-based rhythm
control, radiofrequency ablation (RA) for pulmonary
vein isolation (PVI) could restore atrioventricular and
interventricular synchrony, in PABA study [17]. HF pa-
tients underwent PVI had better left ventricular function,
6 minutes walk distance and higher LVEF in contrast to
AVN ablation with pacemaker implant at 6 months. RA
has been proved to be the most efficient therapy to elimi-
nate AF in HF patients so far, circumferential pulmonary
vein isolation with additional line ablation has became
the established approach [18] based on the finding that
most cases of atrial fibrillation are triggered by ectopic
foci originating from pulmonary veins [19]. Traditionally,
for HF patients with AF, the therapeutic strategy is fo-
cused on correcting heart failure and lowering heart rate
rather than converting AF, because it is commonly be-
lieved that left ventricular dysfunction plays a pivotal
role in the initiation and maintance of AF [20]. This
study demonstrated high success rate of RA in the treat-
ment of AF in TIC patients including 4 subjects with
underlying IDC, and RA could exert significant benefi-
cial impact on left ventricular dysfunction recovery,
which supported the fact that AF was an important com-
ponent in the pathogenesis of TIC.
In one study [21] of patients with AF refractory to
pharmacological treatment, catheter ablation was equally
effective in patients with HF (LVEF < 45% with NYHA
class II or higher symptoms) as it was in patients without
HF, meanwhile, the LVEF was significantly increased by
21% at 12 months. Our study demonstrated 14.5% im-
provement of LVEF at the 6-month follow-up. Another
clinical trial [22] indicated that ablation procedure was
successful in maintaining sinus rhythm in 73% patients
with impaired left ventricular function at 14 months, in
our study, after completion of RA, only 4 patients suf-
fered recurrence of arrhythmia which subsequently was
controlled by amiodarone, the arrhythmia-free rate was
84%.
Atrial flutter is another common atrial arrhythmia in
clinical practice, compared with AF, which seems to be
more susceptible to suffering from TIC due to more rapid
ventricular response [23]. Our research revealed that all 7
atrial flutters were cavotricuspid isthmus-dependent. Ty-
pical isthmus linear ablation could successfully resolve
atrial flutter. 3 subjects with TIC were identified as atrial
tachycardia in EPS, in which 2 were CT origin and the
other one arising from SVC, and these sites are common
foci of atrial tachycardia [24]. In this study, only 2 pa-
tients receiving CPVI were detected mild pericardial
effusion and 1 AT case presented transient phrenic nerve
palsies undergoing ablation within SVC, which proved
RA was a relative safe procedure for TIC subjects.
In the follow-up, we observed that heart function im-
proved dramatically within one week after the procedure.
Before RA, a total of 17 subjects were classified as
NYHA class IV and III, and 7 days later the number de-
creased to 11, meanwhile, LVEDD reduced significantly
from 51.7 ± 4.5 mm to 45.2 ± 3.3 mm, which indicated
rapid reverse remodeling of left ventricular after resolu-
tion of tachyarrhythmia. Other indexes referring to heart
function including LVEF, 6-MWT and BNP simultane-
ously improved during this period. In the following 6
months, the above mentioned indexes further improved,
however, there was no statistical significance between 3
and 6 months. Our results indicated that most patients
could restore normal heart function within 3 months,
even 4 subjects with underlying IDC benefited much
from interruption of tachyarrhythmia, who demonstrated
increased exercise capacity and resolution of heart failure
symptoms after ablation. On admission, all of them were
NYHA class IV, however, 7 days, 3 months and 6
months after the procedure, the numbers of NYHA class
IV were 1, 0 and 0 respectively. Our findings were com-
patible with the prior animal experiments, which proved
that heart failure could result from rapid atrial pacing and
prompt cessation of pacing could result in improvement
of left ventricular function 1 day after termination and
restore normal function within weeks [12].
In this study, all patients had received intensive medi-
cation for heart failure over 3 months on admission whi-
ch was proved to be ineffective before ablation, one pro-
minent characteristic of all subjects was poor-controlled
ventricular response, and 24-hour ambulatory ECG
monitor indicated average heart rate reached 112.5 ±
23.2 bpm. After ablation, previous medical therapy re-
mained unchanged in all patients, however, heart rate
significantly decreased and was maintained in normal
range with regular rhythm, within one week after proce-
dure, reverse of heart failure could be observed in all
affected patients, which proved that atrial arrhythmia
with rapid and irregular ventricular response plays a cen-
tral role in the pathogenesis and development of CIT.
Our study confirmed that CIT was a common form of
left ventricular dysfunction in patients with atrial tachy-
arrhythmia, if pharmacological therapy could not resolve

X. M. Shi et al. / World Journal of Cardiovascular Diseases 3 (2013) 529-535 534
and slow the progression of heart failure, RA was an
effective alternative.
REFERENCES
[1] Miyasaka, Y., Barnes, M.E., Gersh, B.J., Cha, S.S., Bai-
ley, K.R., Abhayaratna, W.P., Seward, J.B. and Tsang,
T.S. (2006) Secular trends in incidence of atrial fibrilla-
tion in Olmsted County, Minnesota, 1980 to 2000, and
implications on the projections for future prevalence.
Circulation, 114, 119-125.
http://dx.doi.org/10.1161/CIRCULATIONAHA.105.5951
40
[2] Bounhoure, J.P., Boveda, S., Albenque, J.P., et al. (2006)
Arrhythmia-induced dilated cardiomyopathies. Bulletin
del Academie de Nationale de Medecine, 190, 1225-1235.
[3] Ehrlich, J.R., Nattel, S. and Hohnloser, S.H. (2002) Atrial
fibrillation and congestive heart failure: Specific consid-
erations at the intersection of two common and important
cardiac disease sets. Journal of Cardiovascular Electro-
physiology, 13, 399-405.
http://dx.doi.org/10.1046/j.1540-8167.2002.00399.x
[4] Grogan, M., Smith, H.C., Gersh, B.J. and Wood, D.L.
(1992) Left ventricular dysfunction due to atrial fibrilla-
tion in patients initially believed to have idiopathic di-
lated cardiomyopathy. The American Journal of Cardi-
ology, 69, 1570-1573.
http://dx.doi.org/10.1016/0002-9149(92)90705-4
[5] De Ponti, R., Cappato, R., Curnis, A., et al. (2006) Trans-
septal catheterization in the electrophysiology laboratory:
Data from a multicenter survey spanning 12 years. Jour-
nal of the American College of Cardiology, 47, 1037-
1042. http://dx.doi.org/10.1016/j.jacc.2005.10.046
[6] Mclaran, C.J., Gersh, B.J., Sugrue, D.D., et al. (1985)
Tachycardia induced myocardial dysfunction. A reversi-
ble phenomenon? British Heart Journal, 53, 323-327.
http://dx.doi.org/10.1136/hrt.53.3.323
[7] Khasnis, A., Jongnarangsin, K., Abela, G., et al. (2005)
Tachycardia-induced cardiomyopathy: A review of lit-
erature. Pacing and Clinical Electrophysiology, 28, 710-
721. http://dx.doi.org/10.1111/j.1540-8159.2005.00143.x
[8] Scheinman, M.M. (1998) Atrial fibrillation and conges-
tive heart failure: The intersection of two common dis-
eases. Circulation, 98, 941-942.
http://dx.doi.org/10.1161/01.CIR.98.10.941
[9] Umana, E., Solares, C.A. and Alpert, M.A. (2003) Tachy-
cardia-induced cardiomyopathy. The American Journal of
Medicine, 114, 51-55.
http://dx.doi.org/10.1016/S0002-9343(02)01472-9
[10] Simantirakis, E.N., Koutalas, E.P. and Vardas, P.E. (2011)
Arrhythmia-induced cardiomyopathies: The riddle of the
chicken and the egg still unanswered?” Europace, 14,
466-473. http://dx.doi.org/10.1093/europace/eur348
[11] Fenelon, G., Wijns, W., Andries, E. and Brugada, P. (1996)
Tachycardiomyopathy: Mechanisms and clinical implica-
tions. Pacing and Clinical Electrophysiology, 19, 95-106.
http://dx.doi.org/10.1111/j.1540-8159.1996.tb04796.x
[12] Shinbane, J.S., Wood, M.A., Jensen, D.N., Ellenbogen,
K.A., Fitzpatrick, A.P. and Scheinmann, M.M. (1997)
Tachycardia-induced cardiomyopathy: A review of ani-
mal models and clinical studies. Journal of the American
College of Cardiology, 29, 709-715.
http://dx.doi.org/10.1016/S0735-1097(96)00592-X
[13] Moe, G.W., Montgomery, C., Howard, R.J., et al. (1993)
Left ventricular myocardial blood flow, metabolism and
effects of treatment with enalapril: Further insights into
the mechanisms of canine experimental pacing-induced
heart failure. Journal of Laboratory and Clinical Medi-
cine, 121, 294-301.
[14] Iyer, V.R. (2008) Ventricular dysfunction: Tachycardia-
induced cardiomyopathy. Indian Pacing and Electro-
physiology Journal, 8, S122-S129.
[15] Redfield, M.M., Kay, G.N., Jenkins, L.S., et al. (2000)
Tachycardia related cardiomyopathy: A common cause of
ventricular dysfunction in patients with atrial fibrillation
refered for AV node ablation. Mayo Clinic Proceedings,
75, 790-795. http://dx.doi.org/10.4065/75.8.790
[16] Freudenberger, R.S., Wilson, A.C. and Kostis, J.B. (2007)
Comparison of rate versus rhythm control for atrial fib-
rillation in patients with left ventricular dysfunction (from
the AFFIRM Study). American Journal of Cardiology,
100, 247-252.
http://dx.doi.org/10.1016/j.amjcard.2007.02.101
[17] Khan, M.N., Jais, P., Cummings, J., et al. (2008) Pulmo-
nary-vein isolation for atrial fibrillation in patients with
heart failure. The New England Journal of Medicine, 359,
1778-1785. http://dx.doi.org/10.1056/NEJMoa0708234
[18] Verma, A., Macle, L., Cox, J., et al. (2011) CCS Atrial
Fibrillation Guidelines Committee. Canadian Cardiovas-
cular Society atrial fibrillation guidelines 2010: Catheter
ablation for atrial fibrillation/atrial flutter. Canadian
Journal of Cardiology, 27, 60-66.
http://dx.doi.org/10.1016/j.cjca.2010.11.011
[19] Bourke, J., Dunuwille, A., O’Donnell, D., et al. (2005)
Pulmonary vein ablation for idiopathic atrial fibrillation:
Six month outcome of first procedure in 100 consecutive
patients. Heart, 91, 51-57.
http://dx.doi.org/10.1136/hrt.2003.023093
[20] Ehrlich, J.R., Nattel, S. and Hohnloser, S.H. (2002) Atrial
fibrillation and congestive heart failure: Specific consid-
erations at the intersection of two common and important
cardiac disease sets. Journal of Cardiovascular Electro-
physiology, 13, 399-405.
http://dx.doi.org/10.1046/j.1540-8167.2002.00399.x
[21] Hsu, L.F., Jais, P., Sanders, P., et al. (2004) Catheter
ablation for atrial fibrillation in congestive heart failure.
The New England Journal of Medicine, 351, 2373-2383.
http://dx.doi.org/10.1056/NEJMoa041018
[22] Chen, M.S., Marrouche, N.F., Khaykin, Y., et al. (2004)
Pulmonary vein isolation for the treatment of atrial fibril-
lation in patients with impaired systolic function. Journal
of the American College of Cardiology, 43, 1004-1009.
http://dx.doi.org/10.1016/j.jacc.2003.09.056
[23] Scheuemeyer, F.X., Grafstein, E., Heilbron, B., et al.
(2011) Emergency department management and 1-year

X. M. Shi et al. / World Journal of Cardiovascular Diseases 3 (2013) 529-535 535
outcomes of patients with atrial flutter. Annals of Emer-
gency Medicine, 57, 564-571.
http://dx.doi.org/10.1016/j.annemergmed.2010.09.027
[24] Zhao, Z., Li, X. and Guo, J. (2009) Electrophysiological
characteristics of atrial tachycardia originating from the
superior vena cava. Journal of Interventional Cardiac
Electrophysiology, 24, 89-94.
http://dx.doi.org/10.1007/s10840-008-9324-0