SPECIAL COMMENTARY
Supraventricular tachycardia causing heart failure
Mahmoud Houmsse, Jaret Tyler and Steven Kalbfleisch
Department of Cardiovascular Medicine, Section of
Electrophysiology, The Ohio State University,
Columbus, Ohio, USA
Correspondence to Mahmoud Houmsse, MD, 473 W.
12th Avenue, Columbus, OH 43235, USA
Tel: +1 614 293 4967; fax: +1 614 293 5614;
e-mail: mahmoud.houmsse@osumc.edu
Current Opinion in Cardiology 2011,
26:261–269
Purpose of review
Supraventricular tachycardia (SVT) causing heart failure is an important cause of
tachycardia-induced cardiomyopathy.
Recent findings
Advances in anti-arrhythmic drugs to achieve either rate or rhythm control, curative
ablative therapy directed at the underlying tachycardia mechanism to restore sinus
rhythm, and atrioventricular junction ablation with permanent pacemaker placement for
better rate control have improved the outcome of SVT management and subsequently
improved the heart failure symptomatology and in some cases reversed remodeling of
the cardiac dysfunction.
Summary
The aim of this review is to provide the reader with clinical presentation as well as the
common SVTs causing heart failure, pathophysiology of SVT causing heart failure,
evaluation and management of SVT causing heart failure, and prognosis of SVT causing
heart failure.
Keywords
heart failure, supraventricular tachycardia, tachycardia-induced cardiomyopathy
Curr Opin Cardiol 26:261–269
ß 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins
0268-4705
Introduction
Supraventricular tachycardia (SVT) causing heart failure
and tachycardia-induced cardiomyopathy (TIC) are often
used interchangeably. Although SVT is the most common cause of TIC, it is a broad term that also includes
heart failure caused by ventricular arrhythmias. Ventricular arrhythmias causing cardiomyopathy and heart failure will be discussed in a separate article in this journal.
Long-standing persistent SVT is a well known cause of
nonischemic cardiomyopathy and heart failure [1–4].
SVT-related TIC is a treatable and often reversible
cardiomyopathy that is usually a diagnosis of exclusion
in a patient with reduced systolic function and an appropriate arrhythmia. In many patients, it is often difficult to
determine which came first, the cardiomyopathy or the
arrhythmia, and therefore a firm diagnosis of TIC cannot
be made until improvement in systolic function is
demonstrated after control of the arrhythmia. The
increasing prevalence and costs of heart failure worldwide
have focused medical efforts on preventive measures and
a search for potentially reversible causes of heart failure.
Chronic tachycardia has long been linked to the development of congestive cardiomyopathy through chamber
dilatation and ventricular dysfunction resulting from structural and cellular changes that occur as a result of the rapid
0268-4705 ß 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins
heart rates [1–5]. The first human report of SVT causing
TIC was in 1913 when Gossage and Hicks [6] noted left
ventricular dilation and hypertrophy in a young patient
with atrial fibrillation. Experimental studies on SVT causing TIC using animal models were first described in 1962
[7]. These animal models showed that sustained, rapid
pacing could reproducibly produce variable degrees of
systolic and diastolic dysfunction and that the degree of
cardiac dysfunction was dependent on the rate and
duration of pacing, with faster rates and longer durations
causing greater degrees of dysfunction [8,9,10]. Initial
hemodynamic changes could occur as early as 24 h into
rapid pacing, with continued deterioration in ventricular
function occurring over the following weeks to months
[10]. Recovery was equally predictable, with improvement
in ventricular function within 1–2 weeks after cessation of
pacing [10]. Cellular and structural dysfunctions, however,
have been found to persist after the early recovery period
in many cases and this is thought to play a role in the risk of
recurrent cardiomyopathy following the initial successful
treatment for SVT-related TIC [8,10,11].
Clinical presentation
Many patients with SVT-related TIC present with signs
and symptoms of heart failure, including exertional dyspnea, orthopnea, and edema. It can often be difficult to
determine whether the tachycardia is the cause or the
result of cardiomyopathy.
DOI:10.1097/HCO.0b013e328345b010
262 Cardiac failure
TICs have been associated with essentially any SVT that
is frequent and fairly persistent. The most common
supraventricular arrhythmias causing TIC are atrial fibrillation and atrial flutter; however, the subgroups of paroxysmal SVT (PSVT) such as atrial tachycardia (Fig. 1a),
atrioventricular nodal re-entrant tachycardia (AVNRT),
and atrioventricular re-entrant tachycardia (AVRT)
(especially the ‘permanent junctional reciprocating
tachycardia (PJRT)’ variant, Fig. 2a) can also be a cause
[9,11,12,13]. SVT-related TIC can occur over a range
of ages, from in-utero to the elderly, and is generally
thought to take months of a fairly persistent arrhythmia to
develop [14,15]. The type of arrhythmias causing TIC
varies with the age of the patient, with certain forms of
PSVT being more common in younger patients and atrial
fibrillation and flutter being more common in older
patients. Although no absolute heart rate cutoff exists,
many consider persistent rates greater than 100 beats/min
are necessary to develop relatively early-onset left ventricular dysfunction; however, even slower incessant
arrhythmias could lead to the insidious development of
heart failure if left unchecked over long periods [11].
Animal models have been studied extensively in the assessment of SVT-related TIC. These studies have shown that
rapid pacing can cause reduction in systolic function and
cardiac output with a secondary increase in filling pressures
and systemic vascular resistance and that cessation of
pacing reverses cardiomyopathy [16–19]. Such findings
have also been described in numerous clinical reports of
SVT-related TIC. In these clinical cases, termination of the
tachycardia resulted in an improvement in clinical symptoms, reduction in left ventricular chamber size, and an
increase in left ventricular systolic function [20].
The degree of left ventricular dysfunction has clearly
been shown to correlate with the rate and duration of the
tachycardia, but ironically, in a clinical setting, very rapid
arrhythmias rarely lead to TIC because these patients
usually develop rate-related symptoms and present for
treatment early before a myopathy develops [21]. One of
the most important factors for the development of TIC is
the total tachycardia burden over time. In patients with
relatively slow and asymptomatic tachycardias, the
arrhythmia may be incessant and the patient may not
present until heart failure symptoms develop. Other factors that may also contribute to the development of TIC
include the type of arrhythmia, atrioventricular relationship during the arrhythmia, pattern of the arrhythmia
(paroxysmal vs. persistent), irregularity of the QRS complexes, and presence of underlying heart disease [22].
Pathophysiology
Before reviewing the available data regarding the gross
and cellular changes that occur in SVT-related TIC, it is
Key points
Long-standing persistent supraventricular tachycardia (SVT) is a well known cause of nonischemic
cardiomyopathy and heart failure, which is known
as tachycardia-induced cardiomyopathy (TIC).
SVT-related TIC is a treatable and often reversible
cardiomyopathy that is usually a diagnosis of exclusion, evaluation, and management of SVT causing
heart failure.
The most common supraventricular arrhythmias
causing TIC are atrial fibrillation and atrial flutter.
Standard workup for cardiomyopathies should
include a thorough history and physical, laboratory
assessment, echocardiogram, and ischemic evaluation. If initial workup is negative, then TIC should
be considered.
Many patients with SVT-related TIC present with
signs and symptoms of heart failure, including exertional dyspnea, orthopnea, and edema. It can often
be difficult to determine whether the tachycardia is
the cause or the result of cardiomyopathy.
The goal of treatment is to control the tachycardia
through rate or rhythm control, thereby improving a
patient’s symptoms, reversing ventricular dysfunction, and preventing future cardiomyopathy.
Despite the apparent normalization of systolic function with control of the tachycardia, cellular and
structural abnormalities of the myocardium may
persist and cause early recurrence of cardiac dysfunction when optimal medical therapy of cardiomyopathy and heart failure is stopped.
A small subset of treated SVT-related TIC patients
had sudden cardiac death after resolution of ventricular dysfunction, supporting the observation of
enduring cellular and molecular abnormalities.
Indefinite heart failure medical treatment and frequent follow-up of SVT-related TIC patients
should be implemented after tachycardia control
or elimination. Implantable cardioverter defibrillator therapy needs to be considered for primary
prevention in patients who have persistent
reduction or recurrence of depressed left ventricular
ejection fraction, despite control of the tachycardia.
important to keep in mind that the interaction between
the myocardial cellular and extracellular matrix (ECM)
via the basement membrane is essential to generate and
maintain adequate left ventricular contractility.
Pacing-induced TIC in animal models results in enlargement of the cardiac chamber, thinning of the chamber
wall with an elevation in wall stress, and decline in the
cardiac pump performance as a result of a significant
increase in myocardial water accumulation [2,23,24]. In
animal studies, SVT-related TIC also resulted in changes
in cellular function and ECM composition (see below) in
Supraventricular tachycardia causing heart failure Houmsse et al. 263
Figure 1 Paroxysmal atrial tachycardia and curative ablative therapy of incessant repetitive pulmonary vein tachycardia
(a) Paroxysmal atrial tachycardia originating from right superior pulmonary vein (RSPV). This was confirmed during electrophysiology study. The P wave
axis mimics a sinus node P wave, but the rhythm is clearly abnormal, indicative of an incessant repetitive pulmonary vein tachycardia. (b) Curative
ablative therapy of incessant repetitive pulmonary vein tachycardia. Twelve-lead electrocardiogram during radio frequency ablation at the right superior
pulmonary vein. Immediately after the onset of the ablation, there was termination of the atrial tachycardia with restoration of sinus rhythm as seen in the
last four beats.
the heart, and these changes demonstrated significant
reversal after tachycardia termination [25,26].
(3) distortion of the sacrolemma–basement membrane
interface, which promotes extracellular remodeling
and scar formation.
Cellular changes are
ECM changes are as follows:
(1) significant increase in myocyte length,
(2) significant reduction in the anchoring of the myocyte
to the basement membrane, and
(1) SVT-causing TIC resulted in a reduction in collagen
concentration and cross-linking, diminished myocyte
264 Cardiac failure
Figure 2 ECG of a supraventricular tachycardia patient during sinus rhythm
(a) Twelve-lead ECG of a 29-year-old man with frequent and nearly incessant paroxysmal supraventricular tachycardia. This ECG demonstrates a
classic long RP tachycardia, the differential diagnosis of which includes permanent junctional reciprocating tachycardia (PJRT), atypical atrioventricular
node re-entrant tachycardia (AVNRT) and atrial tachycardia (AT). Electrophysiologic testing is required to differentiate the tachycardia type, but,
clinically, the incessant nature of the tachycardia is most consistent with either PJRT or AT. In this case, the patient was found to have PJRT and the
accessory pathway was successfully ablated near the coronary sinus ostium. (b) Twelve-lead ECG of the same PJRT patient during sinus rhythm:
please notice the short PR interval without pre-excitation (no delta wave). PJRT patients almost never have a delta wave. Therefore, the lack of a delta
wave does not rule out atrioventricular re-entrant tachycardia (AVRT).
basement membrane adhesion capacity, and
increased proteoglycans.
(2) These changes improved with the resolution of SVT
and resulted in an increased collagen concentration
and a normalization of myocyte adhesion capacity
and proteoglycan distribution.
Incessant SVT-related TIC was also associated with
significant structural alterations to the myocardial capillary vasculature and myocyte injury. These alterations
in capillary structure and distribution were associated
with an increase in coronary vascular resistance,
reduced myocardial blood flow, and an increase in
capillary diffusion distances. These changes in capillary
structure and myocardial blood flow may explain, at
least in part, the ventricular dysfunction and myocardial
injury observed with chronic SVT [27]. Spinale et al.
[28] reported on their observations of subendocardial
injury in SVT-related TIC. Their findings showed
the potential relationship between the structural
changes in capillary vasculature, abnormal myocardial
blood flow and subsequent subendocardial injury, and
Supraventricular tachycardia causing heart failure Houmsse et al. 265
left ventricular remodeling induced by SVT-related
TIC.
Changes in mitral valve function have also been reported
in TIC. Most of these reports describe functional mitral
regurgitation as a result of changes in the left ventricular
chamber geometry [29,30], annular dilatation [31], and
papillary muscle tethering [32,33], leading to decreased
leaflet coaptation in the septal–lateral orientation [34].
Stephens et al. [35] did report on structural changes in
the mitral valve leaflet during TIC. These changes
include greater cell density, loss of leaflet-layered structure, and greater collagen and elastic fiber turnover.
Evaluation
The incidence and prevalence of SVT-related TIC are
not exactly known; however, as it is treatable, and often
reversible, it should be aggressively pursued as a possible
cause of a cardiomyopathy if any significant history of a
dysrhythmia is present. Although arrhythmias have been
shown to be a contributing factor in approximately 6%
of hospital heart failure admissions, the percentage of
patients having an arrhythmia as the primary cause of a
their cardiomyopathy would be expected to be considerably smaller. Unexplained cardiomyopathy work-up
needs to be comprehensive, including common causes
(ischemic heart disease, hypertensive heart disease, and
valvular heart disease) and uncommon causes [infiltrative
heart disease, toxic insults (e.g., alcohol, chemotherapy),
familial disease, tachycardia-induced cardiomyopathy].
Idiopathic cardiomyopathy is the final diagnosis if the
above work-up is negative. The diagnosis of a pure TIC is
really one of exclusion and requires the presence of an
appropriate arrhythmia and the absence of other significant cardiac disease. Even with the existence of underlying cardiac disease, the presence of a persistent tachycardia can lead to worsening cardiac function and the
patient may have a combined cardiomyopathy, with TIC
playing at least a partial role. There is no definitive test
for a TIC and the real evidence that a TIC was present
can only be seen after 2–3 months of follow-up by
demonstrating improvement in left ventricular function
after appropriate arrhythmia control.
The approach to a patient with new, systolic cardiomyopathy includes a thorough history and physical and
guided diagnostic tests. While taking the history, one
needs to keep in mind that some SVTs are much more
common in specific clinical settings. Some variables that
can influence the type of tachycardia involved in the
development of a TIC are listed below.
(1) Age: SVT can occur at any age, but the relative
proportion of different types of SVT is strongly influenced by the age of the patient. Re-entrant tachycardias due to accessory pathways, such as PJRT are more
common in younger patients, as are incessant atrial
tachycardias. Atrial fibrillation and flutter (Fig. 3) are
much more common in older patients (>60 years old)
and those with underlying cardiac disease. Porter et al.
[36] evaluated 1856 patients with PSVT and found
that there was a strong relationship between age and
PSVT mechanism; AVRTs were more common in
younger patients, whereas the prevalence of AVNRT
increased with age.
Figure 3 Twelve-lead ECG of a right atrial flutter
Please note saw tooth flutter waves. Negative P wave in leads II, III, and aVF.
266 Cardiac failure
(2) Sex: AVRTs tend to be more common in men,
whereas AVNRT and atrial tachycardias are seen
more commonly in women [36].
(3) Co-morbidities: Re-entrant forms of PSVT are
usually found in patients without structural heart
disease. An exception to that rule is that some forms
of congenital heart disease, such as Ebstein’s
anomaly, have an increased prevalence of accessory
pathways and associated AVRTs [37]. Atrial fibrillation and flutter are more commonly seen in patients
with other co-morbidities such as diabetes mellitus,
hypertension, valvular disease, coronary artery disease, and sleep apnea [38–41].
A 12-lead ECG can detect an arrhythmia and a presumptive diagnosis of the tachycardia type can be often be
made on the basis of certain ECG features. ECGs can also
reveal substrate for arrhythmias (e.g., pre-excitation) and
suggest other nonarrhythmia-related causes of cardiomyopathy including ischemic disease, left ventricular
hypertrophy and hypertensive heart disease, and infiltrative diseases such as amyloidosis. The basic ECG, however, cannot determine the overall arrhythmia burden;
therefore, long-term monitoring with either a Holter
monitor or an auto-event recorder is needed.
Analysis of the 12-lead ECG can assist in understanding
the possible mechanism of an SVT causing TIC. Some
features that should be evaluated when looking at the
ECG are listed below.
(1) Heart rate: heart rate is not reliable in predicting the
mechanism of a tachycardia, but it is important in
predicting the risk of developing a TIC. Although it
has been shown in experimental studies that the
faster the rate the greater the likelihood of developing a TIC [42], in clinical practice it is usually the
slower, asymptomatic incessant arrhythmias that
typically lead to development of a TIC [9].
(2) Persistent SVT vs. PSVT: Truly paroxysmal tachycardias rarely lead to a TIC, as they rarely cause
enough tachycardia burden to result in reduced left
ventricular function. Incessant tachycardia has been
defined as continuous tachycardia or continuous paroxysms of tachycardia separated by a few normal
sinus beats [43]. A classic incessant SVT is PJRT.
This is an arrhythmia that is caused by a slowly
conducting accessory pathway usually located near
the coronary sinus ostium. These patients may have
truly incessant tachycardia with essentially no periods
of sinus rhythm or they may have frequent episodes
of PSVT that last for long periods and result in a large
tachycardia burden (see Fig. 2a). Long-term monitoring is usually the best way to determine whether a
tachycardia is frequent or incessant, but, in some
cases, the 12-lead ECG can reveal that an arrhythmia
is frequent and repetitive, as is demonstrated by the
ECG shown in Fig. 1a.
(3) Long RP vs. short RP tachycardia: The RP-to-PR
ratio is not diagnostic of any tachycardia type but does
help in creating a differential diagnosis of the
possible tachycardia types. Long RP tachycardias
are far more likely to be incessant, and the differential diagnosis of these includes PJRT, atypical
AVNRT, and atrial tachycardia. A very short RP
tachycardia or a tachycardia in which the P wave is
not identifiable is most consistent with either typical
AVNRT or orthodromic reciprocating tachycardia.
These tachycardias are usually infrequent and paroxysmal in nature and therefore rarely lead to a TIC.
(4) P wave morphology: The typical normal sinus rhythm
P wave morphology is positive in the lateral limb
leads I, aVL, and positive in the inferior limb leads II,
III, and aVF. It is often biphasic in lead V1 and
positive in the rest of the precordial leads. A P wave
morphology different from a sinus rhythm P wave is
indicative of an abnormal rhythm mechanism. A
description of the various P wave morphologies
and location of the tachycardia focus is beyond the
scope of this review. However, some basic rules
regarding P wave morphology and tachycardia
location are as follows:
(a) A negative P wave morphology in the inferior limb
leads (II, III, and aVF) predicts that the origin of the
tachycardia’s activation of the atrium is from the
inferior portion of the atrium, often in close proximity
to the coronary sinus ostium.
(b) A negative P wave morphology in the lateral limb
leads (I and aVL) is indicative of a left atrial location
for the tachycardia focus.
Standard workup for cardiomyopathies should include a
thorough history and physical, laboratory assessment,
echocardiogram, and ischemic evaluation. If initial
workup is negative, then TIC should be considered.
Cardiac MRI is increasingly being utilized for assessment
and diagnosis of unexplained cardiomyopathies. MRIs
can noninvasively assess for infiltrative myopathies
such as sarcoidosis and hemochromatosis, myocarditis,
obstructive causes including valvulopathies and hypertrophic cardiomyopathies, ischemic disease and scar burden, and high-output states including intracardiac shunts,
along with potential arrhythmogenic causes such as right
ventricular dysplasia. Potential limitations are patients
with prior cardiac rhythm devices.
Treatment/follow-up
The goal of treatment is to control the tachycardia
through rate or rhythm control, thereby improving a
patient’s symptoms, reversing ventricular dysfunction,
Supraventricular tachycardia causing heart failure Houmsse et al. 267
and preventing future cardiomyopathy. This management strategy can be obtained through:
(1) anti-arrhythmic drugs to achieve either rate or rhythm
control,
(2) curative ablative therapy directed at the underlying
tachycardia mechanism to restore sinus rhythm, and
(3) atrioventricular junction ablation with permanent
pacemaker placement for better rate control.
Any of these approaches can help improve or normalize
symptoms. Which approach to use is dependent on the
patient’s comorbidities, degree of cardiac dysfunction,
clinical status, type of tachycardia, and risk profile for
either drug or ablation therapy.
In PJRT patients who develop TIC, antiarrhythmic
therapy often fails to suppress or control the tachycardia.
Meiltz et al. [13] followed 49 patients with PJRT for 49þ/
38 months after RF ablation. In this series, eight of the
49 cases had incessant PJRT that was complicated with
TIC. RF ablation was successful in ablating the arrhythmia in all eight cases (four patients required two ablation
sessions) and regression of left ventricular systolic dysfunction was observed during follow-up in all cases.
Radio frequency ablation has also been shown to be
effective in treating focal atrial tachycardias (AT) associated with TIC. Medi et al. [9] followed 331 patients
with focal AT after RF ablation. In that series, approximately 25% of the tachycardias were incessant, and
approximately one-third of patients with an incessant
tachycardia had evidence of a TIC. Most of the patients
with TIC were young (39 22 years), and the arrhythmiarelated heart rates in the TIC patients tended on average
to be slower than the atrial tachycardia rates in those
without a TIC. This last finding most likely relates to the
fact that patients with rapid tachycardia rates tend to
present earlier for care and therefore are less likely to
develop a cardiomyopathy. After successful ablation, left
ventricular systolic function returned back to normal in
97% of patients at a mean of 3-month follow-up.
Rate control for atrial fibrillation or flutter can be obtained
with a cocktail of atrioventricular node slowing medications. Nearly all patients should be placed on a betablocker unless otherwise contraindicated. Additional rate
controlling medications include digoxin, calcium channel
blockers, and even amiodarone in some resistant cases
when there is a desire to avoid an atrioventricular junction
ablation and pacemaker implant. No standard rate control
goal exists; however, most practitioners aim for a resting
heart rate 80 beats/min or less, moderate exercise heart
rates less than 120 beats/min, and average heart rates less
than 100 beats/min on a 24 h Holter. Recurrent
unchecked tachycardia has been shown to accelerate a
decline in ventricular dysfunction; thus frequent assessments of rate control with Holter and event monitors
is warranted in many patients [12,44]. Additionally,
effective rate control can periodically be assessed with
an in-office 6-min walk or outpatient exercise treadmill
evaluation.
In patients with left ventricular dysfunction and atrial
fibrillation with rapid rates refractory to medical therapy,
atrioventricular junction ablation with placement of a
pacemaker has been shown to significantly improve cardiac function in appropriately selected patients. In many of
these patients, placement of a bi-ventricular (Bi-V) pacing
system may be preferred and lead to greater improvement
in cardiac function compared with right ventricular pacing
alone. The improvement in cardiac function after atrioventricular junction ablation and pacing may not only be
due to heart rate control but may also be related to the
regularization of the rhythm [45,46].
In at least one study of patients with refractory atrial
fibrillation and heart failure, curative pulmonary vein
isolation ablation was shown to be superior to atrioventricular junction ablation with Bi-V pacing based on both
subjective and objective follow-up assessments [47]. In
the modern era when potentially curative approaches are
available, these should be considered prior to palliative
approaches such as atrioventricular junction ablation,
especially in younger patients where long-term device
therapy may be problematic. For atrial flutter, which is
more easily cured with ablation than atrial fibrillation,
studies have shown improvement in the ejection fraction
in approximately 60% of patients with reduced left ventricular function prior to the ablation. In many of these
patients, the improvement in ejection was great enough
to eliminate the need for implantation of a primary
prevention defibrillator [13].
Conclusion
Despite the apparent normalization of systolic function
with control of the tachycardia, cellular and structural
abnormalities of the myocardium may persist. This is
supported by observations of precipitous decline in systolic function with recurrent arrhythmias, whereas the
initial process took months or years to develop [12].
Such early recurrence of cardiac dysfunction is thought to
be secondary to persistent cellular abnormalities, structural disarray, and diastolic dysfunction that persisted
well after the tachycardia was treated and systolic function normalized [9,21,44]. This is further supported by
an observed decline in systolic function with cessation of
cardiac remodeling medications (i.e., beta-blockers and
angiotensin-converting enzyme inhibitors) even in the
absence of tachycardia recurrence [48]. Finally, a small
subset of treated SVT-related TIC patients had sudden
268 Cardiac failure
cardiac death after resolution of ventricular dysfunction,
supporting the observation of enduring cellular and
molecular abnormalities [12]. Therefore, medical treatment should be indefinite, with close observation and
frequent follow-up of SVT-related TIC patients. Implantable cardioverter defibrillator therapy needs to be considered for primary prevention in patients who have
persistent reduction of left ventricular ejection fraction
despite control of the tachycardia, but this decision
should generally be made after the patient has been
given enough time, usually 3 months or more, to allow
recovery of cardiac function.
15 Ott P, Kelly PA, Mann DE, et al. Tachycardia-induced cardiomyopathy in a
cardiac transplant recipient: treatment with radiofrequency catheter ablation.
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Papers of particular interest, published within the annual period of review, have
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of special interest
of outstanding interest
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Focal incessant or frequent paroxysmal atrial tachycardia was associated with only
10% TIC. Patients who had slower ventricular rate during incessant or frequent
paroxysmal atrial tachycardia had higher incidence of developing TIC. This was
higher in young men. Ninety-seven percent of the patients with TIC restored their
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9
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