Dear Izzy,
Thanks for the clarification. Since you have already read through the
e-medicine article, I will try to focus on other sources. For
convenience, here is a link to the eMedicine article:
http://www.emedicine.com/med/topic188.htm
I'll go through your question point-by-point:
==========
Causes
==========
Focal atrial tachycardias are a type of supraventricular arrythmia.
In a normal heart, a signal to beat is generated in the pacemaker
(sinus) node located in the atrium. This electrical impulse causes
the atrium to beat and is transmitted to the atrioventricular (AV)
node, where the signal is briefly delayed (to allow the atria to
finish contracting and filling the ventricles). Following the delay,
the signal is sent to the ventricles, which then contract. In atrial
fibrillation, the atria beat at a very high, irregular rate. This
generates many electrical impulses, which are sent to the AV node.
Because of the delay built in to the AV node, most of the signals
don't get sent to the ventricle. This situation is referred to as
atrial fibrillation. There can be, however, other pathways around the
AV node, which allow more or all of the atrial signals to be sent to
the ventricles without delay or filtration. This results in atrial
fibrillation with fast ventricular response. The terminology refers
to the source of the tachycardia, i.e., multifocal atrial tachycardia
implies that there are multiple points in or near the atrium
initiating aberrant signals. You question refers to focal atrial
tachycardia (FAT), which implies that there is a single source
generating an aberrant electrical signal. Because the source is above
the AV node, focal atrial tachycardia is referred to as a
supraventricular tachycardia.
A good, authoritative source of information on several of your
questions is the national guideline report for supraventricular
tachycardias, published jointly by the American College of Cardiology,
the American Heart Association, and the European Society of
Cardiology. You can find the whole report here:
http://scholar.google.com/url?sa=U&q=http://www.acc.org/clinical/guidelines/arrhythmias/sva_index.pdf
Page 29 of this report discusses FAT:
AT is frequently found on Holter recordings and seldom associated with
symptoms. Sustained focal ATs are relatively rare; they are diagnosed
in about 10 to 15% of patients referred for catheter ablation of SVT.
The prevalence of focal AT has been calculated to be 0.34% in
asymptomatic patients versus 0.46% in symptomatic patients. Focal ATs
account for 10 to 23% of SVTs in children with normal hearts and a
much higher percentage in children with congenital heart disease."
"Focal ATs are characterized by regular atrial activation from atrial
areas with centrifugal spread. Focal ATs are usually manifest by
atrial rates between 100 to 250 bpm and rarely at 300 bpm. Neither the
sinus nor the AV node plays a role in the initiation or perpetuation
of the tachycardia. "
There are many potential causes of FAT, as the above report discusses on page 29:
"In adults, focal AT can occur in the absence of cardiac disease, but
it is often associated with underlying cardiac abnormalities ..."
"Atrial tachycardia, usually with AV block, may be produced by
digitalis excess. This arrhythmia may be exacerbated by hypokalemia.
Focal ATs may present as either paroxysmal [sudden] or permanent
tachycardias."
Page 31 discusses the distribution of locations for the origin of the
aberrant electrical signal responsible for FAT:
"Focal ATs are not randomly distributed but rather tend to cluster
over certain anatomical zones. The majority of rightsided ATs
originate along the crista terminalis from the SA node to the AV node,
but other right atrial sites include the atrial septum, atrial
appendages, Koch?s triangle, and the tricuspid annulus. Conversely,
several venous structures have been demonstrated to have atrial
myocardial extensions that may contain a tachycardia focus, such as
SVC or coronary sinus ATs. In the left atrium, foci are often found in
the pulmonary veins, in the atrial septum, or on the mitral annulus;
in many cases, they are generators for AF. "
Page 31 of the above report also discusses the etiology of FAT in more detail:
"Focal ATs are characterized by radial spread of activation from a
focus, with endocardial activation not extending through the entire
atrial cycle. The mechanism of focal discharge is difficult to
ascertain by clinical methods. Available information suggests that
focal activity can be caused by abnormal or enhanced
automaticity,triggered activity (due to delayed afterdepolarization),
or micro?re-entry. Automatic ATs could arise from atrial foci in which
spontaneous phase 4 depolarization occurs in cells with normal or
abnormal resting membrane potentials. The progressive increase in
atrial rate with tachycardia onset (ie, ?warmup?) and/or progressive
decrease before tachycardia termination (ie, ?cool- down?) are
suggestive of an automatic mechanism. Typical automatic ATs may arise
spontaneously or increase their rate of discharge in response to
adrenergic stimulation. However, inducibility of re-entrant and
triggered ATs is also enhanced by catecholamines. Automatic ATs tend
to be incessant, especially in children, whereas those attributed to
triggered activity may be either incessant or paroxysmal."
Medications have also been known to cause FAT:
"The drug most commonly associated with induction of focal AT is
digitalis. This drug-induced AT is usually characterized by
development of AT with AV block; hence, the ventricular rate is not
excessively rapid. Serum digoxin levels are helpful for diagnoses.
Treatment consists of discontinuing the digitalis. In cases of
persistent advanced AV block, digitalis binding agents may be
considered."
==========================
Treatments / Surgical Procedures
==========================
Again from the ACC report I cited above, a general word about treatments for FAT:
"The efficacy of antiarrhythmic drugs is poorly defined because the
clinical definition of focal ATs is often not very rigorous. No large
studies have been conducted to assess the effect of pharmacologic
treatment on patients with focal ATs, but both paroxysmal and
incessant ATs are reported to be difficult to treat medically [using
medications alone]."
Page 31 of the ACC report discusses the current standard of care for
treatment of FATs. A summary of treatment recommendations can be
found on page 32, for both acute (e.g., unstable patients in the
hospital who need immediate treatment) and prophylactic treatment.
This table also includes the level of evidence and cites the studies
used to arrive at the recommendations. If your interested in a guide
to the various levels of evidence (how good the data is), you can find
a table of grades and levels here:
http://www.nsite.ca/sackett/uploads/collections/76897196.pdf
The primary "surgical" intervention is referred to as catheter
ablation. This involves inserting a long wire in a vein in the leg
and advancing it up to the area responsible for the electrical signal
causing the FAT. This area is then destroyed using radiofrequency
energy to generate heat locally. Here is an article about this
technique from Medscape / WebMD:
http://www.medscape.com/viewarticle/478828_4
This technique often requires 3-D electrical mapping of the heart to
identify the source of the FAT.
Here is an article about this from the Indian Heart Journal:
http://www..com/Jan-Feb2003/Catheter%20Ablation%20of%20Atrial%20Tachycardia%20Using/catheter_ablation_of_atrial_tach.htm
The following article also discusses in some detail what is known
about FAT and treatment options, with a focus on electrical mapping
and catheter ablation (from the American Heart Association journal
Circulation):
http://circ.ahajournals.org/cgi/content/full/109/1/84
or in PDF format:
http://circ.ahajournals.org/cgi/reprint/109/1/84
Here is an article, again from the AHA journal Circulation, discussing
radiofrequency ablation:
http://circ.ahajournals.org/cgi/content/full/95/3/572
Although largely supplanted by the less invasive radiofrequency
ablation technique, historically, a Maze procedure has been used for
treatment of FAT.
Here is an article discussing this procedure in 41 patients from Circulation:
http://circ.ahajournals.org/cgi/content/full/101/13/1559?ck=nck
or in PDF format:
http://circ.ahajournals.org/cgi/reprint/101/13/1559?ck=nck
Here is the reference to the first paper describing the procedure:
Cox JL, Schuessler RB, D?Agostino HJ, Stone CM, Chang B-C, Cain ME,
Corr PB, Boineau JP. The surgical treatment of atrial fibrillation,
III: development of a definitive surgical procedure. J Thorac
Cardiovasc Surg. 1991;101:569?583.
The abstract can be found here:
http://jtcs.ctsnetjournals.org/cgi/content/abstract/101/4/569?ijkey=e0bc6b790c86332bd195ae85fcda9fadb6b826ee&keytype2=tf_ipsecsha
Another source - This online textbook of cardiac surgery discussing
the use of RF catheter ablation therapy vs. surgical intervention:
http://cardiacsurgery.ctsnetbooks.org/cgi/content/full/2/2003/1253?ck=nck
"RF lesion size is well suited for focal endocardial tachyarrhythmias.
Tachyarrhythmias utilizing a reentrant circuit with a wide isthmus or
localized deep in the myocardium may be more difficult to ablate.
Advancements in catheter technology have improved the success rates of
RF ablations. Primary of these was the inclusion of a thermistor or
thermocouple within the ablation electrode to monitor catheter-tissue
interface temperature. This allows the maximal energy delivery without
the buildup of excessive temperature that results in coagulum and
increases in impedance. Other advances have been the development of
larger catheter tips, which increase the surface area, reducing
current density and increasing cooling by surrounding blood pool.
Irrigated catheters bathe the catheter tip internally or externally
with a saline solution to cool the catheter-tissue interface,
preventing coagulum formation and enhancing energy delivery. Catheters
themselves have been designed to be steerable and allow precise
positioning of the tip to the region of interest. Future advances in
catheter technologies will be discussed later in the chapter."
Essentially, due to improvements in RF catheter technology, patients
who require invasive surgical intervention have become more rare.
===================================
Links to thyroid disease and vitamin E usage
===================================
The Clinical Journal of Endocrinology and Metabolism published an
article in 2002 discussing the often unappreciated link between
thyroid disease and cardiac dysrhythmias in general. Here is a link
to the full text of the article:
http://jcem.endojournals.org/cgi/content/full/87/3/963
or in PDF format:
http://jcem.endojournals.org/cgi/reprint/87/3/963
Figure 1 from this paper shows the risk of developing atrial
fibrillation (of all types) vs. Thyroid Stimulating Hormone (TSH; a
marker of hyper- or hypo-thyroidism).
A quote from this paper:
"In the adult population, AF is the most common cardiac rhythm
disturbance and after sinus tachycardia is the most prevalent
dysrhythmia in those with hyperthyroidism. Between 10% and 15% of
hyperthyroid patients develop AF."
This quote refers to data originally cited in this paper, from the New
England Journal of Medicine:
http://content.nejm.org/cgi/content/abstract/331/19/1249?ijkey=cfaaf4aa7cea278352acaf936f647a3b84d1f0a2&keytype2=tf_ipsecsha
The full text is here:
http://content.nejm.org/cgi/content/full/331/19/1249?ijkey=cfaaf4aa7cea278352acaf936f647a3b84d1f0a2
Essentially, hyperthyroidism leads to an increase in catecholamines in
the system, which leads to increased automaticity in atrial myocytes,
meaning that the muscle cells of the atrium are more prone to
arrhythmias when exposed to increased catecholamines (such as
epinephrine, adrenaline).
Temperature can also play a role. Here is an abstract of an article
discussing this mechanism:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=12928594&dopt=Citation
There is very little data regarding any connection between Vitamin E
and focal atrial tachycardia.
Some sites (http://www.medical-library.net/sites/framer.html?/sites/_atrial_fibrillation.html)
recommend using Vitamin E instead of Coumadin for anti-coagulation (to
prevent the formation of mural thrombi, which can cause strokes,
etc.):
"Of course there should be no consumption of alcohol, coffee, tobacco,
or unnecessary drugs as these items can aggravate the condition. A
safer, nutritional, alternative to coumadin is high dose vitamin E in
the range of at least 2000 IU per day. This provides anticoagulation,
but in a fashion safer than coumadin. However if a person is already
anti-coagulated, there must be a transition phase supervised by a
physician and the proper lab tests to be sure that clotting ability is
not too far compromised while both the coumadin and vitamin E are on
board at the same time."
Such use of Vitamin E is far from the standard of care in medicine and
is not advised.
A general study, released January, 2005, looking at the effects of
Vitamin E is somewhat disturbing:
Ann Int Med. Jan 5, 2005;142: 1 (Early Release)
"The effect of vitamin E supplementation on cardiovascular and cancer
risk is unclear. Some studies suggest a positive benefit. However,
several trials have shown non-significant trends toward an increase in
mortality with high-dose vitamin E. This meta-analysis of 19 trials
(9 vitamin E alone and 10 in combination with other supplements)
evaluated data from 135,967 total participants to determine the
dose-response relationship between vitamin E supplementation and
mortality. There was a statistically significant trend toward
increased mortality with increasing dose (starting with doses greater
than 150 IU/day.) Three of the 11 high-dose trials contained other
supplements that might increase risk (e.g. beta-carotene.) Most of
the participants had chronic diseases, so it is uncertain if these
findings can be generalized to healthy adults. Also, the threshold of
increase risk could not be precisely determined. The authors conclude
that high-dose (400 IU/d) vitamin E supplementation should be avoided.
Discussion [Neil Skolnik, M.D.]
This meta-analysis raises an important caution regarding the safety,
or lack thereof, of seemingly safe vitamin supplementation. In an
accompanying editorial, the author points out that a third of all
adults in the United States take vitamin supplements, leading to over
$18 billion dollars in sales. Vitamin E is the most widely used of the
vitamins, taken as a supplement for 22% of adults over age 55. Vitamin
E is largely used as an antioxidant, based on laboratory data that
shows that oxidative reactions are involved in causing a variety of
conditions that become more common with age including cardiovascular
disease, cancer, dementia, and COPD. Clinical trial data do not
support the hypothesis that antioxidants help prevent disease. Many
people have felt that, even with a paucity of clinical evidence to
support their benefits, vitamin E is unlikely to cause harm. This
though, does not appear to be the case. This meta-analysis shows that
Vitamin E in high doses does not prevent disease, and may actually
increase mortality."
http://www.amh.org/findphysician/PCUv10n1.htm
A discussion of this article can be found here:
http://heartdisease.about.com/od/otherriskfactors/a/vitaminE.htm
Here is another, brief, discussion of this article, from a
cardiovascular journal club:
http://www.journalclub.org/categories/medical/cardiovascular/page/3/
" I just got around to looking at the vitamin E study that was
publicized at the AHA meetings two weeks ago and published online at
the Annals website (to be published in print in January).
It is a meta-analysis of randomized trials of vitamin E, that looks at
overall mortality. Trials were analyzed by vitamin E dosage. There
were 8 low-dose trials where the vitamin E dose was less than 400 IU
daily, with a total of 95,000 subjects; there was no effect on
mortality. Pooling the results of the 11 trials (about 41,000
subjects) where the dose was 400 IU or greater, there was an increase
in mortality in the vitamin E group. The actual calculated number was
63 deaths per 10,000 persons.
My take on this:
The actual derived number is not meaningful, since results are pooled
across a heterogeneous group of subjects, methods and doses. The
number 63 per 10,000 should not be taken as is, especially since the
confidence interval is 6-119!
On the other hand, the graphic representation of the 19 trials is
highly instructive (a picture really is worth a lot of words). Even if
one doesn?t place any stock in the pooling of results, just looking at
the graphic summary of the trials is very convincing. I believe this
is the biggest value of metanalyses: providing a graphic summary of
multiple studies.
Since the inflection point for increased risk seems to be around 400
IU daily, and since that is a rather common vitamin E dose, it?s not
clear exactly what to think about that dose. But I do feel fairly
comfortable telling people who ask about 400 IU of vitamin E or more
that I wouldn?t recommend it for prevention and would consider
stopping it if they are taking this dose."
Regarding the use of Vitamin E in patients with heart disease, this
quote sums up the current state of knowledge:
"...There are no national recommendations regarding the use of vitamin
E. There were older studies suggesting it was helpful for patients
with heart disease, but more recently several large studies suggested
there was no benefit. In fact there was one study which found that
vitamin E blunted the benefits seen when patients were taking Niacin
and Zocor together.; However this was only one study and with
relatively small numbers. We are specifically recommending to avoid
vitamin E in patients with a low HDL who are taking medications to
raise their HDL. The jury is still out on whether there is any
benefit to patients with normal HDL levels."
[Dr. Ronald H. Fields]
http://www.stmaryhealthcare.org/body.cfm?id=250
There are some studies that suggest that Vitamin E may be beneficial
in patients with arrhythmias:
A study from France:
Walker MK, Vergely C, Lecour S, Abadie C, Maupoil V, Rochette L.
Vitamin E analogues reduce the incidence of ventricular fibrillations
and scavenge free radicals. Fundam Clin Pharmacol. 1998;12(2):164-72.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9565770
Here is the abstract:
"The aim of our study was to analyse the protective effects of
different alpha-tocopherol analogues 1) against fibrillations induced
by an ischemia-reperfusion sequence, and 2) to further investigate in
vitro the radical scavenging properties of these analogues by two
sensitive methods. Concerning 1: isolated rat hearts underwent 10 min
of coronary ligation followed by reperfusion and the alpha-tocopherol
analogues were infused 15 min before occlusion. Functional parameters
including heart rate and fibrillations were recorded. Concerning 2:
the beta-phycoerythrin assay was utilised to determine the oxygen
radical absorbing capacity (ORAC) of these vitamin E analogues against
peroxyl radicals. Electron paramagnetic resonance (EPR) was used to
measure their scavenger abilities on hydroxyl radical and superoxide
anion production. Concerning 1: ventricular fibrillation times were
reduced for all analogues treated hearts at concentrations of 1 microM
and 5 microM, with Trolox being the most efficacious. Concerning 2: in
our experimental conditions of intense production of free radicals,
scavenging IC50 values for hydroxyl radical were 1.15, 2.17 and 4.04
mM for Trolox, MDL 74270 and MDL 74366 respectively. Superoxide anion
IC50 values were 1.0 and 6.75 mM for Trolox and MDL 74270. Our results
show that water-soluble analogues of vitamin E are effective in the
prevention of coronary ligation induced reperfusion arrhythmia, under
our experimental conditions. Moreover, our data demonstrate that these
vitamin E analogues are effective scavengers for a variety of
radicals. Our studies support the view that compounds that can either
inhibit the formation or scavenge free radicals can protect the heart
against arrhythmia associated with ischemia-reperfusion."
Other studies have been done in rats, rabbits, and dogs. The bottom
line: taking the RDA of Vitamin E is unlikely to have a significant
effect (good or bad) on atrial fibrillation or heart disease. Taking
excessive amounts may be harmful.
Here is a more complete list of predisposing factors in atrial
fibrillation from the recent article below:
Page RL. Clinical practice. Newly diagnosed atrial fibrillation. New
England Journal of Medicine. 351(23):2408-16, 2004 Dec 2.
"In most cases, atrial fibrillation is associated with cardiovascular
disease, in particular hypertension, coronary artery disease,
cardiomyopathy, and valvular disease (primarily mitral); it also
occurs after cardiac surgery and in the presence of myocarditis or
pericarditis. When atrial fibrillation complicates severe mitral
regurgitation, valve repair or replacement is indicated. [8] In some
cases, atrial fibrillation results from another supraventricular
tachycardia. When it is associated with the Wolff-Parkinson-White
syndrome, rapid conduction down the accessory pathway may result in
hemodynamic collapse. [9]
Other predisposing conditions include excessive alcohol intake,
hyperthyroidism, and pulmonary disorders, including pulmonary
embolism. Obstructive sleep apnea may also be related, in which case
the provision of continuous positive airway pressure reduces the risk
of the recurrence of atrial fibrillation. [10] Both vagal and
sympathetic mechanisms of paroxysmal atrial fibrillation have been
described (neurogenic atrial fibrillation), [11] as have familial
forms of the condition. [12] "Lone" atrial fibrillation (i.e., that
occurring in the absence of a cardiac or other explanation) is common,
particularly in patients with paroxysmal atrial fibrillation - up to
45 percent of such patients have no underlying cardiac disease."
========
Prognosis
========
Going back to the ACC report I first cited,
"For patients with drug-refractory AT or incessant AT, especially when
tachycardia-induced cardiomyopathy has developed, the best therapy is
catheter ablation of the focus."
FAT, in terms of prognosis, falls in the category of atrial fibrillation.
A good discussion of atrial fibrillation, which includes discussion of
FAT can be found here:
http://www.westhertshospitals.nhs.uk/WHC/archive/evidence/07%2520arrhythmias/AF%2520strategies-Lancet%25202002.pdf
Generally, treatment is advised. Here is a summary of the risks if
this type of condition is not treated, from the paper below:
Golzari H. Cebul RD. Bahler RC. Atrial fibrillation: restoration and
maintenance of sinus rhythm and indications for anticoagulation
therapy. Annals of Internal Medicine. 125(4):311-23, 1996 Aug 15.
"Embolic Events
Atrial fibrillation is the most common cardiac condition that
predisposes a person to systemic embolism. In the Framingham Study
[3], rheumatic heart disease with atrial fibrillation was associated
with a 17.5-fold increase in risk for stroke. Flegel and coworkers [4]
estimated the relative risk for stroke in chronic nonrheumatic atrial
fibrillation to be 6.9; this is close to the estimate of 5.6 found in
the Framingham study [3]. The risk for cerebral embolism is emphasized
by the association of asymptomatic cerebral infarctions with
nonvalvular atrial fibrillation [5]. The rate of stroke in paroxysmal
atrial fibrillation had been estimated to be about 2% per year [6],
but a recent analysis of trials of warfarin for stroke prevention [7]
suggests an annual rate of 5.7%.
The risk for stroke is lower with lone atrial fibrillation, which is
defined as the absence of any other clinical evidence for a primary
cardiac disorder. Data from the Framingham Study [8] showed a fourfold
increase in risk for stroke, but Kopecki and associates [9] did not
find any increased risk. The latter used a more restricted sample of
patients with lone atrial fibrillation; all patients with pre-existing
hypertension or diabetes and those older than 60 years of age were
excluded. Additionally, transient ischemic attacks were excluded as an
end point. Analysis of pooled data from antithrombotic trials confirms
that patients younger than 65 years of age who do not have a history
of hypertension, diabetes, transient ischemic attack, or stroke are at
very low risk for stroke [7]. The different incidences of stroke in
these and other prospective studies [10] have been interpreted as
suggesting that atrial fibrillation is not the principal risk factor
for stroke but is a risk marker for other associated cardiovascular
diseases that lead to stroke [11,12].
Hemodynamic Dysfunction
Ventricular filling is reduced as a consequence of both the shortened
diastolic time seen with rapid ventricular rates and the loss of
active atrial transport; the latter can be more disabling in older
patients because the contribution of the atrium to ventricular filling
increases with age [13]. Mean left atrial and pulmonary wedge
pressures rise, and cardiac output and mean arterial pressure may
decrease. A rapid ventricular response is particularly hazardous when
ventricular filling has already been compromised, as is the case with
mitral stenosis or abnormal ventricular relaxation. Hemodynamic
instability with the onset of atrial fibrillation is more likely to
occur in the presence of left ventricular systolic dysfunction or
previous myocardial infarction or when left atrial contraction is
responsible for more than 40% of ventricular filling [14].
Reduced exercise capacity can result from an abnormally high
ventricular rate at rest or during exercise [15] or from underlying
heart disease [16]. Restoration of sinus rhythm by direct-current
cardioversion reduces maximal heart rate, improves exercise capacity
[17-19], and enhances cardiac output [20,21]. These improvements may
be delayed for weeks and may be related to the gradual return of
atrial transport and improved left ventricular systolic function
[18,19].
Cardiomyopathy
Tachycardia-mediated cardiomyopathy has been considered an uncommon
complication of chronic atrial fibrillation, but noninvasive imaging
suggests that its prevalence is greater than previously acknowledged.
Phillips and Levine [22] first emphasized that atrial fibrillation can
cause congestive heart failure in patients with apparently normal
hearts and that restoration of sinus rhythm can be curative. Chronic,
uncontrolled tachycardia [23-26] and chronic atrial fibrillation with
sustained, rapid ventricular rates [22,27-31] can result in severe
cardiomyopathy, which is usually reversible after either rate control
[27,28] or restoration of sinus rhythm [28,30,31].
Death
The mortality rate of patients with atrial fibrillation is twice that
of the general population, perhaps because of the association between
atrial fibrillation and vascular disease [32,33]. Atrial fibrillation
enhances myocardial vulnerability and decreases the fibrillation
threshold, which can facilitate the induction of ventricular
tachyarrhythmias and sudden death [34,35]. Patients with the
Wolff-Parkinson-White syndrome are particularly at risk; the rapid
ventricular rates, which result from conduction through accessory
pathways with short refractory periods, lack of concealed conduction,
or both, can degenerate into ventricular fibrillation [36]. Sudden
death also may occur as a result of the proarrhythmic effects of
medications used to maintain sinus rhythm [37,38].
In summary, the hazards associated with atrial fibrillation emphasize
the desirability of restoring and maintaining sinus rhythm in most
patients."
Quality of life is the major factor in terms of deciding to be treated
or not. The following excerpt, from the ACC report above, details the
pros and cons of treatment and gives statistics on outcome for various
treatment options:
"Improvement of quality of life is usually the major therapeutic goal
of treatment for SVT. Although it was reported early that catheter
ablation improves quality of life (528,529) and is cost effective
compared with other strategies (530), these studies were observational
rather than randomized (528,530) or were limited to more symptomatic
patients on stable antiarrhythmic medical therapy (529). A later study
compared the effect on quality of life between catheter ablation and
pharmacologic therapy as an initial strategy for patients with SVTs
(531). Both treatments improved quality of life and decreased
frequency of disease-specific symptoms, but ablation improved quality
of life in more general health categories and resulted in complete
amelioration of symptoms in more patients (74 vs. 33%) than did
medication. Potential long-term costs were similar for medication and
ablation (531). Among patients who had monthly episodes of SVT, RF
ablation was,however,the more effective and less expensive therapy
compared with long-term drug therapy (532). Another prospective study
compared the long-term effects on health outcome of catheter ablation
and medical therapy as an initial treatment for patients with newly
documented PSVT, excluding those with drug-refractory symptoms
referred specifically for ablation (533). At 5-year follow-up,
patients who received ablation had improved quality-of-life scores and
a reduction in disease-specific symptoms when compared with patients
who continued to take medical therapy. More patients reported complete
elimination of symptoms with ablation therapy (70%) than did those
taking medical therapy (43%). Over 5 years,the average cumulative cost
for patients in the medical therapy group was statistically
significantly lower than in patients initially treated with ablation
therapy:$6249 plus or minus $1421 per patient versus $7507 plus or
minus $1098 per patient (533). It was concluded that patient
preference remains the critical determinant in choosing a particular
treatment in cases of mildly to moderately symptomatic PSVT (533)."
"Baseline quality-of-life scores appear to be lower for patients with
atrial flutter and AF than for those with other arrhythmias who are
undergoing RF ablation (528). Several studies have described
improvement in symptoms and quality of life after catheter ablation of
atrial flutter (427,534537). Ablation of atrial flutter resulted in an
improvement in quality of life as well as reductions in
symptom-frequency scores and symptom-severity scores compared with
preablation values (536). There was a reduction in the number of
patients visiting accident and emergency departments, requiring
cardioversion, or being admitted to a hospital for a rhythm problem.
Patients with atrial flutter and concomitant AF before ablation and
those with atrial flutter alone both derived significant benefit from
atrial flutter ablation (536). Others reported that patients who had
atrial flutter associated with AF before ablation had less improvement
than those without AF (535). Moreover, in a prospective, randomized
comparison of antiarrhythmic therapy versus first-line RF ablation in
patients with atrial flutter,the sense of well-being and function in
daily life improved after ablation but did not change significantly in
patients treated with drugs (427). Ablation was associated with a
better success rate and effect on quality of life,a lower occurrence
of AF,and a lower need for rehospitalization at follow-up (427)."
I hope this information was helpful. Please feel free to ask for clarification.
-welte-ga |
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