Atrial Fibrillation (AFib) Support Group
Atrial fibrillation (AF or afib) is an abnormal heart rhythm (cardiac arrhythmia) which involves the two small, upper heart chambers (the atria). Heart beats in a normal heart begin after electricity generated in the atria by the sinoatrial node spread through the heart and cause contraction of the heart muscle and pumping of blood.
Just found this Group and thought I'd post here.
Going on 4 years with AFIB not that bothersome when I go into it but
I suffered a TIA/mini-stroke in September that resolved itself in 10 mins.
Been on Xarelto ever since nothing prior to this.. I guess it's time I get this done as I probably waited too long now just turned 56 and in excellent shape was a Chads 0. All my blood work was excellent leading up this this event. But that past Labor day in September weekend I was in and out of AFIB for 4 days so I knew I was in trouble.
Going on 4 years with AFIB not that bothersome when I go into it but
I suffered a TIA/mini-stroke in September that resolved itself in 10 mins.
Been on Xarelto ever since nothing prior to this.. I guess it's time I get this done as I probably waited too long now just turned 56 and in excellent shape was a Chads 0. All my blood work was excellent leading up this this event. But that past Labor day in September weekend I was in and out of AFIB for 4 days so I knew I was in trouble.
This is the place to learn everything you need to know. There are some really supportive and knowledgeable people here. So welcome to our group!
Kelly
Hope you are able to benefit from others' experiences on this forum!
I know way too much about this insidious disease we call the beast so just looking to contribute and learn even more. The one thing I don't quite have a handle on who is the best EP's in New York Area?
I'm looking to hear real life experiences with certain doctors. Thanks
and I have no experiences to share...
ah, well some, but not here...I wouldn't dare!
But I have stopped by just to say,
I hope you are having a really nice day,
Please keep on posting, we like it that way!!!1
Ultimately, you have to make your own decision, but I would use the above Heart Rhythm Society specialist locator to find an EP for your type of afib (in your area).
petey
You know your stuff on here.
I think Reddy and Dukkapati are a tag team so to speak?
Just curious why you let yourself stay in afib for 22 straight months?
Not good to let your heart remodel that long.....
I've been on Flecanaide for almost 2 years now and it's pretty safe and effective and the key is it prevents electrical and structural remodeling so you can eventually have a successful ablation.
Flecainide is safe and effective
MADRID, SPAIN. Flecainide (Tambocor) is a class
1C antiarrhythmic drug that blocks the inflow of
sodium into heart cells thereby slowing conduction
through the heart. It increases the atrial effective
refractory period (the time span during a heart beat
in which AF cannot be initiated). The drug is highly
bioavailable in its oral form (90-95% bioavailability)
and has a half-life of 12 to 27 hours. Flecainide
was first introduced in Europe in 1982, but its
acceptance in North America has been very slow
The AFIB Report May 2011 Page 7
with sales taking a dramatic drop (75%) after the
publication of the CAST trial which showed
increased mortality among patients who had
suffered a heart attack prior to initiating treatment
with class 1C drugs (flecainide, propafenone). It is
now clear that the increased mortality seen in CAST
was caused by pro-arrhythmic events in elderly
patients with significant pre-existing cardiovascular
comorbidity. Thus, flecainide is now recommended
in current guidelines as a first-line treatment option
for the conversion of atrial fibrillation (AF) to normal
sinus rhythm (NSR) and for the maintenance of
sinus rhythm in afibbers with no heart disease and
normal left ventricular function.
The progression of AF through more frequent and
longer episodes to persistent and, in some cases,
permanent AF is caused by electrical and structural
remodeling of the atrium. Flecainide helps prevent
electrical remodeling by slowing conduction across
the myocardium and increasing the refractory
period. It helps prevent structural remodeling by
reducing calcium ion accumulation in the myocytes
and the associated oxidative stress. However, like
any drug, flecainide does have the potential for
adverse effects. It can initiate atrial flutter and, as it
does not slow conduction through the AV node, the
flutter may result in 1:1 conduction which is clearly
dangerous and highly uncomfortable. The risk of
this complication is likely associated with preexisting,
perhaps asymptomatic, right atrial flutter
and can be eliminated through a right atrial isthmus
ablation. Beta-blockers and calcium channel
blockers are also effective in preventing 1:1
conduction. The risk of a pro- arrhythmic event also
increases with depressed left ventricular ejection
fraction, so flecainide is not recommend for AF
patients with this condition.
Nevertheless, the overall safety profile of flecainide,
when given to appropriately selected patients, is
very favourable with a recent study finding overall
mortality in flecainide-treated patients to be lower
than the expected rate in the general population.
The official recommendation is that the oral drug,
when first prescribed, should be administered in a
hospital setting with a gradual increase from 50 mg
twice a day to the maximum dose of 150 mg twice a
day (if needed). For patients not able to tolerate
high doses or having impaired kidney function, a
time-release version is available. Some physicians
routinely prescribe digoxin or a beta-blocker with
flecainide to avoid the possibility of flutter-induced
1:1 conduction.
Intravenous infusion of flecainide is highly effective
in chemically converting acute-onset (less than 48
hours duration) AF and restores NSR within an hour
in 95% of patients. There is also evidence that
flecainide given prior to electrical cardioversion
increases the likelihood of first shocks being
successful in converting the patient to NSR (65%
conversion vs 30% with placebo). Oral
administration is also effective if used soon after
episode onset. A single loading dose of 200 to 300
mg converts 50-60% of patients within 3 hours and
75-85% within 6 to 8 hours. Although generally
safe in healthy afibbers, reversion to NSR may be
preceded by a longish pause in heart beat or, in a
small minority (0.2%), in 1:1 conduction, particularly
if reversion to NSR happens during exercise.
Flecainide is also effective in maintaining NSR after
conversion with only a 38% relapse rate (over a
minimum 6-month follow-up) as compared to
relapse rates of 58% for sotalol and 61% for
propafenone.
Long-term therapy with oral flecainide has been
shown to significantly reduce the frequency of AF
episodes with 65% of patients being responsive to
therapy in the short-term and 49% responding in the
long-term. There is also evidence that flecainide
suppresses palpitations, tachycardia, and episodeassociated
chest pain.
The group of electrophysiologists, with members
form France, Germany, Italy, the Netherlands and
Spain, compiling this report concludes that
administration of flecainide is a safe and effective
option in younger AF patients without co-existing
structural heart disease.
Aliot, E, et al. Twenty-five years in the making: flecainide
is safe and effective for management of atrial fibrillation.
Europace, Vol. 13, 2011, pp. 161-73
My EP, my PCP, Dr Calkins at Johns Hopkins, UPenn 2nd opinion, and Cleveland Clinic 2nd opinion... all said, given my situation (below), rate control is the best course of action at this time/and 22 months ago.
age 64
asymptomatic
first diagnosed with persistent afib in a routine physical
moderately enlarged left atrium
treated sleep apnea
well controlled heart rate
They all said the same thing. Ablation is for symptom reduction or elimination and many times is a long term cure (if paroxysmal). They all still subscribe to the AFFIRM trial and they believe waiting is a valid option as persistent afib ablation has a low cure rate and they expect gains in that area.
I was told that they will look at my atrium again, but all is stable at this time. I asked about fibrosis and Utah scoring. The answer was that fibrosis does accumulate that fast.
Bottom line is that the risk (in ablation) is not warranted, in their opinion, given the success probability and possible outcome "gain".
I have heard this remodeling argument before. It appears I had the afib way before it was diagnosed (as it was first diagnosed as persistent and I had no clue even though I am very active). Therefore, the remodeling had already occured. That window was missed the day I was diagnosed. "Further" remodeling is the issue now.
There is disagreement in the electrophysiology world. In addition, everyone's situation is different (based on factors as I mentioned above). My gut tells me that if the people who told me rate control was the way to go (and they make their living doing ablations and are well respected), it is probably the best thing to do... and then there is the whole topic of rhythm control drugs and their side effects/risks and the fact they prescribe them before and after the ablation. Top that off with the fact that, given the silent nature of afib after ablation, the consensus is people should stay on blood thinners after ablation and for life (as your CHADS score goes up due to age, etc).
So what's the big gain?
petey
I went to Cornell[NYPresbyterian and saw Dr. Christopher Liu, a younger EP, and really liked him. Smart, easy to work with, not full of himself. I had an ablation with him and was very satisfied.