-
Advances in
antiarrhythmic drug therapy.
-
Minimizing
and managing complications in A-Fib ablation.
-
update about
current ongoing clinical trials.
-
Reviews of
selected basic and clinical science papers on A-Fib which
came out in 2011.
-
The use of
Registries (detailed open-book record keeping) in clinical
practice.
-
Panel and
audience discussion of challenging cases in A-Fib ablation.
(This session late Saturday afternoon, though not as well
attended as the previous day's which saw over 1,200
attendees, showcased some of the best, most experienced
A-Fib doctors illustrating and discussing some of their most
difficult cases.)
(The author is
especially indebted to Dr. Peter Stevenson, the Editor of the
Boston AF Symposium News, the official newspaper of the
Symposium. This is the first year the Symposium published a
newspaper. The news, interviews, advertisements and session
coverage was amazingly well done and informative. [I have to
admit to being totally jealous of Dr. Stevenson's ability to
stay up all night producing spot-on summaries of important
presentations and get them printed by the next morning.]
The Symposium
also featured a great degree of presenter/audience interaction
and participation. Each attendee had a remote clicker with 1
through 5 choices. A presenter would, for example, pose a case
and give five different treatment options, then allow time for
everyone to vote. The percentage of attendees voting for each
choice would be almost immediately shown on screen. The
presenters and audience would then discuss the results.
CATHETER-BASED OCCLUSION
In a presentation on the Surgical Management of the Left
Atrial Appendage, Dr. Ralph Damiano, Jr. of Barnes Jewish
Hospital in St. Louis, MO discussed, among other subjects, a
disturbing case where a catheter-based occlusion device was
inserted onto the Left Atrial Appendage (LAA) from inside the
heart, but the insertion was unsuccessful. Part of the occlusion
device was left protruding from the LAA into the Left Atrium
with bare metal wires exposed.
In another disturbing incident at the Symposium, the live
satellite presentation from Milan, Italy showed a different LAA
occlusion device being inserted into a patient’s LAA. Though we
saw in the pre-op how the catheter was flushed out with saline
to prevent air bubbles from leaking into the Left Atrium, that's
exactly what happened during the live case.
EDITOR’S COMMENTS:
Even though inserting
the Watchman device, for example, is a relatively simple
procedure with a high success rate and relatively few
complications, if a problem or mistake does happen, it can have
a catastrophic result for a patient. For example, a device
improperly inserted will most likely have to be removed by major
heart surgery. An air bubble inside the heart can potentially
cause an embolism, clot and stroke.
This Editor in the past thought that the Watchman occlusion
device was a wonderful development for an A-Fib patient who
couldn’t or didn’t want to be on warfarin. It also was more
effective than warfarin in reducing the risk of stroke. But installing a
foreign object inside the heart seems inherently dangerous.
Unlike a catheter ablation which has a low risk of adverse
events that usually can be corrected without any lasting damage,
a mistake or problem inserting an occlusion device inside the
heart can cause disastrous problems for patients.
And there are now other options for patients such as a wider
choice of anticoagulants or devices that close off the LAA from
outside the heart such as the surgical AtriClip or the
Lariat II. Patients should not have an occlusion device
installed unless the doctor can guarantee a 100 percent success
rate without complications. Anything less may result in
catastrophic complications for patients.
This editor predicts that, with the many different options
now available to A-Fib patients, the FDA will not approve
occlusion devices inserted from within the heart. Even though
the failure risk is small, a failure can result in complications
devastating for patients.
PRESENTATIONS
OBESITY, SLEEP APNEA AND
A-FIB
Dr. Stanley Nattel from the University of Montréal Canada made
an insightful scientific research presentation on “Obesity and
Obstructive Apnea – Mechanisms of AF Promotion in Experimental
Models” at the 2012 Boston A-Fib Symposium. It’s well known
that obesity and obstructive sleep apnea increase the risk of
developing A-Fib. But what isn't known is what specific
mechanisms promote A-Fib, such as hypoxia, autonomic imbalance,
left ventricular dysfunction, intravascular volume change,
and/or strongly negative intrathoraic pressures.
FAT RATS
In a brilliant
experiment Dr. Nattel studied rats bred to be fat. These Zucker
obese rats weighed almost twice as much as the normal lean rats
in the experiment. Both the obese and lean rats were subjected
to either obstructive sleep apnea or non-obstructive sleep
apnea, versus a control group of both lean and obese rats not
subjected to apnea. The obstructive sleep apnea generated a
strong negative chest pressure caused by forced inhalation
against the closed airway, while in the non-obstructive sleep
apnea group the rats could still get some air through a side
port. He then induced A-Fib by pacing in all the rats.
SLEEP APNEA PRODUCES A-FIB
No rats had
inducible A-Fib in the absence of apnea, indicating that, at
least in this experiment, obesity by itself did not result in
inducible A-Fib. Also, it was impossible to cause A-Fib in the
obese or lean rats that had an open side port airway. But almost
all the obese rats subjected to obstructive sleep apnea
exhibited A-Fib. A small number of the lean rats subjected to
obstructive sleep apnea also developed A-Fib.
From this
experiment one can possibly conclude that obstructive sleep
apnea substantially increases A-Fib Inducibility, and
significantly more so in obese rats. If we can apply the results
of this experiment to humans, we can conclude that obstructive
sleep apnea combined with obesity makes someone significantly
more at risk of developing A-Fib. On the other hand, just being
obese may be a less significant factor in developing A-Fib.
WHAT MECHANISMS INDUCE A-FIB?
Dr. Nattel went
further and tried to identify the actual A-Fib mechanisms behind
obstructive sleep apnea and obesity. Some of the rats were
subjected to pharmacological autonomic blockade while others
received muscle relaxants. Some of the rats who received the
pharmacological blockade could no longer be induced into A-Fib,
but a majority could. One can conclude that, “autonomic nervous
system changes contribute to A-Fib promotion, but only account
for a part of it.”
But the rats who
received the muscle relaxant did not develop A-Fib. This may be
because they didn’t experience the negative pressure generated
in obstructive sleep apnea when the airway is closed off.
LEFT ATRIAL ENLARGEMENT
But why was A-Fib
more inducible in the obese rats? The left atrial dimensions of
the obese and lean rats control group were not significantly
different, but with progressive apnea there was an almost
two-fold increase in atrial dimensions which increased more in
the obese rats than in the lean ones. Dr. Nattel tried to
prevent this left atrial dilation by inserting a balloon
catheter into the inferior vena cava thereby reducing venous
blood return. This prevented A-Fib in 80% of the previously
inducible rats. He concluded that there is, “strong, suggestive
evidence that it is in fact left atrial distension that is
responsible for the A-Fib susceptibility of the obese rats
during obstructive apnea.” “A-Fib promotion is primarily due to
acute left atrial enlargement, caused by forced inhalation
against a closed airway, combined with left ventricular
diastolic dysfunction and obesity.”
EDITOR’S
COMMENTS:
Dr. Nattel’s
innovative experiment showed how sleep apnea is highly likely to
cause A-Fib primarily by enlarging and remodeling the left
atrium particularly in the obese but also in lean subjects as
well.
If you or
someone you know snores and/or stops breathing while sleeping
and particularly if they are obese, it’s almost guaranteed they
are remodeling and harming their heart and will eventually
develop A-Fib.
They need to have a sleep apnea study done ASAP and correct
their breathing problem.
GENETICS OF A-FIB---40% Increased Risk of Developing A-Fib If
Relative Has It
Genetic
research in A-Fib, though in its preliminary stages, has the
potential to be a game changer for patients with A-Fib.
Dr. Patrick Ellinor of Mass General, Boston
gave a presentation on the “Genetics of A-Fib: How Will We
Translate GWAS Findings to Clinical Practice?”
A-FIB IS INHERITABLE
“If you have any
immediate family with A-Fib, you have a 40% increased risk
of developing A-Fib yourself. And the younger that
someone in your family gets A-Fib, the more likely you are to
have A-Fib.”
SCREEN FOR A-FIB?
If someone has
A-Fib, should all their immediate family members be screened for
A-Fib? Since in the US alone over three million people have
A-Fib, it isn’t possible or practical to screen all family
members for A-Fib. And even if we could screen everyone, we
don’t yet have the means to prevent A-Fib from developing or
even to identify patients with pre-A-Fib.
EDITOR'S COMMENTS:
If anyone in your immediate family has A-Fib, you are very
likely to develop A-Fib yourself. You have to be more aware and
vigilant than the average person.
If, for example, you feel palpitations or a racing heart
rate, take it very seriously. Don’t hesitate or delay in going
to an Electrophysiologist (EP) to have yourself checked out.
Make sure you tell your EP or Cardiologist that your relative
has A-Fib.
SPECIFIC
GENETIC CHROMOSOMES ASSOCIATED WITH A-FIB
Dr. Ellinor
identified the specific genetic chromosomes currently found to
be associated with A-Fib:
1q21
16q22
And particularly 4q25
People with a
particular combination of 3 genetic variants on chromosome 4q25
are six times more likely to develop A-Fib.
FURTHER RESEARCH NEEDED
But current
research has only revealed “associations.” Further research is
needed to determine:
1.
Are these chromosomes
associated with and/or do they cause an increased risk of A-Fib
stroke, heart failure and death?
2.
Are these genetic variants
associated with or do they indicate that a certain treatment
should be used or that a certain outcome is more likely?
3.
How important are these genetic
variants in the development of A-Fib?
4.
How do these genetic variants
affect what types of arrhythmia develop? Do Paroxysmal A-Fib,
Permanent A-Fib, or A-Flutter have different genetic profiles?
5.
And most importantly, how do
these genetic variants work? What Is the mechanism behind them?
“Right now all we have is an
association.” “We don’t have a fundamental understanding as to
how the variants themselves lead to the (A-Fib) disease.”
EDITOR’S COMMENTS:
If you have A-Fib, you must warn
all your immediate family members that they have a good chance
of getting it also. Even though we don’t know yet how to
definitively prevent A-Fib, there are some precautions your
family members can take:
1.
Avoid binge drinking and heavy
partying.
2.
Avoid antihistamines and
anything that can stimulate or trigger A-Fib. (see
A-Fib
Triggers) (This doesn’t necessarily include coffee. Some
research indicates coffee may prevent A-Fib.)
3.
Be more attentive to overall
health. Obesity, for example, is often a contributing factor to
A-Fib. Sleep apnea is known to lead to A-Fib.
4.
Check for deficiencies in
essential minerals (electrolytes) like magnesium or potassium?
Are calcium levels too high (which may be a trigger for A-Fib)?
5. Avoid
or learn to cope with stress (not always possible).
There is a tendency in all of us to
not tell others if we are ill, perhaps because we perceive it as
somewhat humiliating and a weakness in ourselves. But no one
should be ashamed of having A-Fib. Most likely it isn’t anything
we brought on ourselves. It’s genetic! It’s nobody’s fault!
We are not being
fair to our family members by not telling them about our A-Fib.
Don’t just mention it in passing. Sit down with them and tell
them what A-Fib is like, and that they are at risk. If you love
your family, you owe it to them. This applies particularly to
your brothers and sisters with whom you may have a loving but
somewhat competitive relationship. Anyone in your immediate
family must be warned.
BEST CLINICAL
SCIENCES PAPERS ON A-FIB
Dr. Eric Prystowsky of the Care Group presented the Best
Clinical Science Papers on AF for 2011. He started with an
initial literature search of 886 articles, then whittled them
down to 52 articles which he reviewed in detail.
In a study of the blood thinner
Rivaroxaban versus Warfarin (ROCKET AF),
Rivaroxaban was “noninferior” to Warfarin and actually was
somewhat better at reducing stroke risk. (Patel MK et al. NEMJ
2011; 365:883-91)
In a study of the blood thinner
Apixaban versus Warfarin (ARISTOTLE), Apixaban
was better than Warfarin both in reducing stroke risk and in
reducing major bleeds. (This is better than
"noninferiority.") (Granger CB et al. NEMJ 2011; 365:981-92)
(Apixaban seemed to test better than Rivaroxaban and Dabigatran.
Dr. Prystowsky said he was “very much looking forward to using
it.”)
In a study of
Irbesartan’s
effectiveness as an antiarrhythmic med (ACTIVE I), it wasn’t
significantly different than a placebo. (Irbesartan is an
“angiotensin II receptor antagonist” which blocks the action of
certain natural substances that tighten blood vessels, allowing
blood to flow more smoothly and the heart to pump more
efficiently.) (ACTIVE I Investigators NEMJ 2011; 364: 928-38)
Dr. Prystowski suggested that drugs like Irbesartan need to be
applied much earlier as preventive medicine ("upstream therapy")
rather than after patients already have A-Fib.
In a study of
Dronedarone in high-risk
patients with permanent A-Fib (PALLAS), patients taking
dronedarone were dying at more than twice the rate of those on a
placebo. The ratio of stroke and hospitalization for heart
failure was also more than twice as high. (See
Time to Stop Taking Dronedarone (Multaq)? and
No One with A-Fib Should Be Taking Dronedarone.) (Connolly
SJ NEMJ 2011; 365: 2268-76)
Several studies involved
Ablation and
Pulmonary Vein Reconnection. One study of 831
patients who had a Pulmonary Vein Isolation in 2005 by Hussein
(and Natale) was encouraging for patients. The
recurrence/reconnection rate was low (less than 10%) and in a
five year study there was no recurrence/reconnection after 36
months. (Hussein AA (Natale) Circ Arrhythmia Electrophysiol
2011; 4:271-8) This study took place at many different A-Fib
centers, though they all used similar
Pulmonary Vein Antrum Isolation procedures. Instead of
making encircling lesions around each of the pulmonary veins,
wider ablations encircle each of the two left and two right
pulmonary veins in the Antrum area around the veins.
Waiting 30 Minutes
to Check PV Ablations
In a small but important study by Yamane, each PV was
checked 30 minutes after the ablation with the stimulant ATP. If
reconnected, the PV was ablated again where the reconnection
occurred. This process was repeated every 30 minutes until 90
minutes.92% of patients were free of A-Fib recurrence without
antiarrhythmic drugs after 370 days (a little over a year).
(Editor's
Note: This may be a major medical breakthrough.
This simple technique of waiting 30 minutes and retesting seems
to nearly eliminate the problem of recurrence/reconnection and
produces a very high success rate. [Several later presentations
presented different techniques of waiting 30 or 60 minutes for
retesting.] The mean procedure time was only around 3 hours. In
practice, doctors can do other important tasks, even work on
other patients, during this 30 minute wait time. Any procedure
that achieves an over 80% success rate is a major improvement
for patients.) (Yamane T
et al. Circ Arrhythm Electrophysiol 2011; 4: 60-68)
A study by Akoum presented the
Utah 4 Stages of
Fibrosis Recurrence Rates as determined by
DE-MRI. (See
MRI (MAGNETIC RESONANT IMAGING) APPLIED TO A-FIB.)
Recurrence rates were significantly higher in patients with
Stage 4 (the most or highest) levels of fibrosis/remodeling.
(Akoum N et al. J Cardiovasc Electrophysiol 2011;
22:16-22)
MRI-Detected Subliminal
Lesions
Three studies by
Gaita, Siklody, and Deneke found that, using MRI, subliminal
small lesions or clots, undetectable except with MRI, did occur
in the brain after a Pulmonary Vein Isolation procedure
primarily when using a Multielectrode Phased-RF Catheter. (See
Silent Clots from Multielectrode Phased-RF Ablation Catheters.)
But these silent lesions detected by MRI were not linked to any
neurologic defect or cognitive decline, and most (94%) reversed
over time. (Gaita F et al. J Cardiovasc Electrophysiol 2011; 22:
961-68. Siklody CH et al. J Am Coll Cardiol 2011; 58: 651-8.
Deneke T et al. Heart Rhythm 2011; 8: 1705-11)
In a study by Lomuscio, patients were given
Acupuncture after a Cardioversion.
Specific needle points were identified. 80 patients with
persistent A-Fib were randomized into four groups: Acupuncture,
Sham Acupuncture, Amiodarone and No Treatment. The patients
receiving Acupuncture or Sham Acupuncture had 10 sessions of
15-20 minutes weekly starting within 48 hours of cardioversion.
The most freedom from recurrence occurred with the
Amiodarone group. The Acupuncture group came in second but
approximated the results of the Amiodarone group. The No
Treatment group had significantly more recurrence, while the
Sham Acupuncture group had the worst recurrence rate.
(Editor's Note:
Acupuncture, though not quite as effective as Amiodarone, might
be a welcome option for patients who can’t tolerate or don’t
want to risk the toxic side effects of Amiodarone. Cardioversion
has a notoriously high recurrence rate. "50 to 75 percent of
patients eventually develop Atrial Fibrillation again."32
Ten weekly Acupuncture sessions seems a small price to pay to
avoid going back into A-Fib.
But one surprising result of this study was the poor
results of the Sham Acupuncture group. One would expect a
placebo effect from these ten Sham Acupunctures. But instead the
misdirected Acupuncture needle pricks produced more recurrence
than No Treatment. The lesson to be learned is for patients to
make sure their Acupuncturist knows what spots to hit and has a
proven track record in treating A-Fib. Unfortunately these
Acupuncturists are hard to find.) (Lomuscle A et al. J
Cardiovasc Electrophysiol 2011; 22: 241-7)
Kidney Disease GFR (Glomerular Filtration Rate) Relates to
Recurrence After Cardioversion
In a study by
Schmidt, freedom from recurrence after a cardioversion related
to higher levels of GFR (Glomerular Filtration Rate). GFR is a
measurement of how well the kidneys function or the stage of
kidney disease. (Schmidt M J Cardiovasc Electrophysiol 2011; 22:
1092-8)
In a related study by Baber,
Chronic Kidney Disease (CKD) was associated with A-Fib
in adults (REGARDS study). (Baber U et al. Circ
Arrhythm Electrophysiol 2011; 4: 26-32) (This is an important
medical breakthrough observation for patients. Kidney
disease can be added to the list of causes or triggers of A-Fib.
One doctor in
the question-and-answer session said that kidney disease is
associated with fibrosis, inflammation and the release of
factors in the blood which affect other organs, and may be why
kidney disease is associated with A-Fib.)
In a study by Daoud (TRENDS), they found a
temporal relationship between Atrial Tachycardias/A-Fib and
Cerebrovascular Events (strokes). (This is not
at all surprising. People with A-Fib have 5-6 times more chance
of having a stroke [unless treated]. But what is needed is more
long term monitoring. One can't always expect an A-Fib stroke to
occur right after an A-Fib episode.) (Daoud EG Heart Rhythm
2011; 8: 1416-23)
A study by Huxley (ARIC) found that
Whites developed
A-Fib more than Blacks. (Huxley RR Circulation
2011;123: 1501-8) (It isn't clear why, since blacks have more
risk factors for A-Fib such as hypertension. Genetic research
might some day explain why this occurs.)
In a related study Rader found that,
after cardiac surgery Whites developed A-Fib more than Blacks
(1.74 ratio). (Rader Circ Arrhythmi
Electrophysiol 2011; 4: 644-52)
A study by Diepen raises serious
danger
for A-Fib patients undergoing noncardiac surgery and even minor
outpatient procedures.
(It’s well recognized that someone with heart
failure, for example, has a greater risk of dying during
noncardiac surgery (9.3%), and that both patients and surgeons
in these cases must be aware of this added risk. But what this
study shows is that patients with A-Fib also have a high risk of
death (6.4%).This is a major medical breakthrough
observation for A-Fib patients. Anyone with A-Fib and their
surgeons should be made aware of this added risk. But few A-Fib
patients now receive this warning. As a reference point, people
with CAD (Coronary Artery Disease) have a risk of death of
2.9%.]
Perhaps the most disturbing part of this study was the
risk of death for minor outpatient procedures. For heart failure
it was 4.1%. If one has A-Fib. the risk of death from minor
outpatient procedures is 2.2%!!!
This study did not
speculate about why having A-Fib adds more risk.
Caveat about this study: This
study did not compare the risk of having A-Fib to that of a
normal healthy person's risk. The editor has written the authors
of this study to see if these figures are available.)
(Diepen et al. Circulation 2011; 124: 289-96
DRONEDARONE CLINICAL
TRIALS ANALYSIS
Dr. Peter Kowey of Lankenau Medical Center gave a
detailed analysis of the various clinical trials of dronedarone.
Dronedarone is not simply “amiodarone lite,” but is a unique med
with its own characteristics and uses.
Unlike amiodarone, dronedarone is not characterized by “Iodine
Moiety (part or component)” or Thyroid safety issues. While
amiodarone is 65% successful in suppressing A-Fib, dronedarone
is 50%. Dronedarone is taken twice a day with meals, while
amiodarone is taken once a day after loading. Unlike amiodarone,
dronedarone may have only a minor interaction with warfarin.
Dronedarone is probably as efficacious as other antiarrhythmics like
sotalol or class 1C drugs.
Clinical Trials
The ANDROMEDA study was terminated
early, because there was a 2-fold increase in mortality in the
dronedarone group.
In the ATHENA study dronedarone
significantly reduced Cardio Vascular (CV) hospitalizations by
37%.
The PALLAS study was terminated early
due to excess deaths, strokes and heart failure hospitalization.
It was intended to assess the efficacy and safety of dronedarone
in patients with permanent A-Fib.
Patients taking
dronedarone were dying at more than twice the rate of those on a
placebo. The ratio of stroke and hospitalization for heart
failure was also more than twice as high. (See
Time to Stop Taking Dronedarone (Multaq)? and
No One with A-Fib Should Be Taking Dronedarone.)
New Drugs In Clinical Trials
Dr. Kowey described new
drugs being tested in clinical trials as amiodarone congeners
(similar to amiodarone).
- Benzofuran derivatives
(Budiodarone)
- Ranolazine
- Atrial specific agents (vernakalant, IKach, IKur
blockers
Conclusions
Dr. Kowey realistically
appraised the expected future use and utility of dronedarone:
“Dronedarone’s promise
as a safe and simple drug that could be used by a broader group
of physicians will not be realized.”
“Dronedarone’s use should be restricted to cardiologists and
electrophysiologists who are accustomed to intensive patient
monitoring for efficacy and safety.”
DIFFICULT CASES IN
A-FIB MANAGEMENT
One of the most interesting sessions at the Boston A-Fib
Symposium is always the “Difficult Cases in AF Management –
Antiarrhythmic Drugs, Anticoagulation, and Clinical Decision
Making.” In this panel doctors Jeremy Ruskin, A. John Camm,
Hans Kottkamp, Kevin Heist, Peter Kowey, Eric Prystowsky, and
Albert Waldo described individual cases and discussed what were
the best treatment options for these particular patients.
Patient #1
76-year-old man in A-Fib 100 bpm feeling tired & with shortness
of breath
The first case was presented by Dr. Kowey and
involved a 76-year-old man with shortness of breath and
tiredness. He was found to be in A-Fib with rates of around 100
bpm. He was on the rate control med atenolol and had moderate
high blood pressure. His labs were normal.
The options the audience could vote to treat Patient #1 were:
rate control with blood thinners, cardioversion, or “refer for
catheter ablation.” Most of those voting picked cardioversion.
Some picked rate control.
In the discussion it was pointed out that patient #1
needed to be on rate control meds because his heart beat was
high. But he was already on atenolol which did not help his
shortness of breath and tiredness. The general consensus was to
do a cardioversion. But one Dr. pointed out that it would be
wrong to wait too long, because a-fib is likely to become
progressively worse over time. If the cardioversion didn’t work
or didn’t last very long and his symptoms were still bad, he
could then be referred for a catheter ablation within a
relatively short period of time. Most of the participants agreed
that patient #1 needed to be on blood thinners for life unless
his circumstances changed. One doctor stressed how all patients
need to be involved in the decision process and need to
understand the advantages and disadvantages of each treatment
option.
What Actually Happened to Patient #1
Dr. Kowey said that patient #1 was given an
anti-hypertensive drug and an oral anticoagulant. The
beta-blocker atenolol was stopped and was substituted by the
antiarrhythmic med sotalol which has beta-blocker
characteristics. Patient #1 was cardioverted successfully, and
then continued taking sotalol. However, after two months patient
#1’s a-fib recurred, but he did not have any symptoms, and his
blood pressure was now well-controlled. When asked to vote on
his changed condition, most of the participants voted that
patient #1 continue on rate control and warfarin or rate
control and dabigatran/rivaroxaban.
Patient #1 was taken off of sotalol and started on dronedarone.
He continued on blood thinners. He continues to do fine without
significant symptoms and no hospitalizations.
Patient #2
86-year-old woman with silent A-Fib & short A-Fib episodes
Dr. Eric Prystowsky presented
the case of an 86-year-old woman who came in to have her
pacemaker checked. Her pacemaker showed that she had silent
A-Fib, the longest episode being 2.4 hours.
85% of the attendees voted to put her on a blood
thinner. (Current guidelines recommend that anyone experiencing
A-Fib episodes longer than 48 hours be put on blood thinners.)
Several doctors and audience members had divergent
views on this important subject. One doctor pointed out that
elderly women have a greater risk of having a hemorrhagic stroke
from blood thinners than from an A-Fib ischemic stroke. (The
newer blood thinners like dabigatran might work better than
warfarin in reducing the risk of a hemorrhagic stroke.) Another
doctor said that data showed that A-Fib episodes shorter than 24
hours had little chance of causing a stroke.305
But another doctor cited a study where an A-Fib episode as short
as 6 minutes could produce a 2.5 risk of stroke. (The author
is not familiar with this study and has written this doctor for
more info.)
The Symposium attendees then voted on whether
they currently use a 24 hour or 48 hour long episode to
determine the need for anticoagulation. 38% said they used 24
hour, 62% said they used 48 hour.
Dr. Prystowsky pointed out the importance of
discussing and documenting in the patient’s folder all the
anticoagulation options and how patients could be affected by
each. This should be done not only for the patient’s benefit,
but as a protection from law suits.
Another doctor pointed out that patients often have
a hard time determining when exactly an A-Fib episode started or
how long it actually lasted (unlike this elderly woman whose
pacemaker revealed the duration of her A-Fib episodes).
The general consensus was that the duration of an
A-Fib episode that causes a risk of stroke is contested. There
needs to be more hard data and studies developed to resolve this
issue.
(Editor’s
Comments: Doctors do the best they can to protect
patients from having an A-Fib stroke.
But taking blood thinners is not an absolute
guarantee that one will never have an A-Fib stroke. Warfarin
reduces the risk of an A-Fib stroke by 60%-70%.295
But that isn't 100%. There is that 30-40% you still have
to worry about. And
with many blood thinners there is an increased risk of bleeding,
GI problems, and developing an hemorrhagic stroke.
The only guarantee of not having an A-Fib stroke
is to no longer have A-Fib, or to perhaps have one’s Left Atrial
Appendage (LAA) closed off or removed. 90%-95% of A-Fib clots
come from the LAA.)
Patient #3
45-year-old male endurance runner with A-Flutter
Dr. A. John
Camm presented a case of a 45-year-old male competitive
endurance athlete in great shape who used to run 70-75
miles/week but who experienced sudden palpitations in his heart.
His EKG showed he had A-Flutter.
The choices of treatment presented to the Symposium voters were:
* Beta-blocker - bisoprolol
* Flecainide
* Amiodarone
* Atrial flutter Right Atrium ablation procedure
Most voted for an atrial flutter ablation. That's what was done
for patient #3.
But Dr. Camm presented data from a study which showed that
endurance athletes don't have as good results and, if they
continue to run after ablation, don't do as well as patients in
other sports or no sports patients. (Heidbuchel H. et al. Int
J Cardiol 2006; 107:67-72)
What happened to patient #3
Now aged 50
his EKG showed A-Fib and nocturnal pauses, probably brought on
by his running. He also had a large left atrium. In the
discussion doctors pointed out that telling a runner to stop
running doesn't work. Running is an important part of their
life. What you have to tell them is they risk developing A-Fib.
(See
Vigorous Exercise and A-Fib.)
Dr. Camm pointed out that endurance athletes have five times
more risk of developing Lone A-Fib, that 5%-10% of middle age
endurance athletes will develop A-Fib. Runners develop increased
vagal tone, and the pressure and volume overload they apply
produce atrial stretch and dilation, inflammation, and atrial
fibrosis.
Several doctors pointed out that A-Fib often lurks in the
background, is a part of A-Flutter, or often develops after an
A-Flutter ablation. (Editor's
Note:
From this
patient's perspective, a patient having an A-Flutter ablation
should also have an A-Fib ablation at the same time. A
Flutter ablation is a relatively simple procedure compared to
A-Fib ablation. It can usually be done at
the end (or at the beginning) of an A-Fib ablation. See
Flutter Ablation should be Combined with Left Atrium A-Fib
Ablation.) Some
doctors said they would never do an A-Fib ablation when only
A-Flutter is present. Others said they routinely do both Flutter
and A-Fib ablation at the same time, particularly in the case of
athletes.
Dr.
Kottkamp pointed out that the size of the left atrium wasn't a
problem, that he was more interested in the overall health of
the left atrium as shown in an EKG. The bigger atrium is not
always more sick than the smaller atrium. He does ablations if
the left atrium is 50 or 52 mm.
Patient #4
60-year-old male in chronic A-Fib for 12 years with
cardiomyopathy
Dr. Hans
Kottkamp presented a case of a 60-year-old male in long-standing
persistent (chronic) A-Fib with dilated cardiomyopathy. (He
hadn't seen a cardiologist in three years.) He was diagnosed
with A-Fib nearly twenty years ago. He had a low ejection
fraction (25-30%), worsening heart failure, shortness of breath
during minimal exercise, and peripheral edema (swelling).
The choices of treatment presented to the voters at the
Symposium were:
* Electrical cardioversion
* Catheter ablation (both PV Isolation & substrate modification)
* AV-Node ablation + pacemaker
* AV-Node ablation + CRT-D (Cardiac Resynchronization Therapy
with Defibrillator (regular biventricular pacing paces the right
atrium and right ventricle, CRT pacing also paces the left
ventricle to keep both in sync)
What happened to patient #4
Because patient #4 had been in long-standing
persistent A-Fib for so long and had developed cardiomyopathy
(and probably because he wasn't likely to accept and cooperate
with intensive monitoring), he was given an AV-Node ablation +
CRT-D.
Three months after the AV Node ablation his heart was
significantly improved. His ejection fraction improved to
45-50%.
Patient #5 (actually 10 different
cases) CHADS2
scores of 0-1 and still suffered strokes
Dr. Jeremy Ruskin presented sobering, discouraging
cases for doctors and patients.
10 A-Fib patients with low CHADS2 scores (0-1) all suffered CVAs
(Cerebrovascular Accidents---strokes), TIAs (Transient Ischemic
Attacks---mini-strokes), or Embolic MI (Myocardial
Infarction---heart attack).
(Editor's Comments:
One of the cases Dr. Ruskin cited was a young man only 35 years
old who suffered an A-Fib stroke. Is this a wake-up call for
doctors and patients? Should anyone who has A-Fib be on a
serious blood thinner (not aspirin which isn't very
effective)? It's hard to think of this 35-year-old having to
take warfarin for the rest of his life. How would taking
warfarin for so long affect him?
But maybe the newer oral anticoagulants [dabigatran,
rivaroxaban, apixaban]
might lend themselves to daily dosage over a longer period of
time. Could these new anticoagulants replace aspirin as a
recommended blood thinner for A-Fib patients with low CHADS2
scores/supposedly low risk of stroke?)
Aspirin not effective or
safe
Dr Albert Waldo cited studies that "aspirin at 150-200 mg/day is
neither effective nor safe." (Sato H et al. Stroke
2006;37:447-51.) Aspirin was no better than a placebo and caused
a marginally increased risk of major bleeding.
In a Danish registry study of 132,372 A-Fib patients followed
for 12 years, "the use of aspirin to prevent stroke in patients
with A-Fib remains very poorly justified...Aspirin alone did not
decrease the risk of TE (Thromboembolism---stroke) compared to
no treatment." (Olesen JB et al. Thromb Haemost
2011;106:739-49)
One study showed Apixaban to be much better in reducing stroke
risk than aspirin. (Connolly SJ et al. N Engl J Med. 2011
364:806-17) (Perhaps apixaban, if FDA approved, might be a
welcome substitute for aspirin in patients at low risk of an
A-Fib stroke.)
YOGA & STRESS
REDUCTION IN A-FIB
(More to follow)
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