Boston AF Symposium, JANUARY 17-18, 2003
The annual international Boston A-Fib Symposium is one of the -most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information. Unlike other heart related conferences, it concentrates only on A-Fib. But if you haven’t read and understood most of A-Fib.com, it may be difficult reading.
Each presentation is listed by both the last name and by the topic of the presenter. If a doctor made more than one presentation, they are listed as (1) and (2). You can access a presentation either by the doctor’s name or by the topic. (All presentations are not summarized.)
Dr. Crijns discussed the results from the RACE study (Rate Control Versus Electrical Cardioversion for Persistent Atrial Fibrillation).
In this study of patients with Persistent A-Fib, one randomized group received oral anticoagulants and rate control drugs; the other received oral anticoagulants, Electrical Cardioversion and antiarrhythmic drugs ( first attempt, sotalol; second attempt, flecainide or propafenone; third attempt, amiodarone.) Electrical Cardioversion, rather than antiarrhythmic drugs, was used to restore patients to sinus rhythm; while the antiarrhythmic drugs were used to maintain patients in sinus rhythm. Serious problems (“primary end points”) such as heart failure, stroke, etc. were approximately the same with the exception of severe antiarrhythmic side effects (0.8% vs. 4.5%). 39% of the antiarrhythmic group was in sinus rhythm versus 11% of the rate control group. (This was not a randomized study to compare rate control and/or antiarrhythmic drugs to placebos.)
A subgroup analysis of patients with hypertension revealed more serious problems (primary end points) in the antiarrhythmic group, while those with normal blood pressure had fewer problems. “Hypertension may be associated with increased risk of the primary endpoint” in patients taking antiarrhythmic drugs.
Dr. Calkins described experimental developments using MRI (Magnetic Resonant Imaging) to produce live 3-D images of the heart during catheter ablation procedures. Current practice uses Fluoroscopy, a form of X-ray, to produce 2-D images of the heart. Fluoroscopy over time can expose both patients and staff to significant radiation.
“Stereotactic Ablation with MRI/CT Guidance” consists of:
a) A miniature passive magnetic field sensor in the ablation catheter
b) An external ultralow magnetic field emitter (location pad)
c) A processing unit containing the three dimensional MR images.
The location pad is placed under the subject. Three electromagnetic coils in the location pad each generate ultralow magnetic fields. Three orthogonal antennae in the tip of the ablation catheter identify its position and orientation in space in relation to these magnetic fields. These antennae also display the catheter’s position on the 3D-MR images in real time. In this experiment Fluoroscopy was used to confirm the catheter’s position.
In the structural and animal models used in this experiment, the MR imaging was very accurate and precise. This study demonstrated that it is now possible to combine an electromagnetic navigation system with true live 3-D MR images.
(Author’s Note: This could be a very important development for A-Fib. Patients and staff using this system would be exposed to less X-ray radiation. Doctors seeing live, real time 3-D images of the heart could more easily and effectively perform catheter ablations.)
Dr. Pappone described the PVI technique used in Milan called “anatomically based circumferential PV ablation.” Circumferential lesion lines are made around the ostia (opening) of each Pulmonary Vein to isolate these veins from the left atrium while reducing the risk of PV stenosis (swelling). The circumferential lines are made at a distance of more than 5 mm from each PV ostia.
Dr. Pappone’s success rate for patients monitored over a three year period was 87%. He had approximately equal success with both Paroxysmal (occasional) and Chronic (all the time) A-Fib. A typical procedure took only forty minutes.
In what he termed “electroanatomical remodeling” Dr. Pappone found that successful circumferential PV ablation significantly reduced left atrial size and improved its transport function (how well the heart pumps out blood) over a three year monitoring period.
(Author’s Note: This is one of the first significant findings about the long term effects of PVIs. For those of us suffering from A-Fib, it’s welcome news that some of the bad remodeling effects of A-Fib can perhaps be reversed by a successful PVI.)
Dr. Jaïs from the Bordeaux group and other doctors said that they have not been able to replicate Dr. Pappone’s results in their facilities.
(Author’s Note: The fact that other doctors to date have not been able to replicate Dr. Pappone’s work does not call into question his work and results. Dr. Pappone may have developed a unique combination of equipment, facilities, techniques and personal skills that may not translate easily to other environments.)
Dr. Chen discussed using right atrial linear ablation to cure Right Atrium dominant A-Fib. (Patients with focal and Pulmonary Vein A-Fib are not candidates for Right Atrium ablation.) Simply making linear lesions to compartmentalize the Right Atrium isn’t very effective.
Using noncontact mapping, Dr. Chen found that A-Fib reentry circuits go through the low right atrium isthmus and through the crista terminalis gap between low voltage zones. Dr. Chen makes short lesion lines (1-4 cm) in these areas to successfully eliminate right atrium A-Fib in 80% of patients.
Dr. Argenziano described minimally invasive and robotic surgery for A-Fib.
The standard Maze operation, though successful in a high percentage of cases, is invasive. It involves breaking through the sternum, cardiopulmonary bypass, stopping the heart from beating, cutting the heart into sections, and/or making multiple incisions. This open heart surgery is traumatic for the patient and can have complications.
Dr. Argenziano’s surgical approach starts by cutting into the left atrium near the right pulmonary veins to perform pulmonary vein isolation, usually in patients having other cardiac operations. He makes an encircling lesion around the four pulmonary vein openings, and makes another lesion from the encircling lesion to the mitral annulus. He then either amputates the left atrial appendage or makes a circular burn at the base of the appendage to isolate it. He adds a connecting line from the pulmonary vein isolating line to the appendage isolation line. This ablation rarely adds more than 20 minutes to the main cardiac operation. He uses RF, microwave, ultrasound, or laser energy to make the lesions. His success rates approach 80%.
Though the majority of these operations are performed along with other heart operations, he also uses this procedure for patients who only have A-Fib and no other heart problems. He gains access to the heart through a 6 cm incision in the chest. This procedure can be done while the heart is still beating. He also uses robotics to perform the procedure.
(Author’s Note: A person using robotics looks like someone playing video games, only dressed in white. It’s remarkable how this surgical approach is becoming similar to and converging with the PVI procedure.)
In patients undergoing a right atrial operation and in those with a history of atrial flutter (“in whom right-sided initiating foci are common”), he makes a longitudinal incision in the right atrium and a RF lesion from the bottom of this incision to the tricuspid annulus.
After the operation, 69% of his patients experience at least one episode of A-Fib, probably due to the time it takes for the lesions and scars to heal and achieve complete electrical isolation. To keep patients in sinus rhythm, he administers amiodarone in the operating room, followed by a 24-hour intravenous drip and 6 weeks of low-dose oral therapy. He also administers three months of anticoagulation for all patients, whether they are in sinus rhythm or not.
Dr. Jaïs described how the Bordeaux group’s current Pulmonary Vein Isolation techniques are achieving success rates of 82% in curing patients with Paroxysmal (occasional) or Persistent A-Fib. (Success is measured if a patient is in sinus rhythm without taking any antiarrhythmic medications six months after a PVI.) An even higher success rate of 91% is achieved when including patients who are in sinus rhythm while still using antiarrhythmic drugs.
In a PVI the four myocardial sleeves extending into the Pulmonary Veins are ablated (“disconnected”). But A-Fib often returns due to “non PV foci” (other areas of the heart besides the Pulmonary Veins that produce A-Fib signals) or due to “recurrence of initial PVI” (areas of the heart that were ablated but for some reason start producing A-Fib signals again). These areas or foci are often difficult to identify, localize and ablate.
To block these non PV foci, the Bordeaux group then makes a linear lesion connecting the lateral mitral annulus to the ostium (opening) of the left inferior Pulmonary Vein. This is called a “mitral isthmus ablation.” This linear lesion blocks these A-Fib signals from spreading to the rest of the heart.
Coronary Sinus mapping and ablation are used to verify the completeness of the linear lesion and to correct any gaps. “…ablation through the Coronary Sinus is often crucial to achieve mitral isthmus block.”
The Bordeaux group has found that 50% of patients with Chronic (all the time) A-Fib need at least two procedures to be cured of their A-Fib.
Dr. Jaïs in his second presentation described a study now being conducted to compare antiarrhythmic drug therapy with catheter ablation for A-Fib.
Patients with Paroxysmal (occasional) A-Fib will be randomized into two groups, one treated with antiarrhythmic drugs (flecainide, propafenone, quinidine, dofetilide, amiodarone and/or sotalol), the other with radiofrequency catheter ablation (PVI and left atrial linear lesions). Patients will be treated at multiple centers and monitored for a period of one year. Mapping will be used to identify and ablate specific areas of the heart producing A-Fib signals (Segmental Ablation). Up to three ablation procedures of medical treatments using drugs can be performed. Linear lesions will be performed if needed as judged by the doctor.
The principal objective is to compare how often A-Fib reoccurs in the two groups. The study will also examine the two group’s quality of life, the effectiveness of amiodarone in particular, the secondary effects of both approaches, the rate of withdrawal from oral anticoagulants, and in cases of failed ablations whether previously ineffective drugs work to keep patients in sinus rhythm.
Patients must be in Paroxysmal A-Fib for at least six months and resistant to at least 2 antiarrhythmic drugs of different classes. (Author’s note: these are the criteria used by many centers today before performing a PVI.)
Patients will be treated by antiarrhythmic drugs or by radiofrequency ablation for 90 days. In cases of ablation treatment failure, doctors can switch to antiarrhythmic drugs after 90 days. In cases of drug treatment failure, doctors can switch to ablation after 90 to 180 days. Patients will be monitored for a year.
Dr. Nattel’s second presentation discussed using drugs to counteract atrial remodeling from A-Fib.
One type of remodeling is Atrial Tachycardia (rapid heart rate), the mechanism by which “A-Fib begets A-Fib.” It appears to be initiated by Calcium Channel current overload (Ca²+) and usually involves a lack of regulation or control of L-type Ca²+-current. (“L” stands for Long Lasting or High Voltage Activation which is the main pathway for Calcium Channel current in the heart.) Dr. Nattel indicated that genetic reprogramming may be involved in long-term (days) remodeling.
A second type of remodeling is caused by CHF (Congestive Heart Failure) and involves structural remodeling in the form of atrial fibrosis, and ionic (chemical) remodeling where increased Sodium and Calcium Channel currents (Na+, Ca²+) trigger A-Fib.
There are different types and mechanisms of remodeling which respond differently to treatment. Drugs with T-type Ca²+ channel blocking action, like mibefradil and amiodarone, do seem to prevent Atrial Tachycardia remodeling (“T” stands for Transient or Low Voltage Activation Calcium Channel current), though clinical studies are somewhat contradictory. But with regards to structural remodeling, “atrial fibrosis, once established, may be largely irreversible.”
Dr. Wyse discussed the AFFIRM (Atrial Fibrillation Follow-Up Investigation of Rhythm Management) trial which enrolled 4,060 patients in Canada and the US. Patients had to be over 65 or at high risk of stroke. Patients were randomized to rhythm or rate control groups. Doctors could choose from drugs on a list of drugs approved for use in A-Fib. (AFFIRM and other future studies will help identify which particular drugs were effective.) Doctors were encouraged to keep all patients on anticoagulation. The study looked primarily at mortality, how many patients died in each group. Most patients with A-Fib were Persistent (needs cardioversion), but some (around 20%) were Paroxysmal (starts and stops by itself).
There was no significant difference in deaths between the rate and rhythm control groups, though there were more deaths in the rhythm group. There were more hospitalizations and adverse drug effects in the rhythm control group. The authors concluded that “the advantages of rate control in such patients has been under-appreciated.” In fact “rate control may be preferred in some patients.” “Rate control should more frequently be considered as a primary therapy…in patients such as those enrolled in AFFIRM.” “…rate control is at least as good as rhythm control, and has some potential advantages.”
Most of the strokes occurred in patients who either stopped warfarin or had an INR below 2.0. There was no significant difference in strokes between either group. (Patients in the rhythm control group could be taken off of warfarin after 1, but preferably 3, months of continuous sinus rhythm. Only 70% of the rhythm group were on warfarin therapy, compared to 85-95% of the rate control group.) The rate of intercerebral bleeding was 0.3%.
One important conclusion of the AFFIRM trial was that, “anticoagulation should not be stopped when the patient is in sinus rhythm, because…the majority of strokes occurred when the warfarin was stopped or subtherapeutic.
“Quality of life and functional capacity shows no differences between the two treatment (groups).” Only a small number of patients (<5%) received non-drug therapies such as a PVA.
One important figure was the high number of patients in the rate control group who were in sinus rhythm.
(Author’s notes: Newer antiarrhythmic drugs such as dofetilide (Tikosyn) were probably not a part of this study.
Not all antiarrhythmic (rhythm control) drugs are created equal. They work differently and have different success rates. Also, individuals often react differently to medications. A drug that may be ineffective and even toxic to one person may be beneficial to another.
From a patient’s perspective, most people in A-Fib want to be in sinus rhythm. A rate control therapy that keeps the heart from racing too fast but that doesn’t stop the A-Fib, probably isn’t an option that most people in A-Fib would be happy with unless there were no other options.
Since the A-Fib patients in this study were older (over 65) or at high risk of stroke, the lack of significant difference in death between the rate and rhythm control groups could be attributed to the patients’ age and overall state of health rather than to the use of rate or rhythm control drugs. In other words, older patients in poor health might have died irrespective of whether they were using rate or rhythm control drugs. However, the increase in hospitalizations and adverse drug effects in the rhythm group do indicate that antiarrhythmic drugs are associated with more adverse side effects than rate control drugs.)
Dr. Crijns and his associates compared rate control to rhythm control drug therapy in patients with Persistent (lasting 24 hours or longer) A-Fib. In the rate control group patients received digitalis, and/or a calcium-channel blocker and/or a beta-blocker. In the rhythm control group patients received sotalol. If sotalol didn’t work, then flecainide or propafenone was tried, then amiodarone. Electrocardioversion was used in the rhythm control group to restore sinus rhythm. All patients received anticoagulant (blood thinning) drugs.
Looking only at whether rhythm or rate control prevented death or serious heart problems, “Rate control is not inferior to rhythm control…and may be appropriate therapy in patients with a recurrence of persistent A-Fib after electrical cardioversion.” The study also examined quality of life issues such as which group felt better, led a more satisfying life, etc. and did not find major differences between the groups.
In patients with persistent A-Fib undergoing repeated electrical cardioversions and taking antiarrhythmic medications, the A-Fib tends to reoccur and the drugs tend to have bad side effects. Despite the electrical cardioversion and rhythm control drug therapy, at the end of the study only 39% of the rhythm control group were in sinus rhythm (as compared to 10% in the rate control group). “Obviously, safer and more effective methods of maintaining sinus rhythm are needed, and such methods may help reduce morbidity in the future.” Since in this study antiarrhythmic drugs and electrical cardioversion didn’t succeed in keeping patients in sinus rhythm, future rhythm control drugs that work better may get better results than rate control drugs.
One very important finding of the Crijns study is that it didn’t seem to matter whether a patient was in sinus rhythm or in A-Fib in terms of the risk of death and serious heart problems. “This finding suggests that the cardiovascular risk is not reduced with rhythm control even when sinus rhythm is maintained.” This may be because effective rate control may also prevent heart failure.
Another important finding of the Crijns study is that patients with risk factors for stroke may have a stroke when anticoagulation therapy is stopped. In this study anticoagulants were stopped after a patient was in sinus rhythm for one month. But six people in this group had strokes, and all but one were in sinus rhythm. This study found that almost all patients with persistent A-Fib had one or more risk factors for stroke. “Therefore, anticoagulant therapy can be stopped only rarely.”
A large number of strokes occurred in both groups, perhaps because so many patients had risk factors for stroke. There was also a smaller amount of bleeding episodes. “Most strokes occurred at an INR below 2.0. Likewise most bleeding episodes occurred at an INR that exceeded. 3.0.” This study stressed how important it is to carefully monitor the anticoagulant levels in patients with A-Fib.
In this study, “the use of antiarrhythmic drugs contributed significantly to the incidence of major cardiac end points in the rhythm-control group but not in the rate control group.” Patients in the rhythm-control had more major heart problems. In this particular study patients on rhythm control who had hypertension or who were female, had a much higher number of “primary end-point events.” But since this research wasn’t designed to study these subgroups, the report only suggested that these subgroups be further studied.
The authors of this study stressed that it only applied to patients with persistent A-Fib, and didn’t necessarily apply to patients with new A-Fib. “Rather than rate control, cardioversion in combination with prophylactic (rhythm control) drugs is one of the first options in such patients.”
The first presentation at the Boston A-Fib Symposium introduced what could be breakthrough concepts for the understanding of A-Fib.
In what Dr. Jalife called “Optical Mapping,” we could actually see how A-Fib signals work in a heart. In a fascinating, very insightful media presentation, you could see the various frequencies swirling around in a sheep’s heart in A-Fib. (I will try to obtain a copy of this video and include it in A-Fib.com as soon as I find the time to learn flash animation.) Each A-Fib frequency was assigned a different color, what Dr. Jalife called dominant frequency maps. In the right atrium the frequencies were all mixed up and colliding with each other (random reentry), but in the left atrium the frequencies moved in a rotor pattern as though they were rotating around a point in the left atrium. Dr. Jalife introduced the term “mother rotor” as his hypothesis for the mechanism of A-Fib. The higher frequencies of A-Fib were in the left atrium, whereas the right atrium had slower frequencies.
Dr. Jalife hypothesized that, at least in some cases, A-Fib in the left atrium comes from high frequency sources (rotors), whereas the right atrium fibrillates because of signals received from the left atrium and at lower frequencies than the left atrium.
The sheep’s heart was pushed into A-Fib by burst pacing and by administering Acetylcholine (ACh), a chemical involved in the transmission of nerve impulses in the body. Dr. Jalife and his colleagues showed how in this sheep’s heart acute A-Fib came from high frequency rotors in the left atrium, while the right atrium fibrillated because of conduction from the left atrium. This is because the left atrium is more affected by ACh than the right atrium. Dr. Jalife hypothesized that the mechanism of chronic A-Fib may be similar to what we saw in this sheep’s heart even in the absence of ACh, because so-called “electrical remodeling” affects the left atrium more than the right.
(Dr. Alexey Zaitsev collaborated with Dr. Jalife. He did the above experiment and generated the data.)
Dr. Olgin also discussed optical mapping of A-Fib. His emphasis was on the cellular and intercellular level. He showed examples from a dog with chronic Mitral regurgitation (A-Fib is often seen with congestive heart failure, mitral valve disease and hypertension). In the close-ups of A-Fib cell tissue, one could clearly see significant differences in the cells (tissue or myocyte discontinuities or “non-uniform anisotrophy”) and inflamed cells due to fibrosis and inflammation.
In contrast to the classical theory of A-Fib as due to multiple wavelet reentry, Dr. Olgin hypothesized that this chronic A-Fib was due to these cell or tissue differences which slow and disrupt normal conduction patterns in the heart.
(Note: Dr. Olgin is moving to the Un. of California San Francisco June 1, 2003. He will be the Chief of Cardiac Electrophysiology. UCSF will have an A-Fib Center. He has been performing PVA(I)s since 1997 and has done several hundred. Among other initiatives he will study the genetics of A-Fib. He is moving his NIH-funded lab on researching the mechanisms of A-Fib to UCSF and will start an A-Fib research group.)
Dr. Allessie, known for clinically identifying that “A-Fib begets A-Fib,” talked about new medications for A-Fib.
His first visuals showed how easily and quickly a goat’s heart can be remodeled to persistent (Chronic) A-Fib after only one or two weeks of burst pacing (similar to a pacemaker except that signals are generated to produce A-Fib). He showed how certain current class IC drugs like Flecainide actually widen the “excitable gap,” the time period during an ECG heart beat signal when the heart is easily stimulated into A-Fib.
Some class III drugs like Sotalol shorten the “refractory period,” the time period during an ECG heart beat when the heart is not easily stimulated into A-Fib. He also said that Class III drugs lose their efficacy because of electrical remodeling, and don’t work at high A-Fib rates.
He showed his results of an promising experimental “Early Class III” drug produced by Aventis now called AVC 118. It prolongs the refractory period, doesn’t lose its efficacy after remodeling or at high A-Fib rates, and is safe. It can be used to chemically cardiovert someone in A-Fib. (It may be quite some time before this drug is approved for use in the US.)
Despite his reservations about current drugs, Dr. Allessie did say that “(new) Drugs are the only hope we have because of the high number of people in the general population who have A-Fib.”
Answering a question from the audience, Dr. Allessie said Verapamil (a calcium-channel blocker rate control drug) may work to help someone with Paroxysmal (occasional) A-Fib from getting an attack. But, if one is in A-Fib, Verapamil makes it worse, it speeds up the A-Fib rate.
Dr, Nattel examined the cellular activity of the Pulmonary Veins as compared to other areas of the left atrium. He looked at the “cardio myocyte sleeve(s)”—an area of heart tissue extending into the Pulmonary Veins. He found that these areas of the Pulmonary Veins differed significantly from other areas of the left atrium in some of their cellular currents and potentials.54 His findings indicate there is a cellular predisposition in the Pulmonary Veins to trigger and perpetuate A-Fib, but “further work is needed to determine the underlying mechanisms of such activity.”
Discussing stroke prevention for patients with A-Fib, Dr. Ezekowitz said warfarin therapy (INR between 2.0-3.0) reduces the risk of stroke by 68%.
Patients with lone A-Fib under 65 years old “generally do not require any form of (stroke) protection.”
(Author’s Note: There is some disagreement about this age cutoff. Some experts are now advocating 60 as the age cutoff.)
Many patients in this group use aspirin, but there is no evidence that it works. Aspirin at 325mg is sufficient for patients with A-Fib under age 75 without risk factors. However, aspirin was found to be only 2% more effective than a placebo. Patients over age 75 need warfarin therapy.
But the reality in practice is that the elderly are the least likely to be anticoagulated. “…between 15 and 45% of patients are actually anticoagulated.”
Reasons cited for not anticoagulating patients are a fear of bleeding and the difficulty of monitoring patients to keep their INR at the proper levels. But according to Dr. Ezekowitz the actual risk of hemorrhagic stroke is 0.39%. A new generation of anticoagulants in development doesn’t require monitoring and could solve many of the difficulties associated with warfarin therapy. Melegatran is an oral thrombin inhibitor in Phase III trials.
Mechanical alternatives to stroke prevention are in development such as a device to shut off the left atrial appendage so that blood will not pool or clot there (the left atrial Occluder).
Dr. Lemery discussed his preliminary studies of “Bi-Atrial Non-Contact Mapping” (mapping both atria by using basket-shaped catheters with 64 electrodes in each atrium to determine how the atria are activated by A-Fib signals). He found three main types of atrial activation.
- left atrial drivers cause the right atrium to fibrillate following conduction over interatrial connections,
- the right atrium independently sustains A-Fib, even after pulmonary vein isolation (ablation),
- both atria fibrillate independently without activation over interatrial connections.
He is currently analyzing how often the different activation patterns occur.
Dr. Prystowsky discussed the ACC/AHA/ESC Guidelines in the Management of Atrial Fibrillation selecting medications for patients primarily on the basis of safety.
1. For patients with minimal or no heart disease, the object is to “minimize organ toxicity,” to select drugs that will not harm the rest of the body such as flecainide, propafenone and sotalol. They can cause “proarrhythmia” (an increase in heart rhythm problems), “but in patients without heart disease this risk is extremely small.”
If these drugs don’t work, then amiodarone and dofetilide can be considered. And “in experienced hands one might choose (Pulmonary Vein) Ablation (Isolation) for a primary cure.”
2. For patients with congestive heart failure, only dofetilide and amiodarone have been demonstrated to be safe in randomized trials.
a. For patients with congestive heart failure and significant lung disease, “I would likely consider dofetilide as my first choice,”
b. For patients who have congestive heart failure and who are “hypokalemic” (have low levels of potassium), he would choose amiodarone.
3. For patients who have coronary artery disease, sotalol is recommended because of its beta blocking and antiarrhythmic effect. Amiodarone and dofetilide combined with a beta blocker can also be used. Propafenone and flecainide aren’t recommended.
4. For patients with hypertension, he recommended propafenone or flecainide.
a. For patients with hypertension and substantial left ventricular “hypertrophy” (increase in size), amiodarone is preferred because it has the least proarrhythmic effect.
Dr. Prystowsky discussed some new antiarrhythmic drugs that might be available soon in the US.
Azimilide is a Potassium Channel Blocker not chemically related to sotalol, amiodarone, or dofetilide, though it is a Class III drug. It prolongs the QT interval and refractoriness (the time during a heart beat when the heart is not easily stimulated into A-Fib). (In an EKG signal the QT interval represents the time the ventricles are pumping and at rest.) Azimilide is absorbed well by the body and can be given as a once-a-day dose. It is effective with A-Fib patients, and is safe for patients who have had a heart attack and whose left ventricles don’t function well.
He also mentioned that digitalis in his opinion is grossly over prescribed, that only 1-2% of A-Fib patients have Vagal A-Fib, that he personally hasn’t prescribed Class 1A drugs as first line therapy in nearly ten years.
Dr. Ellinor has been studying individuals with Lone A-Fib to identify “phenotypic” or genetic predictors for A-Fib. Recently, he and his colleagues have found that many patients with Lone A-Fib appear to have a family history of A-Fib. Using families with inherited A-Fib, they have identified a new genetic locus (or region) for A-Fib, distinct from the Chromosome 10 or KCNQ1 regions.
Dr. Ellinor welcomes individuals with a family history of A-Fib (generally 3 or more members of a family) to participate in the study to identify genes for A-Fib. You can contact him directly to learn more about the study.
Patrick T. Ellinor, MD, PhD
Cardiac Arrhythmia Service
Massachusetts General Hospital
55 Fruit St., GRB 109
Boston, MA 02114
E-mail: pellinor at partners dot org (Dr. Ellinor’s E-mail address is spelled out to prevent automatic search engines from flooding him with advertisements.)
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Last updated: Sunday, February 15, 2015