Doctors & patients are saying about 'A-Fib.com'...


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Dr. Douglas L. Packer, MD, FHRS, Mayo Clinic, Rochester, MN

"Jill and I put you and your work in our prayers every night. What you do to help people through this [A-Fib] process is really incredible."

Jill and Steve Douglas, East Troy, WI 

“I really appreciate all the information on your website as it allows me to be a better informed patient and to know what questions to ask my EP. 

Faye Spencer, Boise, ID, April 2017

“I think your site has helped a lot of patients.”

Dr. Hugh G. Calkins, MD  Johns Hopkins,
Baltimore, MD


Doctors & patients are saying about 'Beat Your A-Fib'...


"If I had [your book] 10 years ago, it would have saved me 8 years of hell.”

Roy Salmon, Patient, A-Fib Free,
Adelaide, Australia

"This book is incredibly complete and easy-to-understand for anybody. I certainly recommend it for patients who want to know more about atrial fibrillation than what they will learn from doctors...."

Pierre Jaïs, M.D. Professor of Cardiology, Haut-Lévêque Hospital, Bordeaux, France

"Dear Steve, I saw a patient this morning with your book [in hand] and highlights throughout. She loves it and finds it very useful to help her in dealing with atrial fibrillation."

Dr. Wilber Su,
Cavanaugh Heart Center, 
Phoenix, AZ

"...masterful. You managed to combine an encyclopedic compilation of information with the simplicity of presentation that enhances the delivery of the information to the reader. This is not an easy thing to do, but you have been very, very successful at it."

Ira David Levin, heart patient, 
Rome, Italy

"Within the pages of Beat Your A-Fib, Dr. Steve Ryan, PhD, provides a comprehensive guide for persons seeking to find a cure for their Atrial Fibrillation."

Walter Kerwin, MD, Cedars-Sinai Medical Center, Los Angeles, CA


AF Symposium & other medical conferences articles

2020 AF Symposium Challenging Case: 75-Year-Old, A-Fib Increases, Develops Bradycardia, 12-sec Heart Pause

2020 AF Symposium: AF Management 

Challenging Case: 75-Year-Old, A-Fib Increases, Develops Bradycardia, 12-sec Heart Pause

by Steve S. Ryan

One of the most interesting sessions at the AF Symposium is the “Challenging Cases in AF Management: Anticoagulation, Arrhythmic Drugs and Catheter Ablation for AF” where leading doctors discuss very frankly their most difficult cases that year.

While several cases were discussed, here I summarize just one case.

Dr Eric Prystowsky

Dr Eric Prystowsky 

Patient History: 75-Year-Old Female

Case presented by Dr. Eric Prystowsky, St. Vincent Hospital, Indianapolis, IN

Dr. Prystowsky described the case of a 75-year-old female with A-Fib of at least three years duration. Before she came to Dr. Prystowsky, she was on Sotalol 40 mg 2/d and aspirin.

She was doing fine until a few months before when her A-Fib attacks became more frequent and with a more rapid rate. She also developed bradycardia and had a 12-second pause in heart beat.

Any pause over 5 seconds can cause dizziness, fainting and falls and is usually an indication that a pacemaker is necessary.

Pacemaker and Pericardial Effusion: She had a pacemaker installed (but not by Dr. Prystowsky). During the implanting of the pacemaker, she developed a pericardial effusion (bleeding from the heart into the pericardium sac). She was not on anticoagulants.

Two weeks after implanting the pacemaker, she felt lousy with recurring palpitations.

Treatment by Dr. Prystowsky

Flecainide added: Dr. Prystowsky put her on flecainide 100 mg 2/day. She had slightly elevated blood pressure. She was also on aspirin, metoprolol, and Atorvastatin (to lower blood pressure by treating high cholesterol and triglyceride levels).

The patient had repeatedly been offered a catheter ablation, but she declined each time.

Reset Pacemaker: The pacemaker was controlling her atrium 93% of the time. Her Ejection Fraction was 55%-60% (a good range).

Dr. Prystowsky reprogrammed her pacemaker to change her AV interval. He stopped the aspirin, and put her on apixaban (Eliquis) 5 mg 2/d. He ordered a stress echo test to check her heart.

She felt better for 5 days.

Moderate Pericardial Effusion; Medications Adjusted

The patient then developed a moderate (“significant”) pericardial effusion.

Dr. Prystowsky stopped the apixaban (probably the cause of the pericardial effusion). Because she still had some symptomatic episodes of A-Fib (although much better), he then increased the flecainide to 150 mg.

Contributing Role: Referring to the cause of the patient’s pericardial effusion, Dr. Prystowsky faced the fact that “I did it.”

She experienced bad side effects with the increased dosage of flecainide. He put her on 100 mg 3/day to reduce the side effects.

The patient had repeatedly been offered a catheter ablation, but she declined each time.

Minimizing Pacing; Medication Adjusted

The patient’s ventricular pacing produced a wide QRS which Dr. Prystowsky said “worried the hell out of me.” He tried to minimize the pacing she received.

To learn about the heart’s QRS, see my article Understanding the EKG Signal.

A CT scan revealed that her pacemaker incisions were fine, and that she had no more pericardial effusion. He re-started apixaban. She felt great.

He wound up putting her on amiodarone 200 mg which she tolerated well (previously she didn’t react well to Sotalol).

Dr. Prystowsky’s Lament

He described what he called his “shpilkes” index (Yiddish for anxiousness). When he talks to his fellows, “If you go home and worry about your patient at midnight, you ought to re-think everything.”

One Year Later and Lesson Learned

A year later she came in complaining of palpitations. Her pacemaker revealed that she only had 2 minutes of A-Fib in six months. Dr. Prystowsky told her, “I can’t do better than that.”

Dr. Prystowsky told the attendees that he would never again put a woman of her age on flecainide 150 mg.

He wrote me that it’s been over a year, and the patient is doing great.

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2020 AF Symposium Abstract: Combination Device to Both Electrically Isolate and Occlude the LAA

2020 AF Symposium Abstract

Combination Device to Both Electrically Isolate and Occlude the Left Atrial Appendage (LAA)

by Steve S. Ryan

Heart showing location of Left Atrial Appendage (LAA)

Researchers in this study described the Left Atrial Appendage (LAA) as the 5th Pulmonary Vein. It plays a similar role as the PVs in generating A-Fib signals, but is the source of many clots that lead to stroke. Currently implanting an LAA occlusion device is a stand-alone procedure.

How the AuriGen Combination Device Works

An abstract by AuriGen Medical described a study with dogs of a very innovative device which both closes off and electrically isolates the Left Atrial Appendage (LAA) in a one-shot procedure.

The AuriGen Ablation, Delivery and Occlusion System consists of an LAA implant which closes off the LAA with a PET (polyethylene terephthalate) membrane, and an RF Ablation System to circumferential ablate the ostium of the LAA with an RF electrical array.  Once implanted, the catheter electrodes are removed through a self-closing access conduit, leaving the occluder in play.

On day 7, the dogs underwent surgery to open the chest (thoracotomy) and observed that the LAA occluder device hadn’t moved. This also indicated that the ablation may have resulted in permanent electrical isolation of the LAA.

Editor’s Comments:

One can’t help but admire how A-Fib researchers and device manufacturers are developing innovative devices to improve A-Fib patient treatment.
From a patient’s perspective, it’s important that doctors and researchers recognize the importance of the LAA as a source of A-Fib signals (potentials). It seems to me that all too many EPs either ignore or put a low priority on mapping and ablating the LAA. Whereas other EPs such as Dr. Andrea Natale, after ablating the PVs, then focus on the LAA before examining any other areas of the heart. They recognize that the LAA often plays a major role in triggering A-Fib signals
Brilliant Idea to Combine LAA Closure with Electrical Isolation: The AuriGen combination occluder/LAA ablation device probably won’t be used in simple, recent onset, paroxysmal A-Fib cases because just isolating the PVs is usually enough to return patients to normal sinus rhythm (NSR).
Instead, the AuriGen combination device would be very useful in more complex cases where patients have had A-Fib for longer periods or who are more at risk of developing LAA clots. The AuriGen device can both close off and isolate the LAA in one procedure.
Practical Use by EPs: It’s is a long way from being available for A-Fib patients.
When and if the AuriGen device becomes available for patients, in practice EPs will probably first do a PVI to isolate the PVs, then proceed to use the AuriGen combination device to close off and isolate the LAA in the same procedure.

This will increase the effectiveness of ablation particularly in cases of persistent A-Fib. And, more importantly for patients, both procedures can be done at the same time.

Resource
Thompson, J,  et al. Pre-Clinical Evaluation of the AuriGen Medical Combination Device Designed to Electrically Isolate and Occlude the Left Atrial Appendage. Aurigen Medical. Abstract AFS2020-09 in the AF Symposium 2020 brochure, p. 34.

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2020 AF Symposium Abstract: High Hemorrhagic Risk Factors from NOACs

2020 AF Symposium Abstract

High Hemorrhagic Risk Factors from NOACs

by Steve S. Ryan

VIDEO A-Fib Clot Formation & Stroke Risks

NOAC Hemorrhagic Stroke Risk

When I read in this abstract from Massachusetts General Hospital in Boston, these NOAC findings almost jumped off the page at me! We know that NOACs are high risk meds (though they are certainly better than having an A-Fib stroke). But, add to that, also a high risk of Hemorrhagic risk factors, too?

This is a most important and relevant study for A-Fib patients.

Brain MRI to Detect NOAC Hemorrhagic Stroke Risk

Researchers from Massachusetts General Hospital in Boston used MRI to identify markers of increased intracerebral hemorrhage risk (ICH).

This was a single center study conducted from January 2011 to May 2019. In the study were 282 patients of which 76% had Atrial Fibrillation; Of the 282 patients, 49 were taking NOACs and 233 were taking warfarin. All demographic variables, vascular risk factors, etc. were similar between the two groups.

Study Findings

Analyzing the MRI data of the 282 participants revealed:

• cerebral microbleeds (67%)
• moderate-to-severe white matter hyperintensities (76%)
• cortical superficial siderosis (excess iron in body tissue) (18%)

In particular, of the 49 patients taking NOACs:

• 97% had at least one of these markers
• 60% had two
• 4% had all three

Conclusion

Established MRI markers of increased ICH (intracerebral hemorrhage) were common in the NOAC study group.

High hemorrhagic risk markers were present in an overwhelming 97% of NOAC patients.

Editor’s Comments:

Does taking a NOAC long-term mean you’ll eventually develop a hemorrhagic stroke?
No, the researchers didn’t go that far. This was a limited study as the number of patients who were on NOACs was 49 compared to those on warfarin which was 233.
Red Flag Warning: But this study should raise a red flag for anyone taking NOACs long term. Almost all patients on NOACs (97% in this study) had “evidence of neuroimaging markers of high ICH risk.”
The authors recommended that prescribers (and patients) look at nonpharmacological stroke prevention methods. Eliminating the need for lifelong NOAC anticoagulation “may decrease the incidence of fatal/disabling hemorrhages in A-Fib patients.”

For more on NOACs and stroke, see my article Anticoagulants Increase Risk of Hemorrhagic-Type Strokes.

Resource
Das, A.S et al. Etiology and Imaging Risk Markers of Non-Vitamin K Antagonist Oral Anticoagulant-Related Intracerebral Hemorrhage. AFS2020-17. AF Symposium 2020 brochure, p. 42.

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2020 AF Symposium: Terminate Persistent A-Fib by Ablating Higher Frequency Modulation Areas

2020 AF Symposium

Terminate Persistent A-Fib by Ablating Higher Frequency Modulation Areas

by Steve S. Ryan

Background: Previous studies by Dr. Jose Jalife, University of Michigan, Ann Arbor, MI.:
• A-Fib Produces Fibrosis—Experimental and Real-World Data: Dr. Jose Jalife’s ground-breaking research studies with sheep demonstrated conclusively that A-Fib produces fibrosis;
Experiments in Atrial Remodeling in Sheep and the Transition From Paroxysmal to Persistent A-Fib: Dr. Jalife’s later research showed how A-Fib progresses in time from paroxysmal to persistent A-Fib.

Jose Jalife MD

At this year’s AF symposium, Dr. Jalife presented findings by research colleagues showing how leading-driver regions of A-Fib have higher frequency modulation (iFM) areas which, when ablated, usually terminate persistent A-Fib.

His presentation was entitled “Using Instantaneous Amplitude and Frequency Modulation to Detect the Footprint of Stable Driver Regions as Targets for Ablation of Persistent AF.” Dr. Jose Jalife, University of Michigan, Ann Arbor, MI.

Clinical Study

Researchers have used sheep and pigs in previous studies. This time to detect rotors in sheep, researchers developed algorithms based on amplitude modulation (iAM) and frequency modulation (iFM).

They then switched to pigs who underwent high-rate atrial pacing to develop persistent A-Fib.

Frequency modulation (iFM) /instantaneous amplitude modulation (iAM) approach to patients with persistent atrial fibrillation

Using the PentaRay Catheter (Biosense Webster) to produce high-density electroanatomical atrial mapping, they found that regions of higher than surrounding average iFM were considered leading-drivers.

These iFM areas also had the highest dominant frequency. “They are the footprints of rotors.”

Not all rotors are drivers. Only those with the highest frequency and greater stability are A-Fib drivers. “IFM helps identify the regions with the highest frequency drivers.”

Researchers constructed two leading-driver + rotational-footprint maps (rotors) 2.6 hours apart from each other to test for stability and to guide ablation. Leading-driver regions remained in approximately the same spots in each map.

The trial showed high iFM areas are responsible for maintaining persistent A-Fib

Study Results

When these areas were ablated, persistent A-Fib terminated in 12 of the 13 cases (92.3%). Rotational-footprints (rotors) were found at every leading-driver region, but not all rotors had higher iFM. “In pigs, ablation of leading-driver regions usually terminates persistent A-Fib and prevents its sustainability.”

Conclusion

Dr. Jalife concluded that high iFM areas are responsible for maintaining persistent A-Fib. And using iFM results in higher sensitivity and specificity without the need for high resolution and costly panoramic mapping.

Editor’s Comments:

(I had never heard of the term “frequency modulation” (iFM) applied to A-Fib before.)
High Areas of iFM a New Discovery in A-Fib: The researchers have re-defined the field of mapping and catheter ablation.
This research shows that higher regions of iFM help identify the regions with the highest frequency drivers (rotors) and are more easily mapped in persistent A-Fib.

Dr. Jalife and his colleagues have given EPs and researchers a new tool to better ablate persistent A-Fib, the most difficult arrhythmia to fix.

Resource and Footnote
Dr. Jalife added: “The work I described in my presentation was not mine, but the result of a team effort led by a young Spanish physician and scientist named David Filgueiras Rama. David trained with me a few years ago but now has his own independent laboratory at the National Cardiovascular Research Center (CNIC) in Madrid, Spain. The idea of using iFM modulation to localize drivers was an inspiration of Jorge Quintanilla who is the first author in the paper you have cited. Together, Jorge and David generated the hypothesis, designed the experiments and wrote the paper. My roll was primarily advisory, and I helped with the final draft of the manuscript. Thus, I was only acting as a messenger at the AF Symposium.

Quintanilla, JG et al. Instantaneous Amplitude and Frequency Modulations Detect the Footprint of Rotational Activity and Reveal Stable Driver Regions as Targets for Persistent Atrial Fibrillation Ablation.  Circ Res. 2019 August6 30; 125(6):609-627. Epub 2019 Aug 1. https://www.ncbi.nlm.nih.gov/pubmed/31366278  doi: 10.1161/CIRCRESAHA.119.314930.

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2020 AF Symposium: Protecting the Esophagus by Cooling It

2020 AF Symposium

Protecting the Esophagus by Cooling It

Mark Gallagher. MD

“We know that most strategies (to prevent fistula) don’t work,” Says Dr. Mark Gallagher from St. George’s University Hospital in London, United Kingdom.

At the 2020 AF Symposium, he described an innovative strategy he and his colleagues developed to prevent fistula. He presented the completed IMPACT study which investigated whether Attune Medical’s ensoETM esophageal cooling system could effectively reduce the incidence and severity of thermal injuries to the esophagus during cardiac ablation.

What is Atrial Esophageal Fistula?
Atrial-Esophageal Fistula is the worst complication of a catheter ablation. Unlike most other ablation complications, this can kill you.

What is Atrial Esophageal Fistula? During an ablation, heat from the RF catheter applied to the back of the heart can damage the esophagus which often lies just behind the posterior wall of the left atrium. (This can also happen to some extent with Cryo ablation.)

How Atrial Esophageal Fistula can kill You: If RF heat damages the esophagus, ulcer-like lesions form in the esophagus. Then 2-3 weeks post-ablation, gastric acids (reflux) can eat away at these lesions creating a fistula (hole) from the esophagus into the heart. Without major intervention, blood can pump from the heart into the esophagus leading to death.

IMPACT Double Blind Randomised Controlled Trial

In their clinical trial, Dr. Mark Gallagher and colleagues divided 120 patients into two groups: a control group and a experimental group.

IMPACT stands for Improving Oesophageal Protection During Catheter Ablation for Atrial Fibrillation.

The Control Group: The control group received only standard care, in this case a temperature probe in the esophagus. If the temperature in the esophagus went too high, they would stop the ablation till the temperature went back down (current practice).

This would often lead to the EP not being able to effectively isolate all A-Fib signal areas in the heart which were too close to the esophagus. And often, by the time the temperature went up, damage had already been done to the esophagus.

The Experimental Group: Patients in the second (experimental) group instead received a 3-foot long silicone soft tube in their esophagus connected to what was basically a refrigerator. This closed loop system pumped cooled water (25  ͦ F) down one loop of the tube, then back through another loop to the console whenever the EP worked near the esophagus. The EP controls the temperature.

Double-Blind for Both Operators and Evaluators

This was a double-blind study. The EP doing the ablation didn’t know if they were working on a Control or Experimental patient. And the doctors evaluating the procedure for possible esophagus damage also were blinded.

After 7 days, an endoscopy was performed on each patient’s esophagus (an endoscopy examines the inside of an organ). They were looking for lesions and for gastroparesis (delayed emptying of the stomach).

IMPACT Study Results

The Control group who received the standard temperature probe had multiple epithelial lesions, while the Experimental group who experienced the closed loop cooling system had only one minor lesion.

The Experimental group also needed less fluoroscopy (X-ray) time. And, more importantly, the EP was able to ablate longer in areas near the esophagus (such as the posterior wall of the left atrium). That improved the success rate of the ablation and ablation efficacy.

Editor’s Comments

Most fistula patients die. And for those who live through the emergency treatment, they are often compromised for life. But with the esophageal cooling system, patients and doctors may never again have to worry about the dreaded complication Atrial-Esophageal Fistula!
Cooling the Esophagus, a Major Medical Breakthrough! Cooling the esophagus is simple and relatively easy to do. And, barring future research findings, it seems full proof.
The Attune Medical’s ensoETM esophageal cooling system is certainly cheaper than having to care for patients with a fistula.
The Attune Medical ensoETM esophageal cooling system can provide both cooling during RF ablation, and heating during Cryo ablation.
Probably among the major proponents of the esophagus cooling system will be hospital administrators. Treating patients with a fistula is a huge expense and a nightmare for hospital staff.
A fistula is an all-hands-on-deck emergency involving not just the EP department but surgeons and many hospital staffers. A surgeon may have to perform emergency surgery to insert stents in the esophagus in order to close off the fistula, or the surgeon may have to cut out part of the damaged esophagus, which is particularly risky
(I remember one EP describing how he and his staff were running down a hospital corridor with their fistula patient close to dying, in order to get the patient to an operating surgeon.).
Esophageal Cooling Means Better Ablations: And as a bonus, using the esophageal cooling system enables EPs to do a more thorough better job. They can ablate all areas of the heart rather than avoiding areas too close to the esophagus or using lower power with shorter duration or less contact force.
When Will Esophageal Cooling be Available? For catheter ablation application, probably not soon. In the U.S and probably worldwide, Attune Medical’s ensoETM esophageal cooling system is already in use and approved for specific purposes, for example, in cases of brain damage where a patient needs to have their whole body cooled down. But not for catheter ablation
In the United Kingdom, it will first have to be approved by NHS. In the U.S., it may not need to go through the FDA approval process again. (But this is a very speculative observation.)

Will Ablation Centers Implement? It will probably require a great deal of marketing to make EPs and ablation centers aware of and actually start using the esophageal cooling system. And because Atrial-Esophageal Fistula is such a rare complication, centers may not be willing to invest in an esophageal cooling system.

References
If you are looking for Dr. Mark Gallagher’s talk in the AF Symposium brochure, it was not listed. It was presented on Friday, January 24, 2020 in the session “Advances in Pulmonary Vein Isolation (Session II.)”

See also Zagrodzky, J. et al. Fluoroscopy Reduction During Left Atrial Ablation After Implementation of an Esophageal Cooling Protocol. AFS2020-03 AF Symposium brochure abstract, p. 28. St. David’s South Austin Medical Center, 2020.

Late-Breaking Clinical Study Evaluates Attune Medical’s ensoETM for Use During Cardiac Ablation Procedures. EPDigest. February 3, 2020. https://www.eplabdigest.com/late-breaking-clinical-study-evaluates-attune-medicals-ensoetm-use-during-cardiac-ablation-procedures

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2020 AF Symposium: After Diagnosis, How Soon Should an A-Fib Patient Get an Ablation?

2020 AF Symposium

After Diagnosis, How Soon Should an A-Fib Patient Get an Ablation?

by Steve S. Ryan

When you were diagnosed with A-Fib, did your doctor say, “Let’s wait a year or two and try different drugs before we send you for a catheter ablation.” Is this attitude justified by current research?

Karl-Heinz Kuck, MD

Dr. Karl-Heinz Kuck of St. Georg Hospital in Hamburg, Germany discussed this most important topic for patients in his presentation “ATTEST Trial―Impact of Catheter Ablation on Progression from Paroxysmal to Persistent AF.”

Heavy Decision for Electrophysiologists (EPs): When to Ablate

Dr. Kuck started by describing how he personally is affected by the strategic decisions he has to make every day. As an EP, “when should we ablate a patient with A-Fib?” Should we just look at symptoms (not considering anything that is caused by A-Fib).

Will this decision contribute to a patient moving into persistent forms of A-Fib?

This happens all too often―within one year, 4% to 15% of paroxysmal A-Fib patients become persistent.

Persistent A-Fib Patients at Higher Risk

Patients who progress to persistent A-Fib are at a higher risk of dying, they have more risk of stroke, it’s more difficult to restore them to normal sinus rhythm.

In the Rocket AF trial, the mortality rate of persistent A-Fib was triple that of paroxysmal patients.

ATTEST stands for “Atrial Fibrillation progression randomized control trial“

ATTEST: RF Ablation vs Antiarrhythmic Drugs

The ATTEST clinical trial included 255 paroxysmal patients in 36 different study locations. They were older than 60 years and had to have been in A-Fib for at least 2 years (mean age 68). They had failed up to 2 antiarrhythmic drugs (either rate or rhythm control).

Patients were randomized to two groups: radiofrequency ablation (RF) (128) or antiarrhythmic drugs (127). They were followed for 3 years (ending in 2018).

ATTEST Findings: RF Ablation vs Antiarrhythmic Drugs

At 3 years, the rate of persistent A-Fib or atrial tachycardia was lower (2.4% ) in the RF group vs the antiarrhythmic drug group (17.5%).

The RF group was approximately 10 times less likely to develop persistent A-Fib compared to the antiarrhythmic drug group.

For patients in the antiarrhythmic drug group, 20.6% progressed to persistent A-Fib or atrial tachycardia compared to only 2.2% in the RF group.

Recurrences occurred in 49% of the ablation group vs. 84% in the drug group. Repeat ablations were done on 17.1% of the ablation group.

Dr. Kuck’s Conclusion

Early radiofrequency ablation was superior to antiarrhythmic drugs to delay the progression to persistent atrial fibrillation among patients with paroxysmal A-Fib.

His advice: “Ablate as early as possible.”

Editor’s Comments

Don’t Leave Someone in A-Fib―Ablate as Early as Possible: Dr. Kuck’s ingenious research answers once and for all whether or not A-Fib patients should be left in A-Fib, whether seriously symptomatic or not (e.g., leaving A-Fib patients on rate control drugs but still in A-Fib.)
These patients are 10 times more likely to progress to persistent A-Fib. That’s why today’s Management of A-Fib Guidelines list catheter ablation as a first-line choice. That is, A-Fib patients have the option of going directly to a catheter ablation.
Know Your Rights—Be Assertive: I occasionally hear of Cardiologists who refuse to refer patients for a catheter ablation, who tell patients a catheter ablation is unproven and dangerous.
When you hear something like that, it’s time to get a second opinion and/or change doctors.
As an A-Fib patient, you should know your rights and be assertive—that according to the guidelines, you have a right to choose catheter ablation as your first choice.
Your doctor may try to talk you into first trying antiarrhythmic meds before offering you the option of a catheter ablation. That is so wrong!
 Why risk progressing into persistent A-Fib? There are so many bad things that can happen to you when left in A-Fib. As Dr. Kuck points out, you’re at a higher risk of dying, there’s more risk of stroke, it’s more difficult to restore you to sinus.
And we haven’t even talked about heart damage from fibrosis, the risk of electrical remodeling of the heart and, the all-too-real dangers of taking antiarrhythmic drugs over time.
Thanks for Sharing, Dr. Kuck! I am particularly grateful to Dr. Kuck for sharing his own anxieties and decision-making strategies when trying to determine when a patient should get a catheter ablation, how this affects him personally.
Making decisions about patients whom one cares about isn’t always easy. But Dr. Kuck’s research should now make these decisions easier both for EPs and for patients.

The Bottom Line for Patients: It’s safer to have an ablation than to not have one. For more see my article Live Longer―Have a Catheter Ablation!

References
ESC 2019: Catheter ablation may be up to 10 times more effective than  drug therapy alone at delaying AF progression.  Cardiac Rhythm News. September 2, 2019, 3634.

Dobkowski, Darlene. ATTEST: Radiofrequency ablation superior to antiarrhythmic drugs for AF progression. October 10, 2019. Healio, Cardiology Today. https://www.healio.com/cardiology/arrhythmia-disorders/news/online/%7B5fa2c711-a459-4c62-bb46-8fad6c69c9ea%7D/attest-radiofrequency-ablation-superior-to-antiarrhythmic-drugs-for-af-progression

Kuck, K-H. Late-Breaking Science in Atrial Fibrillation 1. Presented at: European Society of Cardiology Congress; Aug. 31-Sept. 4, 2019;

Paris Peykar, S. Atrial Fibrillation. Cardiac Arrhythmia Institute/Sarasota Memorial Hospital website. Last accessed Jan 5, 2013. URL:http://caifl.com/arrhythmia-information/atrial-fibrillation/↵

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2020 AF Symposium: “Virtual Heart” Assists Actual Ablations

AF Symposium 2020

“Virtual Heart” Assists Actual Ablations

by Steve S. Ryan

We have previously described the innovate, exciting work of Prof. Natalia Trayanova of Johns Hopkins Un. in Baltimore, MD. See ‘3D Virtual Heart’ Predicts Location of Rotors (2017 AF Symposium) and The Virtual Heart Computerized Simulation (2015 AF Symposium).

N. Trayanova, MD

At the 2020 AF Symposium, Prof. Natalia Trayanova of Johns Hopkins University presented “Computationally Guided Personalized Targeted Ablation for Persistent AF.” This computerized model is used to simulate an individual patient’s heart. This ‘Virtual Heart’ can then be used to guide an individual patient’s therapy.

Significant for Persistent A-Fib: For patients with Persistent Atrial Fibrillation, this computerized model is especially important. In a simple case of A-Fib, ablating/isolating the Pulmonary Veins (PVs) is usually all that’s necessary to restore a patient to sinus.

But with persistent A-Fib, it’s frequently required to do more than isolate the PVs. Persistent A-Fib patients often have fibrosis (fibrotic substrate) which perpetuates re-circulating electrical waves (rotors). The Virtual Heart identifies these fibrotic areas which sustain A-Fib.

How the Virtual Heart Works

Dr. Trayanova and her team start by doing an MRI scan. Then they hyper-enhance segments which correspond to areas of fibrotic remodeling in a patient’s heart.

The next step is to develop a computational mesh that incorporates representations of ion channels, calcium cycling and other electrophysical aspects of an individual’s atria. All this is incorporated into patient-specific geometry of the model.

Virtual-Heart-OPTIMA-approach-flowchart.

What the Model Can Reveal: They run the model to see what the arrhythmia looks like.

• Does the fibrotic substrate anchor rotors in particular locations?
• What are the spatial characteristics of the regions where they are located?
• Can these spatial metrics guide where the proper ablation should be?
• Can we reliably predetermine ablation targets?

Dr. Trayanova’s team merges these virtual atria with an advanced imaging technology (CARTO 3 System) to predict where the catheter should ablate.

The “Virtual Heart” Identifies Rotors: Prof. Trayanova found that re-entrant drivers (rotors) persisted in areas of higher fibrosis density and entropy (lack of order or predictability). They didn’t persist in regions of non-fibrotic sites and regions of deep fibrosis. The Virtual Heart is designed to completely eliminate the ability of the fibrotic substrate to sustain A-Fib.

Dr. Trayanova compared the predictive ability of her models to actual ECGI mapping cases from the Bordeaux group. Overall, her prediction of where rotors would be found coincided with where rotors were actually found by ECGI.

First-In-Human Virtual Ablation

Dr. Trayanova made major news when she announced the first-in-human clinical study of her Virtual Heart system! The first ten patients were part of an FDA approved clinical study of 160 persistent A-Fib patients called OPTIMA―Optimal Target Identification via Models of Arrhythmogenesis.

These ten patients had MRI heart scans which showed the fibrosis/scarring in their hearts.

This is a personalized approach tailored for each patient. The amount and structure of fibrosis is different in each individual.

Schematic summarizing the process of importing OPTIMA ablation targets into CARTO.

Creating Digital 3-D Models: Dr. Trayanova and colleagues then created digital 3-D models (Carto) and duplicated digitally the substrate and areas of fibrosis in individual patients.

They filled this model with digital virtual heart cells which mimicked and became a computerized duplicate heart. This digital heart behaved just like that individual patient’s real heart.

This digital heart behaved just like that individual patient’s real heart.

Then, they stimulate/pace the virtual heart electrically in many different locations to see where a stimulus produces an irregular heartbeat or rotor.

Rounds of Virtual Ablation: At this point, they performed several rounds of virtual ablation to digitally ablate those areas. Again, they tested to see if the digital ablation scars generated sites of emergent activity.

By the third round, there are no more hidden areas that can cause abnormal electrical signals. “We repeat the process till the substrate is no longer inducible for AF.” This also targets latent atrial arrhythmias, such as those that might emerge following initial ablation.

The Patient’s Digital Model: Finally, they export the digital model of the patient’s heart with all the A-Fib sites/rotors marked for the EP doing the actual ablation. In the EP lab, the EP uses this map to guide the catheter to the areas that need to be ablated.

Success of First Ten Patients

Persistent A-Fib patients, in general, are the most difficult to return to normal sinus rhythm. Around 50% of these patients have recurrences and have to return for additional ablations (which often cause yet more scar tissue).

Of Dr. Trayanova’s first 10 persistent patients in the OPTIMA procedure, only one patient had to return for a Flutter ablation (this was mostly because they ran out of time during the first ablation). In particular, all the rotor sites were correctly identified and ablated.

Editor’s Comments:

Persistent A-Fib patients are perhaps the most difficult to make A-Fib free.
Today, it’s common for even the best Master EPs to bring back persistent A-Fib patients for a second and even a third ablation before restoring them to sinus.
This may change with deployment of the Virtual Heart system.
The Virtual Heart system extensively and repeatedly maps where all A-Fib signals are coming from in a particular patient’s heart. With this mapping, the EP knows exactly where to ablate, including “hidden” areas which could emerge after a preliminary ablation, and areas that would cause electrical misfiring in the future.
Very important, with the Virtual Heart ablation there is no or very little recurrence of A-Fib.
The Virtual Heart system represents a major breakthrough in the treatment of persistent A-Fib patients.
The potential of Dr. Trayanova’ s research for A-Fib patients is incredible!
Imagine getting an MRI and knowing where your A-Fib is coming from, how your A-Fib affects and works in your heart both now and in the predictive future, how various A-Fib drugs can be expected and predicted to affect your heart, how much and what kind of fibrosis you have, how you can expect your fibrosis to progress and affect you over time, what therapies should be done in your particular case.
Imagine…if you need a catheter ablation, your EP knows exactly where to ablate in your heart.
Imagine…being able to accurately predict whether or not or how fast you will progress from paroxysmal to persistent A-Fib.
Imagine…all based on computer models that mirror your own heart.

Dr. Trayanova’s research has the potential to radically change the way A-Fib is treated. Almost all the uncertainties EPs and A-Fib patients now have to deal with can potentially be eliminated with the virtual computer reconstruction of individual A-Fib hearts.

References
Trayanova, N. A. Custom Cardiology: A Virtual Heart for Every Patient; Personalized computer models will let cardiologists test life-saving interventions. IEEE online, 28 Oct 2014. Accessed Feb 26, 2015, URL: http://www.ieee.org/about/index.html

Scudellari, Megan. Personalized Virtual Hearts Could Improve Cardiac Surgery―Digital replicas of patients’ hearts can identify hidden, irregular heart tissue for surgeons to destroy. IEEE Spectrum, August 22, 2019 / 12:00 GMT https://spectrum.ieee.org/the-human-os/biomedical/imaging/virtual-hearts-improve-cardiac-surgery

If you find any errors on this page, email us. Y Last updated: Wednesday, August 26, 2020

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2020 AF Symposium: Device-Detected A-Fib and Stroke Risk

AF Symposium 2020

Device-Detected A-Fib and Stroke Risk: How Long For a Clot to Form?

by Steve S. Ryan

Daniel Singer MD

How long does it take for a clot/stroke to develop? Dr. Daniel Singer from Massachusetts General Hospital in Boston, MA addressed this most important question both for A-Fib patients and their doctors in his AF Symposium presentation― Update on Device-Detected AF and Stroke Risk as a Function of AF Burden-Clinical Implications.” 

Implanted Devices Help Study Clot Formation

Dr. Singer discussed how implanted rhythm devices such as pacemakers have aided Electrophysiologists (EPs) collect data on clot formation timelines. (Mobile and non-implanted devices such as the Kardia or Apple Watch may open up these studies to a much broader population.)

AF detection devices: minimally invasive devices to permanent implanted devices; source: AHA

Read: How Clots Form and Cause Strokes
When someone is in A-Fib, blood is not being effectively pumped out of the left atrium. This blood can collect in areas such as the Left Atrial Appendage (LAA) where a pool of blood can form a clot.

When the left atrium starts beating in normal sinus rhythm again, this clot can be pushed downstream into the left ventricle which then pumps this clot into the brain causing an ischemic stroke.

But these clots aren’t formed instantaneously. It takes a while for blood to pool and clot to a significant size. For example, if you have a ten-minute attack of A-Fib, it’s unlikely a clot/stroke will develop.

In cases of permanent A-Fib, normal sinus rhythm doesn’t need to return to move the clot into the ventricle and from there to the brain. This makes patients in permanent A-Fib at high stroke risk.

The ASSERT Study: How Long Does It Take for a Clot to Form?

Dr. Singer discussed the ASSERT study (the Asymptomatic Atrial Fibrillation and Stroke Evaluation in Pacemaker Patients and the Atrial Fibrillation Reduction Atrial Pacing Trial).

The study enrolled 2,580 patients, 65 years of age or older, with hypertension and no history of A-Fib, in whom a pacemaker or defibrillator (ICD) had recently been installed.

Detecting Silent A-Fib: The pacemaker and ICD devices were programmed to detect silent A-Fib (Subclinical Atrial Tachycardia [SCAF]) when the heart rate reached 190 beats or more per minute lasting more than 6 minutes.

Silent A-Fib is called Subclinical Atrial Tachycardia (SCAF). Different from clinical A-Fib, it’s often of short duration and often is asymptomatic.

The devices were checked at a clinical visit 3 months later. These patients were then followed up for around 2.5 years.

ASSERT Study Result: They found that it took more than 17.72 hours to significantly increase annual stroke risk.

The ASSERT study basically said that it takes around 24 hours of silent A-Fib (SCAF) to develop a serious risk of stroke. Patients with silent A-Fib for over 24 hours had around a 3.1% risk of developing a clot/stroke.

In a later analysis of the ASSERT study by Van Gelder (2017), patients with a SCAF of from 6 hrs to 24 hrs were not significantly different from patients without SCAF.

TRENDS Study, A-Fib and Stroke Risk

Using much the same implanted device strategies as in the ASSERT study, the TRENDS study enrolled patients (2,486) with one or more stroke risk factors. They used a 30-day window to measure silent A-Fib (AT/AF burden).

Ischemic stroke is the most common type of stroke for A-Fib patients.

Findings: Having silent A-Fib for 5.5 hours or more on any 30-day window appeared to double stroke risk (12% of patients in the study had a stroke). (Stroke rates in this study were far below the 4% anticipated annual rate.)

A-Fib Cause or Marker of Stroke Risk? In the TRENDS study (and in the ASSERT study) nearly ¾ of the patients didn’t have A-Fib before the study. This raises the issue of whether A-Fib causes or is just a marker for stroke risk.

Silent A-Fib Hard to Detect

In the ASSERT study, the median time to detect silent A-Fib within the first 3 months was 36 days.

For many patients, just getting an ECG in your doctor’s office or wearing a standard monitor for a few days may not detect if you have silent A-Fib.

This is a major public health issue.

The ASSERT study raises the possibility that patients who suffer ischemic strokes may have silent A-Fib. For those who had an A-Fib-associated stroke, 25% had their A-Fib detected at the time of the stroke. A-Fib-associated strokes account for about 20% of all ischemic strokes.

Unfortunately, from a public health perspective, longer-term monitors like the Medtronic Reveal LINQ (which lasts 3 years) are currently too expensive for screening the general population. Wearable or hand-held ECG monitors may ultimately fill this need.

Pacemakers Don’t Work to Prevent A-Fib

Another finding of the ASSERT study is that pacemakers (continuous overdrive pacing) “does not prevent clinical atrial fibrillation” episodes. (This was the primary question the ASSERT study was constructed to answer.)

Low CHA2DS-VASc and A-Fib Stroke Risk

Dr. Singer pointed out that, even with a high AF burden, there isn’t much stroke risk if the CHA2DS-VASc score is low.

He acknowledged that most Symposium attendees would probably consider that a 1-2-hour episode of silent A-Fib would be a risk factor for stroke.

While others would consider any A-Fib at all as requiring that the patient be put on anticoagulants.

Limitations of the ASSERT Study

The ASSERT study was not designed to study how long it takes for a clot/stroke to form.

The cut-off point at >17.72 hours is somewhat arbitrary. How many patients had strokes from 17.42 hours to 24 hours or 48 hours? What is the precise number of hours in A-Fib where the risk of stroke significantly increases?

ASSERT and TRENDS studied patients with pacemakers and defibrillators. These patients may have other heart problems that the average A-Fib patient doesn’t have.

Editor’s Comments:

Silent A-Fib (Subclinical Atrial Tachycardia [SCAF]) is really dangerous! This is an important public health issue.
I advocate everyone reaching age 65 have long-term monitoring for silent A-Fib. How many strokes could be prevented and lives saved simply by detecting silent A-Fib before it kills or disables people?
Silent A-Fib Is Dangerous―Get Tested at Age 65! If you are 65 or older, get tested for silent A-Fib. In the ASSERT study it took 36 days of monitoring to detect silent A-Fib (SCAF).
However, we don’t currently have rigorous trial evidence that such screening for A-Fib leads to lower stroke risk. The U.S. Preventive Services Task Force doesn’t yet recommend wide scale screening for A-Fib.
Shorter Episodes of A-Fib Not Generally Dangerous: Despite studies such and ASSERT and TRENDS, we still need many more studies on how long it takes for a clot/stroke to form. Probably the most useful data to date comes from the ASSERT study stroke risk where it took round 24 hours of silent A-Fib before clot/stroke risk was significantly increased.
Should All A-Fib Patients be on Anticoagulants? Patients with shorter episodes of A-Fib or those who develop A-Fib after a successful catheter ablation, may not need to be on anticoagulants at all.

Remember that anticoagulants are high risk drugs that shouldn’t be taken unless there is a real risk of stroke.

Hemorrhagic stroke: Another risk of A-Fib is a hemorrhagic stroke where blood bleeds/flows into the brain. For more, see my article, Anticoagulants Increase Risk of Hemorrhagic-Type Strokes

References for this report
Healey, J.S. et al. Subclinical Atrial Fibrillation and the Risk of Stroke. The New England Journal of Medicine 2012; 366:120-129. https://www.nejm.org/doi/full/10.1056/NEJMoa1105575

Gotto, Jr., Antonio M. Bottom Line Health, Vol 26, November 2012, p. 4.

Van Gelder, I.C. et al. Duration of device-detected subclinical atrial fibrillation and occurrence of stroke in ASSERT. European Heart Journal, Volume 38, Issue 17. 1 May 2017, Pages 1339-1344, https://academic.oup.com/eurheartj/article/38/17/1339/3059370. doi.org/10.1093/eurheartj/ehx042

If you find any errors on this page, email us. Y Last updated: Wednesday, August 26, 2020

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2020 AF Symposium Live Case: LAA Closure with New Generation Device

John Foran MD

AF Symposium 2020

Live Case: LAA Closure with New Generation Device

In this live case Dr. John Foran from Royal Brompton Hospital in London, implanted the Watchman FLX to close off the Left Atrial Appendage (LAA) (Boston Scientific). It was in conjunction with several presentations on Left Atrial Appendage Closure (LAAC) devices.

The moderator for this live case was Dr. Walid Saliba of the Cleveland Clinic. The Panelists were Dr. Jacqueline Saw of Vancouver General Hospital and Dr. Dhanunjaya Lakkireddy of the Kansas City Heart Rhythm Institute.

Patient History

This male patient with persistent A-Fib had recently suffered a hemorrhagic (bleeding) stroke. He had been in A-Fib for 20 years and had a long history of hypertension. He had a CHADS-VASc score of 4 and a HAS-BLED score of 3. He was formerly on warfarin for 17 years, then switched to edoxaban (Savaysa) for one year when he had his “catastrophic” cerebral bleed. Happily, he eventually made a good recovery.

Dr. Foran would not state that his patient’s hemorrhagic stroke came from his years of being on anticoagulants. He raised the alternative possibility that the man’s stroke could have come from a hypertension bleed. Dr. Foran said he tries to insert a Watchman device as soon as possible after a cerebral stroke.

Patient Drug Treatments

His doctors stopped his anticoagulant when he was approved for Left Atrial Appendage Closure. He was put on Apixaban (Eliquis) 2/day for a short period of time.

As of April 2020, the Watchman FLX device is not yet approved for use in the U.S.

Dr. Foran said, “we always anticoagulate in the lead-up to an implant procedure.” The apixaban was continued through the procedure.

Post-op, the patient will be given apixaban as well as aspirin during six weeks after the procedure. Then he will be on apixaban for 6 months.

The Next Generation: Watchman FLX Occlusion Device

Dr. Foran displayed the earlier Watchman 2.5 version (left) and compared it to the new Watchman FLX (right).

Comparison of Watchman 2.5 (left) and Watchman FLX (right)

The Watchman FLX has a closed cell architecture with no sharp points at the top. The threaded insert is much smaller with less metal visible. (In the older Watchman device, it was found that thrombi (clots) could form on the metal insert visible after the Watchman was inserted.)

The Watchman FLX is designed to conform better to individual anatomies.

Watchman FLX -18 J-hooks in 2 rows

It uses 18 hooks offset in two different planes as compared to the older Watchman 2.5 which had 10 hooks. This allows the FLX to hook deeper into the LAA.

Dr. Foran said the older Watchman had sharp points at the top which meant you couldn’t push it forward very hard into the heart tissue̶-particularly in someone with a small LAA (like this patient).

Because the Watchman FLX is more flexible, he no longer uses the earlier Watchman 2.5 version.

Inserting the Watchman FLX

When the Symposium audience joined the live ablation, the patient had already been prepped in the EP lab. The catheters were already in place in the heart.

Illustration of Watchman inserted into Left Atrial Appendage

We watched as Dr. Foran, using fluoroscopy (x-ray) and echocardiogram, inserted the Watchman FLX into the opening of the LAA. He used saline and color flow for contrast to show where the sheath was.

Dr. Foran showed how there were air bubbles inside the sheath which he flushed out with saline.

Next, he opened up the Watchman FLX inside the LAA. He pushed in the Watchman FLX for 10 seconds to better imbed the device’s hooks. He then tugged on it a couple of times to make sure the anchors were well seated.

To complete the procedure, he then released the Watchman FLX and withdrew the sheath.

Editor’s Comments

My own electrophysiologist (EP), Dr. Shephal Doshi at Pacific Heart in Santa Monica, CA, told me it normally takes him only around 20 minutes to insert a Watchman. The new Watchman FLX appears to be even easier to install.
The biggest improvement in the Watchman FLX, in my opinion, is the smaller threaded insert with much less metal visible. Patients will likely have significantly reduced risk of clots forming on metal, which was an annoying problem that sometimes occurred with the earlier Watchman.
Approved in Europe but Not in U.S.:  In Europe, Boston Scientific received CE Mark certification in March 2019 and initiated a limited market release of the Watchman FLX™ in the European Economic Area (EEA).
In the U.S., clinical trials of the Watchman FLX are under way in 29 U.S. medicals centers. The trials close in Feb. 2021. I expect eventual approval by the U.S. Food and Drug Administration (FDA).
About 85% of A-Fib strokes are ischemic strokes; this A-Fib patient had a hemorrhagic stroke which is less common.
The Patient’s Hemorrhagic Stroke: Did anticoagulants cause or contribute significantly to this patient’s bleeding stroke?
We simply can’t say for sure whether being on anticoagulants for so many years caused or contributed to this patient’s cerebral hemorrhage (bleeding stroke).
As Dr. Foran pointed out, the patient’s hypertension may have been a factor in his stroke.
But anticoagulants are not like taking vitamins. They work by causing or increasing bleeding. However, they are certainly better than having an A-Fib ischemic (blocking blood flow) clot and stroke.

A-Fib Patients and Hemorrhagic Stroke: Recent research indicates that the risk of a hemorrhagic stroke, particularly in older A-Fib patients, should be considered carefully and can be very dangerous. For more about A-Fib and Hemorrhagic stroke, see my article, Anticoagulants Increase Risk of Hemorrhagic-Type Strokes

Reference for this report
Das, A.S et al. Etiology and Imaging Risk Markers of Non-Vitamin K Antagonist Oral Anticoagulant-Related Intracerebral Hemorrhage. AFS2020-17. AF Symposium 2020 brochure, p. 42.

If you find any errors on this page, email us. Y Last updated: Wednesday, August 26, 2020

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2020 AF Symposium: Live Case: Convergent AF Ablation

AF Symposium 2020

Live Case: Convergent AF Ablation

by Steve S. Ryan

Background: The Convergent Ablation is currently used for patients with persistent and longstanding persistent atrial fibrillation. It combines the efforts of a surgeon and an electrophysiologist (EP).
First, the surgeon accesses the outside (epicardial) of the heart to create lesions on the posterior left atrial wall and around the pulmonary veins (PVs). Second, the EP performs a PV catheter ablation from inside (endocardial) the heart, then maps the surgeon’s surgical ablation lines for any gaps, and if needed the EP completes the surgeon’s lesion set.

Live Via Streaming Video from Tampa, FL

Andrew Makati, MD

Andrew Sherman, MD

Drs. Andrew Makati (Electrophysiologist) and Andrew Sherman (Surgeon) from St. Joseph’s Hospital, Tampa, FL presented a live case of “Convergent AF Ablation―Staged PVI After Surgical Posterior Wall Isolation”.

The on-site moderator was Dr. Felix Yang from Maimonides Medical Center in Brooklyn, NY.

Patient with a Difficult Persistent Case

The patient they were working on was a 72-year-old male with persistent A-Fib/Flutter for 11 years. Previously he had a Cryo Ablation and many Cardioversions. He had tried the antiarrhythmic drug, amiodarone. His left atrial dimension was 5.1 (a normal left atrium measures around 2.0-4.0 cm).

Phase 1: Thoracoscopic Surgery

Video-assisted thoracic surgery (VATS) uses a tiny camera and surgical instruments inserted into your chest through one or more small incisions in your chest wall.

Surgeon Andrew Sherman began by showing slides of a thoracoscopic (through the chest) epicardial operation he had performed earlier in the week on another patient (Phase 1 of the Convergent operation).

He stated that the surgery has now turned more to a subxiphoid approach (the xiphoid is the lowest point of the breastbone). He stated that this surgery is “minimally invasive.”

(Called minimally invasive, video-assisted thoracic surgery uses very small incisions to access the inside of the chest cavity. But to the average patient, the Convergent operation is major surgery with all the potential complications and risks of heart surgery.)

Long Linear Catheter Placed Horizontally

The Atricure EPi-Sense Guided Coagulation System with VisiTrax® technology: How it works.

The catheter used by surgeons to make the burns on the outside of the heart is unlike a standard point-by-point RF catheter used by Electrophysiologists.

The surgeon uses a long linear catheter with multiple RF coils on its side which is placed horizontally to make long, large burns on the heart (AtriCure EPi Sense Coagulation Device).

The burns are normally 90 seconds long at 30 watts. This catheter can also be used for pacing, sensing, and to produce electrograms. Impedance drops (10%) are used to verify lesion effectiveness.

Illustration of surgical lesions to outside of heart

The catheter has a notch on the top which can be used to orient the catheter.

Dr. Sherman had ablated the whole of the posterior left atrium including any other areas of the posterior left atrium he could access. Usually 20 to 40 burns are made. The burns can overlap and can be repeated.

“Charring” the “Red Meat”

Dr. Sherman described normal heart tissue as “red meat” which after the ablation looks “charred”. “We just mow the lawn.” Dr. Sherman said his goal was to ablate to the point of complete “electrical silence.”

Ablated heart muscle is turned into dead, fibrotic tissue. There is no more blood flow, transport and contraction function no longer work, nerve transmission is destroyed, normal heart muscle fibers turn into non-contracting scar tissue. The A-Fib potentials or signal sources are destroyed along with the heart tissue.

Dr. Sherman stated his goal was to eliminate all electrical activity, to basically kill as much heart tissue as he can reach.

Passing the Baton: From Surgeon to Electrophysiologist

In Phase II, Electrophysiologist Dr. Kevin Makati continued Dr. Sherman’s surgical work and eliminated electrical activity in areas of the posterior left atrium wall Dr. Sherman could not reach.

As much as possible, they try to do both the surgery and the catheter ablation on the same day, usually in what he called their Hybrid Lab.

Phase II: Convergent Catheter Ablation

Example of a voltage map during CryoBalloon catheter ablation. Source: K. Makati

Dr. Kevin Makati then described the Convergent catheter ablation (Phase 2).

He used a voltage map to show how, after Surgeon Sherman’s work, there was still electrical activity at the roof of the posterior wall and in the lower wall which he called the “vestibule”.

Using a CryoBalloon catheter, he dragged it to make an ablation line from the Right Superior PV to the Left Superior PV.

“Reducing the critical substrate in the left atrium, you decrease the incidence of fibrillation conduction.” He also ablated in the vestibule to “reduce the substrate available to participate in Atrial Fibrillation.” Basically, he made sure the whole posterior wall was dead and electrically silent.

Thoracoscopic Approach to Close Off the LAA

From the audience, Dr. Mansour asked a question about how the patient seemed to have a “V clip” (AtriClip ProV Device from AtriCure) already installed in his Left Atrial Appendage (LAA).

Dr. Sherman explained that the “V Clip” was installed earlier in the week using a thoracoscopic approach (three port holes in the chest rib area).

A thoracoscopic approach works better than a subxiphoid when closing off the LAA, though this does involve two different surgeries for the patient.

Dr. Sherman stated that they do not do a LAA closure if there are clots in the LAA. They first have to use anticoagulants to dissolve these clots before closing off the LAA.

We watched a pre-recorded segment from earlier in the week as Dr. Sherman attached the “V Clip” to the LAA. He had to do a lot of tugging and wrestling with the LAA which is remarkably resilient. He thought he had all the lobes of the LAA included until someone using Transesophageal Echocardiogram (TEE) pointed out that there was one lobe that hadn’t been included. Once this was done, they closed the “V Clip”. There didn’t seem to be any residual LAA stump left over.

Convergent Reported 80% Success Rate

The on-site moderator Dr. Felix Yang from Maimonides Medical Center in Brooklyn, NY stated:

The term “procedure” is usually reserved for treatments that don’t involve cutting and surgery.

“There have been 10,000 Convergent procedures that have been performed worldwide today. This procedure has undergone an evolution over time…. The LAA closure has become an integral part of this procedure. It’s a good thing to see what happens to this persistent population when you have posterior wall isolation as well as electrical isolation of the appendage.”

To conclude, Dr. Yang stated that the success rate of today’s Convergent Surgery/Ablation is around 80%, and that the complications seen in the first Convergent operations have decreased over the last ten years.

Editor’s Comments:

I’m biased against the Convergent Surgery. I admit it. I consider the Convergent operation barbaric, brutal and excessive. Talk about overkill.
The Surgeon: The surgeon operates on the outside (epicardial) of the heart. Every time I see a live Convergent operation, I get nauseous. I can’t imagine having my posterior left atrium wall destroyed like this. Is it really necessary to completely obliterate (kill) the left atrium wall to make a patient A-Fib free?
I acknowledge that, in some patients, this may indeed be helpful. But is this a case of throwing the baby out with the bathwater?
What’s the point of making all these burns if a patient’s left atrium wall no longer functions?
Do as Much Damage? Or, Do as Little Damage? Surgeons in the Convergent operation try to do as much damage as possible.
EPs do often ablate in the posterior left atrium wall such as by creating a box lesion set. But they try to do as little permanent damage to the heart as possible.
Convergent Surgery Does Lasting Damage to the Heart. In the Convergent surgery, the posterior left atrium is turned into dead, fibrotic tissue.
There is no more blood flow, transport and contraction function no longer work, nerve transmission is destroyed, normal heart muscle fibers turn into non-contracting “charred” scar tissue.
The ability of the left atrium to contract risks being affected (though the posterior wall of the left atrium doesn’t normally contract that much).
Leads to Weakened Hearts: The surgeon does tremendous damage to the posterior left atrium which can never be restored. The heart can’t function normally if the posterior wall doesn’t work anymore.
This may weaken the heart and contribute later to heart problems like congestive heart failure. All too many patients today suffer from weak hearts due to heart muscle damage.
Restore Not Destroy. I admit it. For most patients I’m biased against the Convergent Surgery

Instead of destroying tissue, the goal should be to restore a patient to normal sinus rhythm, to make the heart function normally again. (That’s the goal of catheter ablation.)

If you find any errors on this page, email us. Y Last updated: Saturday, May 2, 2020

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