The Atrial Fibrillation Summit held as part of the Heart Rhythm Society’s annual meeting in Denver, Colorado has just concluded. Why a "summit" would be held in the basement of the Colorado Convention Center seems a bit odd, but perhaps it was to be sure the fancy colored lights behind the speaker’s podium radiated a professional glow.
The event was a virtual “Who’s Who” of catheter ablation, assembled by the two program coordinators, Douglas Packer, MD of the Mayo Clinic, and Hugh Calkins, MD of Johns Hopkins Medical Center.
Eric Prystowsky, MD kicked off the sessions with a great review of the history of atrial fibrillation: its mechanisms and early historical observations by scientists of an earlier era, and put us in our place after demonstrating that most things we know seem to have already been observed by prior electrophysiologic minds from the 1940’s. He also hinted at a work published in Nature 2001 Vol 409 regarding a tarantula peptide that can reduce atrial stretch, and might be a pharmacologic target for reducing atrial fibrillation. Hmmm. But his most important message to those performing atrial fibrillation ablation procedures at the close of his talk was: “PRESERVE THE BRAIN.” Wise man.
Jose Jalife, MD (SUNY, NY) then followed with some elegant videos of his work on tissue cultured atrial cells interspersed with varying amounts of fibroblasts (that make fibrous tissue) and showed how fibrosis within the atrial architecture can contribute to the development of the erratic activations of the atrium, and that fibrosis increases in the settings of hypertension and heart failure.
Peng-Sheng Chen, MD (Krannert Institute, Indianapolis) was supposed to talk on Neural Networks in the generation and treatment of atrial fibrillation, but the message must have gotten out about his thick accent, so we never heard from him. Shin-Ann Chen, MD (Taipei) took over instead and reviewed nice basic scientific work on the contribution of atrial stretch causing atrial after-depolarizations, and might account why the initiation of atrial fibrillation always occurs after a pause and then a sinus beat, then atrial fibrillation.
Virend Somers, MD (Mayo Clinic) did a great job reviewing the mechanisms of why obstructive sleep apnea might exacerbate atrial fibrillation (or might even be a cause it) but cautioned his theories were only based on observational studies and not based on prospective studies. However, the mechanisms postulated were: low oxygen periods (hypoxemia), sympathetic activation, extreme blood pressure surges, transmural pressure gradients (see my prior post) as much as -40 to -80 mmHg during attempts to breath against a closed airway, and systemic inflammation with elevated C-reactive protein levels. Treated sleep apnea (with CPAP) had a 50% reduction in recurrent afib after cardioversion compared to folks who refused or could not tolerate the CPAP machine.
Patrick Ellinor, MD, PhD from Mass General reviewed the genetics of atrial fibrillation. He said something about the long arm of chromosome 10, but then I fell asleep briefly. I’m told he did a good job reviewing this.
After resuscitation with a coffe break, the late morning session kicked off with Michel Haissaguerre, MD (Bordeaux, France) reviewing his step-wise approach to atrial fibrillation.
Carlo Pappone, MD followed with his “Milan (Italy) Approach” to atrial fibrillation – which basically seemed to be that he ablates a lot more than he used to, because, truth be told, he’s had some recurrences. (Who knew!). He ended his discussion remarking that one patient that had chronic atrial fibrillation took him three procedures and a total procedure of 20 hours to render him afib-free, suggesting we still need better tools to approach this population. It was the first time I heard him speak to reality, and it was appreciated.
Warren (Sonny) Jackman, MD (Oklahoma City, OK) then spoke eloquently on the topic of the importance of the vagal ganglionic plexi (nerve inputs) at supporting afib, and demonstrated that stimulating one ganglionic plexus on one side of the heart could cause a pulmonary vein on the opposite side of the heart to increase its firing frequency, suggesting that afferent and efferent limbs of the vagus nerve are at play in maintaining atrial fibrillation. Brilliant work and magnificent observation. I’m just glad I’m not his fellow, because I can’t imaging how long his procedures must last when collecting this information!
Koonlawee Nadamanee, MD (Inglewood, CA) then demonstrated his results with catheter ablation targeting just the small (0.05-0.12mV) electrograms that last between 50 and 120 msec WITHOUT isolating the pulmonary veins. His data suggested about the same outcomes as others, but also showed that sometimes waiting as long as 6 -12 months might be needed to rid a patient of atrial fibrillation after his procedure in some patients. I didn’t see too many other people using solely this approach, but more seem to be incorporating some of his lesion sets.
The afternoon session was mainly made up of reviews of left atrial anatomy, by Siew Yen Ho, PhD (London, UK), followed by the new imaging and robotic techniques used for catheter ablation.
Douglas Packer, MD (Mayo Clinic) listed his pros and cons of the Stereotaxis and Hansen Robotic systems. It seems all of the current robotics suffer from an inability to reliably register anatomic locations from one imaging modality to another imaging or robotic modality. Much work needs to be done here. Bottom line: Stereotaxis had better image integration with 3D electroanatomical mapping systems, but Hansen was less expensive, portable, and could use any catheter, but limited by a slightly higher perforation risk. Some interesting data there: it seems 10-20 grams of force on the ablation catheter gave the best lesions in dogs while limiting performations.
Henry Halperin, MD (Johns Hopkins, MD) spoke to the use of real-time MR for ablating tissue and its benefits for reducing ionizing radiation and spoke to its utility at being able to see lesions in the myocardium. David Haines, MD asked at the end of the session about the resolution of 1.5Telsa MRI scanners, to which is was admitted that the 3-5mm resolution might not be enough to see left atrial walls that are only 2 mm thick in places. Henry seems to think that 3 Telsa MR scanners might improve on this. But the cost???
Vivek Reddy, MD showed some interesting work on rotational CT imaging performed during an AF ablation procedure and uses one fifth the amount for fluoroscopy to image the left atrium compared to spiral CT’s obtained pre-procedure. He also showed how these 3D volumes could then be projected onto fluoroscopic images to better localize the ablation catheter intra-operatively. Kind of cool.
The remainder of the afternoon was spent talling about the possible complications of atrial fibrillation procedures. Tamponande, gastroparesis and pyloric spasm, lasso entrapment, and minimizing embolic events with anticoagulation were all covered by Dr. Dipen Shah, MD. Esophageal perforations, heralded by chest pain, dysphagia (difficulty swallowing) and fever, were nicely reviewed by Dr. John Day, MD (Salt Lake City, UT). It seems they had two back in 2004 after ablating the posterior left atrium with an 8mm tipped catheter at 70W output for 20 seconds with each burn. Each patient presented 2-3 weeks after the (initially) uncomplicated procedure. The first died (we were left to assume) because the diagnosis was not recognized early. The other was treated aggressively with esophageal stenting, broad spectrum antibiotics (including antifungals) and nasogastric tube feedings, and survived, and has been followed 3 years and is still doing well.
Frank Marchlinski, MD (Philadelphia, PA) reviewed management of pulmonary vein stenosis, pericardial tamponde, and the phrenic nerves, and Samuel Asirvatham, MD (Mayo Clinic, Rochester, MN) help cap the anatomical relationships that can lead to these complications.
Whew! Lots covered on Day 1. Now off to poster sessions…
I have been following the comments in another topic as they relate to MTWA.
You seem to be ambivalent about the efficacy of using MTWA screening for patients who might be at risk for SCD.
Now that you are at the HRS meeting and mixing it up with other EPs, do you notice similar sentiments from you colleauges, there?
Just got back from HRS. Here's what I hear: there is still a lot of resistence to deploying this technology. Barriers to entry include (1) the fact that the set-up is not like a conventional EKG (special training required), (2) MTWA is not an easy test to perform, especially in patients on beta blockers since achieving the necessary HR can be difficult and time-comsuming. And after they've held their HR "in zone" for several minutes, they still have to achieve 80-85% MPHR for age or else the study becomes "indeterminant." (3) If an indeterminant arises, who will check to evaluate why? Should you repeat the study another day? (tough logistically) and if an indeterminant means they still need and ICD anyway, then why do it? Also, (4)another individual I spoke with suggested that perhaps the reason the negative predictive value is so good is because only the healthy patients can complete the test (in other words, does it ADD to their risk stratification above a regular treadmill?) and (5) the reimbursement is relatively low for the work involved.
Hey, I'm just calling 'em as I hear 'em.
Also, there are not a lot of people standing around the posters asking questions - so the "buzz" regarding this test just isn't there, as far as I can see.
I am more than willing to discuss this civily here on this blog, but our last thread was just about pulled since it contained candor that added little to a meaningful discussion about MTWA. (Hence, I stopped responding and moved on).
I realize that there is a desire to tap into the psyche of the customers regarding their purchase of this machine. But despite what other commentors on this blog have felt about physicians, especially in regard to MTWA, I do not think doctors are inherently evil individuals. We are trying to do what's best for our patients: no one wants to implant unnecessary ICD's in patients, but no one wants their patients to die either. As I mentioned before, MTWA is dealing with trying to predict an event that, if it occurs even once, can have profound ramifications for our patients and like it or not, EP's have seen many more patients' lives saved by ICD's than hurt by them. Certainly ICD's have their problems: ICDs are expensive, shocks hurt, and ICDs are invasive. But what else has demonstrated efficacy at prolonging life (above and beyond our pharmachologic interventions) in these high-risk patients?
Hope this answers your quesiton.
Thanks for taking the time to weigh in on this. I posted the original question. I had other reasons for asking (not investment-related), and I appreciate your thoughtful feedback.
There are a handful of medical blogs run by docs out there that are absolutely terrific.
Yours is definitely one of them.
Just reading your posts gives me great insight into how my cardiologist processes my situation....my relationship with him is a lot better because of you.
wes, i think you should spend more time trying to help your patients and less time writing lies..If you wanted to be a writer, you got the wrong degree...Your words are filled with deceit, and you do more harm than good to people that dont deserve it....you are a disgrace to your degree...I know more about this subject than you will ever...And Im a long way from being done with you...You should be investigated...
How many deaths have occured on ICD implanted patients that for whatever reason, mfg recall, or battery depletion, it was decided to replace or repair the ICD? I know you have those statistics.
Do you think that your decision process to "play it safe" has possibly cost a life or two, or even more. Do you consider those deaths as an "oh well, better safe than sorry" stratagy. Do you work for an institution or do you have a private practice?
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