The Cardiac Ablation

 

On August 30, 2023, I finally bit the bullet and had a cardiac ablation for atrial fibrillation and atrial flutter. If you are one of those rare readers of this blog you may recall me wrting about it and how it occurred in the first place. I happened to be speedskating 19 years ago on the John Rose Oval and just completed my warm up laps.  I looked at my heart rate monitor and my pulse was 170 BPM.  I pulled up to stretch a little and suddenly my HRM was chirping irregularly and the rate was 240 BPM. I checked my carotid pulse and knew I was in atrial fibrillation. I drove down to the hospital where I was cardioverted with flecainide and metoprolol and have been taking those medications ever since.

In the interim, I have seen a sports cardiologist several times, 5 electrophysiologists (EP), and two general cardiologists as well as my primary care physician and the physicians that cross cover for him. I have also been seen in the emergency department for a heart rate that was down to 25 beats per minute and atrial bigeminy. The physician in the ED thought that I might need a pacemaker, but it turns out that the combination of flecainide and metoprolol can cause significant bradycardia. Once I learned that I started cutting 25 mg tablets into quarters (6.25 mg) and would typically take two of those tablets per day. I also learned that if you take flecainide, you also need to take a beta blocker or a calcium channel blocker to prevent atrial flutter.  Atrial flutter is difficult to diagnose without an ECG because clinically it can seem like sinus tachycardia.  For example, I have had the flu or taken corticosteroids for asthma and developed tachycardia.  When I started running rates of 130 bpm, that seemed a little high for sinus tachycardia.  I decided to get an ECG and it was atrial flutter. I had to figure all of that out, because my initial plan was to taper off metoprolol and that is unrealistic.

At the same time, the combination at times would cause severe bradycardia.  I had a nocturnal heart rate of 35 BPM recorded on a Holter monitor and saw a cardiologist.  We agreed to stay at metoprolol 6.25 mg BID unless there were extraordinary circumstances.  That generally works but my heart rate can still get into the 40s range. That led me to the stage to consider the ablation.  The other factor is that the second EP cardiologist that I saw 15 years ago told me to wait on an ablation because the technology was not good enough. When I saw him this Spring – he thought it had matured and recommended the procedure. He also told me that both the atrial fibrillation and atrial futter could be ablated in a single session rather than two and that was the first time I heard that. 

For about 15 years I have been titrating what most people consider to be microdoses of metoprolol (Physicians typically say: “I have never heard of a dose that small.”) against the flecainide and it has been holding very well. I get about 1 major episode of afib per year that may last 2-3 hours.  I typically take the next dose of flecainide and 12.5 of metoprolol instead of 6.25.   Multiple 24 hr Holter monitors and clinical assessments by cardiologists have not resulted in a better combination.  They were adamant about not increasing the flecainide because of the risk of QRS prolongation and ventricular arrythmias.  There was a consensus to try the ablation – even if the pandemic had persisted.

Researching the procedure followed three lines of evidence.  The first was efficacy and that seems to be a moving target. Conventional wisdom for a long time was that rate control (maintaining a heart rate of < 100 bpm even if you were in atrial fibrillation) and rhythm control (maintaining normal sinus rhythm) produced equivalent results. It turns out that is true only if hemodynamic stability is maintained and for some people it is not.  When that happens, they develop significant symptoms like shortness of breath, lightheadedness, dizziness, chest pain, and can even develop congestive heart failure and renal failure. When all of that is not planned it is riskier to stabilize the person. There is also concern that rate control leads to quality-of-life (QoL) problems associated with both the direct symptoms and indirect symptoms like anxiety about palpitations and the arrhythmia. There seems to be movement in the direction of an attempt to stabilize the rhythm with medication and if that fails try the ablation. There is a QoL rating scale available for atrial fibrillation.  In terms of likelihood of ablating the arrhythmia the frequent quotes are generally 2/3 to ½ of patients, but the data is complicated by the number and intensity of cardiac morbidities.

The second line of evidence was complications and serious complications were noted.  Radiofrequency ablation of arrhythmias in some cases produces a full thickness burn to the heart muscle.  As a result, it can damage adjacent structures including the esophagus and the phrenic nerve.  It can also lead to pericardial effusions and cardiac tamponade. In a very worst-case scenario atrial-esophageal fistula with gas in the left atrium and left ventricle essentially causing an air lock in the pumping mechanism of the heart (4).  

The third line was something I had not considered in the past and that is that atrial fibrillation is progressive. In other words, even if you have good rhythm control with medication, unless something is done to alter the electrical substrate the likelihood of maintaining a normal sinus rhythm after an ablation decreases over time. Accumulating cardiac problems outside of atrial fibrillation can predispose to the condition and make it harder to treat.  

Some additional intangibles were considered. I would like to get back on the ice speedskating. That will take rhythm control and some resilience against exercise induced tachycardia.  Rhythm control is important because atrial fibrillation reduces typical cardiac output by 20-30% based on inadequate filling and pumping cycles due to the irregular heartbeat.   Augmentation of ventricular filling is also adversely affected due to a lack of coordinated atrial contractions.  I am hoping the ablation gets me close to that goal.  There are some theories that interoceptive signaling in the form of accelerated heart rate from any cause can lead to anxiety.  Certainly many people with arrhythmias have anxiety that may seem explainable on a general medical concern basis but there may also be an autonomic component as well as a cognitive component based on the multiple concerns of treating a chronic disorder than can cause stroke and congestive heart failure.    

What has happened so far? I underwent the procedure.  It was 4 hours and 40 minutes in duration from intubation to extubation. The general anesthesia given is shown in the graphics below. The top graphic is the one I made until the official graphical anesthesia record could be located as the second graphic. To do the ablation 4 catheters were placed in the right femoral vein and one in the left. I don’t know the technical details of those catheters only that one is for cryoabalation/isolation of the pulmonary veins in the left atrium, one is for mapping the electrical fields in the surrounding tissue, and one is for a radiofrequency ablation of the a CTI line (cavotricuspid isthmus) in the the right atrium.  That procedure targets atrial flutter.  The plan was do the CTI line ablation first and then puncture the interatrial septum and then enter the left atrium with the cryoablation catheter for the pulmonary vein isolation.  The technical details are more complex since the ablation sites and surrounding areas need to be checked to makes sure that the abnormal conduction sites have been eliminated and no new pathways are evident. The phrenic nerve and esophagus are also checked to make sure there is no damage from ablation that occurs in proximity to these structures. 

Everything seemed to go well during the procedure.  There were no obvious complications just a long time under general anesthesia. Recovery room was uneventful but they decided I needed to stay overnight to monitor bleeding risk from the catheterization site.   That happened when they got me up at the 6-hour mark – blood from the largest site in the right groin dripping onto the floor. More pressure applied and the bleeding stopped and I was discharged the next day.

I tried to capture the post-procedure course by in the following graphics.  In clinical practice it was common for me to see people of all ages who had ablations for various arrhythmias. In some cases, they were told to “go home and throw your medications away!” as a result of the ablation.  That may apply to some arrhythmias but not atrial fibrillation. They told me to expect no changes in the medications for 3 months and that I would be taking the same doses of metoprolol and flecainide.  Later at the time of discharge – they told me that in some cases there is a very rocky course until things heal up from the procedure and that it was not uncommon for people to get palpitations and even a return of the rhythm problems.

As noted in the graphics – the course to date has been rocky.  At this point much more atrial fibrillation than I have experienced in the past 16 years and much longer duration.  In my reading about why athletes get atrial fibrillation and the associated experiment work in that area – running sustained high heart rates causes remodeling of the biological substrate of the heart and that makes continued atrial fibrillation more likely. In 16 years, I rarely had an episode that lasted longer than 2 hours and lately more seem to end in less than an hour. As I type this today, I have been in atrial fibrillation for going on 48 hours continuously and just this morning converted to a rapid ventricular response meaning that my ventricular rate is the same as the atrial rate of 150 bpm.  Estimated maximum heart rate for exercise at my age is about 130 bpm.

As can be seen from the graphic there are additional unexpected side effects primary among which is ocular migraines.  An ocular migraine is a typical migraine scotoma without a headache. It starts out as a small shimmering spot or disk in the visual field and slowly expands to a large, jagged, shimmering circle of light. Within about 20 minutes it is gone. Unlike a retinal detachment or stroke there are no deficit symptoms like permanent blind areas in the visual field.  When I asked several staff people about the cause they attributed it to general anesthesia however it is well documented to occur with congenital defects in the atrial septum (patent foramen ovale or PFO) and iatrogenic defects of the septum caused by catheterization into the left atrium (7-10).  Repair of the defect in some cases reverses the headache. About 75% of the iatrogenic atrial septal defects (ASD) spontaneously close by 12 months.  UpToDate put the risk of persistent ASD at 5-20% at 9-12 months (16).

A critical question for anyone contemplating an ablation procedure on a non-acute basis like I did is the post operative course. I was very aware of the low frequency serious and lethal complications, but not the specific about length of time to recovery and what the symptoms might be.  Most people experience significant if not disabling symptoms for months rather than days or weeks following the procedure. That is based on a small study where they did detailed interviews on what happened to the subjects following the ablation (11).  It is available to read online and I would encourage anyone interested in the procedure or knowing more about the procedure to read it.  One of the authors' conclusions is  

“The majority (85%) of the study sample did improve at six months, but the process was much slower and more difficult than expected. Although the symptom burden post-ablation did decrease over the six months, only 50% of subjects (n=10) were symptom-free and off anti-arrhythmic medications at six months.”  (reference 11)  These findings are qualified by the study sample size as well as the possibility of selection bias since the researchers were looking for people who could tolerate the protocol of completing rating scales and lengthy interviews about potential adverse events.  Reference 11 is also very useful in terms for what kind of recovery time to expect - especially in terms of fatigue and more frequent contact with the healthcare system after atrial fibrillation ablation (12).

That is certainly consistent with my experience. Right at this moment I have been in atrial fibrillation or atrial flutter continuously for 48 hours.  My heart rate is 160 bpm at rest.  I am contemplating taking more medication on my own initiative or going to the ED for cardioversion. I am scheduled for a cardioversion in the cardiology clinic on Wednesday September 13 - but I don't know if I can hold off that long.   I guess I am hoping for a break. There are many mitigating factors. Whatever happens tonight – I hope to add more to this post soon.  This is an important topic that has been neglected for too long.

Final qualifier on this post to point out that this is my experience and it does not mean it would be your experience. Much of the sensationalism about medicine in the media is based on oversimplified dichotomous thinking.  Medications, procedures, tests, doctors and even diagnoses are seen as all bad or all good.  Human biology is very complex and there are few if any medical interventions that address that level of complexity. That typically means that over any population there will be an array of outcomes and most of them will not be explainable. That is a hard pill to swallow but that is the state of the art of modern medicine. 

 

George Dawson, MD, DFAPA

 

Supplementary 1:  Cardioversion today (9/13/2023) successfully terminated about 90 hours of atrial fibrillation (rates of 70-140 bpm) with atrial flutter (rates of 150-160 bpm).  In terms of the original ablation procedure that is probably more hours of these arrhythmias than I have experienced in the past 19 years.  Normal sinus rhythm has been present for the past 10 hours and vital signs are normal.  What follows is a graphic of the entire process starting with the ablation and ending with the cardioversion. There were multiple episodes of atrial fibrillation before it became continuous with shift to atrial flutter.  During the 90 hours most of the rates were 150-160 bpm.  That is consistent with atrial flutter and may have been associated with a change in medications.

Supplementary 2:

The discussion leading up to the ablation:

https://real-psychiatry.blogspot.com/2022/11/a-visit-to-electrophysiologist.html

 

Image Credit:

Click to enlarge any graphic.

Rottner L, Bellmann B, Lin T, Reissmann B, Tönnis T, Schleberger R, Nies M, Jungen C, Dinshaw L, Klatt N, Dickow J, Münkler P, Meyer C, Metzner A, Rillig A. Catheter Ablation of Atrial Fibrillation: State of the Art and Future Perspectives. Cardiol Ther. 2020 Jun;9(1):45-58. doi: 10.1007/s40119-019-00158-2. Epub 2020 Jan 2. PMID: 31898209; PMCID: PMC7237603.

License : https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/), which permits any noncommercial use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

Image is used "as is" from the paper and no changes were made.  

Remaining images were all generated by me.

Hat Tip:  Kenneth A. Vatz, MD - a neurology colleague on Twitter who analyzed the scotoma symptoms and directed me to excellent references connecting atrial septal defects to migraines and scotoma especially reference 10. 

Hat Tip:  Medical records staff at Regions Hospital who persevered, located the graphical anesthesia record and mailed it to me on 9/19/2023.  I just incorporated it into this post today.  I have a similar request into the electrophysiology staff so that I can display the actual mapping of this procedure but have been advised that they are less likely to provide these images.     

Update (11/22/2023):  I had a brief (20 min) episode of atrial fibrillation this AM that resolved spontaneously.  It was rate controlled at about 84 BPM.  It is the only arrythmia I have had since the 4 days of atrial flutter early in September.  I notified the clinic and emailed them a tracing of my Kardia ECG.  I have a scheduled appointment next week and it was supposed to be to taper and discontinue the antiarrhythmic medications.  Also seem to correlate with progressively lower HRV numbers despite more vigorous workouts and higher heart rates.

References:

1:  Alobaida M, Alrumayh A. Rate control strategies for atrial fibrillation. Ann Med. 2021 Dec;53(1):682-692. doi: 10.1080/07853890.2021.1930137. PMID: 34032538; PMCID: PMC8158272.

2:  Barbero U, Ho SY. Anatomy of the atria : A road map to the left atrial appendage. Herzschrittmacherther Elektrophysiol. 2017 Dec;28(4):347-354. doi: 10.1007/s00399-017-0535-x. Epub 2017 Nov 3. PMID: 29101544; PMCID: PMC5705746.

3:  Lim HS, Schultz C, Dang J, Alasady M, Lau DH, Brooks AG, Wong CX, Roberts-Thomson KC, Young GD, Worthley MI, Sanders P, Willoughby SR. Time course of inflammation, myocardial injury, and prothrombotic response after radiofrequency catheter ablation for atrial fibrillation. Circ Arrhythm Electrophysiol. 2014 Feb;7(1):83-9. doi: 10.1161/CIRCEP.113.000876. Epub 2014 Jan 20. PMID: 24446024.

4:  Thomson M, El Sakr F. Gas in the Left Atrium and Ventricle. N Engl J Med. 2017 Feb 16;376(7):683. doi: 10.1056/NEJMicm1604787. PMID: 28199804.

5:  Manolis AS. Transseptal Access to the Left Atrium: Tips and Tricks to Keep it Safe Derived from Single Operator Experience and Review of the Literature. Curr Cardiol Rev. 2017;13(4):305-318. doi: 10.2174/1573403X13666170927122036. PMID: 28969539; PMCID: PMC5730964.

6:  Singh SM, Douglas PS, Reddy VY. The incidence and long-term clinical outcome of iatrogenic atrial septal defects secondary to transseptal catheterization with a 12F transseptal sheath. Circ Arrhythm Electrophysiol. 2011 Apr;4(2):166-71. doi: 10.1161/CIRCEP.110.959015. Epub 2011 Jan 19. PMID: 21248245.

7:  Kato Y, Hayashi T, Kato R, Takao M. Migraine-like Headache after Transseptal Puncture for Catheter Ablation: A Case Report and Review of the Literature. Intern Med. 2019 Aug 15;58(16):2393-2395. doi: 10.2169/internalmedicine.2519-18. Epub 2019 Apr 17. PMID: 30996181; PMCID: PMC6746642.

8:  Hoshina Y, Iijima H, Kubota M, Murakami T, Nagai A. Case of atrial septal defect closure relieving refractory migraine. Clin Case Rep. 2022 Nov 6;10(11):e6484. doi: 10.1002/ccr3.6484. PMID: 36381060; PMCID: PMC9637252.

9:  Azarbal B, Tobis J, Suh W, Chan V, Dao C, Gaster R. Association of interatrial shunts and migraine headaches: impact of transcatheter closure. J Am Coll Cardiol. 2005 Feb 15;45(4):489-92. doi: 10.1016/j.jacc.2004.09.075. PMID: 15708691.

10:  Schwedt TJ. The migraine association with cardiac anomalies, cardiovascular disease, and stroke. Neurol Clin. 2009 May;27(2):513-23. doi: 10.1016/j.ncl.2008.11.006. PMID: 19289229; PMCID: PMC2696390.

11:  Wood KA, Barnes AH, Paul S, Hines KA, Jackson KP. Symptom challenges after atrial fibrillation ablation. Heart Lung. 2017 Nov-Dec;46(6):425-431. doi: 10.1016/j.hrtlng.2017.08.007. Epub 2017 Sep 18. PMID: 28923248; PMCID: PMC5811184.

12:  Wood KA, Barnes AH, Jennings BM. Trajectories of Recovery after Atrial Fibrillation Ablation. West J Nurs Res. 2022 Jul;44(7):653-661. doi: 10.1177/01939459211012087. Epub 2021 Apr 26. PMID: 33899608; PMCID: PMC8801207.

13:  Björkenheim A, Brandes A, Magnuson A, Chemnitz A, Svedberg L, Edvardsson N, Poçi D. Assessment of atrial fibrillation–specific symptoms before and 2 years after atrial fibrillation ablation: do patients and physicians differ in their perception of symptom relief?. JACC: Clinical Electrophysiology. 2017 Oct;3(10):1168-76.

14:  Dorian P, Angaran P. Symptoms and Quality of Life After Atrial Fibrillation Ablation: Two Different Concepts. JACC Clin Electrophysiol. 2017 Oct;3(10):1177-1179. doi: 10.1016/j.jacep.2017.06.007. Epub 2017 Sep 13. PMID: 29759502.

15:  Steinbeck G, Sinner MF, Lutz M, Müller-Nurasyid M, Kääb S, Reinecke H. Incidence of complications related to catheter ablation of atrial fibrillation and atrial flutter: a nationwide in-hospital analysis of administrative data for Germany in 2014. Eur Heart J. 2018 Dec 1;39(45):4020-4029. doi: 10.1093/eurheartj/ehy452. PMID: 30085086; PMCID: PMC6269631.

16:  Levy S.  Overview of catheter ablation of cardiac arrhythmias.  In: UpToDate, Connor RF (Ed), Wolters Kluwer. (Accessed on January 17, 2023) 

 

 

Electrophysiology 2nd opinion – implications for medical and psychiatric practice

 

Pandemic related inaccessibility prevented me from getting timely Cardiology appointments this year.  As a result, I ended up with my scheduled consultation and a second opinion consultation spaced just two weeks apart.  I talked with a 2nd electrophysiologist today. He had records about me dating back to 2009. I had consulted with a cardiologist who was an exercise physiologist and another electrophysiologist at that clinic. After reviewing the recent history of paroxysmal atrial fibrillation again we had a very interesting conversation.

He reviewed the issues of rate versus rhythm control again. The priority is reducing stroke risk and that is done by anticoagulation. When it comes down to trying to maintain a normal sinus rhythm and all the measures that involves the decision is based on "How much does the arrhythmia bother you". He gave many examples that I was familiar with including the person who is not aware of being in atrial fibrillation until you tell them. I have made the diagnosis many times by taking vital signs on people and noticing their irregularly irregular pulse and pulse deficit. Most of the time they have no awareness of the arrhythmia. In some cases, they have been advised of the arrhythmia but decided not to do anything about it. I am in the category of people with what I like to call "cardiac awareness". I know immediately if I am in atrial fibrillation or even having palpitations. I check my own vital signs 3 times a day-in triplicate. We had a discussion of my neurotic tendencies and how much this rhythm problem bothers me – even if I am in atrial fibrillation only a few times a year for a brief period.

This point is also critical when it comes to treating psychiatric conditions. A misrepresentation of medical and psychiatric treatment is that physicians are drumming up business and manipulating populations into unnecessary care. Either that - or the care is just automatic and dependent on a diagnosis or blood test.   One of the favorite fabrications is that the DSM is designed expand treatment and line the pockets of both psychiatrists and pharmaceutical companies. In fact, I have not seen a patient in outpatient practice that was not there because they were distressed, bothered by their current symptoms, and unable to get help anywhere else. In my conversation today with the electrophysiologist we are contemplating a 3-hour procedure under general anesthesia with significant potential complications including bleeding, stroke, the need for pacemaker placement, and death - all based on my subjective assessment of how much this arrhythmia bothers me. Based on level of risk – there are no equivalent decisions in psychiatry.

To reinforce that point, he said that cardiologists have been trying to show that rhythm control is superior to rate control for about 40 years and the evidence was very thin and possible non-existent. Based on the discussion of stroke prevention, that assumes that anticoagulation reduces stroke risk on the atrial fibrillation group to the same level as the normal sinus rhythm or rhythm group. I would give the edge to the rhythm control group on that parameter.  In terms of lifestyle measures rhythm control would potentially eliminate other nuisance rhythms like bigeminy and trigeminy if the origin was in the pulmonary veins.  Additional mapping occurs during the procedure to see if there is another focus for these rhythms.  The atrial flutter would need to be eliminated in a procedure on the right side of the heart. A concern that we did not discuss is a sudden worsening of the atrial fibrillation or atrial flutter to the point that a different antiarrhythmic would need to be used.  I have seen amiodarone added at that point and there are many complications with that medication – including death from pulmonary complications.

We got into a discussion about phenotypes based on the recent New England Journal of Medicine review. The focal point was whether a paroxysmal atrial fibrillation pattern like mine was easier to covert by an ablation procedure and remain in a normal sinus rhythm and remain in that rhythm.  He was aware of the review, but thought that not enough is currently known about phenotypes.  That seem to be a problem with a lot or intermediate or endophenotypes that are used in psychiatry and other fields like asthma or multiple sclerosis.  On the surface there appear to be a lot of easily described apparent subgroups, but the natural history of those groups and the underlying pathophysiology is essentially unknown and considerable heterogeneity in severity, course, and outcomes remains.   

There was a brief discussion of the athlete’s heart.  He had no reason to doubt that the slightly enlarged left atrium and aortic root on my echocardiogram was due to decades of intense athletic activity and knew that was also one of many potential factors leading to atrial fibrillation.

The question of early rather than late ablation was discussed and the idea that there is progressive remodeling in the heart due to atrial fibrillation even in the case of a few episodes per year. He thought that in general, ablation prior to persistent atrial fibrillation resulted in better outcomes and earlier ablation was better than late ablation.  He emphasized that these were across group comparisons and there was a heterogeneity factor at work.  All the ablation that he does is radiofrequency ablation and the result is anywhere from 75-90% effective depending on how well the pulmonary vein isolation goes.  That is balances against a 2-3% risk of adverse effects – largely in the form of bleeding and hematoma formation at the catheter sites.  Chest pain and migraine headaches are also common post procedure.  Very serious complications during the procedure including death and the need for pacemaker placement were at about 1%.  The only death he had seen during the procedure was unrelated to the ablation.

He had a different opinion about the dose of flecainide and moving on to other antiarrhythmics like sotalol.  He thought I could take twice as much flecainide as a standard trial dose 150 mg BID), but agreed that it might not make much difference in the low frequency of atrial fibrillation.  That is quite a difference in flecainide dosing compared to the other group of cardiologists that I consult with.

In terms of recovery time give my current workout schedule he thought it would take a month to get back up to speed.  At that point I could resume my usual activities. If I decided to do that soon it would mean putting speedskating on hold for another winter.

That is where I am at after the second opinion.  Assuming that my insurance is the same across facilities – I have two to choose from and two electrophysiologists willing to try the ablation. My choice is to weigh a moderately successful procedure against the low frequency but significant complications and make the decision. And I know at this point it is an elective procedure based on how disruptive this arrhythmia is to my life. It is possible that at some point due to worsening atrial fibrillation and/or flutter and associated worsening symptoms or cardiac function that it would be less elective.

In terms of comparison with psychiatric practice and the usual critiques – these are the same choices that people would have if they were seeing me in clinic with a few exceptions. I am not treating anyone with invasive procedures or general anesthesia.  The medications prescribed by psychiatrists are generally safer that antiarrhythmics. There is a long list of absurd complaints made by antipsychiatrists that could similarly be applied to this cardiology scenario. But most importantly – in either case the treatment decision by the patient is subjectively based on how much the symptom is bothering them. I do not know how to translate 4 hours of symptoms per year into what I have been told about daily anxiety and depression symptoms every week. Some of those symptoms are also cardiac in origin.  

But I think this highlights a completely neglected dimension of medical and psychiatric practice.  Treatment is based on more than a rational informed consent discussion and weighing the risks and benefits. It is based on more than a scientific diagnosis and confirmatory tests.

It is highly subjective and based on the personal experience of the patient that is rarely know to casual observers.

 

George Dawson, MD, DFAPA

 

 Supplementary:

I thought I would add some additional observations about my recent cardiology consults and how they compare with psychiatric practice. Putting these in the main body of the post would have increased the reading difficulty.

Categorial diagnosis versus something else:  It is fashionable these days to say that medically diagnosed syndromes are a thing of the past and we should be making dimensional diagnoses or systems diagnoses.  Of course, these have been tried in the past. Contrary to a standardized approach – the diagnostic and treatment approach is highly practice dependent as can be noted by comparing the recommendations of the last 2 posts.  In addition, there is a fine structure to categories that is so detailed that it cannot be listed as criteria. Diagnostic categories in medicine have been talked about as prototypes – but it is really an indexing system for each physician to catalogue everything they know about that disease especially in the populations they are treating.

There may be objections to this conceptualization of categorial diagnosis.  Shouldn’t all clinicians be making the same diagnosis based on some sort of standardization?  That is certainly the argument many people make – but it certainly is not realistic.  Experts have seen more cases, know more variations, and have seen more diagnostic errors in the conditions they are diagnosing and treating. They have studied those conditions more thoroughly than anyone else. To suggest that a non-expert can read criteria in a diagnostic manual or administer a checklist of symptoms from that manual and get the same results is a significant misunderstanding of the process.  

Any medical category can be parsed based on severity and using that metric will lead to different assessments and treatments within the same category That is as true for cardiac arrhythmias as well as categories of depression and psychosis. A related issue on the medical side is that all the associated symptoms that might be lumped into lifestyle effects or suggest a psychiatric disorder are basically ignored if they do not show up on a PHQ-3 that is given as part of a preregistration packet.

The good news here is that subjectivity is alive and well in medicine and psychiatry as it should be.  Our biology determines unique presentations of our illnesses as well as our reaction to them.  The physicians treating us have to understand that.

 

A Visit To The Electrophysiologist

I have been waiting for today’s appointment since January 19^th of this year. At that time I saw a cardiologist who recommended that I see an electrophysiologist for atrial fibrillation.  I have had paroxysmal atrial fibrillation - just a few episodes per year for 10 years.  It didn't start out that way.  I was having frequent episodes until the dose of the antiarrhythmic was adjusted.   It all began while I was speedskating one night and my heart rate monitor began chirping uncontrollably.  Since then I have been seen by 4 cardiologists and 4 electrophysiologists.  The first one suggested that I hold off on any ablation procedures until “the technology improves”.  I was back to seeing that doctor today.  The first time I saw him he impressed my with detailed drawings and notes about atrial fibrillation and the time he took to explain it all.  He wrote out all of the details of CHADS-VASc Score for atrial fibrillation stroke risk and tried to convince me to start anticoagulation.  I was not impressed with the addition of one point to the score just based on age so I deferred. I did start apixaban 3 months ago when I realized the systems of medical care was fragmented and if for some reason I did not come out of one of these episodes in a reasonable period of time I might run out of luck and end up with a stroke. This time the visit was a bit different – it went something like this (not a transcript):

EP:  “We have seen each other before – what brings you back?”

Me:  “A few things – the cardiologist I saw in January recommended it, I have some concerns about the Holter results, can I expect a better result from medication changes, and to get your opinion about ablation.”

EP: “How often do you have episodes?

Me:  “This year so far I have had three – one for 2 hours, and 2 for 1 hour each in February, July, and August.  Triggers may be anxiety and nightmares. Exercise is not a trigger acutely but I did have an episode the next day after I increased my pushups from 100/day to 150/day.

EP:  “That is actually pretty good considering you are 10 years out.  We generally see this as a progressive process….

Me:  “ I have been having 2-3 episodes per year for the past 10 years.”

EP:  “Even so there may be progression there.”

Me:  “What about the Holter result?  I noticed there was a brief episode of trigeminy. When this all started I had a much longer episode of bigeminy and was advised it was a benign rhythm.  Is there a ventricular component?  Does something need to be done about that?

EP:  “No this is atrial bigeminy/trigeminy and you are right it is a benign rhythm.  Your Holter shows less than 1% isolated PACs and VPCs so there is nothing to be concerned about there and I don’t think changing any medication would be useful.”

Me:  “My primary care doc called one of your colleagues about increasing the flecainide to 200 mg/day and he said the arrhythmia risk increased at the higher dose.” 

EP:  “I just don’t think it will do much in terms of eliminating 3 episodes per year.  Are you using CPAP?”

Me:  “I don’t sleep without it – my AHI is typically less than 1.  I also my check BP twice a day in triplicate and the systolic is typically in the 100-110 range.  It always seems elevated when I come here.”

EP:  “Everybody’s BP is higher here. Do you drink alcohol?”

Me:  “No.  I had a question about NSAIDS.  I have gout but have not had an attack in a long time. I know what the package insert says about NSAIDs and apixaban – can I safely use them for a few days?”

EP:  “Well I can’t tell you it is OK to use them because it is listed as a contraindication – but you would probably be OK for a couple of days.” 

Me:  “What about an ablation?  The last time you and I talked you advised me to hold off because the technology was improving at the time. Has it improved to the point it is safer?”

EP:  “It improves every year.”  [ draws a diagram of rate versus rhythm control and on the rhythm control arm antiarrhythmics versus ablation].  About 70% of people respond to ablation but in 33% of those patients it requires multiple procedures.  There is a 5% complication rate across all procedures and that includes damage to the esophagus or phrenic nerve but we monitor to prevent that. [Another diagram to show proximity of esophagus and phrenic nerve to the structures to be ablated].   There is also a risk of stroke but you are anticoagulated during the procedure to prevent this.  It is done under general anesthesia. It takes about 3 hours.  At the end of that time, you spend 2 hours in recovery to monitor the catheter sites and if you are OK – you can go home.”

Me:  “I have also had two episodes where the afib converted to atrial flutter at a rate of 130 – I understand that takes a right sided procedure in addition to the pulmonary vein isolation on the left?”

EP:  “They can both be done at the same time [demonstrates lesion and current pathway on his drawing].”

Me:  “I have seen photographs of the radiofrequency ablations and they appear to be full thickness burns….”

EP:  “We use a cryo procedure for the pulmonary vein isolation.  Any other questions?”

Me:  “On the Eliquis – my initial concern with it was ’nuisance bleeding’ described in the package insert but I noticed that I am bleeding a lot less than with aspirin.  Is that common.”

EP: “Yes.”

Me:  “Well at this point – I guess it’s up to me to decide on the ablation.  Let me think about it and get back to you.”

EP:  “OK here is my direct number.  Either way let’s get back together in about 6 months.”

That was the approximate content of the encounter. I am used to memorizing these details and summarizing them from long and detailed discussion in a psychiatric context.  I also compared the process with the first time I met this physician.  We were both wearing masks and this was significant and of course he worked through the entire pandemic and I bailed out after the first 18 months.  Both of those factors seemed significant.  The first time I saw him I was probably wearing my white hospital coat because I worked in the same hospital and would never take time off for an appointment in the building.  This time, he either forgot I was a physician or possibly had the view that psychiatrists don’t know much about medicine. At any rate the interview seemed pressured and he was running 30 minutes late.  I had advised his nurse that I thought I had dysgeusia (altered taste) from the apixaban.  That was not passed on and I forgot to ask about it again. I also wanted to ask about exercise and resuming speedskating now that I am retired but I also forgot to ask that question. But every cardiologist I have asked that question to in the past 16 years says the same thing: “Exercise as much and ask vigorously as you want to.”  I have come to realize that is not necessarily the best advice.

The overriding goals never seem to make it into medical appointments.  There always seem to be the assumption that you address a medical problem separate from your overall life.  For example, my goal is to live as long as possible and be as active as possible.  Never touched on.  With any cardiology problem there is also the issue of cardiac neurosis – will I at some point consider myself disabled from cardiac symptoms when I am not? Is it possible to do something that will make my symptoms worse? It helps to have a clear answer to that problem.  The closest I ever get is the exercise advice (that I question) – although today it seems that the episode frequency is minor and stable and the Holter results are nothing to be concerned about.

There was potentially some controversy in the appointment that I could have brought up.  The progression of atrial fibrillation irrespective of frequency seemed new and may not have been consistent with a recent New England Journal of Medicine review.  In that review it seemed like paroxysmal atrial fibrillation was a stable phenotype compared with persistent atrial fibrillation.  On the other hand remodeling at the molecular level potentially occurs every time there is an episode and for that reason my goal is to do everything possible to minimize them.

Was there another reason to post this?  There are a couple of reasons that I use my own medical experiences for didactic purposes.  The first is to illustrate the uncertainty in all medical diagnosis and treatment. Psychiatry is constantly (and erroneously) criticized for not having a discoverable lesion or testable abnormality as a cause of most non-medical psychiatric disorders. In this case, I am talking about two conditions (atrial fibrillation and atrial flutter) that seem to have a clear medical cause or do they? There are several pathways (genetics, heart disease, excessive exercise) leading to atrial fibrillation.  What is the true etiology in my case? The excessive exercise is largely based on preclinical studies in animals and observing a higher incidence of atrial fibrillation in endurance athletes. If I opt for an ablation – the first part of that will be an electrophysiology study to detect the conduction problems to be ablated. It is not a specific treatment for a lesion – it isolates the lesion or interrupts the circuit pathway.  The medication is similarly non-specific.  As the electrophysiologist said today: “Of course the medication will not cure anything. I can’t say whether the ablation will work. We can’t be certain of anything.”  Just a few weeks ago I saw a debate saying the psychiatric medications don’t “cure” anything. Cardiology and the rest of medicine seems to be in the same boat.

The other reason to use my own data is that I don't have to worry about consent and I don't have to disguise anything - although I have deidentified the ECG with respect to the physician and hospital. 

Death was not discussed as a possible outcome and I know that it happens.  Within the past few years there was a case posted in the NEJM that showed airlock in the ventricles based on and injured esophagus and air entering the heart from that pathway. There was also a celebrity who died following an ablation for atrial fibrillation.  Like most procedures, people who do them a lot are probably more successful, but there are never any guarantees.  Henry Marsh the British neurosurgeon has written about his complications and states that even in procedures where everything seems to go right there can be a bad outcome. Over the course of my lifetime I have experienced good and problematic surgical outcomes. It is a far cry from a coin toss - but they happen.

The phenomenology of the episodes was basically irrelevant today. I have them correlated with nightmares, anxiety, and other stimuli leading to increased adrenergic input.  None of the seemed relevant.  There was no discussion of sleep or how to get rid of the nightmares. Most people may have the expectation that cardiologists don’t cover this area.  Psychiatrists do and that’s why I am trying to figure that part out myself. On the other hand – I spend a lot of time talking with people about their cardiac symptoms and often tell them to call their physician immediately at the end of my session.

The nurse who got me into the room was very pleasant and professional. She went out of her way to make me feel comfortable. Her efforts were appreciated.  She was also charged with getting an ECG done before I saw the electrophysiologist.  She did this expertly and then offered me a copy of the ECG.  The electrophysiologist gave me an additional copy!  I posted a copy here (it is unremarkable) but I will add that if this had happened in a primary care clinic within the same healthcare organization – it would have elicited eye rolls, the statement: “Let me ask my supervisor if I can do that.”, followed by a rejection of that request. Again this is all the same healthcare organization presumably schooling each clinic differently in the nuances of HIPAA.  There should be no reason why you can’t walk out of the clinic with test results and I appreciate the efforts of the Cardiology Clinic.

That is where things stand today. I am playing it by ear and tracking my blood pressure, heart rate and rhythm, sleep apnea, nightmares, anxiety level, neurosis, headaches, and long COVID symptoms. I have decisions to make and will probably get a second opinion on the ablation issue as well as where to have it done.  Should it be at my local health care organization or at a larger referral center where they do a lot more of them?

But that is another story….

 

George Dawson, MD, DFAPA

References:

1:  Michaud GF, Stevenson WG. Atrial Fibrillation. N Engl J Med. 2021 Jan 28;384(4):353-361. doi: 10.1056/NEJMcp2023658. PMID: 33503344.

2:  Thomson M, El Sakr F. Gas in the Left Atrium and Ventricle. N Engl J Med. 2017 Feb 16;376(7):683. doi: 10.1056/NEJMicm1604787. PMID: 28199804.

   

Incident Atrial Fibrillation and Intoxicants

I remain very interested in the cardiac and brain complications of medications and substances that are commonly used to get high or create altered states.  I am also very interested in the popular trend to characterize cannabis as some previously undiscovered medication that can cure everything ranging from anxiety to obstructive sleep apnea.  I was naturally interested when I saw this paper (1) looking at the issue of incident atrial fibrillation and common intoxicants.

The authors examine a very large database in California that included anyone who had been seen in an emergency department, ambulatory surgery center, or hospital over a period of 10 years (2005-2015).  After they eliminate minors, subjects with persistent atrial fibrillation, and subjects with missing data they had a total of 23,561,884 people. 998,747 of those people had incident atrial fibrillation (defined as the first encounter for atrial fibrillation).  Since their study design is a retrospective observational study they also recorded substance use was considered present if Substance use was considered present if there was coding for any indication of use of methamphetamine, cocaine, opiates, or cannabis.  Knowing the atrial fibrillation and substance use diagnoses – the authors calculate the hazard ratio for each of the substances of interest.

Hazard ratios are basically the ratio of the people exposed to intoxicants who developed atrial fibrillation over the unexposed who developed atrial fibrillation.  So any number greater than 1 means that the population exposed to intoxicants had greater risk.  The corrected hazard ratios were noted to be 1.86 (methamphetamine), 1.74 (opioids), 1.61 (cocaine), and 1.35 cannabis. The authors adjusted for common atrial fibrillation risk factors and ran an additional negative control analysis and looked at the scatter of data pints for these 4 substances and hazard ratios of developing appendicitis, connective and soft tissue sarcoma, and renal cell carcinoma and showed no consistent pattern for these illnesses.

There are a couple of interesting considerations relevant to this study.  The first is the mechanism of action in each case. With stimulants there is a direct hyperadrenergic effects and depending on the individual and dose of the drug varying degrees of tachycardia, palpitations, and hypertension.  Long term users frequently end up with cardiomyopathy from these effects and in some cases ventricular arrhythmias and congestive heart failure. There can also be acute vascular effects like ischemia either due to the increased cardiac demand or pre-existing arteriosclerosis. Atrial fibrillation has not typically been placed in that group of morbidities from stimulant use. Patient with atrial fibrillation often notice emotional precipitants for discrete episodes or atrial fibrillation although a recent study showed that the only reliable precipitant was alcohol use (2). There were significant limitations with that study with attrition and length of the study although I generally agree that alcohol is a clear participant.  Precipitants need to be carefully approached and I suspect that attentive physicians have noted variable phenomenology on an individual basis. 

The high hazard ratio for opioids is a little puzzling. Hyperadrenergic states can occur with the euphorigenic effects and withdrawal effects as well. Direct comparison with stimulants may be difficult due to rapid dose escalation and some degree of tachyphylaxis.  Cannabis is not surprising to me at all. Many initial cannabis smokers notice that their heart is pounding and don’t know why.  They find it unexpected given the conventional wisdom that cannabis is supposed to be a benign substance. Many initial users also get increased anxiety and, in some cases, have a panic attack that may be due to the cardiac sensations. The primary heart pounding sensation is because cannabis causes hypotension and they are experiencing reflex tachycardia. The effects may be less predictable because cannabis use can affect both sympathetic and parasympathetic pathways that can potentiate arrhythmias. A case report of cannabis induced atrial flutter (3) was described as occurring in a woman with a history of hypertension that eventually had to be terminated by an intravenous antiarrhythmic.   

Atrial fibrillation and other cardiac arrhythmias are another good reason for avoiding intoxicants including alcohol (in the supplementary analysis alcohol had a Hazard Ratio of 2.37).  It could be argued that it is basically a numbers game – since most people who use these intoxicants do not develop incident atrial fibrillation.  As of this moment, even if you have had your DNA analyzed for what are known about atrial fibrillation genes – you can’t be certain that you are not susceptible to the problem. And as outlined above there are many additional cardiac problems and that are possible from using these compounds.  The safest path is to avoid these intoxicants all together.

 

George Dawson, MD, DFAPA

 

 

References:

1:  Lin AL, Nah G, Tang JJ, Vittinghoff E, Dewland TA, Marcus GM. Cannabis, cocaine, methamphetamine, and opiates increase the risk of incident atrial fibrillation. Eur Heart J. 2022 Oct 18:ehac558. doi: 10.1093/eurheartj/ehac558. Epub ahead of print. PMID: 36257330.

2: Marcus GM, Modrow MF, Schmid CH, Sigona K, Nah G, Yang J, Chu TC, Joyce S, Gettabecha S, Ogomori K, Yang V, Butcher X, Hills MT, McCall D, Sciarappa K, Sim I, Pletcher MJ, Olgin JE. Individualized Studies of Triggers of Paroxysmal Atrial Fibrillation: The I-STOP-AFib Randomized Clinical Trial. JAMA Cardiol. 2022 Feb 1;7(2):167-174. doi: 10.1001/jamacardio.2021.5010. PMID: 34775507; PMCID: PMC8591553.

3: Fisher BA, Ghuran A, Vadamalai V, Antonios TF. Cardiovascular complications induced by cannabis smoking: a case report and review of the literature. Emerg Med J. 2005 Sep;22(9):679-80. doi: 10.1136/emj.2004.014969. PMID: 16113206; PMCID: PMC1726916. [full text] 

An Outstanding Paper on Atrial Fibrillation

 

I have been fascinated by atrial fibrillation since I was a third-year medical student. I was doing a Medicine rotation and examining a middle-aged man.  Listening to his heart sounds was the first time I heard the irregularly irregular heart rhythm characteristic of atrial fibrillation. It was such an outrageous and unexpected sound compared to what I was used to that I felt a little panicky. Why wasn’t this patient experiencing more symptoms and even more unexplainably – why doesn’t he sense that there is something wrong with his heart beat?  Since then, I have treated hundreds of patients with atrial fibrillation.  I ask them all if they can sense the irregular heart beat and in the people I see about half of them can.  Being a psychiatrist, diagnosing and treating atrial fibrillation is technically not my “job”.  But it is currently such a prevalent condition that a brief examination typically triggered by vital signs and noting a pulse irregularity followed by an electrocardiogram is all that is needed. Atrial fibrillation has considerable mortality and morbidity associated with the most feared complication of stroke. A good friend of mine developed renal failure from a combination of atrial fibrillation and atrial flutter and required ablation procedures to restore normal sinus rhythm.  Two relatives had strokes associated with atrial fibrillation resulting in disability and ultimately death. Both had atrial fibrillation for about 30 years.  One of them was 92 years old, using digoxin for rate control, and not on anticoagulants. The other was 92 years old, using diltiazem for rate control, and on warfarin at therapeutic doses. He had two strokes about 10 years apart on the warfarin and multiple episodes of nuisance bleeding or excessive bleeding from minor injuries due to anticoagulation that did not require medical attention.   Another friend had pulmonary complications from an antiarrhythmic drug that he was taking for a new onset of atrial fibrillation and died as a result of those complications. Sixteen years ago – I developed lone atrial fibrillation while speedskating and have been on antiarrhythmics since that time.

When you see all of those problems associated with a condition and have had it yourself, you tend to read more about it than the average person.  Reading about atrial fibrillation is generally a frustrating task. The evidence base for treating the condition seems to be in a state of flux. For years the research seemed to say that rate control and rhythm control led to equivalent outcomes. When life style measures were included, the rhythm control strategies seemed superior. Even the question of anticoagulation with novel oral anticoagulants of NOACs for stroke prevention based on a scoring system has been called into question recently.

That brings me to the topic of this blog post and that is the single best summary of information about atrial fibrillation that I have seen anywhere - at least for nonspecialists in that area.

The paper was written this year in the New England Journal of Medicine (1). It starts out with a case description of a 63-year-old man with a new onset of atrial fibrillation. The authors discuss the disease in detail and treatment recommendations consistent with their discussion. What I really like about this paper is that they are discussing phenotypes of atrial fibrillation and I do not see that happening very often in real clinical situations. The phenotypes they discuss are paroxysmal atrial fibrillation, persistent atrial fibrillation, and long-standing persistent atrial fibrillation.  They have an excellent figure in their paper that was unfortunately prohibitively expensive for me to try to post here, but the basic idea is that there are distinct anatomical and electrophysiological substrates for each of those phenotypes. In the paper the phenotypes are labeled as “clinical profiles”. His phenotypes have prognostic considerations since the authors make the point that there is a gradation in the likelihood of conversion to normal sinus rhythm and maintaining that rhythm with paroxysmal atrial fibrillation being the most likely to convert and maintain a normal sinus rhythm and long-standing persistent atrial fibrillation being the least likely to convert. Just knowing that much about atrial fibrillation is a significant advance compared with most of the clinical discussions that I hear.

The second feature in this paper that I really like is that atrial fibrillation is not necessarily a benign condition. For years the discussion has been controlling the rate or rhythm and in most cases they have been considered to be equivalent. Many clinicians have their first experience with atrial fibrillation like I had. They are doing a physical examination outpatient for another reason and they notice they are in atrial fibrillation. Depending on physiological factors that patients irregularly irregular heart rate may already be rate controlled. I have talked with many people over the years who knew that their heart rate was irregular because their spouse noticed it and they did not do anything about it for years. Atrial fibrillation is a risk factor for embolic strokes as well as dementia, death, and heart failure. Persistent tachycardia can cause cardiomyopathy and reduced cardiac output can lead to renal failure.  The authors suggest that a heart rate of 110 bpm or greater might lead to cardiomyopathy but they also suggest it can occur at a lower rate. This is an interesting observation because the most recent review in UpToDate on sinus tachycardia suggests it is generally a benign condition, however an irregular tachycardia because of reduced cardiac output is likely a different matter.

In addition, the patient can be symptomatic from reduce cardiac output with lightheadedness, dizziness, fatigue, decreased exercise tolerance, palpitations, hypertension, and an exacerbation of symptoms of underlying coronary artery disease. The lesson for psychiatrists is if you notice that a patient has atrial fibrillation it cannot be approached casually. Atrial fibrillation is associated with significant medical comorbidities such as underlying structural coronary disease, obesity, sleep apnea, hypertension, hyperlipidemia, and diabetes mellitus. If the patient has had limited contact with primary care physicians the comorbid conditions may have gone unnoticed. It makes sense to ask about additional symptoms in the review of systems as well as family history and whether that patient is seen primary care physician or cardiologist recently.  I would have no problem referring a patient with tachycardia, expected symptoms, or risk factors to an emergency department for acute stabilization if I could not get them seen in a primary care clinic.

The authors go into treatment of atrial fibrillation as basically a rate control strategy, a rhythm control strategy, and a strategy to address comorbid medical conditions.  They review rate control with beta-blockers and calcium channel blockers and prefer beta-blockers. They consider a number of antiarrhythmics and the risks and benefits of those medications.  They consider catheter ablation - either radiofrequency pulmonary vein isolation or cryoablation as being more effective for treating and preventing recurrent atrial fibrillation. The recurrence rates are relatively high even after the ablation procedures, so continued antiarrhythmic medications may be necessary.

Once a patient has stable treated atrial fibrillation, the main task for the psychiatrist is to make sure that any prescribed medications do not interfere with the cardiac medications at either the pharmacokinetic or pharmacodynamic level. QTc prolongation is a primary consideration since several of the agents used prolong the QTc interval or affect other cardiac conduction.  At the pharmacokinetic level there is the possible risk of decreased metabolism of beta-blockers and increasing bradycardia and hypotension. If I have any doubts all about medication combinations I am usually in touch with the patient’s cardiologist or primary care physician before making those changes. All of the patients I see with atrial fibrillation also have their blood pressure and pulse taken at every visit along with the description of symptoms and potential medication side effects. That means I never practice in an environment where I can't do that. I will also review how well their comorbid conditions are being treated particularly hypertension, sleep apnea, and diabetes mellitus. I will provide them with concrete advice on how to approach those problems and whether or not they need to be seeing their primary care physician sooner than scheduled.

This is also an opportunity to discuss any comorbid substance use problems. Alcohol is a definite precipitant of atrial fibrillation. I have had patients never experience another episode by stopping alcohol. I have also had patients report that they can tell when their alcohol level reaches a certain point because they will go into atrial fibrillation for several hours until that alcohol is metabolized. Stimulant medications are also a risk because they increase sympathetic tone, increase heart rate, increase blood pressure. All three of those changes can trigger an episode of atrial fibrillation.  Cannabis can have a fairly potent sympathomimetic effect by acutely lowering blood pressure leading to a reflex tachycardia. Atrial fibrillation has been reported as one of several cardiac arrhythmias associated with cannabis use (2). Interestingly, the authors of the NEJM article state that caffeine is not a precipitant. There are no qualifiers on that statement and I think it is based primarily on epidemiological evidence. Caffeine intake is always important to quantify because of its wide variability across the population and general reputation of being a benign compound. There are segments of the population that consume large quantities of caffeinated beverages every day and experience the expected side effects of anxiety (in some cases panic attacks), agitation, insomnia, and hyperadrenergic effects but they seem unaware that these symptoms are related to their caffeine consumption. Certainly consumption at that level can directly or indirectly precipitate an episode of atrial fibrillation.

That is my brief review of the NEJM article in atrial fibrillation. I encourage all psychiatrists to get a copy of this paper, read it, and keep it for reference. I am not suggesting that psychiatrists treat this condition.  I am suggesting that they recognize it - even if it has not been diagnosed and know what to do when that occurs. The reality is that in adult psychiatry no matter what your practice setting there will be a significant number of people with atrial fibrillation and other arrhythmias as well as all of the known comorbidities. You cannot treat those people unless you know about these conditions, the comorbidities, and how to avoid complications.

 George Dawson, MD, DFAPA

 

References:

1:  Michaud GF, Stevenson WG. Atrial Fibrillation. N Engl J Med. 2021 Jan 28;384(4):353-361. doi: 10.1056/NEJMcp2023658. PMID: 33503344.

2:  Richards JR, Blohm E, Toles KA, Jarman AF, Ely DF, Elder JW. The association of cannabis use and cardiac dysrhythmias: a systematic review. Clin Toxicol (Phila). 2020 Sep;58(9):861-869. doi: 10.1080/15563650.2020.1743847. Epub 2020 Apr 8. PMID: 32267189.

Supplementary:

Common and uncommon medications listed in this article used in atrial fibrillation for rate control, antiarrhythmic properties, and anticoagulation.  I added additional warnings and general type of medications that might require avoiding based on pharmacokinetic or pharmacodynamic considerations. Important to keep in mind that all medications vary in their ability to affect these mechanisms as well as therapeutic mechanisms. That includes significant differences between medications in the same class. That leads to qualifiers like "all possible mechanisms leading to complications or serious adverse effects may not be listed" (in this package insert or computerized drug interaction program). Almost every time I am seeing a patient on these medications - it requires a study of the medication combination, even if they are taking a psychiatric medication that appears to be working. Baseline cardiac symptoms related to the arrhythmia also need to be established as well as the patient's plan to obtain assistance if they worsen.

Additional qualifier (if it is not obvious). Psychiatrists prescribe beta blockers (metoprolol, propranolol, pindolol, etc). Psychiatrists can diagnose atrial fibrillation. Psychiatrists do not manage atrial fibrillation but need to know what to do acutely and how to avoid complications of the following medical therapies from drug interactions with psychiatric medications. Practically all of the antiarrhythmics in the following table are prescribed by Cardiologists and subsequently managed by primary care physicians although many patients continue to see Cardiologists in follow up. Like all areas of medicine the limits of technical expertise need to be recognized.  I worked with Cardiologists who became psychiatrists and they restricted their practice to medications prescribed by psychiatrists.  

Graphics Credit:

Bunch TJ, Cutler MJ. Is pulmonary vein isolation still the cornerstone in atrial fibrillation ablation? J Thorac Dis 2015;7(2):132-141. doi: 10.3978/j.issn.2072-1439.2014.12.46

Open Access per this Creative Commons License: https://creativecommons.org/licenses/by-nc-nd/4.0/