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.

   

Cardiac Screening In Psychiatric Patients

There is a paper that just came out (1) that I consider a must-read for all psychiatrists.  Some experts might qualify that and say that it is only necessary to know the subjects if you are treating the medically ill, the elderly, pediatric patients, patients with cardiovascular disease, or patients with cardiac risk factors. The problem with those qualifications is that you have to know everything in this paper (and others) in order to make that determination. Beyond that you have to been trained in how to determine if your patient is seriously ill or not. In the case of all medical specialists, serious illness generally means treatment by another specialist or in a more intensive setting. For that reason, the cardiac aspects of care in this paper are required knowledge.

Three of the authors of this paper are cardiologists, two are psychiatrists, and one is a clinical pharmacist. They have produced a very practical document on identifying problems with tachycardia, QTc prolongation, sudden cardiac death, myocarditis, and dilated cardiomyopathy.  They provide very specific endpoints and suggest some basic intervention that can be done before the patient is referred to cardiology. Examples would be assessment of tachycardia, suggested treatment thresholds, common treatment interventions like beta-blockers and calcium channel blockers, and referral to cardiology if there is a progression to other cardiac symptoms, nonresponse to the initial therapy, or an arrhythmia beyond sinus tachycardia. They provide similar guidance on the other common conditions and relate them to second-generation antipsychotics (SGAs). 

All of the authors are from the United Kingdom.  I am not familiar with the standard settings for practicing psychiatry in the UK, but in the US there is a high degree of variability. For example, in practicing on inpatient settings it is not a problem to order ECGs or even stat ECGs. Echocardiograms and other imaging studies of the heart are easily obtained as well as cardiology consultation. In a previous inpatient setting where I practiced, I requested a cardiology consultation for a young woman with a QTc of 520 ms who required treatment with antipsychotic medications. She was seen immediately and an electrophysiology study was done. After that study I was advised by cardiology that I could safely treat the patient with olanzapine. At the other end of the spectrum, I know there are psychiatrists reading this who have no access ECGs, medical testing, or cardiology consultants. They are often practicing in an office that lacks a sphygmomanometer or staff routinely checking patient vital signs. Many of those office settings are essentially nonmedical and any psychiatrist practicing there - would need to bring in their own equipment and probably take their own vital signs.  A basic standards would be that every practice setting for psychiatry in the country should have the tools to make the measurements recommended in this paper, but I am not aware that any standard like that exists.

The second obstacle to realizing these guidelines is the way electronic health records (EHR) are set up. Major organizations and the EHR companies themselves produce templates that are typically designed for business purposes rather than medical quality. A visit to a psychiatrist in that organization results in that template being filled out with a business rather than a clinical focus. In other words, sections of bullet points are completed based on what coders believe will capture the necessary billing from insurance companies. One of the key sections is often the review of systems (ROS). Because these documents are not designed by physicians and there are no uniform standards, a functional review systems is often not there. In the case of cardiac symptoms, there needs to be a clear section that encompasses all the symptoms described by the authors in this paper. As an example, take a look at the cardiac symptomatology that I recorded in this post and the modified extended review of systems that I typically ask patients about.

Any inpatient or outpatient assessment done by a psychiatrist should include a thorough medical history, a review of systems that is focused on medical rather than psychiatric systems, a set of vital signs including noting whether or not the cardiac rhythm or pulse is regular or irregular and a further description of the irregularity.  A focal exam for additional heart and lung findings and determination of pulses and peripheral edema may be indicated.  The take home point is that this history taking combined with a few additional findings should be all that is necessary to order further tests like an ECG, refer for an acute assessment, or refer to a primary care physician or cardiologist for further assessment.  If the patient is being followed for the metabolic complications of SGAs, there may already be a fasting blood glucose, and lipid profile in the chart to assess additional risk factors.  Over the years I have also found that recording a theory about why I think the patient is symptomatic is also very useful.  In my practice that has ranged from medication side effects to an acute myocardial infarction.

With those issues we can proceed to consider the assessments and treatments recommended by this group. I am not going to repeat the content of the paper here.  I recommend that any interested psychiatrist or psychiatric resident get a copy of this paper and study it in detail if you are not already familiar with the concepts. I will list a few of the points that I found to be interesting after doing these assessments for a long time.

Tacycardia is a common problem in psychiatric patients and the population in general. Here the authors were focused on tachycardia as a side effect of SGAs and haloperidol.  They produced a table showing the incidence of tachycardia across a number of SGAs and haloperidol and illustrate that clozapine by far has the highest prevalence of tachycardia. In the table haloperidol, asenapine, and sertindole at the lowest incidence of tachycardia at about 1%. They point out this problem is generally self-limited but it suggests a number of investigations that should be considered before monitoring for improvement over time. The recommended treatments (bisoprolol, ivabradine) are not recognizable medications for physicians in the US. In the US, beta-blockers are commonly used. They suggested treatment is predicated on whether patients are symptomatic or not with palpitations. Although UpToDate describes sinus tachycardia as a benign condition with no worse outcome than a control group, this tachycardia is drug-induced. My main concern with persistent drug-induced tachycardia is tachycardia induced cardiomyopathy. My other concern is that common causes of tachycardia in the patients I see include excessive use of caffeine (alcohol, or other substances), deconditioning, and sleep deprivation. Establishing a baseline prior to any of these prescriptions is important.  There is always a lot of debate about whether or not electrocardiogram should be done. I agree with the authors that the ECG is an inexpensive screen and should be done to make sure that it is a sinus rhythm. Another bit of information that may not be available is whether the pulse is irregular or not. Many clinics have automatic blood pressure and heart rate measuring devices and not all of them make that determination.

The section on the QTc interval was interesting because the authors provide very clear guidance on measuring QTc, the problems with that measurement, and very clear guidelines on what to do about that measurement. They cite the threshold for stopping or reducing treatment with QTc prolonging agents as an interval greater than 500 ms or relative increase of greater than 60 ms. They also use the American Heart Association definitions of prolonged as QTc > 450 ms in men and > 460 ms in women.  They point out that the most common calculation of QTc (Bazett’s formula) overcorrects heart rates greater than 100 BPM and they suggest that other formulae may be used for that situation. Like many psychiatrists I have ordered hundreds of ECGs for determining baseline cardiac conduction. The vast majority have been normal. The ones that were not - were typically unrelated to the medication I was prescribing. Many conduction abnormalities were related to increasing age and latent cardiac problems. The other common scenario where I am concerned about cardiac conduction is polypharmacy. It is possible for a person to be taking multiple medications for psychiatric indications - all of which may affect cardiac conduction. The drug interaction software for most EHRs as a very low threshold for this type of interaction.

The myocarditis section of this paper was very interesting. In Table 1 - the authors included prevalence figures for myocarditis in the same table where they documented the prevalence of tachycardia for each medication. The figures are based on isolated case reports. The review the controversy about clozapine and widely variable reports of incidence. The incidence quoted for Canada and the USA was 0.03%. Different criteria used to diagnose myocarditis was considered an important point of variance. A set of clinical criteria is provided in the paper as well as when to refer to a cardiologist. In addition to the ECG, serum troponin, C-reactive protein, echocardiogram, and cardiac MRI are considered. The referral indicators included elevated troponin, CRP, and abnormalities at echocardiogram. My interpretation is that psychiatrists in the US who have access to those measures and ready access to cardiologists could potentially use those markers. The most reasonable approache is to be able to recognize the symptoms of myocarditis clinically and be able to refer the patient to cardiology were most of the testing could occur. The clinical description of myocarditis in the paper sounded very similar to typical viral myocarditis with chest pain, dyspnea, flu-like illness, fever, and fatigue. These are nonspecific symptoms especially during influenza season. The clinician has to have a high index of suspicion based on treatment with clozapine. The paper contains an ECG tracing of saddle -shaped ST elevation considered to be a finding consistent with myocarditis. It was visible in most leads.

The approach to dilated cardiomyopathy was very similar in terms of recognizing the symptoms of congestive heart failure and the necessary investigations. There was guidance and when to request an echocardiogram based on BNP and in NT-ProBNP measures as well as when referral to cardiology was indicated. The standard of care in the US is the psychiatrist recognizing what is happening but not treating dilated cardiomyopathy. In most clinical with limited resources, this is a good reason to have a referral relationship with a primary care clinic - especially one that can do the testing on site. There are many primary care and even urgent care clinics that cannot do the testing suggested in this paper.

In the case of myocarditis and dilated cardiomyopathy, the question of whether a patient should be re-challenged if they need the offending medication and their underlying cardiac condition has improved. The authors suggest close consultation with a cardiologist at that point. Given the data my own practice has been to not re-challenge with the offending medication but to try a different treatment modality. The concern in the article is that the patient’s ability to function from a psychiatric standpoint may require use of that specific medication. I do not think that enough is known about the outcome of either condition to resume the original medication, but if favorable outcome studies or case reports exist, I might revise that opinion.

All things considered this is an outstanding article on the cardiotoxicity of SGAs. The graphics in the paper also excellent with management flow diagrams and well-designed tables.  The authors restate that cardiotoxicity is very low.  It is the job of every psychiatrist who prescribes these medications and others to make sure that patients are monitored for these complications. There is always a question of what constitutes adequate informed consent when we are talking about a potential complication rate of 0.03%. At that level it is certainly possible that many psychiatrists have never seen these complications and never will. I think it is reasonable to let people know that medications they are taking can cause rare but potentially serious side effects including death. The informed consent issue was not touched on in the paper but a day-to-day practice it is an important one.  From a practical standpoint I generally advise people that if they are taking a medication with rare but potentially life threatening side effects, they have to take all physical symptoms seriously. Physical symptoms cannot be attributed to common explanations like colds, the flu, or gastroenteritis.

This paper had a very specific focus and it did not touch on the other metabolic and neurological complications of these medications that require additional screening.  One of the reasons I posted my ROS document on this blog was to make ti easy for any clinic or psychiatrist to build their own template with the relevant questions needed for their own patient population. 

For some psychiatrists and clinics the work in cardiac screening just got a lot harder.  For others who have been doing all of this for decades - there will be very little difference.

George Dawson, MD, DFAPA

References:

1:  Sweeney M, Whisky E, Patel RK, Tracy DK, Shergill SS, Plymen CM.  understanding and managing cardiac side effects of second-generation antipsychotics in the treatment of schizophrenia. Br J Psych Advances 2019: 1-15.

2:   Patel RK, Moore AM, Piper S, Sweeney M, Whiskey E, Cole G, Shergill SS, Plymen CM. Clozapine and cardiotoxicity - A guide for psychiatrists written by cardiologists. Psychiatry Res. 2019 Jul 24:112491. doi:10.1016/j.psychres.2019.112491. [Epub ahead of print] Review. PubMed PMID: 31351758.

A Stress Test.... Free Associations

I was just starting to breathe a little heavier.  The nurse running the test has been talking to me - continuously for the last nine minutes.  She was bright, pleasant, a great conversationalist but more to the point - everything she said seemed highly relevant. From time to time she would ask how I was doing, check my blood pressure and tell me what my heart rate was.  Some time at about the 9 minute mark she said that I might need to break into a jog for the next level.  It was a 16% grade at 4.1 mph.  The treadmill tilted up and it was a smooth transition.  I was still walking at a fast pace.  "Your heart rate is 160 are you OK?"  I was feeling very good.  Still talking in full sentences and not feeling stressed at all.  My left knee was sore and I said: "My knee is sore and I don't want to break into a jog.  I will complete this stage and call it a day."

I did have room at the end and am fairly confident I could have knocked off the next stage.  I have done it many times in the past starting with a test at about ago 42.  There were a number of considerations holding me back.  The knee.  It was nothing big.  When you exercise a lot as an adult - episodic knee pain is all part of it.  Secondly, a history of paroxysmal atrial fibrillation.  I probably got it in the first place from running heart rates too high for my age.  I did not want to flip into another episode of atrial fibrillation.  Third, the target rate.  Before starting, the supervising nurse told me that the target heart rate for a guy my age was 140 bpm and I was over that with no signs of ischemia or more importantly a widening QRS interval (I take flecainide).  Fourth, I was just happy to be there.  Even though I have had 5 exercise stress tests over the last 25 years, the last one was at the Mayo Clinic about 10 years ago.  These things are a lot less certain with age. As I was on the treadmill, I kept thinking of a review I read in the Medical Clinics of North America many years ago: "40% of 85 year olds have significant coronary artery disease".  Of course those are the 85 year olds who survived to that age.

I had other associations while I was walking and talking. I take a cardiac history on every person I talk with. Some are more detailed than others. I know a number of ways that stress tests can be failed. I know from talking with people what happens when your ECG suddenly shows signs of ischemia. Generally the next step is a Cardiologist spraying nitro into your mouth.  I also know that passing a stress test is a generally a good sign, but it is not a guarantee. Nothing in medicine is.  Too many people have told me about cardiac problems in the absence of a positive stress test, including an infarction in the absence of any occlusions.  Irrespective of the result, I would maintain humility and strive even more to avoid the trans fats that are quantitatively too low to make it on the food label.  And of course all of that bakery with thick frosting - the first display you encounter in any supermarket.           

I had the exercise stress test two weeks ago.  Four days earlier I was doing my usual dictation of an assessment in my office and as I stretched back - I experienced an intense sharp burning pain going down the left side of my sternum.  It lasted about 5- 10 seconds.  I have been having this pains for at least a year all over the chest, left shoulder and back.  At one point they were clearly musculoskeletal in origin and I could replicate them by certain movements or flexing certain muscles.  But then the discriminatory ability was gone.  All of the tricks I learned in medical school and residency about the  difference between musculoskeletal pain and true cardiac pain or angina did not apply.  One of the things they never teach you is that when you get old - all of the routine pains that you live with every day meld into vague pains all over your torso.  Was that chest pain or did it originate in my back, neck or shoulder?  Arthritic pain or pain from trying to do too many pull ups last night?  At some point I just decided to go in to see my internist to see if we could figure it out.

My internist has known me for 30 years.  Any chest pain in the early part of that period was immediately dismissed as musculoskeletal pain.  He knew I was a compulsive exercise fanatic and between the ages of 30 and 55 probably cycled 200 miles per week or the equivalent. In the winter, I would speedskate as much as possible.  My goal was to end the season by doing as many laps as possible in an hour on the John Rose Oval - one of the few refrigerated speedskating outdoor tracks in North America.  Doing that kind of exercise gets the heart rate up to very high levels.  During interval training up to 190+ beats per minute.  Whenever the subject came up during those years my internist would say: "You do a stress test every time you exercise".

That all changed at age 55.  I was out doing a warm up on the speed skating track.  I looked down at my heart rate monitor and it read 170 bpm.  One lap later it was chirping loudly and now it read 240 bpm.  I felt my carotid pulse and it was the irregularly irregular rhythm of atrial fibrillation.  That led to 2 hospital admissions, 2 cardioversions, 2 consultations with a sports cardiologist at the Mayo Clinic and 2 exercise stress tests on a bicycle at Mayo.  I ended up on flecainide  with the advice to consider an ablation procedure at some point in the future as long as the flecainide continued to work and "if the technology improves".  That is a direct quote from one of my electrophysiologists.

During the bicycle stress tests, I ran my heart rate up to 170 bpm and could have gone higher, but was concerned about triggering another episode of atrial fibrillation that would no longer respond to flecainide.  On echocardiography, I have features that are seen in some series of cyclists who do high levels of dynamic exercise - primarily an large left atrium and a slightly enlarged aortic root.  During dynamic exercise, there is a steady increase in blood pressure despite the fact that stroke volume peaks at about 120 bpm and main contributor after that point is heart rate and sympathetic nervous system output.  My adaptation was to try to keep my heart rate at 140 bpm or lower when exercising and lately 130 bpm.  It is good to know I can go higher even for brief periods of time.

So the coronary arteries may be OK, but that leaves paroxysmal afib and the enlarged aortic root/aorta.  We have only recently discovered the role of the layered extracellular matrix in aortic anatomy. Like most of these structures disruption of those layers can result in permanent weakness.  It is also known that high levels of dynamic exercise results in aortic enlargement.  I have not seen any outcome studies of those individuals - but it would be useful to find an expert. 

My next step is to see a Sports Cardiologist about the afib and aorta.  I anticipate that he or she will wonder about why there is an old man in the examination room trying to get as much performance as possible out of an aging cardiovascular system.  If that question comes up, the response is simple:

"I don't want to die on the side of the road from a blown aorta because I tried to race a 40 year old up a hill.  I need your most conservative estimate on how I can prevent that."

And so it goes......


George Dawson, MD, DFAPA


Supplemental:

Previous exercise stress test done on a bike at the Mayo Clinic in 2012 showed a similar result (possibly low BP and heart rate this time but I find that it is easy to over rev on a bike as opposed to a treadmill).


         

Financial Marginalization of Psychiatry

I wrote this original article in 2005 for the Minnesota Psychiatric Society newsletter in response to two developments.  First, it is one of the only articles that you will ever see quoting actual prices in terms of bills and what the actual reimbursement is.  Contrary to the myth of expensive health care, I have had people tell me how shocked they were at how little of a bill the insurance company actually paid.  The author here gives the actual dollar amounts.  Second, there is an obvious boom in Cardiology services at a time when psychiatric services were being strictly rationed according to managed care "carve out techniques." At the  time this article was originally written 100,000 patients per year received implantable cardioverter devices (ICDs) at a cost of $2 billion and a pulse generator replacement cost of an additional $1.4 billion.  Using the figures from this article that is the equivalent of 794,000 psychiatric hospitalizations per year.  The original article and the reference begins with the paragraph below.

A recent Twin Cities article on the escalation of technology and real costs for cardiac care in Minnesota highlighted just how severe the resources have been skewed away from psychiatric care. If you have been following the Minnesota Psychiatric Society's initiatives in this area over the past few years it will probably come as no surprise - but even in that context I found the following numbers somewhat shocking:

1. Minnesota (a state with maximal managed care penetration) - has 40% fewer mental health beds per capita than the nation.

2. In the past 5 years - 5 new cardiac care facilities have opened at a cost of $263 million.

3. An analysis of Medicare cost data for one hospital (United) shows why cardiac care is expanding and psychiatric care is shrinking. Here is a direct quote from the article:

"A look at Medicare cost data for one local hospital shows why. It cost United Hospital $8,091 to implant a pacemaker, but the hospital received $11, 538 for each procedure, according to 2003 data provided by the American Hospital Directory.

On the other hand, it cost United $10, 132 to treat a patient with psychosis, but the hospital received only $4, 282 per case. These are federal Medicare figures but the same disparities exist in payments by private health plans."

That's why you are seeing all of those shiny new Heart centers and no new psychiatric hospitals. Combined with the psychiatric outpatient penalty - it probably also goes a way toward explaining why the system is so fragmented and the seriously ill cannot find a psychiatrist.  Also notice that the insurers were described as worried about how to contain Cardiology costs, but the reality here is that all of these Cardiology services are owned by the major managed care companies.

George Dawson, MD

Hauser RG.  The growing mismatch between patient longevity and the service life of implantable cardioverter-defibrillators.  Journal of American College of Cardiology 2005; 45 2022-5.

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