The Recent Takedowns of Adult ADHD

 

Psychiatry seems doomed to argue endlessly about whether certain conditions exist or not and whether they can be characterized by written criteria. The latter condition is the most easily dismissed since clinical training is necessary to recognize conditions. You cannot just sit in an office, read the DSM and call yourself a psychiatrist. Whether conditions exist or not is more debatable but often slides into rhetoric that suggests inadequate training, ignorance, and/or significant conflict of influence or undue influence by the pharmaceutical industry. Consideration of the undue influence can easily be applied at the global level since Pharma has massive marketing efforts, direct to consumer advertising in the US, and at least one major political party pulling for them.

That brings me to the recent commentaries about adult ADHD (1, 2). The first reference (1) doubts that adult ADHD exists for the most part and sees the diagnosis primarily as the result of a marketing scheme by Eli Lilly for atomoxetine and ignoring affective temperaments and other states that may affect attention. Atomoxetine was invented as a norepinephrine reuptake inhibiting antidepressant and like other members of this class of drugs – it did not work for depression. Since it is not technically a stimulant it was tested for ADHD and found to be effective. It is unique relative to other ADHD medications and not surprisingly it was heavily marketed while on patent. The patent expired on May 2017. The years on the market patent protected were 2002-2017. The first references to the diagnosis of adult ADHD were noted in the 1980s. Reference 2 suggests that the diagnosis of ADHD in children in the US is around 2-3% with adult numbers half that based on the work of one author.  Contrasting numbers of a lifetime prevalence in adults as 8.1% and surveys estimating current prevalence at 4.4% are described as “absurdly high” but qualified on methodology (surveys vs interviews).  Some authors have the opinion that books published about adult ADHD like Ratey and Hollowell's  Driven to Distraction were a major source of public interest in the diagnosis and instrumental in getting it into the public vernacular. 

Before I get started – let me say that the only stake I have in this argument is making sure that the complexity of the situation is adequately described. Practically all the pro/con arguments in psychiatry are gross oversimplifications and based on what I know about the literature – I had no reason to expect that this was any different.  I am already on record on this blog describing how to diagnose and treat ADHD and not fall into the common problems of misdiagnosis, prescribing to people with substance use problems, or prescribing to people who view these medications as performance enhancers. I have successfully treated adult ADHD with both on and off label medications and can attest to the fact that it is a valid and treatable diagnosis.

Let me start out by looking at the prevalence estimates. These figures are very popular in the press to indict diagnosticians in the United States compared with some European countries and sell more papers. The problem with prevalence estimate is that the range can vary significantly due to methodological differences in the surveys. That question was looked at (3) and the title of that paper asked if ADHD was “an American condition”.  The authors reviewed 22 studies based on DSM-III criteria and 19 studies based on DSM-IV criteria.  Twenty prevalence estimates were done on the US and 30 were done in other countries.  They demonstrated that the range of prevalence across all studies was approximately the same and that ADHD was not just an American condition. Since then numerous prevalence studies have been done in other countries – more recently using DSM-5 criteria showing similar ranges.

On the issue of adult ADHD, a recent review looked at the issue adult ADHD and symptomatic adult ADHD prevalence by the 6 WHO regions (4).  Their overall goal was to determine the worldwide prevalence of adult ADHD. They looked at the issue of persistent or childhood onset ADHD and symptomatic adult ADHD with no evidence of childhood onset and estimated the prevalence of those two groups separately.  The pooled prevalence of persistent adult ADHD was 4.6% and for symptomatic ADHD it was 8.83%.  These authors also looked at prevalence by a list of demographic factors, diagnostic criteria, addition to geographic areas as well as the decreasing prevalence by age groups.   

 

Study	Target Population	Prevalence % (US vs Non-US) ranges or pooled
Faraone, et al (2002)	DSM-III ADHD DSM-III-R ADHD DSM-IV	(9.1-12.1) vs. (5.8-11.2) (7.1-12.8) vs. (3.9-10.9) (11.4-16.1) vs. (2.4-19.8)
Polanczyk, et al (2007)	Pooled prevalence estimates of ADHD by geographic location.  N= number of studies in each WHO designated location	North American (N=32)  6% Europe (N=32)  4.5% Oceana (N=6) 4.5% South American (N=9) 12% Asia (N=15) 4% Africa (N=4) 8% Middle East (N=4) 2.5%
Song, et al (2021)	Pooled estimates and ranges of Adult ADHD worldwide by WHO designated geographic areas	North America (N=3) 6.06% Europe (N=10) 7.12% Oceana (N=4) 9.67% South America (N=3) 6.06% Asia (N=1) 25.6% Africa (N=1) 9.17% Middle East (N=2) 16.58%

 

This study raises the issue of whether ADHD can be acquired rather than be a childhood onset illness. The reality is that there are many paths to acquired attentional deficit that have been treated over the course of my 35 years in the field.  The best examples are neurodegenerative diseases, strokes, and brain injuries. Neuropsychiatrists have written about treating the associated cognitive, mood, and motivational deficits with stimulants.  But a more relevant question is whether mechanisms exist that can result in people with none of these acquired brain injuries.  The answer comes from modern genetics. Polygenic risk scores (of all diseases) suggest that there are high risk individuals who show no evidence of an illness as adults. These examples of incomplete penetrance are usually explained as environmental factors, additional genetic dynamics such as aging or protective factors. I see no reason why these factors could not occur in an ADHD genotype after childhood. The other significant genetic factor is spontaneous mutation or as a recent commentator put it: “You don’t die with the genome you were born with.” Psychiatry has focused on familial studies for the past 50 years, but it is likely that significant numbers of most conditions occur as the result of spontaneous mutations rather than strictly hereditary transmission. That is borne out in clinical practice every day.

The authors (1) make the argument that ADHD is not a “scientifically valid” diagnosis. They explain “these symptoms have not been shown to be the result of a scientifically valid disease (adult ADHD) and better explained by more classic and scientifically validated psychiatric conditions, namely diseases or abnormalities of mood, anxiety, or mood temperament.”  Mood temperament is a stretch.  It is rarely commented on in adult psychiatry and then in extreme cases.  It is not contained in the DSM. Part of the reason is selection bias.  Psychiatrists are seeing people who have failed multiple other treatments and I have referred to this as being the treatment provider of last resort. 

Another factor is that ADHD is a quantitative rather than qualitative disorder – that is the cognitive symptoms are at the extreme end of normalcy and it is difficult to draw a line to demarcate illness from normal in many cases. A comparable example from medicine is hypertension.  The cutoff for what is considered hypertension has varied significantly over the decades (9, 10) and even now considers antihypertensive side effects as a qualifier for treatment.  That means that for any 2 people with the same marginally elevated blood pressure only one might get consistently treated. At one point hypertension was considered by some physicians to be a necessary compensatory mechanism that should not be treated (10). On the issue of quantitative aspects of psychiatric disorders in general – dimensional approaches are often suggested as a solution and the question is whether they work any better than the impairment criteria used in the DSM.  That is especially true in a clinical setting where a patient is presenting with a clear problem that they are asking for help with

On the issue of validity, studies have been done demonstrating reliability and validity (8) on both the DSM criteria as well as various rating scales for adult ADHD that are consistent with the diagnosis. There have also been detailed discussions of how to approach the problem clinically (11).  Those discussions include how to differentiate mood disorders from ADHD and how to approach the functional impairment criteria in the clinical interview.

That brings me to the issue of temperaments mentioned in reference 1.  Temperaments have been researched in various contexts in psychiatry over the past decades.  Most psychiatrists of my generation first heard about them on child psychiatry rotations and the work of Stella and Chess. In adults, temperaments are more descriptions of hyperthymia, cyclothymia, and dysthymia and are generally considered in the differential diagnosis of subclinical mood disorders.  The best example is hyperthymia and it has been referred to both as a temperament and a personality. Hyperthymic people are generally high energy, require less sleep, and are social, talkative, and outgoing. They may be very productive and have increased libido relative to their peers. In clinical interviews they may say that their friends think they are “bipolar” and need to be treated. But careful interviewing demonstrates that they lack the symptom severity and degree of impairment necessary for a diagnosis of bipolar disorder.  Ideally the initial interview results in that formulation and the psychiatrist can advise the person about why treatment is not necessary.

Reference 12 looks at the issue of temperaments in a retrospective controlled study of patients being treated with stimulants who were referred to a mood disorders clinic.  The authors acknowledge the selection bias in their study design. I can not think of a better design to pick up misdiagnosed patients than this one. To cite one example – of the 87 amphetamine treated referrals only 50% had a past diagnosis of ADHD. The authors acknowledge that there is no standard way to determine affective temperaments and decide to use the TEMPS-A with a cutoff of 75% of the items. If you are able to find a copy of the TEMPS-A (it is not easy) – you will find a list of 50 true-false questions like “I’m usually in an upbeat or cheery mood.” The questions are reminiscent of the Minnesota Multiphasic Personality Inventory (MMPI) except there are far fewer questions. The scoring guide suggests that the TEMPS-A can discriminate between hyperthymic, cyclothymic, dysthymic, and irritable temperaments. It is validated in the usual ways.  The relevant question is whether any diagnosis made with this checklist would deter you from treating a comorbid condition - like Adult ADHD?  It is one thing to survey a misdiagnosed group with the TEMPS-A and consider the clinical implications, but another to consider the presenting problem possible ADHD and whether it should be treated.

The arguments in reference 2 about overdiagnosis, the existence of adult ADHD, and the idea that ADHD can occur in adults without a childhood diagnosis can be challenged with the facts and references provided here.  The fact that we are in the midst of a multigenerational drug epidemic in an increasingly intoxicant permissive society does not mean that a diagnosis, treatment, or problem does not exist. It does mean that all psychiatrists from the moment they enter practice must exercise extreme caution when prescribing substances that reinforce their own use. 

The most likely cause of overdiagnosis is not because adult ADHD does not exist, not because of drug promotion (most are generic including the non-stimulant alternatives), or because MDs are careless.  There are basically two reasons.  First – the difficulty of diagnosing quantitative conditions. Second – sociocultural factors that exist in the US. Performance enhancement is built on the myth that you can tune your brain (or any organ) with supplements, nutrients, or medications to become a superior human being. The reality is you can alter your conscious state to believe that – but in the case of stimulants it is unlikely. The only real performance enhancement occurs because you can stay awake longer to read more and there is some evidence that your belief system is altered so that you believe you are smarter (14). These are just two of the reinforcing properties of stimulants that can lead to accelerated use and addiction.

That is my brief summary of the complexity of this situation. For more on my approach to adult ADHD (I only treat adults) – see this post.

 

George Dawson, MD, DFAPA

 

References:

1:  Ruffalo ML, Ghaemi N.  The making of adult ADHD: the rapid rise of a novel psychiatric diagnosis.  Psychiatric Times 2023 40(9): 1, 18-19.

https://www.psychiatrictimes.com/view/the-making-of-adult-adhd-the-rapid-rise-of-a-novel-psychiatric-diagnosis

2:  Frances A.  Containing The Adult ADHD Fad — With a Rejoinder from ChatGPT. 9/21/23. 

https://www.psychotherapy.net/blog/title/containing-the-adult-adhd-fad-with-a-rejoinder-from-chatgpt

3:  Faraone SV, Sergeant J, Gillberg C, Biederman J. The worldwide prevalence of ADHD: is it an American condition? World Psychiatry. 2003 Jun;2(2):104-13. PMID: 16946911  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1525089/

4:  Song P, Zha M, Yang Q, Zhang Y, Li X, Rudan I. The prevalence of adult attention-deficit hyperactivity disorder: A global systematic review and meta-analysis. J Glob Health. 2021 Feb 11;11:04009. doi: 10.7189/jogh.11.04009. PMID: 33692893; PMCID: PMC7916320.

5: Polanczyk G, de Lima MS, Horta BL, Biederman J, Rohde LA. The worldwide prevalence of ADHD: a systematic review and metaregression analysis. Am J Psychiatry. 2007 Jun;164(6):942-8. doi: 10.1176/ajp.2007.164.6.942. PMID: 17541055.

6:  Kim DS, Burt AA, Ranchalis JE, Wilmot B, Smith JD, Patterson KE, Coe BP, Li YK, Bamshad MJ, Nikolas M, Eichler EE. Sequencing of sporadic Attention‐Deficit Hyperactivity Disorder (ADHD) identifies novel and potentially pathogenic de novo variants and excludes overlap with genes associated with autism spectrum disorder. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. 2017 Jun;174(4):381-9.

7: McGough JJ, Barkley RA. Diagnostic controversies in adult attention deficit hyperactivity disorder. Am J Psychiatry. 2004 Nov;161(11):1948-56. doi: 10.1176/appi.ajp.161.11.1948. PMID: 15514392.

8: Kooij JJ, Buitelaar JK, van den Oord EJ, Furer JW, Rijnders CA, Hodiamont PP. Internal and external validity of attention-deficit hyperactivity disorder in a population-based sample of adults. Psychol Med. 2005 Jun;35(6):817-27. doi: 10.1017/s003329170400337x. PMID: 15997602.  

9:  Saklayen MG, Deshpande NV. Timeline of History of Hypertension Treatment. Front Cardiovasc Med. 2016 Feb 23;3:3. doi: 10.3389/fcvm.2016.00003. PMID: 26942184; PMCID: PMC4763852.

10:  Kotchen TA. Historical trends and milestones in hypertension research: a model of the process of translational research. Hypertension. 2011 Oct;58(4):522-38. doi: 10.1161/HYPERTENSIONAHA.111.177766. Epub 2011 Aug 22. PMID: 21859967.

11:  Murphy KR, Gordon M.  Assessment of adults with ADHD. In: Barkley RA. Attention-Deficit Hyperactivity Disorder, 3^rd edition.  The Guilford Press, New York, 2006: 425-450.

12:  Mauer S, Ghazarian G, Ghaemi SN. Affective Temperaments Misdiagnosed as Adult Attention Deficit Disorder: Prevalence and Treatment Effects. J Nerv Ment Dis. 2023 Jul 1;211(7):504-509. doi: 10.1097/NMD.0000000000001626. Epub 2023 Apr 11. PMID: 37040539.

13:  Akiskal HS, Mendlowicz MV, Jean-Louis G, Rapaport MH, Kelsoe JR, Gillin JC, Smith TL. TEMPS-A: validation of a short version of a self-rated instrument designed to measure variations in temperament. J Affect Disord. 2005 Mar;85(1-2):45-52. doi: 10.1016/j.jad.2003.10.012. PMID: 15780675.

14:  Ilieva I, Boland J, Farah MJ. Objective and subjective cognitive enhancing effects of mixed amphetamine salts in healthy people. Neuropharmacology. 2013 Jan;64:496-505. doi: 10.1016/j.neuropharm.2012.07.021. Epub 2012 Aug 1. PubMed PMID: 22884611.

 

 

 

 

Heart Rate Variability

 

I have been following heart rate variability (HRV) on my watch and three different apps for the past several years. HRV is defined as the slight variations between R waves in the standard ECG recording.  I have included an example below, illustrating the R-R’ intervals (or RRI) and how they might vary over time.

Since HRV became widely available as a measurement off a watch that is commonly worn by millions of people, the research on this measurement and the variable studied has increased significantly.  For my purposes – HRV is thought to be an indicator of heart health and conditioning and possibly a marker of overtraining – but advice about that varies significantly. Some studies have shown that decreased HRV is associated with an increased risk of arrhythmias.  My recent cardiac ablation and cardioversion seemed to present an ideal situation for further study. 

Before getting into those details the physiology of HRV needs to be considered. The dominant heart rhythm of a normal heart is determined by the sinoatrial (SA) node. This node contains a population of spontaneously depolarizing cells that determine the rhythm and rate of the heartbeat. In addition to the neurophysiology of that cell population several additional factors affect both the rate and HRV.  Primary among them is autonomic innervation from both the sympathetic and parasympathetic systems and their effect at the SA node. Parasympathetic fibers from the vagus nerve modulate slower firing through the neurotransmitter acetylcholine (ACh). Sympathetic fibers increase the rate of firing through the neurotransmitter norepinephrine (NE).  NE has a longer half-life than ACh, but vagal tone is thought to be the most significant determinant of HRV.  That is in line with several clinical observations including lower baseline heart rates in conditioned athletes and higher heart rates in people with less conditioning or in stressful situations.

What happened to my heart rate and HRV during the recent cardiac ablation for atrial fibrillation and subsequent cardioversion?  To answer that question, I had to figure out how to get the data off my Apple Watch 5.0.  The only approach I could find was to downloaded all of the collected Health App data as a CSV file and then plot it in Excel.  There are some online sites that you can download the data to and then use the remote software for plotting, but I preferred to retain control over the data. If you decide to do that and have several years of data like I did – it takes a long time.  It took about 5 hours in my case to download about 1G of data to a zip file.  From there it is easy to open that file with Excel or other software and do the plots. A useful addition to the Health App would be able to download specific time intervals.

I have done 2 plots so far based on average daily HRV and hourly HRV as shown below.

 The plots are interesting because it clearly shows an effect from the ablation, a 96-hour period of atrial fibrillation and atrial flutter, and the cardioversion. At the minimum the baseline HRV drops to a different baseline after the ablation. That is followed by a significant spike with the recurrence of afib/flutter.  And then there is a return to the lower baseline after the electrical cardioversion.  I rarely had any significant episodes over the course of a year and whenever I went back and reviewed HRV it was not significantly changed. Since all those episodes were typically less than 2 or 3 hours it may not have been long enough to see an HRV effect.  Conversely spikes of 50-100 msec in the HRV recording were common and not associated with arrhythmias. In the case of the post ablation period the sustained rates were associated with spikes, but since atrial flutter is regular, the associated R-R’ intervals probably showed a more characteristic HRV.

I would expect to see an increase in vagal tone and therefore HRV just related to the sustained high rates over 4 days. If increased vagal tone correlates with increased HRV that does not seem to be the case in these graphs. The graphs also seem to indicate to me that there may be a structural element to HRV – either in the anatomical configuration of the conducting cells, their altered physiology, or a combination.

The main implication for me at this point is to cautiously restart my conditioning efforts and see what impact that has on the HRV baseline.  A second question is whether my HRV will approach the pre-ablation baseline.  Electrocardiograms (ECG) may provide some clues in that direction.  I have listed them below for references. Significant changes occurred in the immediate post ablation ECG and the post cardioversion ECG.

An additional thought is whether non linear analysis of the RR intervals would yield more information and easily interpretable graphics. I have used some of these attractor plots in the past and also applied them to single electrode analyses of normal controls and patients with Alzheimer's disease. In terms of ECG analysis - see figure 5 in reference 2. In terms of theory - these attractor diagrams also imply changes in biological complexity at either the structural or functional level - see the diagrams at the bottom of this post. 

 

George Dawson, MD, DFAPA

ECG time course (1 -> 5 are in sequence):

1.  Baseline - preop ECG 

2.  Post ablation ECG (following day):

3. Post ablation ECG - note anterior T wave changes thought to be consistent with procedure.

4.  Precardioversion ECG showing atrial flutter at a high rate (day 5 of this arrhythmia; post op day 14).

5. Post cardioversion ECG showing NSR but flipped T waves in V1-V3.

6. ECG follow up 2 weeks after cardioversion showing T wave normalization in anterior leads.

Heart Rate Variability

Some recent recovery in HRV after a long period of low numbers in the 7-37 msec range following ablation and cardioversion.

References:

 

1:  Fojt O, Holcik J. Applying nonlinear dynamics to ECG signal processing. Two approaches to describing ECG and HRV signals. IEEE Eng Med Biol Mag. 1998 Mar-Apr;17(2):96-101. doi: 10.1109/51.664037. PMID: 9548087.

2:  Nayak SK, Bit A, Dey A, Mohapatra B, Pal K. A Review on the Nonlinear Dynamical System Analysis of Electrocardiogram Signal. J Healthc Eng. 2018 May 2;2018:6920420. doi: 10.1155/2018/6920420. PMID: 29854361; PMCID: PMC5954865.

3:  Aston PJ, Christie MI, Huang YH, Nandi M. Beyond HRV: attractor reconstruction using the entire cardiovascular waveform data for novel feature extraction. Physiol Meas. 2018 Mar 1;39(2):024001. doi: 10.1088/1361-6579/aaa93d. PMID: 29350622; PMCID: PMC5831644.

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) 

 

 

Happy Labor Day 2023!

 

Over the years of writing this blog I have put out a Labor Day message to describe any progress in the physician workspace in the past year.  The practice environment for physicians has deteriorated significantly over the past 3 decades and those changes are generally locked in by the healthcare business managers backed by both Congress and state governments. I have used the following graphic several times on this blog to illustrate what happened over specific time frames and it is probably time to add some additional details.

The impact of managed care on medical practice has been clear for the past 30 years.  In many cases that model is being adopted by physicians in private practice settings. For example, it is common now to see a specialist initially but in follow up see one of the physician extenders working with them. That can make health care a lot less personal and it leads me to think about the reason why physicians are trained to provide continuity of care in the first place.

But even more than that issue is the explosion of online services provided for flat rates that focus on seemingly basic problems in exchange for payment. On my streaming services that typically involves a company that offers prescriptions for depression, anxiety, hair loss, and erectile dysfunction.  A second company offers beta blockers for performance anxiety.  Given the side effect potential for these medications – I am curious about how comprehensive the initial evaluations are and the follow up visits.

I was recently hospitalized and had a first hand look at what the modern hospital workplace looks like.  When I was in training there were discrete teams by specialty and they consisted of physicians at all levels of training.  A typical team might have 1-2 med students, 1-2 interns, a resident, a senior resident or fellow, and the attending. The work load would depend on whether your service admitted people to the hospital (typically internal medicine, surgery, neurology, renal medicine, cardiology, psychiatry) or consulted to those teams (infectious disease, endocrinology, pulmonology, rheumatology, cardiology, psychiatry).  The admitting services were the most intense because of irregular admissions and complicated unstable patients. Teams generally had places to meet, where patients were presented to the attending and there were formal didactics. Bedside teaching occurred on rounds.

During my hospitalization, I was not seen by a single physician in my room. When I went out into the hallway, both sides of the hall were lined by people facing computer screens. There was one consulting team standing outside a patient door – visible only because it was obvious the fellow and attending were discussing cases. The level of crowding was striking and it left me with the impression that all these people could not possibly be physicians.  Managed care shaped the form of these teams and who was in that hallway. First, they eliminated the usual admitting services and replaced them all with hospitalists. Then they replaced at least some physicians on those teams with non-physicians. Those moves benefit business decisions but I have not seen a single adequate study on the impact it has on medical care.

Training physicians in hospitals has typically involved hands on learning, consultation from senior and expert physicians, and active learning environment, and in many cases the opportunity for research.  All these areas need to be preserved in the practice environment in order to stimulate practicing physicians to maintain high standards. An environment that leads to burnout, sleep deprivation, and moral injury is not adequate to the task. The question always has been whether physicians have any kind of leverage that could lead to appropriate modifications. That question has never been put to the test and in fact, healthcare organizations in the United States generally flaunt their power over physicians rather than attempting to negotiate with them.

Will a union make a difference? My experience with unions started out in my family of origin.  My father was a member of the Brotherhood of Locomotive Firemen and Engineers (BLFE). He worked as a locomotive fireman and then an engineer.  He had to be a union member in order to work.  He generally was not very happy about it. The railroad industry was run on a seniority system and as railroad utilization decreased – younger workers like my father had a difficult time finding job assignments. Even though they were technically employed by a railroad and reimbursement for the work was good, it seemed like only the most senior engineers benefitted to the point that they could make a good living.  As a result, the contracts negotiated by the unions did not mean that much to my father. He also tended to see the union as corrupt because, the union officials clearly made far more than he was making trying to work in their system.  Railroads unions were also compartmentalized - so a strike against one railroad did not mean a strike against all.  As a result, workers from the railroad that was the object of the strike could work for competing railroads during the strike. If similar rules apply to physicians a uniform practice environment is no guarantee, but the onerous aspects might be eliminated.   

Unions for physicians and residents are becoming increasingly popular but they have more restrictions that in a blue-collar environment. The National Labor relations Board (NLRB) enforces the National Labor Relations Act (NLRA) and decides what public sector employees can form unions (1). Independent contractors, supervisors, and managers are excluded because the focus of the act was on laborers. The general categories are loosely defined so it takes an NLRB investigation to determine who can be in the union. Tenure and tenure track employees were eliminated by a Supreme Court ruling. Only salaried employees who do not do a significant amount of supervision are allowed to be union members. If a union is allowed, the goals in terms of collective bargaining, representation, and impact on hospital policies need to be determined.  Although the momentum for unions is building, there is a considerable amount of inertia from the managed care era. During that time, we had many physicians who were eager to escape a deteriorating practice environment to become administrators and basically enforce business policies. It remains to be seen if unions can have a favorable impact on local health care policy and practices – but just establishing more is a step in the right direction.    

More resistance to Maintenance of Certification by various boards and the American Board of Medical Specialties is also growing. I went to the alternate system National Board of Physicians and Surgeons (NBPAS) certification in 2018 and have not looked back. At the same time, I realize that I was outside of any system demanding that I recertify through an ABMS board and as a result – in a unique situation relative to younger colleagues. A petition was started in July to end ABMS MOC and so far there are 20,000 + signatures. There was an initiative in the APA to stop MOC about 10 years ago, but the administrative process prevented it from being put on a ballot. The basic problems with MOC is that there is no evidence it is necessary for quality care, in fact most health care organizations have abandoned true quality programs. Second, it is not reflective of clinical practice. Most physicians – even generalists end up in a niche and focus their educational efforts and mastery in that area. It makes no sense to keep taking examinations outside of that area. Third, it is a substantial time and financial commitment and it clearly generates a lot of revenue for ABMS specialty boards. Fourth, there is some suggestion that MOC should be tied to state licensing (Maintenance of Licensure or MOL). This would allow states and health care organizations even more power in controlling physicians – even during their private times when they would need to spend time studying for barely relevant examinations. Elimination of MOC is another positive step in the direction of restoring a more reasonable practice environment.

Beyond a better practice environment and what it takes to make that politically – the profession of medicine is at stake.  I have written about a lot of the technicalities – but this is deeply personal. Going to medical school and studying medicine was the best thing I could have done with my life. By identifying with the practicing physicians in my various training programs I learned how to live and breathe medicine and psychiatry 24 hours a day. Always thinking about it, never far from a journal article that I wanted to read, and always focused on how that translated to clinical practice – usually a very hard problem I was seeing in practice. From the very first patient contact, the importance of communicating with people in an empathic, unhurried and comprehensive way was obvious.  We cannot afford to lose that transformative effect that medicine has on people.  We cannot dumb things down for the business world and make human biology less complex. I know there are many docs out there that think like me.  Whether we can unionize or cancel MOC – we can never lose sight of the fact that we need to preserve a transformative profession for the sake of future generations of physicians and their patients.

 

 

George Dawson, MD, DFAPA

 

References:

1:  Bowling D 3rd, Richman BD, Schulman KA. The Rise and Potential of Physician Unions. JAMA. 2022 Aug 16;328(7):617-618. doi: 10.1001/jama.2022.12835. PMID: 35900755. 

The True Big Pharma Backers Show Themselves

 

Here is a hint – they are not psychiatrists or even physicians.  They are Republicans.  That may come as a shock to those of you who have absorbed all of the pharma conflict of interest stories about physicians over the past 20 years. Psychiatry in general was selected for much of that criticism. The average physician in the US had no significant conflict of interest even when trivial compensation like meals during continuing medical education (CME) courses were tallied. Some members of Congress even went so far to investigate some psychiatrist’s personal employment arrangements to point out any potential conflicts of interest when it came to pharmaceutical manufacturers.

Today we finally have some clarification on who really backs Big Pharma and wants to assure their large profits.  It should come as no surprise that it is Congress – specifically members of the pro-business GOP.  For years, Congressional conflict-of-interest has been sanitized by their disclosures as if that somehow prevented them from passing pro-Pharma legislation and regulations. For the record the amount of lobby money to the major parties varies from year to year.  For 2022 a total of $26,297,445 was donated from the pharmaceutical industry with $15,175,518 to the Democrats and $10,994,723 to the Republicans. That is an average donation of $29,159 to $105,910.  By contrast the Open Payments site recording payments to health care professionals claims that drug and medical device companies gave physicians $12.59 billion in 2022, but they are counting funds used to pay for research as well as profits from ownership of patents and medical devices (a total of $8.87 billion).  Looking at general payments alone, the physicians receiving any type of reimbursement averaged about $441. The current reporting rule is that any amount exceeding $10 or an aggregate of $100 in the case of meals must be reported.

I previously asked the question whether a slice of pizza given to a doctor at grand rounds was more likely to get results for the pharmaceutical industry than the average donation to Congress ($46,579 at the time).  I made the point that despite the continuous criticism of psychiatrists, they happen to be way down on the list of physicians getting these donations with about 37% receiving general payments and 3.6% receiving payments totaling more than $10,000.

But all the corruption by trivial payments discussion was based on shaky research. It is quite easy to demonstrate that physicians want to try new drugs as they come into the marketplace and show that marketing efforts correlate with prescriptions. We had a No Free Lunch movement to prevent corruption by pizza slices. We had a great deal of agitation about ghost writers, pharmaceutical companies not publishing negative studies, faulty research, side effect reporting, etc. Almost all of that involved psychiatry and often several self-appointed critics from the field.  There are undoubtedly problems with clinical trials in all specialties, but during that 20-year span from about 1998-2018 it seemed as if there was an active conspiracy to sell psychiatric medications.  To some extent that continues but it has less legitimacy in the field particularly since drug detailing and sales have been eliminated from most clinics and hospitals.

All of that commotion was probably good cover for Congress who was actually receiving payments that could make a difference.  And during that time pharmaceutical companies recorded record profits.

What is different now?  The Biden administration has decided that it wants to negotiate prices for Medicare Part D prescriptions. They are on solid ground. The Veterans Administration (VA) negotiates drug prices and has 399 drugs on their formulary.  A GAO study showed that they paid 54% less per unit than Medicare. HHS has already selected the drugs that will be negotiated in the initial round and as expected most of them are the high expenditure drugs in the plan.

The Republicans claim that these negotiations will decrease access to care and raise drug prices although there is no evidence that the VA negotiations have done that. They also claim that there will be reduced innovation, research and development, and job losses. They seem to have missed the overall picture that pharmaceutical companies in other countries succeed – even when there are negotiated prices with the health plan in those countries. Of the top 15 pharmaceutical companies in the world 8 are in the United States and the remainder in Switzerland, UK, France, Denmark, and Japan. The numbers given for fewer new drugs, fewer new indications, and drop in R&D spending seem highly speculative to me.  For example, the drop of $663B in R&D spending is the equivalent of about half of the total revenue for the top 15 companies.   I seriously doubt they are spending that much on R&D. During the 20 year period that I am referring to companies left entire therapeutic areas and it was common knowledge that marketing was going to drive pharmaceutical sales. There is an entire section about decreased jobs.  Are the Republicans really suggesting that Americans should pay (by far) the highest amounts for prescription drugs in order to fund a jobs program? And finally, the suggestion that the plan is “legally dubious”.  Apparently Congress is set up to help industries optimize profits rather than protect people who can’t pay a thousand dollars or more for a Medicare Part D copay.         

This post also has implications of pharmacy benefit managers or PBMs.  You remember them?  They are the business entities charged with “managing” your pharmacy benefits allegedly to make medications most “cost effective”.  PBMs make about $315 B annually for doing nothing more than managing prescription drug programs for employers and other large entities with health insurance programs. In practice they are a price multiplier rather than a price reducer.  PBMs control the spread or difference between what the insurance pays for a medication and what they reimburse pharmacies. In some cases, their reimbursement for pharmacies is lower than the actual cost of the medication. Since they are leveraging large number of patients, local pharmacies typically do not have much of a choice if they expect to do business – even though an affiliation with a PBM is draining. PBMs can own their own pharmacies and reimburse those pharmacies more than community pharmacies.   For a physician the most onerous aspect of PBMs occurs with prices for drugs and their positions on formularies for hospitals and clinics.  A formulary is a restricted list of medications available for physicians in that health plan to prescribe for their patients.  That can mean a patient has to change their prescription for it to be covered or some newer medication may not be covered at all.  During negotiations with manufacturers, PBMs can get a rebate from the manufacturer if they get their product exclusively in the formulary. That rebate is kept by the PBM rather than shared with the people paying for the drug.  

The pharmaceutical landscape is a minefield that is set up to optimize corporate profits. Pharmaceutical companies are essentially guaranteed high margins based on patent exclusivity and high prices.  PBMs generate a lot of revenue, add no value, and many pharmacists would add are a drain on their businesses. Let's face it - these businesses like most of healthcare in the US were essentially invented in Congress.  If they are not a recipe for making money - I don't know what is.  The Medicare Part D price negotiations through the Inflation Reduction Act is the first bright spot I have seen in a long time.  Republicans clearly want to maintain the status quo and that means extremely expensive medications and copays for anyone who is in the Medicare Part D coverage gap. If you were ever surprised by one of these copays like I was recently – support the Biden Administration’s attempt to control high drug prices.

George Dawson, MD, DFAPA

Supplementary 1:  An obvious point that I forgot in the original post in terms of backing Big Pharma is the idea that any physician would back limited access to a needed medication because of financial (rationing) restrictions.  Toward the latter half of my career, if anything physicians have made extraordinary efforts to get medications for their patients including having to manage large collections of samples and try to supply some patients from those samples.  Incredibly - some critics saw that as another perk from pharmaceutical companies that was corrupting physicians.  Some politicians on the other hand who are getting very large donations from pharmaceutical companies have no hesitation in suggesting that American patients should continue to pay exorbitant costs for pharmaceuticals - even if it means not being able to afford medication and compromised health.   

Supplementary 2:  Must watch video on regulatory capture or how Congress profits from disrupting free markets and establishing monopolies. Pharma and electronic health record (EHR) companies are cited examples, but there are additional examples including broadband and AI:

 https://www.youtube.com/watch?v=F9cO3-MLHOM