NEJM Case: Brain, Heart, and Parsimony

Cardiology factors prominently in psychiatry and psychiatric care. I have been fortunate on many occasions to work with psychiatrists who were also cardiologists and to have access to outstanding cardiologists as consultants. That gave me a great appreciation for what was possible in the detection treatment of cardiac problems. It also help me appreciate the importance of treating psychiatric disorders in patients with cardiac problems. The recognition that some medications can cause problems and the need for ECG screening was another change in psychiatric practice. Prior to that knowledge, there were some medications that delayed cardiac conduction to the point that they are no longer used.

One of the commonest scenarios I currently see is at the interface of anxiety and the effect it has on the heart. About 20 to 30% of the people I see have severe anxiety and panic attacks. About two thirds of them have made at least one trip to the emergency department because they thought they were experiencing a heart attack. They are generally young people with limited cardiac risk factors. When I asked them about the symptoms that led them to the ED, the most common answer is “my heart was pounding out of my chest and I thought I was having a heart attack”. Palpitations are another common symptom. They are harder to get at and people who have talked to cardiologists are better at describing them. I demonstrate by making an irregular thumping noise on my chest with my hand to indicate what it might feel like. The associated symptoms of panic attacks like swelling, lightheadedness, dizziness, chest tightness, shortness of breath, hyperventilation, and dizziness all reinforce the thought of a heart attack. Once the ED staff determine the patient is having a panic attack the way they are educated is critical in reducing ongoing symptoms. But that is another story.

An associated symptom in anxiety is what I like to call “cardiac awareness”. It happens in anxious people whether they have an anxiety disorder diagnosis or a stressor making them anxious. Laying in bed at night waiting to fall asleep many people can sense their heart beating without taking their pulse. They can sense other pulse points in the body and frequently they can sense large pulsations. This is a normal physiological process but anxiety can lead to a focus on it. I also lead to attaching other meetings to it such as the occasional palpitation is seen as evidence of heart disease leading to increased anxiety. In that situation it becomes very difficult to sleep leading to more anxiety and frequently - a faster heart rate the next day.

Cardiac pathology can compound the problem because there are various conditions like atrial fibrillation that can lead to people paying much more attention to their heart rate and rhythm. Atrial fibrillation is interesting in that regard because there are two management strategies. In a rate control strategy the person is given a medication to generally keep their heart rate less than 100 bpm but the rhythm could still be irregular and experienced as frequent palpitations. In a rhythm control strategy the person is either given a medication or treatment to maintain a regular sinus rhythm and palpitations would be much less frequent to nonexistent. Current thinking on treating atrial fibrillation is that the outcomes of both strategies are equivalent in terms of mortality but that patients with a rhythm control strategy rate themselves as having a higher quality of life.

That brings me to the New England Journal of Medicine case listed in the references below.  This case continues a recent trend in incorporating more psychiatric expertise into these cases with psychiatrists as discussants. The patient was a 62-year-old man with depression and anxiety. The depression dated back 15 years with onset after he learned that his wife had cancer. His wife eventually died. Whichever psychiatrist are about seven years and eventually found that citalopram and clonazepam are effective. He continued with his primary care physician and eventually discontinued the citalopram. He was seen by one of the discussants due to recurrent anxiety depression and lethargy. Vital signs were noted to be abnormal with an irregular pulse of 130 bpm blood pressure 108/75. An ECG was done that showed new onset of atrial fibrillation. 

Echocardiography showed an enlarged left atrium and left ventricle, low normal LV ejection fraction, mild left ventricular hypertrophy, and no valvular disease. The subsequent ECG showed a prolonged QTc interval of 466 ms. At a subsequent visit he had an additional significant stressor also had started to binge drink. At that time he had weekly panic attacks that correlated with increased alcohol intake. When he was seen in the psychiatric clinic had weekly panic attacks that consisted of “racing heart, lightheadedness, restlessness, shaking, and generalized weakness and so the episodes lasted for several hours. A family history of depression and suicide was noted. He was noted to be drinking 4 to 6 standard drinks per week with occasional binges. Aripiprazole was added to the clonazepam and citalopram.

The patient subsequently had a near syncopal episode three weeks later I was noted to be hypertensive and tachycardic. The ECG showed atrial fibrillation and sinus pauses of six and seven seconds. A permanent pacemaker was placed in the metoprolol was discontinued.

He was noted to be improved on the psychiatric medication changes but the metoprolol is discontinued because of fatigue. Three weeks later he had increasing anxiety and the feeling that his heart was racing and “thumping” in his chest and that he was excessively worried. They aripiprazole was increased at that time.

Like most of these cases there is a differential diagnosis exercise included and the discussant in this case is a psychiatrist.  The exercise focuses on the fact that the central symptoms in this case-anxiety, palpitations, racing heart, restlessness, and fatigue are not specific for cardiac or psychiatric diagnosis. In fact all DSM diagnoses included criteria to rule out any medical causes of the syndrome. In this case all the usual suspects are discussed. From the medical side hyperthyroidism, return atrial fibrillation, dilated cardiomyopathy, Torsade de pointes, and rare medical causes are discussed. The duration of the patient’s symptoms rules out a lot of the acute causes. From psychiatric standpoint panic disorder, substance intoxication, and substance withdrawal were the primary considerations. The discussant Dr. Chen uses the term that we don’t hear enough of lately and that is parsimony specifically “The best diagnosis would parsimoniously explain the patient’s symptoms and the time course of his illness”. He concludes that there is a clear correlation with discontinuing metoprolol and experiencing recurrent atrial fibrillation.

From a cardiology standpoint the decision was made to improve rhythm control with sotalol and the rationale for choosing that agent was provided. He experienced a decrease number of episodes of atrial fibrillation that he was correlating with anxiety.

The discussion highlights the correlation of anxiety with atrial fibrillation. That anxiety is a product of experiencing the palpitations and also can be an etiological factor in the episodes of atrial fibrillation. Depression and anxiety also predict who experiences more severe symptoms of atrial fibrillation. Patient medications also discussed in terms of the prolonged QTc interval. The authors comment on the FDA warning about QTc prolongation with higher doses of citalopram. They point out that although citalopram prolongs QTc interval more than other antidepressants there is little evidence that it leads to torsade de pointes or sudden cardiac death. They also point out that the literature shows that when this warning led to decreasing the dose of citalopram the result was no worsening of cardiac outcomes but less than optimal psychiatric outcomes including more frequent hospitalizations and increased sedative hypnotic prescriptions.

Overall this was an excellent discussion of the cardiology-psychiatry interface. Psychiatrists are likely to see increasing numbers of patients with atrial fibrillation. I currently see number of patients who are taking multiple cardiac medications. Any patient with this degree of complexity it is important to discuss the possibilities in order to determine the likely sequence of events. In patients with cardiac risk factors who are hypertensive and appear to be describing panic attacks caution is necessary to make sure that there are no underlying cardiac conditions that need to be attended to. As illustrated in this case I have seen patients with severe panic attacks (but no atrial fibrillation) due to the abrupt discontinuations of metoprolol. In patients who have recently discontinued antihypertensive therapy and have panic attacks - clarifying whether there has been any exposure to beta blockers is important.  

Another relevant factor in this patient's demographic is that the sympathetic tone of the peripheral nervous system in humans seems to increase with age. That may predispose older populations to tachycardia, palpitations, hypertension, and anxiety either directly or indirectly by experiencing the cardiac symptoms.

Being able to make an assessment and determination of patient stability, whether or not they need urgent care, what further testing is needed, and what further referrals are necessary is a skill that every psychiatrist should have.

George Dawson, MD, DFAPA

Reference:

1: Chen JA, Ptaszek LM, Celano CM, Beach SR. Case 9-2019: A 62-Year-Old Man with Atrial Fibrillation, Depression, and Worsening Anxiety. N Engl J Med. 2019 Mar 21;380(12):1167-1174. doi: 10.1056/NEJMcpc1900140. PubMed PMID: 30893540. Full Text

See also for the critical references in this case.



Graphics Credit:

The human heart line drawing in the above graphic is from Shutterstock per their standard agreement.

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).


         

Waiting To Call An Ambulance Is Not Much Of Plan

I don't like to write about my own health problem - but it is a ready example and I already have another blog about it so here goes.  I also don't need to worry about violating my own confidentiality.  It involves a personal medical problem called paroxysmal atrial fibrillation.  I have consulted 5 different Cardiologists and the rhythm problem is not due to valvular or coronary artery disease.  It is probably due to excessive exercise - specifically exercise with sustained high heart rates.  After a period of frequent episodes, I started taking a generic brand of flecainide 4 1/2 years ago and have not had an episode since.  During that time I have had two episodes of influenza and 1 episode of acute bronchitis requiring prednisone therapy with no recurrence of atrial fibrillation.

Lately I have been seeing patients and about 40% of them have an upper respiratory virus and the various complications.  I knew it was just a matter of time.  Earlier this week I developed a cough, sneezing, facial burning, and a headache but no additional flu like symptoms.  It is not flu season here, but respiratory viruses abound.  Monday, Tuesday and Wednesday morning - I was awakened at 4 AM with an intense flurry of palpitations.  Taking the pulse showed a pattern of 4 or 5 regular beats followed by what seemed like a pause or dropped beat that I recognize as the early transition (I think) to atrial fibrillation.  In each case I drank a large glass of water, paced for a minute or two and I was back in sinus rhythm - the palpitations resolved.  Initial BP check was about 130/80 with a pulse of 88 rapidly back down to 110/70 with a pulse of 58.  The last readings are my typical baseline and I check them four times a day.  I know how much physical, mental, and emotional exertion affects those readings and I try to stay cool.

When it happened Wednesday, I decided to do the responsible thing and take the day off of work and see my primary care physician.  He did a physical exam, ordered labs and an ECG.  Everything was normal.  That is my ECG from that clinic visit at the top of this post.  It is normal sinus rhythm with a slight bradycardia (less than 60 bpm).  An interesting homage to artificial intelligence is that the ECG machine communicated with the electronic health record (EHR) and determined that there was no appreciable change between this ECG and one I had done 10 months ago.  The cardiologist is out of that loop.  The bottom line is that the tests were all negative and the plan was to see what happened and consider a Holter monitor if it persisted.  A Holter monitor in this clinic is a 48 hour recording of the ECG looking for discrete events that might suggest a cause of the rhythm disturbance.  It also allows the patient to mark any episodes of subjective disturbance on that record.

Yesterday morning I felt a little tachycardic at about 5 AM and got up and checked.  Heart rate was 66 and blood pressure was fine.   This AM, a flurry of palpitations wakes me up.  They are gone in two minutes after pacing and drinking water.  There was no chest pain or lightheadedness.  In fact when I had the initial episode about 10 years ago, I was speedskating and my heart monitor showed a rate of well over 200 bpm.  No chest pain or lightheadedness at that time and I drove to the hospital and told them I was in atrial fibrillation.

Today I respond to my primary care physician's note though the EHR and describe what happened.  I recall that he is not in, so I go back to the EHR,  agree that I can be billed if this is not a problem that I have been seen for in the last 7 days and attempt to cut and past my note to my primary care doctor into a separate email to his team.  The EHR cuts me off because it says that I can only use 255 characters.  It is the Twitter of EHRs.  I edit it down and send it - no response to my request for the Holter monitor.  I call the clinic and get on the phone with a triage nurse.  The conversation goes something like this (not a transcript):

Me: (Relating the history and Holter monitor request).
Triage RN:  "Well what is the emergency here?  It is Friday afternoon, there is no way that we are  going to get a Holter monitor today.  It will be Monday at the earliest. Your doctor can call it in then"
Me (a little steamed): "Maybe you could suggest criteria that I can use to call an ambulance."
Triage RN: "What?"
Me: "You know - when I wake up from a deep sleep with this arrhythmia at 4AM tomorrow morning, what criteria should I use to decide when to call an ambulance?"
Triage RN: "I did not know it was still happening."
Me: "It happened this morning.  That is why I e-mailed and called you.  That is why I stayed home from work."
Triage RN: "Well in that case I will run it by one of the attendings who is here and ask them about what should be done."

After another call back to get more of the usual information about cardiac symptoms, the Triage RN called again and connected me with the Holter Monitor tech.  I can apparently get in next Wednesday.  He told me the entire procedure would take 5 minutes so I would only have to miss a half day of work instead of a full day.  I did not pursue the obvious "Well why can't I just drive down there now and have it put on."  Everyone must be scheduled.  Schedules must be adhered to.

So that is where it stands tonight.  All of the bullshit that passes in the press for medical news does not apply.  There is no IBM Watson computer out there that knows more than I know about this condition or how to treat it.  There is no personalized medicine.  I have not encountered a single cardiologist interested in the genetics of atrial fibrillation or why I might have it.  Most  physicians assume I have neglected hypertension or have done something wrong with regard to my self care and therefore deserve it.  I still encounter physicians who doubt that I have never smoked a single cigarette in my life - even though it is true.  Hard to believe that somebody could bring this on by excessive exercise.  Isn't exercise supposed to be good for you?

I am probably being overly dramatic.  This is most likely a benign atrial arrhythmia.  On the other hand - why am I so certain if my physician wants another Holter?  I did a Holter and a longer event monitor 5 years ago.  I run a heart rate of 130 bpm during 4 hours of exercise per week and have tolerated a sustained heart rate of 140 bpm from a medication side effect - calmly pacing and taking incremental amounts of beta blockers to slow it down.  The final instructions from the triage nurse were to get to a hospital if a sustained heart rate of 120 bpm or greater and call an ambulance if chest pain.

Personalized medicine in the early 21st century is in many ways inferior to medicine the way it was practiced in the 20th century.  In those days, there may have been an interested physician who said: "Spend a night on telemetry and we will see if we can capture the beats and figure out what to do about it."  I saw those people being admitted when I was a medical student and an intern.  That was before you had to be dying to get into a hospital and the admission rules were dictated by case managers.  In those days personalized meant a long term personal relationship with a real physician who  could make things happen.

Now like me - those people are sitting at home waiting for something to happen and guessing about when they should call an ambulance.


George Dawson, MD, DFAPA




Disclaimer:

Don't try any of this at home.  This is not medical advice.  Only your personal physicians and consultants can give you that advice.