Back in 1981 when I was 27 years old and living in the quaint suburban Metro NYC town of Rockville Centre on Long Island, I came home from work from yet another long day in the NY banking world and thought I was having a heart attack. My wife wasn’t home so I drove myself the mile to Mercy Hospital to the ER, where they put me on a EKG machine. Within the hour, a young ER resident came to me and said with no small amount of sarcasm that everything was normal and that I had probably just had an anxiety attack. He couldn’t help himself from telling me that a clue in the future was that if you’re well enough to drive yourself the the ER, the chances are that you’re not having a heart attack. In those days we had a bank doctor (Dr. Carl Nolte…rest his soul) who had been a noted cardiologist before he had had a massive coronary on stage at the annual American College of Cardiology convention. He became my personal doctor since I was young rising star at the bank. He spent a good deal of time with me, specifically on the issue of my heart health, which was fine, but my size always made people wonder. Then in 1988, after a client dinner in the City (I had a not-so-light repast of fettuccine Alfredo), I was on my LIRR train home when I had what I was certain was a heart attack (chest pain, shortness of breath, profuse sweating and a sense of foreboding). Dr. Nolte checked me out the next day and sent me for a battery of tests with a raft of specialists. After six months and multiple similar attacks, we finally figured out that what I had was severe gall bladder disease. I went right to St. Vincents for surgery. This was before arthroscopy, so I have a 9” scare across my gut where the surgeon put both his hands in me. Even though I was seen before surgery by the head of cardiology, when I came out I was told by the recovery room nurse that I had gone into arrhythmia and had to be shocked back into sinus rhythm. When I asked the cardiologist what had happened, he shrugged and said it was probably a bad interaction between the anesthesia and the Tagamet I was on. Was there any reason for concern? Absolutely not, shit just sometimes happens in surgery, he said.
Arrhythmia can stem from many sources, broadly grouped into structural, electrical, and lifestyle/systemic causes. Structural/cardiac causes are the most common, namely coronary artery disease, prior heart attacks (scar tissue disrupts electrical pathways), heart failure, cardiomyopathy, and valvular disease, all of which alter the heart’s architecture in ways that interfere with normal electrical conduction. Electrical/congenital causes of all kinds exist with inherited defects in the heart’s ion channels that generate the heart’s electrical signal. If there are systemic and metabolic triggers involved, they are frequently reversible with electrolyte imbalances (low potassium, magnesium, or calcium are classic culprits), thyroid disorders (both hypo- and hyperthyroidism), sleep apnea, and diabetes all increase arrhythmia risk. Lifestyle factors also play a significant role with things like excessive alcohol (“holiday heart” syndrome), stimulants like caffeine or cocaine, obesity, and chronic stress can all provoke or sustain arrhythmias. Medications and substances (particularly in ill-managed combination) are an underappreciated cause. Many drugs, including some antiarrhythmics themselves can be proarrhythmic or bring on arrhythmia. Inflammation and infection, myocarditis, pericarditis, Lyme disease, and COVID-19 have all been associated with new-onset arrhythmias. Finally, the autonomic nervous system matters a great deal. Many arrhythmias have multiple contributing factors simultaneously, which is why workup typically involves an EKG, Holter monitor, labs, and sometimes imaging.
Of all of those indications, I only had and still have one…the most obvious one…obesity. I went to two Pritikin Clinics for two-week stints to lose weight and then in 1997 I sent myself off to the Duke University Weight Loss Program for a month. Duke prides itself in its medical capabilities, so patients in that Program are assigned a doctor to suss out any and every issue their patients may have. My doctor was a slender and very diligent young woman who was sure I should have a coronary issue. She even sent me for a nuclear medicine thallium stress test. She seemed almost disappointed to find that I had no coronary issues. She was equally stumped that I had genetically low cholesterol, so my lipid profiles always came back very clean. Since then, I have worn a heart monitor, I have had echocardiograms (one done very recently showing no problems) and I go regularly to Lifeline Screenings that show no significant plaque buildup in my peripheral or carotid arteries (thank you, genetically low cholesterol). It seems that over and over again the vehicle establishment is sure I must have a coronary weakness and they just keep coming up short finding anything…though they keep trying.
When I recently went to the ER with my TIA scare, they took my vitals and thought I might have AFib, so they took an EKG and then told me that all looked well. But all my GP needed to hear was the word AFib and I was back in the medical system’s “this guy must have some coronary issues” corner, so she wanted me to wear a heart monitor to check. I wear an Apple Watch, so I just did a quick check on the ECG app. I did it twice to be sure and both times the result came back “no evidence of AFib.” Atrial Fibrillation (AFib) means the upper chambers of the heart (atria) are firing chaotically instead of in a coordinated rhythm. The result is an irregularly irregular heartbeat with no consistent pattern at all. The AV node gets bombarded with hundreds of electrical impulses per minute and passes them to the ventricles in a random fashion. And then there were another favorite…PVCs (Premature Ventricular Contractions), that are extra beats that originate from the ventricles themselves, rather than following the normal electrical pathway down from the atria. On an EKG they appear as wide, bizarre-looking complexes that come earlier than expected and are followed by a compensatory pause. Together, AFib + PVCs means that the baseline rhythm is already chaotic (AFib), and on top of that, the ventricles are occasionally firing on their own out of sequence. It can be tricky to interpret because AFib already produces an irregular rhythm and PVCs are identified by their characteristic wide, oddly-shaped waveform standing out against the background irregular beats. The combination can sometimes cause palpitations, lightheadedness, or a sensation of skipped or extra beats…none of which I have. The clinical significance of AFib (with or without PVCs) depends on their frequency and context. To begin with, occasional PVCs in AFib are common and often benign. In the setting of structural heart disease or heart failure, frequent PVCs carry more weight, but the underlying AFib itself is usually the primary management target (rate control, rhythm control, anticoagulation for stroke risk, etc., etc.). The combination is something a cardiologist would want to evaluate in context looking at all symptoms, heart function (echo), and frequency of PVCs on a Holter monitor. All of that factors into whether any specific treatment for AFib or beyond AFib management is needed.
So guess who’s wearing a Holter heart monitor tonight and will do for two weeks to let my GP figure out what all those who came before her have come to understand about my quirky system…or not. One way or another, I have never shied away from reality, so knowing is always the best option.