Caffeine Effects on PVC Frequency: A Self-Experiment

Palpitations due to premature beats, either ventricular contractions (PVCs) or atrial contractions (PACs), can be extremely vexing even when we know they are benign. For many individuals, these extra-systoles come in waves that are seemingly random and inexplicable. This unpredictability can add to the anxiety they create.

A reader recently shared his attempt to sort out the influence of caffeine consumption on the frequency of his symptomatic PVCs but encounters one of the many “variables” that confound his attempt at biohacking.

I discovered that I had SEVs (PACs) and PVCs about 6 months ago by using the 6-lead Kardia device. I can watch the trace live in real-time, feel the PVC and then see it on the trace (easy to see with the 6 lead version) about a second after I actually feel it. I went to an electrophysiologist and he offered me the option of monitoring with a Zio patch for two weeks.

I followed the incidence of PVCs with my Kardia in parallel with the patch. The results matched up well.

An Imperfect Experiment

See the linked log from the Zio report. Some years ago I cut over to decaf coffee, but I actually drink a lot of it; two large mugs in the morning which turns out to be 6 cups. My guess is that its 30-50 mg caffeine in total.

For the first week of the Zio I kept up my decaf coffee habit and then on the second week (March 8) I cut out all the decaf. As you can see from the data the second week had a dramatic decrease in PVCs. I resumed the decaf drinking the morning of March 11, but did not see an immediate return of the PVC’s until 3 days later.

The results are pretty dramatic. I might have failed to mention that the experiment was conducted during Lent, when I traditionally abstain from all alcohol. So it was not a variable in the experiment.

However, the experiment is imperfect because a second variable was changed in the second week. I got sick of using the Kardia all the time and sick of worrying about this whole situation and pretty much forgot about it. I suspect that measuring the PVCs with the Kardia actually causes them to be worse because I am tensed up while measuring. Other scientists might understand why I call this a Heisenberg problem.

So were the decreased PVCs in week 2 due to the reduced caffeine or the reduced stress due to an attitude adjustment?

For reference, I am 66 years old, extremely active (two jobs), I exercise 5 days a week (you can see the 1 hour elevated heart rate in the report). Oh, and my mother recently told me that she and every single one of her 5 siblings have atrial fibrillation and are on warfarin (Coumadin). So I am highly motivated to make whatever lifestyle adjustments need to defer what may be an inevitable fate due to my genes.

Caffeine and Extrasystoles

A recent observational study looked at the frequency of extrasystoles in relation to habitual caffeine consumption. The introduction to that paper nicely lays out our current understanding of that relationship:

“Patients often associate the symptoms of premature cardiac contractions with emotional stress, physical activity, dietary factors, and caffeine or other stimulant use. Though there is little data to support the role of behavioral modifications or trigger avoidance in reducing or preventing premature cardiac contractions, clinicians often instruct patients with any arrhythmia to avoid caffeine intake. The American College of Cardiology/American Heart Association guidelines on the management of supraventricular arrhythmias state that if a patient’s history is consistent with premature extra beats, one should review and eliminate potential exacerbating factors, such as caffeine, alcohol, and nicotine. Prominent online medical resources for clinicians, such as UpToDate and Medscape, feature similar recommendations for the management of premature beats.While none of these sources explicitly refer to the acute versus chronic effects of caffeine on ectopy, they focus on general avoidance in order to avoid triggering arrhythmias. Caffeine is of particular interest because of its known sympathomimetic effects, leading to increased plasma norepinephrine and epinephrine levels and, as a result, possibly increasing ectopy.”

The study found no relationship between the frequency of PVCs or PACs by 24-hour Holter monitoring versus level of coffee, tea, or chocolate consumption.

The Value of Quantification in Self-Experimentation With PVCs

Despite the absence of a demonstrable relationship between the frequency of extra-systoles and habitual caffeine consumption in the general population, I am convinced that PVCs in certain individuals (including myself) are triggered by higher levels of caffeine. Such a relationship is revealed by the type of self-experimentation performed by my reader.

These so-called “n of 1” or bio-hacking studies when combined with an accurate and precise way of measuring the outcome of interest (like a patch monitor for PVC frequency) yield insights into idiosyncratic or individual responses to chemicals, foods, and medications that don’t show up in large population studies.

When self-experimenting, it is important to be aware of all the variables that might be influencing the measured outcome. My reader was able to maintain zero alcohol intake during the two weeks of his Zio recording. Presumably, his dietary intake and exercise program remained constant. Hopefully his sleep patterns and quality remained constant, though this is quite difficult to control.

But one parameter for all creatures that cannot be controlled is our sympathetic autonomic nervous system response to psychological stressors. For many of my patients, the simple act of measuring their blood pressure (BP) activates the sympathetic nervous system, thereby causing a BP spike. For some, seeing their PVCs on an ECG recording might similarly induce stress.

Anthony C. Pearson, MD, is a noninvasive cardiologist and professor of medicine at St. Louis University School of Medicine. He blogs on nutrition, cardiac testing, quackery, and other things worthy of skepticism at The Skeptical Cardiologist, where a version of this post first appeared.