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2022 November 17

Holter monitor results

I got back the results from wearing the Holter monitor for 14 days today, and they were not what I expected.  I was expecting to see frequent PVCs, particularly when I was resting or sleeping. Instead the report had almost no PVCs but frequent PACs (premature atrial contractions) with runs of supraventricular tachycardia (runs of more than 3 PACs without normal beats in between).  “Isolated SVEs [supraventricular ectopy] were frequent (10.3%, 114645).” “2161 Supraventricular Tachycardia runs occurred, the run with the fastest interval lasting 6 beats with a max rate of 176 bpm, the longest lasting 26.7 secs with an avg rate of 133 bpm.”

Asymptomatic PACs (like asymptomatic PVCs) do not generally call for any treatment, but “many idiopathic PACs are relatively benign in the short term, although they can be associated with an increased risk of cardiac and all-cause mortality if they occur frequently.” [] Most of the medical treatments seem to be focussed on lowering heart rate or blood pressure, neither of which seem appropriate for me (I have normal blood pressure and a low heart rate). The followup recommended for frequent PACs is an echo cardiogram, which I have now scheduled for mid-January (the soonest date that the clinic had available).

My sinus heart rate was about what I expected with “a min HR of 36 bpm, max HR of 160 bpm, and avg HR of 55 bpm”, though the 36 bpm minimum was a little lower than the 40bpm I expected—my sinus rate drops a little lower when I sleep than I expected. The recording of the 36bpm period does not look like my normal sinus rhythm—it looks like a series of ectopic beats with really tiny QRS complexes to me, but it did occur when I was asleep (in the middle of a period of very low heart rate). On another day, there was a recording of 37 bpm which showed normal QRS complexes, so my sinus rate does indeed drop that low.

The max of 160 bpm occurred when I was exercising fairly hard—pushing myself a bit on bicycling uphill to campus.  It is probably not my real maximum heart rate (I was not doing an all-out effort).  I looked up estimates of maximum heart rate and found three formulas: (220 – age), (207 – 0.7 age), and (211 – 0.64 age).  The first is very common, but clearly wrong for me, the second is adjusted for people over 40 years old and pretty accurately matches the observed maximum on the Holter monitor, and the third is adjusted for active people and may slightly overestimate my max heart rate.  If I ever need to take a stress ECG or stress echocardiogram, I’ll argue for them using the second formula rather than the first in estimating my max heart rate, so that the stress level is appropriately set.

One thing I wanted to know that is not reported in the short summary report from the Holter monitor is whether there was any correlation between the sinus rhythm and the ectopic beats—in particular, I wanted to know whether the ectopic beats occurred primarily when my sinus rhythm was very low.  If that is the case, then a pacemaker set to maintain a minimum sinus rhythm might be a possible treatment, should treatment ever be needed.  I downloaded the full report, which shows when the SVT runs occurred, and they seem to be primarily when I’m awake and active, which is the opposite of what I expected based on my observations of PVCs earlier in the year.

I wasn’t sure how one distinguishes a PAC from a PVC on a one-lead Holter monitor, so I watched a video ( from “Catalyst University”, which showed the difference between PVCs and PACs on a one-lead ECG. The crucial differences are whether the P-wave (from atrial depolarization) is observed and whether the resulting QRS complex is more or less normal or much longer duration that usual.  If the P-wave is observed and the QRS spike is normal duration and shape (though usually lower amplitude), then you have a premature atrial contraction.  If there is no P-wave and the QRS complex is much longer than usual, you have a PVC.  By these criteria, the observations I made earlier (see PVC again, for example) were clearly PVCs, and the examples of SVT runs shown in the report were indeed PACs. My most recent home ECG recordings have not shown me PVCs, but if I now have PACs instead, my inability to find PVCs may represent a change in what my heart is doing, rather than a failure in my rather crude code for detecting them.

I looked for genetic causes of PACs, but have not found much. Deletion of the STK11 gene is the only thing I’ve found so far, and there is no hint of that in my genome—I do have a SNP in an intron of a gene whose protein that interacts with it: STK11IP, as well as some SNPs in the intergenic region upstream of STK11.  None of these SNPs seem likely to be a major cause of problems.

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