I found a super interesting paper from 2019 that answers one important question and suggests several others. My cardiologist has offered me treatment options based on % of time in arrhythmia, but I haven’t been certain about what this means. My guess was: # of missed heartbeats divided by # of total heartbeats in the sample. Without recording every heartbeat over a longish period of time, this ratio is very hard to determine, since my PVCs are intermittent and my heart rate varies.
This study hoped to contribute to understanding the relationship between PVCs and cardiomyopathy by looking specifically at the effect of PVCs on the cardiac parasympathetic nervous system. To do this, the researchers induced PVCs in pigs. I can see from their description that PVC burden is defined just as I guessed: # missed beats/ # total beats. (It’s unclear to me if the skipped beat is counted in the denominator, but for my general understanding that’s not important.)
Currently, there are no clear cut-off points that delineate the PVC burden at which cardiomyopathy may develop (4, 6, 17). However, several studies have suggested that a frequency 10%, and especially 24%, is associated with development of cardiomyopathy (4, 17, 37). In line with these studies, we chose to deliver PVCs at an average burden of every 5 beats (~20%) Premature ventricular contractions activate vagal afferents and alter autonomic tone: implications for premature ventricular contraction-induced cardiomyopathy, Salavatian et al., American Journal of Physiology-Heart and Circulatory Physiology, 317(3) 2019
That was good to know.
However, the article was much less sanguine about the consequences of PVCs than my cardiologist. PVCs are associated with higher risk of heart failure, and one of the studies cited in the paper, a 2019 analysis of California health data concluded that:
"a diagnosis of VPCs independently predicts incident systolic HF. This effect is most pronounced in younger patients without co-morbidities, suggesting that VPCs may be an important cause of “idiopathic” HF. (Relation Between Ventricular Premature Complexes and Incident Heart Failure, Agarwal, Vratika et al. American Journal of Cardiology, Volume 119, Issue 8, 1238 - 1242.)
Note: as far as I can tell, VPCs and PVCs are synonyms.
The paper is behind a paywall, but it’s interesting to note that this condition, which is extremely bothersome and sometimes causes my SpO2 to drop to 94 as measured on my cheap blood oxygenation meter (during which time I feel light headed) is not conclusively harmless. Adds to my motivation to learn, at least.
Back to the pig study. The researchers found evidence that autonomic nervous system imbalances can be caused by PVCs and speculate that these can contribute to development of cardiomyopathy. Specifically:
PVCs activate mechanosensory as well as chemosensory neurons in the inferior vagal ganglia, and nodose ganglion sensory neurons are capable of statedependent adaptations and display memory in response to cardiac stimuli. Because of this capacity, any excitation of this population of cardiac afferent neurons persists following the initial insult, further exacerbating the pathology of cardiac arrhythmias and cardiomyopathy.
Yikes. Let’s see if I can reduce these PVCs.
This memory effect, if it is real, doubtless combines with role of the autonomic nervous system in inducing PVCs, since stress and exercise are common triggers. I’ve seen that my own PVCs come in waves that can last many days in a row. If the likelihood of my having PVCs on a given day is increased by my having had them the day before, then it makes sense to try to find a way to dampen the cycle, even making changes that I know I can’t sustain over time, in order to see if they can stop the PVCs for long enough to establish a temporary equilibrium at a lower level of arrhythmia.