The exact mechanism is not well understood. Some studies suggest a relationship between the burden of PVCs and LV dysfunction. That is a high number of PVCs over 24 hours (like 10,000 PVCs and more) over time cause depressed LV function.

I am unaware of any good pathophysiological explanation. We do understand the PVC pathophysiology but how so many of them lead to CM is not well understood.

I think the process is much similar to the mechanical dysynchrony following RV pacing, therefor, PVCs can induce DCM when exceeding 27% in the holter trace

From a cellular perspective, the mechanisms of PVC-induced cardiomyopathy are speculative and based on animal models, from which extrapolation for humans is sometimes limited. It has been postulated that the prolongation and marked beat-to-beat variation in action potential duration, as well as decreased outward and inward (L-type calcium) currents, could result in increased repolarisation heterogeneity. This may be associated with an increased risk of sudden cardiac death due to triggered activity and malignant ventricular arrhythmias. The contractile dysfunction observed in PVC-induced cardiomyopathy could be explained by an altered calcium-induced calcium release from the sarcoplasmic reticulum. In another canine model, it was reported that LVEF impairment could occur within 3 months of induced ventricular ectopy. This suggests that the underlying mechanism is functional rather than structural, given the absence of myocardial fibrosis and changes in apoptosis.