Why the study?
The progression of intraventricular dyssynchrony, radial, and circumferential strain in premature ventricular contraction-induced cardiomyopathy was unknown.
Does frequent premature ventricular contractions (ventricular bigeminy) induce early changes in left ventricular strain and dyssynchrony prior to ejection fraction decline in a canine model?
RCT (n=20)
null
randomly assigned to either persistent PVC or sham group
No
Does frequent premature ventricular contractions (ventricular bigeminy) induce early changes in left ventricular strain and dyssynchrony prior to ejection fraction decline in a canine model?
In a canine model of PVC-induced cardiomyopathy, changes in circumferential strain and intraventricular dyssynchrony precede the decline in left ventricular ejection fraction, suggesting electro-mechanical latency as a novel marker for early contractile remodeling.
Answers are grounded in this paper and cite their sources.
Supports strain/dyssynchrony monitoring for early PVC effects in models; leaves open human translation and clinical utility.
Background Strain imaging has been suggested as a tool to detect early left ventricular (LV) dysfunction due to frequent premature ventricular contractions (PVCs) in patients with preserved LV ejection fraction (EF). However, the progression of intraventricular dyssynchrony (IVD), radial, and circumferential strain (RS, CS) in PVC-cardiomyopathy (CM) are unknown. The aim of this study was to elucidate the progression patterns of CS, IVD, and electro-mechanical latency (EML) in PVC-CM. Methods and results Pacemakers were implanted in 20 canines to reproduce ventricular bigeminy at 200ms (PVCs n = 11) for 12 weeks and compared to a sham group ( n = 9). We obtained echocardiograms at baseline, 4-, 8- and 12-weeks. RS and CS were obtained at the LV mid-cavitary level. IVD was defined as the time between the earliest and latest peak RS. EML was defined as the time between the onset of QRS and the earliest peak RS. LVEF (62 ± 5 to 42 ± 7%, p < 0.01), CS (–18 ± 3 to –12 ± 3, p < 0.01), and EML (219 ± 37 to 283 ± 46ms, p = 0.02) changed significantly in the PVC group. Peak CS (–18 ± 3 to –14 ± 4, p = 0.02) and IVD (49 ± 31 to 122 ± 103, p = 0.05) had a significant change at 4-weeks despite preserved LVEF (51 ± 5%). IVD normalized while EML increased at weeks 8 and 12. Conclusion Our findings consolidate the existing theory that changes in strain precede changes in LVEF in PVC-CM. While IVD becomes abnormal early in the development of PVC-CM, it pseudo-normalizes at advanced stages due to further increases in EML suggestive of cardiac contractility remodeling. These findings are consistent with recent published data where abnormal LV mechanics could be part of a substrate that can predispose to worse outcome in PVC-Cardiomyopathy.
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Kowlgi et al. (2022) conducted an RCT in premature ventricular contraction-induced cardiomyopathy (PVC-CM) (n=20). premature ventricular contractions (PVCs) vs. sham group (no ectopy) was evaluated on Left ventricular ejection fraction (LVEF) (null, 95% CI null, p=<0.001).
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