Myocardial hypertrophy after pulmonary regurgitation and valve implantation in pigs

Background: Patients may suffer from right ventricular (RV) failure and malignant cardiac arrhythmias after late pulmonary valve replacement correcting pulmonary regurgitation (PR). But the underlying mechanisms of the refractory arrhythmias are not well understood.

Methods: The aim of present study was to characterize the RV myocardium after percutaneous pulmonary valve implantation (PPVI) in a porcine model after severe PR for 3months. RV histology was evaluated with morphometric methods and RV function was assessed with electrophysiology, echocardiography, and biochemical measures: The results were compared with age-matched sham-operated animals.

Results: At euthanasia, RV weight was increased compared to sham-animals, median 127 g (115-137) vs. 71 g (69.5-76.5), p=0.0007. RV myocyte diameters corrected for individual variation with the RV/LV ratio were enlarged, 1.06 (1.02-1.13) vs. 0.84 (0.80-0.91), p=0.0006. There were no excess collagen tissue (RV/LV ratio), p=0.77. Electrophysiological stimulation resulted in RV arrhythmia in 67% of the animals compared to 25% in the sham-operated animals, but this difference was not statistically significant, p=0.28. Echocardiography revealed geometrical dilation in end-systolic RV area, mean ± SD, 11.8 ± 4.9 cm(2) vs. 6.0 ± 3.5 cm(2), p=0.05, and end-diastolic area, 23.3 ± 10.4 cm(2) vs. 12.7 ± 2.5 cm(2), p=0.08. RV anterior free wall thickness was not increased, 0.7 ± 0.2 cm vs. 0.7 ± 0.1 cm, p=0.66. Echocardiographic functional parameters and plasma natriuretic peptides were unchanged.

Conclusions: The RV does not completely recover after three months of PR with persistent myocardial hypertrophy one month after PPVI. Future studies should address whether RV chamber and cellular hypertrophy, without fibrosis or interventional scar tissue, may be substrate for arrhythmia.