Abstract 1935: Unloading the Pressure-Loaded Failing Infant Right Ventricle: Recovery of Cardiac Function and Ultrastructure
Introduction: Most evidence suggests that the LV has limited ability to recover from hypertrophy-induced failure. Far less is known about adaptive and maladaptive RV hypertrophy, which is important to various forms of congenital (e.g. tetralogy of Fallot) and adult (e.g. pulmonary hypertension) heart disease.
Hypothesis: We tested the hypothesis that restoring normal RV pressure would promote recovery of cardiac function and myocardial ultrastructure in RV failure caused by pressure overload.
Methods: Ten-day-old rabbits underwent pulmonary artery banding (PAB, n=10) or sham (Sham, n=6). Eight weeks later, half of PAB rabbits underwent debanding surgery (Deband, n=5); the band remained in the others (n=5). At 12 weeks, RV function was measured by tissue Doppler-derived myocardial performance index (TDI-MPI) and peak systolic velocity of tricuspid annulus (TAPSV); LV fractional shortening (LVFS) was also measured. Finally, the hearts were harvested for histology and RV electron microscopic (EM) examination.
Results: At 8 and 12 weeks, RV and LV systolic function were significantly decreased and the RV markedly hypertrophied and dilated in PAB. Normalizing RV pressure load (debanding) promoted rapid recovery of RV size as well as systolic function (Table⇓). EM in PAB/RV failure hearts showed myofibrillar disarray and decreased mitochondrial volume and the ratio of mitochondrial:myofibrillar area; these as well as indices of patholgical remodeling normalized after debanding (Figure⇓).
Conclusion: Unlike LV, it appears that failing RV is able to undergo considerable reverse (beneficial) remodeling when load is normalized. Potential mechanisms merit further study.