Right Ventricular Remodeling in an Ovine Model of Pulmonary Regurgitation

Background: In patients with tetralogy of Fallot, the integrity of the pulmonary valve is often disrupted to relieve right ventricular (RV) outflow tract obstruction effectively. This results in pulmonary regurgitation (PR), chronic RV volume overload, and ultimately RV dysfunction. We investigated the effects of chronic RV volume overload in an animal model of PR.

Methods: Five lambs aged 2.5–3 months (weight 16.2 ± 3 kg) underwent surgical creation of pulmonary valve insufficiency. MR imaging was conducted 11 months after surgery before sacrifice. Muscle tissue from RV and LV was histologically analyzed by automated algorithms for myocardial fibrosis. Data were compared with controls (ctrl) of same age.

Results: All animals completed the study. MRI showed significant PR

(Table 1). Muscular hypertrophy was histologically present in both LV and RV, but no significant myocardial fibrosis

MRI parameter	PR, n = 5	ctrl, n = 6	change (%)	MRI parameter	PR, n = 5	ctrl, n = 6	change (%)
PI (%)	33	0	33	RV wall thickness (cm)	0.67	0.49	+37
RV output (mL/min)	1865	2196	−15	systemic HCV (ml/min)	2023	2692	−25
RVEDD (cm)	3.28	2.58	+27	LVEDD (cm)	3.41	3.37	+1
TAPSE (cm)	1.53	1.55	−1	MAPSE (cm)	1.43	1.22	+17

Conclusion: This sheep model created a hemodynamic relevant PR with subsequent RV volume overload. MRI showed relevant RV but also LV remodeling as well as decreased ventricular function even in a small study group. Although significant myocardial hypertrophy was already present, evidence for myocardial fibrosis may be found after a longer observation time.