Early detection of left ventricular (LV) failure is crucial to improve prognosis of patients with right ventricular (RV) overload.

We aim to assess whether LV function is precociously affected in 2 surgical porcine models of moderate (Fallot repaired) and severe RV dysfunction (progressive pulmonary hypertension HP) at in vivo and in vitro levels.

Three animals of each surgical group were compared with 6 controls/Sham. 4 months after surgeries, LV function was evaluated using echocardiography/strain compared with conductance catheter. At cellular level using isolated cardiomyocytes, calcium transients amplitude with relaxation time associated and sarcomere shortening were recorded using Ionoptix system. T-tubules network integrity (DI-4-ANEPPS) and colocalization (Immunofluorescence) between main Excitation/Contraction (EC) actors (Ca^2+v1.2-Ryr) were analyzed. Contractile reserve was evaluated by adrenergic stimulation in-vivo and in-vitro (Dobutamine-isoproterenol).

Despite RV dysfunctions in both groups, LV present hemodynamic impairment only in HP group (Longitudinal strain 9 versus 18%. Conductance catheter with dobutamin: Elastance arterial 7.7 versus 1,32, SV 14 versus 75ml and tau (relaxation) 49 versus 27, P<0.05).In cardiomyocytes, we observe decrease of Ca²⁺ transient amplitude and cardiomyocytes contraction, acceleration of Ca²⁺ relaxation time, T-tubule network disorganisation and Cav1.2/Ryr decoupling (Fig. 1). In vivo and in vitro, adrenergic stimulations increase dysfunction.

In vitro experiments pointed early abnormalities in LV EC particularly after adrenergic stimulation. A better understanding of cellular alterations could lead to survival improvement.