Abstract 18727: Right Ventricular Pressure Overload is More Important than Volume Overload in Producing Contralateral Ventricular Dysfunction: A Congenital Heart Disease Model

Abstract

Intro: It is known that right ventricular (RV) contractile failure predisposes the left ventricle (LV) to failure. Animal models in an acute setting indicate this phenomenon is due predominantly to RV volume overload causing both changes in LV geometry and suboptimal LV filling. We investigated the relative importance of chronic RV pressure versus volume overload in producing LV dysfunction using d-transposition of the great vessels with an atrial switch (TGA, RV pressure overload) and repaired tetralogy of Fallot with severe pulmonary valve insufficiency (ToF, RV volume overload) as model systems. Methods: We performed a single center retrospective analysis of cardiac magnetic resonance imaging (MRI) data. All adult patients with TGA and ToF who had useful MRI data were screened. Included ToF patients had pulmonary insufficiency without residual pulmonary or infundibular stenosis. Included TGA patients had mild or less aortic or tricuspid regurgitation. We assessed MRI derived LV and RV volume measurements. Correlations were assessed using Pearson’s correlation coefficient. Differences between correlation coefficients were assessed using a Fischer r to z transformation. Results: 32 TGA and 46 ToF patients met enrollment criteria with 35 and 72 MRIs respectively having data adequate for analysis. The groups were similar in terms of sex (58 versus 51% male) and age (29.6 +/- 6.0 versus 31.0 +/- 9.7) respectively. Patients with TGA demonstrated a strong correlation between RV and LV systolic function based on ejection fraction (EF) r=0.75. They also demonstrated a strong correlation between RV end-diastolic volume indexed to body surface area (EDVi) and LV EF (r=-0.56). Although there was a trend toward increased RV EDVi in patients with ToF (119ml/m2 versus 101ml/m2 for TGA p=0.11), ToF patients had a weaker correlation between RV and LV EF (r=0.46; p=0.02 compared to TGA) and a very weak correlation between RV EDVi and LV EF (r=-0.21). Conclusions: The present data indicate that in the chronic setting, RV pressure rather than volume overload is of greater importance in producing LV dysfunction, implicating shared muscle fibers, neurohumoral milieu, or relative unloading of the LV as playing a greater role in this process.