Hemodynamic interplay of ventricular, atrial and aortic function in patients after arterial switch operation: insights from cardiac MRI.

BACKGROUND

Left ventricular, atrial and aortic dysfunction might be important disease drivers in patients with transposition of great arteries (TGA) that possibly influence pathophysiological processes beyond the underlying congenital disease. Therefore, this study aimed to assess their influence and relationship in TGA patients following arterial switch operation (ASO).

METHODS

Patients with TGA after ASO were studied with cardiac magnetic resonance imaging (CMR) to measure (I) extracellular volume fraction (ECV); (II) global peak systolic longitudinal strain (GLS); (III) left atrial reservoir function (LA-EF-reservoir) and (IV) aortic distensibility (AD). Mediation analysis was performed to model the interplay of ventricular, atrial and aortic function.

RESULTS

Eighty-one TGA patients (median age 16 years, 32% female) and 30 heart-healthy controls were included. TGA patients had significantly lower LA-EF-reservoir function (P<0.001) resulting in a shift from active to passive LA function (P<0.001), and AD was impaired in TGA patients (P<0.001). The ratio of active to passive LA function correlated with ECV (P=0.002). Both LA-EF-reservoir and AD correlated negatively with peak systolic GLS. In a mediation model, the effect of AD on peak systolic GLS encompassed both a direct effect on peak GLS (β=-0.2833), and an indirect effect mediated by LA-EF-reservoir (β=0.2087). LA-EF-reservoir had the strongest effect on ventricular function (β=-0.3193) and mediated 29% of the effect of AD on ventricular function (mediated β=-0.066).

CONCLUSIONS

Post ASO, impaired LA function and AD are associated with reduced systolic left ventricular function. These relationships are mediated through both direct effects, such as the direct impact of AD on GLS, and indirect pathways, including the mediating role of LA-EF reservoir function. Consequently, impaired left atrial and aortic function should be viewed not as isolated abnormalities but as interconnected physiological processes that jointly contribute to altered ventricular performance.