The right ventricular response to high afterload: comparison between healthy persons and patients with transposition of the great arteries: a 2D strain study.

ABSTRACT

OBJECTIVE: To evaluate the contraction pattern of the systemic right ventricle (RV) in comparison to healthy controls. METHODS: 31 patients (14 female, mean age 21.5 ± 3.3 years) with congenital corrected (ccTGA) and surgical corrected (D-TGA) TGA and 31 age-matched healthy controls (17 female, mean age 23.1 ± 2.6 years) were included in the study. We compared the contraction pattern of the systemic RV with findings in the right and left ventricle (LV) of healthy controls. Echocardiograms were performed for all patients (19.3 ± 2.5 years after the operation) and all healthy controls. Using a novel computer software (GE Ultrasound, Horton, Norway) that allows automatic frame-by-frame tracking of accoustic markers during the heart cycle longitudinal and circumferential strain and strain rate were defined as parameters of myocardial deformation. RESULTS: In the systemic free RV wall, circumferential strain was greater than longitudinal strain (-25.6 ± 4.2% vs. -15.2 ± 3.9%, P < 0.001), opposite to the contraction pattern of the subpulmonary free RV wall (-17.7 ± 4.1% vs. -28.3 ± 3.3%, P < 0.001). Compared with controls, segmental analysis of the free RV wall resulted in lower systolic longitudinal and higher systolic circumferential strain and strain rate values. In the free LV wall, circumferential strain was lower than longitudinal strain (-19.1 ± 2.7% vs. -26.8 ± 4.5%, P < 0.001) in contrast to the data in the systemic free LV wall (-24.5 ± 3.1% vs. -16.7 ± 3.5%, P < 0.001). CONCLUSIONS: Myocardial deformation parameters were significantly different in systemic and normal RV indicating a dependency of myocardial deformation parameters on right ventricular afterload. The use of myocardial deformation imaging identified a shift from longitudinal to circumferential contraction pattern in the systemic RV in comparison to the LV. This might demonstrate a response to the systemic load creating a myocardial hypertrophy.