OBJECTIVES: Aortic endografting can cause aortic stiffening. We aimed to determine the chronic effect of thoracic endografting on cardiac afterload, function and remodelling. METHODS: Eleven dogs were included, and all except 1 was successfully assessed [endograft, n = 5; sham operation (control), n = 5]. We deployed a stent graft in the descending aorta. The ascending aortic pressure and flow were measured, and aortic input impedance was obtained by frequency analysis to determine characteristic impedance and arterial compliance. Left ventricular pressure-volume relations were measured with an admittance catheter. Measurements were performed before, 10 min after and 3 months after endografting. Following euthanasia, we weighed the left ventricle of each dog and measured the cardiomyocyte cell size. RESULTS: Arterial compliance decreased from 0.47 ± 0.07 to 0.36 ± 0.06 and to 0.31 ± 0.05 ml/mmHg (both P < 0.01 versus baseline), and characteristic impedance increased from 0.11 ± 0.04 to 0.19 ± 0.05 and to 0.21 ± 0.04 mmHg/ml/s (both P < 0.01 versus baseline) 10 min and 3 months after endografting, respectively. Pressure-volume relation analysis showed that arterial elastance increased from 5.3 ± 1.0 to 6.7 ± 1.6 (at 10 min) and to 6.8 ± 1.0 mmHg/ml (at 3 months) (both P < 0.05 versus baseline), but end-systolic elastance and ventriculo-arterial coupling remained unchanged. Left ventricular weight to body weight ratio and left ventricular cardiomyocyte cell width in the endograft group were larger compared with the control's results (5.06 ± 0.27 g/kg vs 4.20 ± 0.49 g/kg, P = 0.009, 15.1 ± 1.7 µm vs 13.9 ± 1.5 µm, P = 0.02, respectively). CONCLUSIONS: The mid-term effect of the descending aortic endografting on left ventricular contractility and efficiency in canine normal hearts was minimal. However, endografting resulted in increased cardiac afterload and left ventricular hypertrophy.
OBJECTIVES: Aortic endografting can cause aortic stiffening. We aimed to determine the chronic effect of thoracic endografting on cardiac afterload, function and remodelling. METHODS: Eleven dogs were included, and all except 1 was successfully assessed [endograft, n = 5; sham operation (control), n = 5]. We deployed a stent graft in the descending aorta. The ascending aortic pressure and flow were measured, and aortic input impedance was obtained by frequency analysis to determine characteristic impedance and arterial compliance. Left ventricular pressure-volume relations were measured with an admittance catheter. Measurements were performed before, 10 min after and 3 months after endografting. Following euthanasia, we weighed the left ventricle of each dog and measured the cardiomyocyte cell size. RESULTS: Arterial compliance decreased from 0.47 ± 0.07 to 0.36 ± 0.06 and to 0.31 ± 0.05 ml/mmHg (both P < 0.01 versus baseline), and characteristic impedance increased from 0.11 ± 0.04 to 0.19 ± 0.05 and to 0.21 ± 0.04 mmHg/ml/s (both P < 0.01 versus baseline) 10 min and 3 months after endografting, respectively. Pressure-volume relation analysis showed that arterial elastance increased from 5.3 ± 1.0 to 6.7 ± 1.6 (at 10 min) and to 6.8 ± 1.0 mmHg/ml (at 3 months) (both P < 0.05 versus baseline), but end-systolic elastance and ventriculo-arterial coupling remained unchanged. Left ventricular weight to body weight ratio and left ventricular cardiomyocyte cell width in the endograft group were larger compared with the control's results (5.06 ± 0.27 g/kg vs 4.20 ± 0.49 g/kg, P = 0.009, 15.1 ± 1.7 µm vs 13.9 ± 1.5 µm, P = 0.02, respectively). CONCLUSIONS: The mid-term effect of the descending aortic endografting on left ventricular contractility and efficiency in canine normal hearts was minimal. However, endografting resulted in increased cardiac afterload and left ventricular hypertrophy.