Abstract
R A L A B ST R A C T S Methods: A computer model of the entire cardiovascular system of a normal neonate (Mynard JP, PhD Thesis, University of Melbourne, 2011) was modified to incorporate aortic coarctation. CCA haemodynamics and wave intensity were assessed for coarctation severities between 0% and 90%. Augmentation index (AI) was calculated by dividing the total pressure rise following the initial inflection point by overall pulse pressure. To evaluate the effect of elevated arterial stiffness, wave speed of all precoarctation arteries was increased by up to 250%. Results: Simulated pressure and wave intensity in the CCA are shown in Fig. 1 for a normal aorta and for 90% coarctation. A single forward compression wave (FCW1) was present in the case of a normal aorta. Coarctation led to partial reflection of the FCW1, and the reflected wave was partially transmitted into the CCA, giving rise to a second forward compression wave (FCW2) whose wave area increased progressively with coarctation severity (Fig. 2). The FCW2 augmented CCA pressure (Fig. 1), producing an increase in AI from 0.22 for 0% coarctation to 0.50 for 90% coarctation, with the most prominent rise occurring when the severity was >50%. Increasing wave speed reduced the FCW1-FCW2 time delay (Fig. 2) and the two waves merged at high wave speeds. Conclusion: Computer modelling data suggest that a reflected wave arising from the site of aortic coarctation may be transmitted into the carotid artery and lead to a substantial pressure augmentation. These wave dynamics may play a role in the higher risk of cerebral aneurysm formation in patients with aortic coarctation. Disclosure of Interest: None Declared
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