Background: Neonatal asphyxia caused acute kidney injury and severe hypertension in a newborn patient. An unusually dilatated ascending aorta developed within a few weeks. Dialysis and hypertensive treatment led to partial recovery of the aortic diameters. It was hypothesized that the aortic dilatation may be associated with cardiovascular changes induced by the acute kidney injury. Mathematical modelling was used to better understand the underlying mechanisms of hypertension and aortic dilatation.Methods: Patient observation included systolic blood pressure recording and echocardiographic exams. To explore underlying mechanisms of aortic dilatation and hypertension, a previous whole-body lumped parameter hemodynamics model was adapted to this study. Computer simulations were designed to permit dissection of individual mechanisms. The hypertension inducing effects of altering systemic vascular resistances, stiffnesses, and heart rate on blood flows and pressures were simulated.Results: In agreement with our clinical diagnosis, the mathematical model showed that an increase of systemic small vessel resistance is the prime cause of hypertension. Further, aortic stiffening may also cause hypertension, it was found to be secondary to the potency of systemic small vessel resistance. The cardiac output, as quantified using pressure-volume loop area, reduced significantly due to hypertension. Simultaneous left ventricle hypertrophy and small vessel blocking increased ascending aorta blood flow as well as pressure indicating an enlarged ascending aorta. In contrast, increased arterial stiffness appeared to lower the aortic blood flow and pressures.Conclusions and discussion: Systemic small vessel resistance is an important factor in arterial hypertension, and may also be a key clinical therapeutic target. Left ventricle hypertrophy may also be simultaneously ameliorated when treating systemic small vessels. Treatment of arterial stiffness appears to provide significant benefit but may be secondary to treatment of the systemic small vessels. The quantitative grading of pathophysiological mechanisms provided by the modelling may contribute to treatment recommendations. Further development and individualization of the model will augment its applicability in clinical practice.
Arterial hypertension and unusual ascending aortic dilatation in a neonate with acute kidney injury: mechanistic computer modelling