Even after successful treatment of aortic coarctation, a high risk of cardiovascular morbidity and mortality remains. Uncertainty exists on the factors contributing to this increased risk among which are the presence of (1) a residual narrowing leading to an additional resistance and (2) a less distensible zone disturbing the buffer function of the aorta. As the many interfering factors and adaptive physiological mechanisms present in vivo prohibit the study of the isolated impact of these individual factors, a numerical fluid-structure interaction model is developed to predict central hemodynamics in coarctation treatment. The overall impact of a stiffening on the hemodynamics is limited, with a small increase in systolic pressure (up to 8 mmHg) proximal to the stiffening which is amplified with increasing stiffening and length. A residual narrowing, on the other hand, affects the hemodynamics significantly. For a short segment (10 mm), the combination of a stiffening and narrowing (coarctation index 0.5) causes an increase in systolic pressure of 58 mmHg, with 31 mmHg due to narrowing and an additional 27 mmHg due to stiffening. For a longer segment (25 mm), an increase in systolic pressure of 50 mmHg is found, of which only 9 mmHg is due to stiffening
