Abstract 2961: Ventricular Stiffness Contributes to Hypertension in Patients with Clinical Science Repaired Coarctation of the Aorta
Background Despite successful repair, patients with coarctation of the aorta (CoA) often show persistent hypertension at rest and/or during exercise. Previous studies indicated that this phenomenon is mainly due to abnormality in arterial bed and its regulatory system. However, blood pressure is determined not only by the state of arterial bed but also by cardiac function to which the blood vessels are coupled. We hypothesized that ventricular stiffness contributes to the hypertensive state in patients with repaired CoA, in addition to increased vascular stiffness.
Methods and Results The left ventricular pressure-area relationship was measured invasively in 37 patients (2–14 years of age) with successfully repaired CoA (defined as 0 mmHg pressure gradient) and compared with that of 41 age-matched control subjects who had small ventricular septal defect with an estimated shunt ratio <5%. Data recorded at rest and during transient preload reduction by inferior vena caval obstruction yielded left ventricular chamber stiffness (Ees) and effective arterial stiffness (Ea). The mean systolic blood pressure (SBP) was significantly higher in CoA patients (118±24 mmHg) than in the control (98±9 mmHg, p<0.01). Ees (45±19 mmHg/mlm2) and Ea (36±19 mmHg/mlm2) of CoA patients were significantly higher than those of the controls (18±7 and 20±7 mmHg/mlm2, respectively, P<0.001). To quantify the contribution of increased ventricular stiffness to the high SBP in CoA patients, SBP was estimated by assuming that Ees of CoA patients was equal to the mean Ees value of the control. The results showed a significant decrease in blood pressure by 12±5 mmHg, indicating that ventricular stiffness accounts for about 60% of the elevated blood pressure in CoA patients.
Conclusions Increased ventricular stiffness greatly contributes to elevated systolic pressure in patients with repaired CoA. Thus, in addition to the recognized arterial stiffness, abnormal neurohumoral activity and autonomic dysfunction, ventricular stiffness could be a viable target for reduction of blood pressure and improvement of prognosis of patients with this disease.