Determinants of aortic root dilatation over time in patients with essential hypertension: The Campania Salute Network.

Background: Determinants of changes of aortic root dimension over time are not well defined.

Design: We investigated whether specific phenotype and treatment exist predicting changes in aortic root dimension in hypertensive patients from the Campania Salute Network.

Methods: N = 4856 participants (age 53 ± 11 years, 44% women) were included. At first and last available echocardiograms, we measured aortic root and a z-score of aortic root (AOz) was generated as the difference between measured and predicted aortic root, derived from a healthy reference population. Aortic root dilatation (ARD) was defined as AOz >75th percentile of distribution.

Results: At baseline, 3642 patients (75%) exhibited normal aortic root, and 1214 (25%) ARD. After a follow-up of 6.1 years (interquartile range 3.0-8.8 years), 366 (11%) patients with initial normal aortic root exhibited ARD, whereas 457(38%) with initial ARD exhibited normal aortic root. At multivariate analysis patients with incident ARD were most likely to be women, obese, with left ventricular hypertrophy, lower systolic but higher diastolic blood pressure and stroke volume index at baseline, and higher average value of diastolic blood pressure during follow-up (p < 0.05); whereas patients normalizing their ARD were non-obese women with lower baseline systolic blood pressure, stroke volume index, average diastolic blood pressure during follow-up and longer follow-up time (p < 0.05). Anti-renin-angiotensin system (anti-RAS) was associated with 45% greater probability to normalize aortic root dimension.

Conclusions: Volume (stroke volume index) and pressure loads (diastolic blood pressure) influence aortic root dimension over time. Aortic root normalization, reflecting a more favourable haemodynamic load, is predictable in non-obese women with lower diastolic blood pressure, taking more anti-RAS therapy. This suggest that sex elicits a different response in aortic walls to pathological stimuli.