Abstract 4439: Insular Cortex Atrophy as an Independent Determinant of Disrupted Diurnal Rhythm of Ambulatory Blood Pressure in Elderly Hypertension
Recently, insular cortex (Ic) is suggested to be a key site in limbic-autonomic integration. Association of Ic damage with diurnal blood pressure (BP) variation disruption, higher level of brain natriuretic peptide (BNP) and catecholamine were reported. We examined the relationship of Ic volume with ambulatory BP measures and these biomarkers. Amubulatory BP monitoring and brain MRI were performed in 55 elderly hypertensives. Right and left Ic volumes were measured using Intensity Contour-Mapping Algorithm. BNP, adrenaline and noradrenaline concentration were evaluated. Subjects were classified into Ic-atrophy group (n=14) and non-atrophy group (n=41) based on total Ic volume (right and left side) of 12.6 cm 3 (lowest quartile). In Ic-atrophy group, 24hr (144.5 vs 134.2 mmHg, p=0.032), sleep (143.4 vs 127.2 mmHg, p=0.002) systolic BP (SBP), nocturnal SBP dipping (1.30 vs 8.54 %, p=0.027) and BNP (60.6 vs 28.1 pg/ml, p=0.008) were significantly, and noradrenaline (373.5 vs 296.5 pg/ml, p=0.084) was marginally different from those in non-atrophy group. Right Ic volume was significantly correlated with 24hr (r=−0.271, p=0.046), sleep (r=−0.420, p=0.001) SBP, nocturnal SBP dipping (r=0.311, p=0.021) and noradrenaline (r=−0.334, p=0.013), while left Ic volume with 24hr (r=−0.279, p=0.039), sleep (r=−0.498, p=0.0001) SBP, nocturnal SBP dipping (r=0.409, p=0.002) and BNP (r=−0.363, p=0.006). In multiple linear regression analysis adjusted for age, gender and body mass index, left Ic volume was significantly negatively associated with sleep SBP (p=0.008) and BNP (p=0.001), and positively with nocturnal SBP dipping (p=0.044). In elderly hypertensives, predominant left Ic atrophy was significantly associated with sleep SBP measures and BNP. Ic damage, specifically in the left side, may partly contribute to disruption of diurnal ambulatory BP rhythm as well as cardiac function via central autonomic dysregulation.