Impaired arterial elasticity in young patients with white-coat hypertension

Background Conflict still exists over whether patients with white-coat hypertension are at increased risk of developing target organ damage compared with normotensive individuals. Methods We studied vascular distensibility in 117 young-to-middle age patients with white-coat hypertension, 174 patients with sustained hypertension, and 51 normotensive controls. To obtain a measure of compliance, a model was used that divides the total systemic compliance into large artery (C-1) and small artery (C-2) compliance. With this aim, radial arterial pulse waves were recorded with a tonometer sensor array by means of an HDI CR2000 device (Eagan, Minnesota, USA). Moreover, pulse wave velocity and the augmentation index were measured using the Specaway DAT system (St Pauls, Sydney, Australia). Results Patients with sustained hypertension had a greater body mass index than patients with white-coat hypertension (P=0.04) or the normotensive individuals (P=0.01). C-1 and C-2 were decreased in the two hypertensive groups as compared with those in the normotensive group (P=0.0002 and 0.03, respectively, versus sustained hypertension; P=0.00007 and 0.0004, respectively, versus white-coat hypertension). Pulse wave velocity and aortic augmentation index were increased in the white-coat hypertension patients compared with the normotensive individuals (P=0.02 and 0.004, respectively). Aortic augmentation index (P=0.008) but not pulse wave velocity was increased in the sustained hypertensive patients compared with that in the normotensive individuals. All indexes of arterial distensibility were similar in the two hypertensive groups. Conclusions Indexes of arterial distensibility are impaired in the white-coat hypertensive group and similar to those in the sustained hypertensive group, indicating that early changes in the arterial wall can occur in white-coat hypertension. This may account for the higher risk of stroke that has been described in this condition. Blood Press Monit 11:243-249 (C) 2006 Lippincott Williams & Wilkins.