Hindawi Publishing Corporation Cardiovascular Psychiatry and Neurology Volume 2012, Article ID 616572, 8 pages doi:10.1155/2012/616572 Research Article Association of Ultrasonographic Parameters with Subclinical White-Matter Hyperintensities in Hypertensive Patients Ioannis Heliopoulos, 1 Dimitrios Artemis, 1 Konstantinos Vadikolias, 1 Grigorios Tripsianis, 2 Charitomeni Piperidou, 1 and Georgios Tsivgoulis 1 1 Department of Neurology, School of Medicine, Democritus University of Thrace, Alexandroupolis, Greece 2 Department of Biostatistics, School of Medicine, Democritus University of Thrace, Alexandroupolis, Greece Correspondence should be addressed to Konstantinos Vadikolias, vadikosm@yahoo.com Received 22 May 2012; Accepted 3 July 2012 Academic Editor: Richard C. Veith Copyright © 2012 Ioannis Heliopoulos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background and Purpose. Cerebral white matter hyperintensities (WMHs) are regarded as typical MRI expressions of small- vessel disease (SVD) and are common in hypertensive patients. Hypertension induces pathologic changes in macrocirculation and in microcirculation. Changes in microcirculation may lead to SVD of brain and consequently to hypertensive end-organ damage. This damage is regarded the result of interactions between the macrovascular and microvascular levels. We sought to investigate the association of cerebral WMHs with ultrasonographic parameters of cerebral macrocirculation evaluated by carotid duplex ultrasound (CDU) and transcranial doppler (TCD). Subjects and Methods. The study was prospective, cross-sectional and consecutive and included hypertensive patients with brain MRI with WMHs. Patients underwent CDU and TCD. The clinical variables recorded were demographic characteristics (age, gender, race) and vascular risk factors (hypertension, diabetic mellitus, hypercholesterolemia, current smoking, and body mass index). Excluded from the study were patients with history of clinical stroke (including lacunar stroke and hemorrhagic) or transient ischemic attack (either hemispheric or ocular), hemodynamically significant (>50%) extra- or intracranial stenosis, potential sources of cardioembolism, and absent transtemporal windows. WMHs were quantified with the use of a semiquantitative visual rating method. Ultrasound parameters investigated were (1) common carotid artery (CCA) diameter and intima-media thickness, (2) blood flow velocity in the CCA and internal carotid artery (ICA), and (3) blood flow velocity and pulsatility index of middle cerebral artery (MCA). Results. A total of 52 patients fulfilled the study inclusion criteria (mean age 71.4 ± 4.5 years, 54% men, median WMH-score: 20). The only two ultrasound parameters that were independently associated with WMH score in multivariate linear regression models adjusting for demographic characteristics and vascular risk factors were increased mean common carotid artery (CCA) diameter (beta = 0.784, SE = 0.272, P = 0.006, R 2 = 23.9%) and increased middle cerebral artery pulsatility index (MCA-PI; beta = 0.262, SE = 0.110, P = 0.025, R 2 = 9.0%). Among all ultrasound parameters the highest AUC (areas under the receiver operating characteristic curve) were documented for MCA-PI (AUC = 0.82, 95% CI = 0.68-0.95, P< 0.001) and mean CCA diameter (AUC = 0.80, 95% CI = 0.67-0.92, P< 0.001). Conclusions. Our study showed that in hypertensive individuals with brain SVD the extent of structural changes in cerebral microcirculation as reflected by WMHs burden is associated with the following ultrasound parameters of cerebral macrocirculation: CCA diameter and MCA-PI. 1. Introduction There is accruing data indicating that white matter hyper- intensities (WMHs), the most common imaging biomarker of small-vessel disease (SVD), are longitudinally associated with increased risk of cognitive decline and gait disturbance [1]. Older age and hypertension are the two clinical factors that have been consistently associated with increased burden of WMHs in asymptomatic individuals [2]. The suggested underlying mechanism linking elevated blood pressure levels with SVD includes hypertension-induced structural vessel changes in microcirculation such as lipohyalinosis and fib- rinoid degeneration [3]. Hypertension also affects macrocir- culation causing arterial remodeling (reflected by increased