Cerebral hemodynamics and silent cerebral white matter lesions in middle-aged essential hypertensive patients

Cristina Sierra1, Alejandro de la Sierra, Angel Chamorro

  • 1Hypertension Unit, Department of Internal Medicine, IDIBAPS (Institut d'Investigacions Biomèdiques August Pi i Sunyer), Hospital Clínic, University of Barcelona, Spain. csierra@clinic.ub.es

Blood Pressure
|November 17, 2004
PubMed

Cerebral white matter lesions (WML) represent a subclinical form of ischemic brain damage that have been associated with risk of future stroke. Studies have shown an association between WML and impaired cerebral autoregulation in hypertensives who had previously suffered a stroke. The aim of the study was to evaluate cerebral hemodynamics in asymptomatic hypertensives according to the presence or absence of WML. Fifty never-treated essential hypertensives (32 men, 18 women), aged 50-60 years, without clinical evidence of target organ damage were studied. All patients underwent 24-h ambulatory blood pressure monitoring, and brain-magnetic resonance imaging to establish the presence or absence of WML. Baseline cerebral blood flow velocity (CBF), pulsatility index (PI; differences between systolic and diastolic velocities), and CBF after acetazolamide infusion (vasomotor reactivity of cerebral vessels), were measured by transcranial Doppler ultrasonography in both left and right middle cerebral arteries, and averaged. Twenty hypertensive patients (40%) were found to have WML on brain resonance. No differences were observed on resting and stimulating CBF between hypertensives with and without WML. In contrast, patients with WML exhibited significantly higher PI compared with hypertensives without WML (0.79 +/- 0.13 vs 0.66 +/- 0.12; p = 0.003). Moreover, PI correlated with 24-h pulse pressure (r = 0.361; p = 0.015). We conclude that the presence of silent WML in middle-aged hypertensives is associated with increased cerebrovascular pulsatility. This increased pulsatility is also associated with higher pulse pressure values, suggesting a pathogenetic link between pulse pressure, pulsatility and the development of WML.

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