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(Stroke. 1996;27:388-392.)
© 1996 American Heart Association, Inc.

Articles

Contribution of Arterial Blood Pressure to the Clinical Expression of Lacunar Infarction

A. Chamorro, MD; A. Saiz, MD; N. Vila, MD; C. Ascaso, PhD; R. Blanc, MD; M. Alday, MD J. Pujol, MD

From the Neurology Service, Department of Medicine, Hospital Clinic Provincial (A.C., A.S., N.V., R.B., M.A.); Epidemiology and Biostatistics Unit, University of Barcelona (C.A.); and Centro Resonancia Magnética Pedralbes (J.P.), Barcelona, Spain.

Correspondence to A. Chamorro, MD, Neurology Service, Hospital Clinic i Provincial, Villarroel 170, 08036 Barcelona, Spain.

Background and Purpose The relation between symptomatic lacunar infarction, silent stroke, and arterial hypertension is controversial.

Methods From 500 patients with ischemic or hemorrhagic stroke admitted to the Downtown Barcelona Stroke Registry between July 1992 and December 1994, we evaluated prospectively the prevalence of silent infarction in 249 patients who had a brain MRI. The association of risk factors with silent infarction was investigated with the use of logistic regression analysis. In a selected group of 43 patients with symptomatic lacunes, we performed at stroke follow-up transcranial Doppler sonography and 24-hour continuous blood pressure monitoring to evaluate whether blood pressure, cerebrovascular tone, and cerebral blood flow at rest and after the administration of 1 g acetazolamide correlated with silent infarction.

Results A total of 147 silent infarctions were observed in 83 patients (33%). Most silent infarctions corresponded to small deep lesions in the territory of the lenticulostriate arteries. Patients with silent infarctions had higher systolic and diastolic blood pressure at stroke onset. However, on multivariate analysis, age greater than 60 years was the only risk factor associated with silent infarction. In a subgroup of 43 patients with symptomatic lacunes and patent extracranial vessels, systolic and diastolic pressure at stroke onset and diastolic pressure and vascular resistance at stroke follow-up were higher when silent infarctions coexisted. However, cerebral blood flow at rest and after acetazolamide injection were unrelated to silent infarction.

Conclusions Silent ischemia in patients with symptomatic lacunar and nonlacunar stroke was only associated with aging. However, a history of arterial hypertension was perhaps unrecognized, since hemodynamic testing and continuous blood pressure monitoring in patients with lacunar stroke suggested that the coexistence of silent lesions indicated a more generalized cerebral arteriolosclerosis.

Key Words: hemodynamics • infarcts, silent • lacunar infarction • risk factors

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