CONTRIBUTION OF ARTERIAL BLOOD-PRESSURE TO THE CLINICAL EXPRESSION OFLACUNAR INFARCTION

Citation
A. Chamorro et al., CONTRIBUTION OF ARTERIAL BLOOD-PRESSURE TO THE CLINICAL EXPRESSION OFLACUNAR INFARCTION, Stroke, 27(3), 1996, pp. 388-392
Citations number
27
Categorie Soggetti
Cardiac & Cardiovascular System","Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
27
Issue
3
Year of publication
1996
Pages
388 - 392
Database
ISI
SICI code
0039-2499(1996)27:3<388:COABTT>2.0.ZU;2-A
Abstract
Background and Purpose The relation between symptomatic lacunar infarc tion, silent stroke, and arterial hypertension is controversial. Metho ds From 500 patients with ischemic or hemorrhagic stroke admitted to t he Downtown Barcelona Stroke Registry between July 1992 and December 1 994, we evaluated prospectively the prevalence of silent infarction in 249 patients who had a brain MRI. The association of risk factors wit h silent infarction was investigated with the use of logistic regressi on analysis. In a selected group of 43 patients with symptomatic lacun es, we performed at stroke follow-up transcranial Doppler sonography a nd 24-hour continuous blood pressure monitoring to evaluate whether bl ood pressure, cerebrovascular tone, and cerebral blood how 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 w ith silent infarctions had higher systolic and diastolic blood pressur e 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 extra cranial vessels, systolic and diastolic pressure at stroke onset and d iastolic pressure and vascular resistance at stroke follow-up were hig her when silent infarctions coexisted. However, cerebral blood how at rest and after acetazolamide injection were unrelated to silent infarc tion. Conclusions Silent ischemia in patients with symptomatic lacunar and nonlacunar stroke was only associated with aging. However, a hist ory of arterial hypertension was perhaps unrecognized, since hemodynam ic testing and continuous blood pressure monitoring in patients with l acunar stroke suggested that the coexistence of silent lesions indicat ed a more generalized cerebral arteriolosclerosis.