Contribution of arterial blood pressure to the clinical expression of lacunar infarction.
OBJECTIVE
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 co-existed. 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.
Chamorro
A
A
Neurology Service, Department of Medicine, Hospital Clinic Provincial, Barcelona, Spain.
Saiz
A
A
Vila
N
N
Ascaso
C
C
Blanc
R
R
Alday
M
M
Pujol
J
J
D000086:Acetazolamide; D000367:Age Factors; D000368:Aged; D001794:Blood Pressure; D018660:Blood Pressure Monitoring, Ambulatory; D002545:Brain Ischemia / Q000150:complications / Q000175:diagnosis; D002543:Cerebral Hemorrhage / Q000150:complications / Q000175:diagnosis; D002544:Cerebral Infarction / Q000175:diagnosis / Q000209:etiology*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D002561:Cerebrovascular Disorders / Q000175:diagnosis / Q000209:etiology*; D015331:Cohort Studies; D003342:Corpus Striatum / Q000098:blood supply; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000150:complications*; D002537:Intracranial Arteriosclerosis / Q000150:complications; D016015:Logistic Models; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D015995:Prevalence; D011446:Prospective Studies; D012307:Risk Factors; D017585:Ultrasonography, Doppler, Transcranial; D014655:Vascular Resistance; D014665:Vasodilator Agents
D014665:Vasodilator Agents; D000086:Acetazolamide