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Comparative Study
Journal Article
[Reactivity of cerebral vessels in patients with circulatory encephalopathy, arterial hypertension and cerebral hypoperfusion risk].
AIM: To study cerebral vasomotor reactivity (CVR) in patients with chronic cerebrovascular disturbances caused by arterial hypertension (AH) and to determine criteria of cerebral hypoperfusion risk during antihypertensive therapy.
MATERIAL AND METHODS: 80 patients with chronic cerebrovascular disturbances because of AH and 15 normotensive subjects without any neurological pathology (control group) were examined using CT of the brain, duplex scanning of extra- and intracranial arteries, echocardiography. CVR was assessed with transcranial dollperography of the blood flow velocity in both middle cerebral arteries before and after nitroglycerine provoked test.
RESULTS: CVR in the patients significantly differed from that of the controls. Main factors responsible for changes in CVR ara the age, form and duration of arterial hypertension, circadian rhythm of blood pressure, occlusive extra- or intracranial arteries disease. CT signs of focal (lacunes) or diffuse (leukoaraiosis) ischemic brain damage, deformations of the neck vessels, left ventricular hypertrophy may be leading markers of severe disturbances in CVR.
CONCLUSION: In patients with chronic cerebrovascular disease disturbances of CVR arise due to arterio/arteriolopathy as a result of AH. Limitation of the vasodilatation potential demonstrates cerebral autoregulation dysfunction. Thus, factors and markers of CVR impairment can be considered as risk criteria of cerebral hypoperfusion during inadequate antihypertensive treatment.
MATERIAL AND METHODS: 80 patients with chronic cerebrovascular disturbances because of AH and 15 normotensive subjects without any neurological pathology (control group) were examined using CT of the brain, duplex scanning of extra- and intracranial arteries, echocardiography. CVR was assessed with transcranial dollperography of the blood flow velocity in both middle cerebral arteries before and after nitroglycerine provoked test.
RESULTS: CVR in the patients significantly differed from that of the controls. Main factors responsible for changes in CVR ara the age, form and duration of arterial hypertension, circadian rhythm of blood pressure, occlusive extra- or intracranial arteries disease. CT signs of focal (lacunes) or diffuse (leukoaraiosis) ischemic brain damage, deformations of the neck vessels, left ventricular hypertrophy may be leading markers of severe disturbances in CVR.
CONCLUSION: In patients with chronic cerebrovascular disease disturbances of CVR arise due to arterio/arteriolopathy as a result of AH. Limitation of the vasodilatation potential demonstrates cerebral autoregulation dysfunction. Thus, factors and markers of CVR impairment can be considered as risk criteria of cerebral hypoperfusion during inadequate antihypertensive treatment.
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