INTRODUCTION: Depression is a prospective risk factor for stroke. Little is known, however, about the pathophysiologic links leading to this association. Cerebrovascular reactivity (CVR) reflects the compensatory dilatory capacity of cerebral arterioles to a dilatory stimulus and is an important mechanism to provide constant cerebral blood flow. In the absence of major arterial stenosis, an impaired CVR has been associated with a higher risk of stroke. We hypothesized that CVR might be continuously reduced in patients with major depression even after successful remission thus contributing to the association between depression and stroke. MATERIALS AND METHODS: We investigated CVR in a group of patients (N=29) in the acute episode of depressive illness and after 21months under euthymic condition. A healthy control group (N=33) was investigated at comparable time intervals. All patients and controls were otherwise healthy. CVR was investigated by calculating the increase in cerebral blood flow velocity after stimulation with acetazolamide. Blood flow velocities were measured by transcranial doppler ultrasound. RESULTS: A group of acutely depressed patients presented a significantly reduced CVR compared to controls. On follow-up 21months later after treatment and remission, CVR in the patient group had significantly improved, whereas CVR in the control group remained unchanged. Confounding factors had no significant influence. DISCUSSION: CVR is impaired during major depression. Since CVR seems to improve after treatment of depression, the contribution to an increased stroke risk among depressive patients may be true for a subgroup only and needs to be further investigated. Copyright 2009 Elsevier Ltd. All rights reserved.
INTRODUCTION:Depression is a prospective risk factor for stroke. Little is known, however, about the pathophysiologic links leading to this association. Cerebrovascular reactivity (CVR) reflects the compensatory dilatory capacity of cerebral arterioles to a dilatory stimulus and is an important mechanism to provide constant cerebral blood flow. In the absence of major arterial stenosis, an impaired CVR has been associated with a higher risk of stroke. We hypothesized that CVR might be continuously reduced in patients with major depression even after successful remission thus contributing to the association between depression and stroke. MATERIALS AND METHODS: We investigated CVR in a group of patients (N=29) in the acute episode of depressive illness and after 21months under euthymic condition. A healthy control group (N=33) was investigated at comparable time intervals. All patients and controls were otherwise healthy. CVR was investigated by calculating the increase in cerebral blood flow velocity after stimulation with acetazolamide. Blood flow velocities were measured by transcranial doppler ultrasound. RESULTS: A group of acutely depressedpatients presented a significantly reduced CVR compared to controls. On follow-up 21months later after treatment and remission, CVR in the patient group had significantly improved, whereas CVR in the control group remained unchanged. Confounding factors had no significant influence. DISCUSSION: CVR is impaired during major depression. Since CVR seems to improve after treatment of depression, the contribution to an increased stroke risk among depressivepatients may be true for a subgroup only and needs to be further investigated. Copyright 2009 Elsevier Ltd. All rights reserved.
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