Carolyn S Kaufman1,2, Stephen X Bai3, Sarah M Eickmeyer3, Sandra A Billinger1,2,3,4. 1. Department of Molecular and Integrative Physiology, University of Kansas, Medical Center, Kansas City, KS, USA. 2. Department of Physical Therapy and Rehabilitation Science, University of Kansas, Medical Center, Kansas City, KS, USA. 3. Department of Physical Medicine and Rehabilitation, University of Kansas, Medical Center, Kansas City, KS, USA. 4. Department of Neurology, University of Kansas, Medical Center, Kansas City, KS, USA.
Abstract
BACKGROUND AND PURPOSE: Chronic hyperglycemia contributes to cerebrovascular dysfunction by damaging blood vessels. Poor glucose control has been tied to impairments in cerebral blood flow, which may be particularly detrimental for people recovering from major cerebrovascular events such as acute ischemic stroke. In this secondary analysis, we explore for the first time the connection between chronic hyperglycemia before acute stroke and the cerebrovascular response (CVR) to exercise 3 and 6 month into the subacute recovery period. METHODS: We recorded middle cerebral artery velocity (MCAv) using transcranial Doppler ultrasound bilaterally at rest and during moderate-intensity exercise in stroke patients at 3 (n = 19) and 6 (n = 12) months post-stroke. We calculated CVR as the difference between MCAv during steady-state exercise and resting MCAv. We obtained hemoglobin A1c levels (HbA1c; a measure of blood glucose over the prior 3 months) from the electronic medical record (EMR) and divided participants by HbA1c greater or less than 7%. RESULTS: Participants with high HbA1c (>7%) at the time of acute stroke had significantly lower CVR to exercise for both the stroke-affected (p = .009) and non-affected (p = .007) hemispheres at 3 months post-stroke. These differences remained significant at 6 months post-stroke (stroke-affected, p = .008; non-affected, p = .016). CONCLUSIONS: Patients with chronic hyperglycemia before acute ischemic stroke demonstrated impaired cerebrovascular function during exercise months into the subacute recovery period. These findings highlight the importance of maintaining tight glucose control to reduce morbidity and improve recovery post-stroke and could have implications for understanding cerebrovascular pathophysiology.
BACKGROUND AND PURPOSE: Chronic hyperglycemia contributes to cerebrovascular dysfunction by damaging blood vessels. Poor glucose control has been tied to impairments in cerebral blood flow, which may be particularly detrimental for people recovering from major cerebrovascular events such as acute ischemic stroke. In this secondary analysis, we explore for the first time the connection between chronic hyperglycemia before acute stroke and the cerebrovascular response (CVR) to exercise 3 and 6 month into the subacute recovery period. METHODS: We recorded middle cerebral artery velocity (MCAv) using transcranial Doppler ultrasound bilaterally at rest and during moderate-intensity exercise in stroke patients at 3 (n = 19) and 6 (n = 12) months post-stroke. We calculated CVR as the difference between MCAv during steady-state exercise and resting MCAv. We obtained hemoglobin A1c levels (HbA1c; a measure of blood glucose over the prior 3 months) from the electronic medical record (EMR) and divided participants by HbA1c greater or less than 7%. RESULTS: Participants with high HbA1c (>7%) at the time of acute stroke had significantly lower CVR to exercise for both the stroke-affected (p = .009) and non-affected (p = .007) hemispheres at 3 months post-stroke. These differences remained significant at 6 months post-stroke (stroke-affected, p = .008; non-affected, p = .016). CONCLUSIONS: Patients with chronic hyperglycemia before acute ischemic stroke demonstrated impaired cerebrovascular function during exercise months into the subacute recovery period. These findings highlight the importance of maintaining tight glucose control to reduce morbidity and improve recovery post-stroke and could have implications for understanding cerebrovascular pathophysiology.
Authors: Bianca Hemmingsen; Søren S Lund; Christian Gluud; Allan Vaag; Thomas Almdal; Christina Hemmingsen; Jørn Wetterslev Journal: BMJ Date: 2011-11-24