Pedro Castro1, Elsa Azevedo2, Jorge Serrador3, Isabel Rocha4, Farzaneh Sorond5. 1. Department of Neurology, São João Hospital Center, Faculty of Medicine of University of Porto, Portugal. Electronic address: pedromacc@gmail.com. 2. Department of Neurology, São João Hospital Center, Faculty of Medicine of University of Porto, Portugal. Electronic address: eazevedo@med.up.pt. 3. Veterans Biomedical Institute and War Related Illness and Injury Study Center, Department of Veterans Affairs, New Jersey Healthcare System, East Orange, USA; New Jersey Medical School, Newark, NJ, USA. Electronic address: Jorge.Serrador@va.gov. 4. Cardiovascular Autonomic Function Lab, Institute of Physiology, Faculty of Medicine of University of Lisbon, Portugal. Electronic address: isabelrocha0@gmail.com. 5. Department of Neurology, Division of Stroke and Neurocritical, Northwestern University Feinberg School of Medicine, Chicago, IL, United States. Electronic address: farzaneh.sorond@nm.org.
Abstract
BACKGROUND: Hemorrhagic transformation and cerebral edema are feared complications of acute ischemic stroke but mechanisms are poorly understood and reliable early markers are lacking. Early assessment of cerebrovascular hemodynamics may advance our knowledge in both areas. We examined the relationship between dynamic cerebral autoregulation (CA) in the early hours post ischemia, and the risk of developing hemorrhagic transformation and cerebral edema at 24h post stroke METHODS: We prospectively enrolled 46 patients from our center with acute ischemic stroke in the middle cerebral artery territory. Cerebrovascular resistance index was calculated. Dynamic CA was assessed by transfer function analysis (coherence, phase and gain) of the spontaneous blood flow velocity and blood pressure oscillations. Infarct volume, hemorrhagic transformation, cerebral edema, and white matter changes were collected from computed tomography performed at presentation and 24h. RESULTS: At admission, phase was lower (worse CA) in patients with hemorrhagic transformation [6.6±30 versus 45±38°; adjusted odds ratio 0.95 (95% confidence internal 0.94-0.98), p=0.023] and with cerebral edema [6.6±30 versus 45±38°, adjusted odds ratio 0.96 (0.92-0.999), p=0.044]. Progression to edema was associated with lower cerebrovascular resistance (1.4±0.2 versus 2.3±1.5mmHg/cm/s, p=0.033) and increased cerebral blood flow velocity (51±25 versus 42±17cm/s, p=0.033) at presentation. All hemodynamic differences resolved at 3months CONCLUSIONS: Less effective CA in the early hour post ischemic stroke is associated with increased risk of hemorrhagic transformation and cerebral edema, possibly reflecting breakthrough hyperperfusion and microvascular injury. Early assessment of dynamic CA could be useful in identifying individuals at risk for these complications.
BACKGROUND: Hemorrhagic transformation and cerebral edema are feared complications of acute ischemic stroke but mechanisms are poorly understood and reliable early markers are lacking. Early assessment of cerebrovascular hemodynamics may advance our knowledge in both areas. We examined the relationship between dynamic cerebral autoregulation (CA) in the early hours post ischemia, and the risk of developing hemorrhagic transformation and cerebral edema at 24h post stroke METHODS: We prospectively enrolled 46 patients from our center with acute ischemic stroke in the middle cerebral artery territory. Cerebrovascular resistance index was calculated. Dynamic CA was assessed by transfer function analysis (coherence, phase and gain) of the spontaneous blood flow velocity and blood pressure oscillations. Infarct volume, hemorrhagic transformation, cerebral edema, and white matter changes were collected from computed tomography performed at presentation and 24h. RESULTS: At admission, phase was lower (worse CA) in patients with hemorrhagic transformation [6.6±30 versus 45±38°; adjusted odds ratio 0.95 (95% confidence internal 0.94-0.98), p=0.023] and with cerebral edema [6.6±30 versus 45±38°, adjusted odds ratio 0.96 (0.92-0.999), p=0.044]. Progression to edema was associated with lower cerebrovascular resistance (1.4±0.2 versus 2.3±1.5mmHg/cm/s, p=0.033) and increased cerebral blood flow velocity (51±25 versus 42±17cm/s, p=0.033) at presentation. All hemodynamic differences resolved at 3months CONCLUSIONS: Less effective CA in the early hour post ischemic stroke is associated with increased risk of hemorrhagic transformation and cerebral edema, possibly reflecting breakthrough hyperperfusion and microvascular injury. Early assessment of dynamic CA could be useful in identifying individuals at risk for these complications.
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