Acute hyperglycemia adversely affects stroke outcome: A magnetic resonance imaging and spectroscopy study

Authors

  • Mark W. Parsons FRACP,

    1. Royal Melbourne Hospital Echoplanar Imaging Stroke Study Group, University of Melbourne, Parkville Vic, Australia
    2. Department of Medicine, University of Melbourne, Parkville Vic, Australia
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  • P. Alan Barber PhD, FRACP,

    1. Royal Melbourne Hospital Echoplanar Imaging Stroke Study Group, University of Melbourne, Parkville Vic, Australia
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  • Patricia M. Desmond MD,

    1. Royal Melbourne Hospital Echoplanar Imaging Stroke Study Group, University of Melbourne, Parkville Vic, Australia
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  • Tracey A. Baird MRCP,

    1. Royal Melbourne Hospital Echoplanar Imaging Stroke Study Group, University of Melbourne, Parkville Vic, Australia
    2. Department of Medicine, University of Melbourne, Parkville Vic, Australia
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  • David G. Darby PhD, FRACP,

    1. Royal Melbourne Hospital Echoplanar Imaging Stroke Study Group, University of Melbourne, Parkville Vic, Australia
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  • Graham Byrnes PhD,

    1. Department of Mathematical Statistics, University of Melbourne, Parkville Vic, Australia
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  • Brian M. Tress MD, FRACR,

    1. Royal Melbourne Hospital Echoplanar Imaging Stroke Study Group, University of Melbourne, Parkville Vic, Australia
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  • Stephen M. Davis MD, FRACP

    Corresponding author
    1. Royal Melbourne Hospital Echoplanar Imaging Stroke Study Group, University of Melbourne, Parkville Vic, Australia
    2. Department of Medicine, University of Melbourne, Parkville Vic, Australia
    • Royal Melbourne Hospital, Parkville Vic 3050, Australia
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Abstract

Controversy exists whether acute hyperglycemia is causally associated with worse stroke outcome or simply reflects a more severe stroke. In reversible ischemia models, hyperglycemia is associated with lactic acidosis and conversion of penumbral tissue to infarction. However, the relationship between hyperglycemia, lactic acidosis, and stroke outcome has not been explored in humans. Sixty-three acute stroke patients were prospectively evaluated with serial diffusion-weighted and perfusion-weighted magnetic resonance imaging and acute blood glucose measurements. Patients with hypoperfused at-risk tissue were identified by acute perfusion-diffusion lesion mismatch. As a substudy, acute and subacute magnetic resonance spectroscopy was performed in the 33 most recent patients to assess the relationship between acute blood glucose and lactate production in the ischemic region. In 40 of 63 patients with acute perfusion-diffusion mismatch, acute hyperglycemia was correlated with reduced salvage of mismatch tissue from infarction, greater final infarct size, and worse functional outcome. These correlations were independent of baseline stroke severity, lesion size, and diabetic status. Furthermore, higher acute blood glucose in patients with perfusion-diffusion mismatch was associated with greater acute-subacute lactate production, which, in turn, was independently associated with reduced salvage of mismatch tissue. In contrast, acute blood glucose levels in nonmismatch patients did not independently correlate with outcome measures, nor was there any acute-subacute increase in lactate in this group. Acute hyperglycemia increases brain lactate production and facilitates conversion of hypoperfused at-risk tissue into infarction, which may adversely affect stroke outcome. These findings support the need for randomized controlled trials of aggressive glycemic control in acute stroke.

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