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Stroke and Diabetes: a Dangerous Liaison

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Stroke and Diabetes: a Dangerous Liaison REVIEW Stroke and diabetes: a dangerous liaison SARAH L MACPHERSON, 1 CHRISTOPHER R SAINSBURY, 1 JESSE DAWSON, 2 GREGORY C JONES 1 Abstract diagnosed diabetes. 3 A prospective study of over 13,000 people Ischaemic stroke is a major cause of disability and death and showed that, in people with type 2 diabetes, the risk of death the incidence rate of ischaemic stroke is doubled in patients from myocardial infarction and stroke is increased two fold, in - who have diabetes. Admission hyperglycaemia in acute dependent of other known cardiovascular risk factors. 4 Thus, stroke patients is associated with higher mortality, longer diabetes increases the risk of stroke and the risk of death from hospital stay and worse functional outcome. However, it stroke . remains unclear whether hyperglycaemia is in fact a marker The definition of hyperglycaemia varies in stroke studies and of stroke severity or whether hyperglycaemia directly con - ranges from 6.1 mmol/L to >10 mmol/L glucose. Based on these tributes to brain damage. Potential mechanisms of hypergly - definitions, hyperglycaemia is found at presentation in 30–60% caemia related brain damage in stroke include acidosis, of all stroke patients. 5 Research has shown that acute hypergly - oxidative stress and reperfusion injury. Evidence suggests a caemia in stroke contributes to worse functional outcomes, potential benefit of treatment of hyperglycaemia with longer hospital admission and higher mortality. 6 There is uncer - insulin in acute stroke patients but the potential for morbid - tainty about what level of blood glucose contributes to un - ity caused hypoglycaemia should be considered. The American Heart Association/American Stroke Association favourable outcomes. Evidence varies regarding whether there guidelines recommend maintaining the blood glucose level is a glucose threshold for worse outcomes or whether the rela - in the range 7.8–10 mmol/L during acute stroke hospitalisa - tionship is linear. 7,8 One group found that the capillary glucose tion whilst the European Stroke Organization guideline rec - level with the highest predictive accuracy for poor outcome was ommends lowering the blood glucose with insulin to below >8.6 mmol/L. 7 Another group showed that odds for favourable 10 mmol/L. More research is needed to explore the impact stroke outcome decrease as admission blood glucose increases of admission hyperglycaemia and hypoglycaemia on stroke (odds ratio of neurological improvement 0.76 per 5.6 mmol/L outcomes and the role of other glucose lowering therapies. increase in glucose). 8 Br J Diabetes 2016; 16 :114-118 This literature review will explore the proposed underlying mechanisms by which alterations in blood glucose may contribute Key words: hyperglycaemia, hypoglycaemia, diabetes, to poor outcomes, summarise both animal studies and clinical stud - ischaemic, haemorrhagic, stroke, mortality, outcomes, insulin ies to date and propose topics for future research. Evidence for treatment of hyperglycaemia on admission with acute stroke will Introduction also be explored. Ischaemic stroke is a major cause of disability and is now the 4th leading cause of death in the USA. 1 Stroke accounted for 5.7 The impact of hyperglycaemia on stroke million deaths in 2005 worldwide, with the incidence rate of Cell death occurs in ischaemic stroke due to depletion of glucose ischaemic stroke approximately doubled in patients who have and oxygen resulting in reduced adenosine triphosphate (ATP) pro - diabetes. 2 Approximately one-third of patients with transient duction. 5 It is unclear exactly how hyperglycaemia causes worse ischaemic attacks or ischaemic stroke who have no previous his - outcomes in acute stroke. 6 Hyperglycaemia related acidosis is a pro - tory of diabetes have prediabetes and over a quarter have newly posed mechanism. Under ischaemic conditions, lactic acid produc - tion from anaerobic metabolism contributes to an acidic pH. Hyperglycaemia accentuates lactic acid production and reduced pH. 1 Department of Diabetes and Endocrinology, Gartnavel General Hospital, Glasgow, UK Brain tissue pH can be reduced from 7.2 to 6.6 during ischaemia. 2 College of Medical, Veterinary and Life Sciences, Institute of Under hyperglycaemic conditions, pH can drop further to <6, 9 Cardiovascular and Medical Sciences, University of Glasgow, Queen potentially causing protein denaturation, acid sensitive ion channel Elizabeth University Hospital, Glasgow, UK activation and iron release, contributing to ischaemic brain Address for correspondence: Dr Gregory C Jones injury. 10,11 Department of Diabetes, Gartnavel General Hospital, 1053 Great Hyperglycaemia also plays a role in oxidative stress by acceler - Western Road, Glasgow, G12 0YN, UK Tel: +44 (0)141 211 3259 ating the production of free radicals since, glucose is the substrate E-mail: [email protected] for their production. 5 Figure 1 summarises key mechanisms likely http://dx.doi.org/10.15277/bjd.2016.089 to be involved in mediating the adverse effects of hyperglycaemia on stroke outcomes. 114 THE BRITISH JOURNAL OF DIABETES REVIEW This was associated with larger infarct size and is in agreement with Figure 1. Coronal schematic of brain with ischaemic stroke 17-20 showing proposed mechanisms by which previous work. One study contradicts this hypothesis, possibly 21 hyperglycaemia (HG) worsens stroke related brain injury due to differences in hyperglycaemia severity. Cerebral autoregulation is the process by which the blood sup - Acidosis ply to the brain is maintained despite changes in perfusion pressure. • HG ↑ lactic acid To achieve this, smooth muscle cells constrict when perfusion pres - production, reducing pH sure is high and relax when pressure is low to keep blood flow con - Oxidative Stress stant. 22,23 Work using rats has shown that, under hyperglycaemic • Glucose is substrate for conditions, cerebral vessels were incapable of responding to production of ROS changes in pressure, impairing cerebral autoregulation. 24,25 • HG results in ↑ substrate In addition to reperfusion injury, hyperglycaemia may also affect Reperfusion Injury outcome after thrombolytic therapy for ischaemic stroke. High • HG during reperfusion blood glucose levels increase coagulation by increasing thrombin ↑ ROS production • HG impairs cerebral production and stimulating the tissue factor pathway. Hypergly - Infarct autoregulation caemia also reduces the activity of tissue plasminogen activator zone • HG contributes to thrombolysis treatment by increasing production of plasminogen haemorrhagic 6 transformation activator inhibitor. Impaired Thrombolysis Clinical studies: mortality, functional status and • HG ↑ thrombin levels, Cerebral artery haemorrhagic transformation promoting coagulation Blood clot • HG stimulates the tissue A strong link between admission hyperglycaemia in ischaemic and factor pathway haemorrhagic stroke patients and negative outcomes has been shown. These outcome measures include infarct size, disability Other Mechanisms and mortality. 5 Regression analyses controlling for other con - • ↑ glucose/ sodium exchange founding factors demonstrate the importance of hyperglycaemia • Abnormal protein in negative outcomes. 26-28 Recently, these findings have been sup - glycosylation ported by an imaging study. 29 The authors used transcranial ROS, reactive oxygen species • Increased cortisol levels Doppler, MRI, and magnetic resonance spectroscopy to show that hyperglycaemia is a strong predictor of infarct growth and poor outcome. The study had a small sample size of only 47 patients Animal studies: stroke, hyperglycaemia and reperfusion but showed that the stroke lesion on diffusion weighted imaging injury grew 2.7 times faster in patients with hyperglycaemia treated with A variety of studies in animals have been done to shed light on the tissue plasminogen activator than in those without. The study was impact of hyperglycaemia on acute stroke outcomes. Early studies strengthened by the use of National Institutes of Health Stroke found that hyperglycaemia at the time of stroke resulted in worse Scale scores. neuronal and vascular injury post-stroke, in keeping with clinical A systematic review and meta-analysis was undertaken to findings. 12,13 Increased infarct size and levels of inflammatory mark - explore stress hyperglycaemia and stroke prognosis in patients 27 ers were observed in hyperglycaemic Zucker obese rats. 6 However, with and without diabetes. another study reported that hyperglycaemia did not affect the in - Twenty-six studies were included. The group found that the farct volume but increased blood brain barrier permeability and unadjusted relative risk of in-hospital or 30-day mortality associ - haemorrhagic transformation. 14 ated with an admission glucose level of 6 –8 mmol/L was 3.07 in Studies in rats has demonstrated that larger infarcts are seen in non-diabetic patients and 1.30 in patients with diabetes for both hyperglycaemic animals in brain territories with collateral circulation ischaemic and haemorrhagic stroke. Thus, even a small increase compared to those in end arterial region. 15 This supports studies in blood glucose level in non-diabetic patients with ischaemic that show lacunar stroke outcomes are not worsened by hypergly - stroke increases mortality three fold. These patients also have an caemia. 16 These strokes affect areas with poor collateral circulation. increased risk of poor functional recovery compared to patients Thus, animal studies are generally in agreement with clinical study
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