Baird Tracey A, Parsons Mark W, Phan Thanh, Butcher Ken S, Desmond Patricia M, Tress Brian M, Colman Peter G, Chambers Brian R, Davis Stephen M
Department of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australia.
Stroke. 2003 Sep;34(9):2208-14. doi: 10.1161/01.STR.0000085087.41330.FF. Epub 2003 Jul 31.
Hyperglycemia at the time of ischemic stroke is associated with increased mortality and morbidity. Animal studies suggest that infarct expansion may be responsible. The influence of persisting hyperglycemia after stroke has not previously been examined. We measured the blood glucose profile after acute ischemic stroke and correlated it with infarct volume changes using T2- and diffusion-weighted MRI.
We recruited 25 subjects within 24 hours of ischemic stroke symptoms. Continuous glucose monitoring was performed with a glucose monitoring device (CGMS), and 4-hour capillary glucose levels (BGL) were measured for 72 hours after admission. MRI and clinical assessments were performed at acute (median, 15 hours), subacute (median, 5 days), and outcome (median, 85 days) time points.
Mean CGMS glucose and mean BGL glucose correlated with infarct volume change between acute and subacute diffusion-weighted MRI (r>or=0.60, P<0.01), acute and outcome MRI (r=0.56, P=0.01), outcome National Institutes of Health Stroke Scale (NIHSS; r>or=0.53, P<0.02), and outcome modified Rankin Scale (mRS; r>or=0.53, P=0.02). Acute and final infarct volume change and outcome NIHSS and mRS were significantly higher in patients with mean CGMS or mean BGL glucose >or=7 mmol/L. Multiple regression analysis indicated that both mean CGMS and BGL glucose levels >or=7 mmol/L were independently associated with increased final infarct volume change.
Persistent hyperglycemia on serial glucose monitoring is an independent determinant of infarct expansion and is associated with worse functional outcome. There is an urgent need to study normalization of blood glucose after stroke.
缺血性脑卒中发生时的高血糖与死亡率和发病率增加相关。动物研究表明梗死灶扩大可能是原因所在。此前尚未研究过脑卒中后持续高血糖的影响。我们测量了急性缺血性脑卒中后的血糖情况,并使用T2加权和弥散加权磁共振成像(MRI)将其与梗死灶体积变化进行关联分析。
我们纳入了25名在出现缺血性脑卒中症状后24小时内的受试者。使用葡萄糖监测设备(CGMS)进行连续血糖监测,并在入院后72小时测量4小时毛细血管血糖水平(BGL)。在急性(中位数为15小时)、亚急性(中位数为5天)和预后(中位数为85天)时间点进行MRI和临床评估。
平均CGMS血糖和平均BGL血糖与急性和亚急性弥散加权MRI之间的梗死灶体积变化相关(r≥0.60,P<0.01),与急性和预后MRI相关(r=0.56,P=0.01),与预后美国国立卫生研究院卒中量表(NIHSS;r≥0.53,P<0.02)以及预后改良Rankin量表(mRS;r≥0.53,P=0.02)相关。平均CGMS或平均BGL血糖≥7 mmol/L的患者,急性和最终梗死灶体积变化以及预后NIHSS和mRS显著更高。多元回归分析表明,平均CGMS和BGL血糖水平≥7 mmol/L均独立与最终梗死灶体积变化增加相关。
连续血糖监测显示的持续高血糖是梗死灶扩大的独立决定因素,并与更差的功能预后相关。迫切需要研究脑卒中后血糖的正常化问题。