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首页> 外文期刊>Journal of the Neurological Sciences: Official Bulletin of the World Federation of Neurology >Hemorheologic profiles of plasma fibrinogen and blood viscosity from silent to acute and chronic cerebral infarctions.
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Hemorheologic profiles of plasma fibrinogen and blood viscosity from silent to acute and chronic cerebral infarctions.

机译:从无声到急性和慢性脑梗死的血浆纤维蛋白原和血液粘度的血液流变学特征。

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摘要

Hemorheologic changes from silent to acute and chronic cerebral infarction have seldom been reported. We evaluated hemorheologic profiles of the whole blood viscosity, plasma viscosity and fibrinogen level in stroke at-risk patients with silent cerebral infarction, patients with acute or chronic cerebral lacunar infarction, and subjects at low risk for stroke. Hemorheologic profiles were measured in 88 subjects: (1) 36 patients with silent cerebral infarction (mean 64.7 years), who provided no clinical history of having had definitive stroke but showing > 5 mm lesions of cerebral infarction or periventricular hyperintensity (PVH) observed in magnetic resonance imaging (MRI) T2-weighted images; (2) 12 patients with acute cerebral lacunar infarction (mean 69.1 years), measured within 3 days and repeated 1 month after onset; (3) 25 patients with chronic cerebral lacunar infarction (mean 66.2 years), measured 12.5 months after onset; and (4) 15 subjects at low risk for stroke (mean 65.8 years) without cardiovascular risk factors or lesions on MRI. Patients with silent cerebral infarction were subdivided into two groups of less advanced and more advanced grades, based on the number of infarctions or the grade of PVH. Whole blood viscosity (shear rates: 22.5-225.0 s-1), corrected blood viscosity for 45% standard hematocrit (Hct), plasma viscosity, fibrinogen, serum total protein, albumin, and Hct were measured. Plasma fibrinogen levels were lower in silent cerebral infarctions than in chronic cerebral infarctions (P < 0.01), and patients with more advanced grades of silent cerebral infarction showed higher levels of plasma fibrinogen than those with less advanced grades (P < 0.01 and P < 0.05). Whole blood viscosity, corrected blood viscosity (Hct 45%), plasma viscosity and fibrinogen levels in acute cerebral infarction within 3 days after onset were higher significantly than those in subjects at low risk for stroke. Plasma fibrinogen level persisted to be elevated up to 1 month after onset, which continued as well in patients with chronic cerebral infarction. Advanced grades of silent cerebral infarction in stroke at-risk patients are accompanied by elevations of plasma fibrinogen level, which increases further after onset of cerebral infarction; such abnormalities persist up to the chronic stage. Elevated plasma fibrinogen level might reflect progression of atherogenesis in patients with advanced grades of silent cerebral infarction, resulted in an increased probability as to be a risk factor for cerebral infarction.
机译:从安静到急性和慢性脑梗死的血液流变学变化鲜有报道。我们评估了全血粘度,血浆粘度和纤维蛋白原水平的血液流变学特征,包括无症状性脑梗死的中风高危患者,急性或慢性脑腔隙性脑梗死的患者以及中风风险低的受试者。在88位受试者中测量了血液流变学特征:(1)36例无症状性脑梗死的患者(平均64.7岁),没有提供明确的中风的临床病史,但显示有5毫米以上的脑梗死或脑室高强度(PVH)病变。磁共振成像(MRI)T2加权图像; (2)12例急性脑腔隙性脑梗死患者(平均69.1岁),在发病后3天内测量并在发病后1个月重复一次; (3)25例慢性脑腔梗死患者(平均66.2岁),发病后12.5个月测量; (4)15名中风风险低的受试者(平均65.8岁),无心血管危险因素或MRI病变。根据梗死次数或PVH等级,将无症状性脑梗死患者分为两组,分别为低度晚期和高度晚期。测量全血粘度(剪切速率:22.5-225.0 s-1),校正后的血液粘度(标准血细胞比容(Hct)的45%),血浆粘度,纤维蛋白原,血清总蛋白,白蛋白和Hct。静默性脑梗死患者血浆纤维蛋白原水平低于慢性脑梗死患者(P <0.01),静默性脑梗死程度更高的患者血浆血浆纤维蛋白原水平高于低沉度患者(P <0.01和P <0.05) )。发病后三天内急性脑梗死的全血粘度,校正的血液粘度(Hct 45%),血浆粘度和纤维蛋白原水平显着高于中风风险低的受试者。血浆纤维蛋白原水平在发病后的1个月内持续升高,在慢性脑梗死患者中也持续升高。脑卒中高危患者的静默性脑梗塞病晚期分级伴有血浆纤维蛋白原水平升高,在脑梗塞发作后进一步升高。这种异常一直持续到慢性阶段。血浆纤维蛋白原水平升高可能反映了晚期静默性脑梗死患者的动脉粥样硬化进展,导致作为脑梗死危险因素的可能性增加。

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