PDF(Pubmed)
Abstract：
BACKGROUND: The origin of pre-existing cognitive impairment in stroke patients remains controversial, with a vascular or a degenerative hypothesis.
OBJECTIVE: To determine whether endothelial dysfunction is associated with pre-existing cognitive problems, lesion load and biological anomalies in stroke patients.
METHODS: Patients originated from the prospective STROKDEM study. The baseline cognitive state, assessed using the IQ-CODE, and risk factors for stroke were recorded at inclusion. Patients with an IQ-CODE score >64 were excluded. Endothelial function was determined 72 h after stroke symptom onset by non-invasive digital measurement of endothelium-dependent flow-mediated dilation and calculation of the reactive hyperemia index (RHI). RHI ≤ 1.67 indicated endothelial dysfunction. Different biomarkers of endothelial dysfunction were analysed in blood or plasma. All patients underwent MRI 72 h after stroke symptom onset.
RESULTS: A total of 86 patients were included (52 males; mean age 63.5 ± 11.5 years). Patients with abnormal RHI have hypertension or antihypertensive treatment more often. The baseline IQ-CODE was abnormal in 33 (38.4%) patients, indicating a pre-existing cognitive problem. Baseline IQ-CODE > 48 was observed in 15 patients (28.3%) with normal RHI and in 18 patients (54.6%) with abnormal RHI (p = 0.016). The RHI median was significantly lower in patients with abnormal IQ-CODE. Abnormal RHI was associated with a significantly higher median FAZEKAS score (2.5 vs. 2; p = 0.008), a significantly higher frequency of periventricular lesions (p = 0.015), more white matter lesions (p = 0.007) and a significantly higher cerebral atrophy score (p < 0.001) on MRI. Vascular biomarkers significantly associated with abnormal RHI were MCP-1 (p = 0.009), MIP_1a (p = 0.042), and homocysteinemia (p < 0.05).
CONCLUSIONS: A vascular mechanism may be responsible for cognitive problems pre-existing stroke. The measurement of endothelial dysfunction after stroke could become an important element of follow-up, providing an indication of the functional and cognitive prognosis of stroke patients.
OBJECTIVE: To determine whether endothelial dysfunction is associated with pre-existing cognitive problems, lesion load and biological anomalies in stroke patients.
METHODS: Patients originated from the prospective STROKDEM study. The baseline cognitive state, assessed using the IQ-CODE, and risk factors for stroke were recorded at inclusion. Patients with an IQ-CODE score >64 were excluded. Endothelial function was determined 72 h after stroke symptom onset by non-invasive digital measurement of endothelium-dependent flow-mediated dilation and calculation of the reactive hyperemia index (RHI). RHI ≤ 1.67 indicated endothelial dysfunction. Different biomarkers of endothelial dysfunction were analysed in blood or plasma. All patients underwent MRI 72 h after stroke symptom onset.
RESULTS: A total of 86 patients were included (52 males; mean age 63.5 ± 11.5 years). Patients with abnormal RHI have hypertension or antihypertensive treatment more often. The baseline IQ-CODE was abnormal in 33 (38.4%) patients, indicating a pre-existing cognitive problem. Baseline IQ-CODE > 48 was observed in 15 patients (28.3%) with normal RHI and in 18 patients (54.6%) with abnormal RHI (p = 0.016). The RHI median was significantly lower in patients with abnormal IQ-CODE. Abnormal RHI was associated with a significantly higher median FAZEKAS score (2.5 vs. 2; p = 0.008), a significantly higher frequency of periventricular lesions (p = 0.015), more white matter lesions (p = 0.007) and a significantly higher cerebral atrophy score (p < 0.001) on MRI. Vascular biomarkers significantly associated with abnormal RHI were MCP-1 (p = 0.009), MIP_1a (p = 0.042), and homocysteinemia (p < 0.05).
CONCLUSIONS: A vascular mechanism may be responsible for cognitive problems pre-existing stroke. The measurement of endothelial dysfunction after stroke could become an important element of follow-up, providing an indication of the functional and cognitive prognosis of stroke patients.
摘要：
背景：中风患者预先存在的认知障碍的起源仍然存在争议，血管或退化假设。
目的：为了确定内皮功能障碍是否与先前存在的认知问题有关，中风患者的病变负荷和生物学异常。
方法：患者起源于前瞻性STROKDEM研究。基线认知状态，使用智商代码评估，纳入时记录卒中的危险因素.排除IQ-CODE评分>64的患者。通过非侵入性数字测量内皮依赖性血流介导的扩张并计算反应性充血指数（RHI），在中风症状发作后72小时确定内皮功能。RHI≤1.67提示内皮功能障碍。在血液或血浆中分析内皮功能障碍的不同生物标志物。所有患者在卒中症状发作72h后行MRI检查。
结果：共纳入86例患者（男性52例；平均年龄63.5±11.5岁）。RHI异常的患者更经常患有高血压或抗高血压治疗。33例(38.4%)患者的基线IQ-CODE异常,表明预先存在的认知问题。在15例RHI正常的患者（28.3％）和18例RHI异常的患者（54.6％）中观察到基线IQ-CODE>48（p=0.016）。IQ-CODE异常患者的RHI中位数明显较低。异常RHI与中位数较高的FAZEKAS评分相关（2.5vs.2；p=0.008），脑室周围病变的频率明显更高（p=0.015），更多的白质病变（p=0.007）和显着更高的脑萎缩评分（p<0.001）在MRI。与异常RHI显著相关的血管生物标志物是MCP-1(p=0.009),MIP_1a(p=0.042)，和同型半胱氨酸血症（p<0.05）。
结论：血管机制可能是先前存在的卒中认知问题的原因。卒中后内皮功能障碍的测量可能成为随访的重要因素。提供中风患者的功能和认知预后的指示。
目的：为了确定内皮功能障碍是否与先前存在的认知问题有关，中风患者的病变负荷和生物学异常。
方法：患者起源于前瞻性STROKDEM研究。基线认知状态，使用智商代码评估，纳入时记录卒中的危险因素.排除IQ-CODE评分>64的患者。通过非侵入性数字测量内皮依赖性血流介导的扩张并计算反应性充血指数（RHI），在中风症状发作后72小时确定内皮功能。RHI≤1.67提示内皮功能障碍。在血液或血浆中分析内皮功能障碍的不同生物标志物。所有患者在卒中症状发作72h后行MRI检查。
结果：共纳入86例患者（男性52例；平均年龄63.5±11.5岁）。RHI异常的患者更经常患有高血压或抗高血压治疗。33例(38.4%)患者的基线IQ-CODE异常,表明预先存在的认知问题。在15例RHI正常的患者（28.3％）和18例RHI异常的患者（54.6％）中观察到基线IQ-CODE>48（p=0.016）。IQ-CODE异常患者的RHI中位数明显较低。异常RHI与中位数较高的FAZEKAS评分相关（2.5vs.2；p=0.008），脑室周围病变的频率明显更高（p=0.015），更多的白质病变（p=0.007）和显着更高的脑萎缩评分（p<0.001）在MRI。与异常RHI显著相关的血管生物标志物是MCP-1(p=0.009),MIP_1a(p=0.042)，和同型半胱氨酸血症（p<0.05）。
结论：血管机制可能是先前存在的卒中认知问题的原因。卒中后内皮功能障碍的测量可能成为随访的重要因素。提供中风患者的功能和认知预后的指示。
