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Objective To observe the changing characteristics of plasma lysophosphatidic acid (LPA) or acidia phospholipid (AP) levels in patients with obstructive sleep apnea syndrome-associated(OSAS)acute cerebral infarction and to explore the pathophysiological mechanisms of OSAS-related stroke so as to provide basis for clinical antithrombotic therapy. Methods Thirty-six patients of OSAS, 32 patients of OSAS-related acute stoke and 36 patients of acute stoke without OSAS diagnosed by clinical and accessory examinations were enrolled in the current study. Thirty-eight age-matched healthy subjects were recruited as controls. The changes of the plasma LPA and AP levels were measured. Results Within 24 hours after symptom onset, the plasma LPA and AP levels in the OSAS-related acute cerebral infarction group (LPA(3. 78 ±0. 56) μmol/L; AP(7. 63 ± 1. 38) μmol/L) were significantly higher than those in the OSAS group(LPA(3. 17 ±0. 65) μmol/L; AP(6. 60 ± 1. 20) μmol/L) ,the not OSAS-related acute cerebral infarction group (LPA (3. 40 ± 0. 59)μmol/L; AP (6. 41 ± 1. 37)μmol/L) and the control group (LPA(2.76±0.45)μmol/L;AP(4.52±0. 83) μmol/L (P < 0. 01)) . The levels of LPA and AP in the OSAS group and the not OSAS-related acute cerebral infarction group were significantly higher than those in the control group(P<0. 01). Seven days after symptom onset, the plasma LPA and AP levels in the OSAS-associated acute cerebral infarction group (LPA(3.08 ± 0. 58) μmol/L; AP(6. 15 ±1. 14)μmol/L) were still higher(P < 0. 01) . The plasma LPA levels were not significantly different among the OSAS-related acute cerebral infarction group, the not OSAS-related acute cerebral infarction group and the control group 21 days after symptom onset, whereas the plasma AP levels in the OSAS-related acute cerebral infarction group (5. 04 ± 0. 83) μmol/L were still significantly higher than those in the not OSAS-related acute cerebral infarction group (4. 57 ± 0. 94) μmol/L and the control group (P < 0.05). Conclusions The significantly elevated plasma LPA and AP levels in patients with OSAS suggested that platelets in vivo are in an activated state and in cerebral ischemia and hypoxia state, especially for the OSAS-related acute cerebral infarction patients. The activated state of platelet may persist for a long time, thus the time window for antithrombotic therapy may be longer.  相似文献   
2.
目的观察阻塞性睡眠呼吸暂停综合征(OSAS)患者血浆脂蛋白相关磷脂酶A2(Lp-PLA2)水平的变化特点,探索OSAS相关性脑卒中的病理生理学机制,为临床抗栓治疗提供依据。方法经临床和辅助检查确诊的OSAS患者40例(OSAS组)、伴OSAS的急性脑梗死患者36例(OSAS伴脑梗死组)以及不伴OSAS的急性脑梗死患者38例(脑梗死组)纳入本研究,另选取年龄、性别匹配的36名健康者作为对照组。采用ELISA法检测各组血浆Lp-PLA2水平。结果发病24h时,OSAS组、OSAS伴脑梗死组以及脑梗死组患者血浆LpPLA2水平均显著高于对照组(均P0.01),且OSAS伴脑梗死组血浆Lp-PLA2水平高于OSAS组和脑梗死组(均P0.01)。至发病后21d,OSAS伴脑梗死组患者血浆Lp-PLA2含量仍高于脑梗死组和对照组(P0.01),而脑梗死组和对照组血浆Lp-PLA2水平比较差异无统计学意义(P0.05)。结论 OSAS患者血浆LpPLA2水平升高,提示其体内存在Lp-PLA2相关性炎性反应,LP-PLA2可作为一种理想的分子标记物用于判断OSAS患者体内炎性反应状态;OSAS伴脑梗死患者炎性反应明显且持续时间较长,可能为早期强化抗炎治疗提供理论依据。  相似文献   
3.
Objective To observe the changing characteristics of plasma lysophosphatidic acid (LPA) or acidia phospholipid (AP) levels in patients with obstructive sleep apnea syndrome-associated(OSAS)acute cerebral infarction and to explore the pathophysiological mechanisms of OSAS-related stroke so as to provide basis for clinical antithrombotic therapy. Methods Thirty-six patients of OSAS, 32 patients of OSAS-related acute stoke and 36 patients of acute stoke without OSAS diagnosed by clinical and accessory examinations were enrolled in the current study. Thirty-eight age-matched healthy subjects were recruited as controls. The changes of the plasma LPA and AP levels were measured. Results Within 24 hours after symptom onset, the plasma LPA and AP levels in the OSAS-related acute cerebral infarction group (LPA(3. 78 ±0. 56) μmol/L; AP(7. 63 ± 1. 38) μmol/L) were significantly higher than those in the OSAS group(LPA(3. 17 ±0. 65) μmol/L; AP(6. 60 ± 1. 20) μmol/L) ,the not OSAS-related acute cerebral infarction group (LPA (3. 40 ± 0. 59)μmol/L; AP (6. 41 ± 1. 37)μmol/L) and the control group (LPA(2.76±0.45)μmol/L;AP(4.52±0. 83) μmol/L (P < 0. 01)) . The levels of LPA and AP in the OSAS group and the not OSAS-related acute cerebral infarction group were significantly higher than those in the control group(P<0. 01). Seven days after symptom onset, the plasma LPA and AP levels in the OSAS-associated acute cerebral infarction group (LPA(3.08 ± 0. 58) μmol/L; AP(6. 15 ±1. 14)μmol/L) were still higher(P < 0. 01) . The plasma LPA levels were not significantly different among the OSAS-related acute cerebral infarction group, the not OSAS-related acute cerebral infarction group and the control group 21 days after symptom onset, whereas the plasma AP levels in the OSAS-related acute cerebral infarction group (5. 04 ± 0. 83) μmol/L were still significantly higher than those in the not OSAS-related acute cerebral infarction group (4. 57 ± 0. 94) μmol/L and the control group (P < 0.05). Conclusions The significantly elevated plasma LPA and AP levels in patients with OSAS suggested that platelets in vivo are in an activated state and in cerebral ischemia and hypoxia state, especially for the OSAS-related acute cerebral infarction patients. The activated state of platelet may persist for a long time, thus the time window for antithrombotic therapy may be longer.  相似文献   
4.
目的 观察伴有阻塞性睡眠呼吸暂停综合征(OSAS)的急性脑梗死患者血浆溶血磷脂含量的变化特点,探索OSAS相关性卒中的病理生理学机制,为临床抗栓治疗提供依据.方法 经临床和辅助检查确诊的36例OSAS患者、32例伴有OSAS的急性脑梗死患者以及36例不伴有OSAS的急性脑梗死患者纳入本研究.测定其血浆溶血磷脂酸(LPA)及其极性相似总磷脂(AP)的含量变化,年龄匹配的健康体检者38名作为健康对照组.结果 发病24 h血浆LPA及AP含量,伴OSAS的脑梗死组患者[LPA:(3.78±0.56)μmol/L;AP:(7.63±1.38)μmoL/L]显著高于OSAS组[LPA:(3.17 ±0.65)μmol/L;AP:(6.60 ±1.20)μmoL/L]、不伴OSAS的脑梗死组[LPA:(3.40±0.59)μmol/L;AP:(6.41±1.37)μmol/L]和健康对照组[LPA:(2.76±0.45)μmol/L;AP:(4.52±0.83)μmol/L](P均<0.01),OSAS组及不伴OSAS的脑梗死组患者显著高于健康对照组(P均<0.01).发病后7 d,伴OSAS的脑梗死组血浆LPA及AP含量仍显著升高[LPA:(3.08 ±0.58)μmol/L;AP:(6.15 ±1.14)μmol/L](P均<0.01);发病后21 d,伴OSAS的脑梗死组、OSAS组、不伴OSAS的脑梗死组血浆LPA含量无差异,伴OSAS的脑梗死组血浆AP[(5.04±0.83)μmol/L]仍高于不伴有OSAS的急性脑梗死组[(4.57±0.94)μmol/L]及健康对照组(P<0.05).结论 OSAS患者血浆LPA、AP含量显著升高,持续时间长,提示其体内血小板处于活化及脑缺血缺氧状态,OSAS相关性脑梗死患者尤为明显,故其抗栓治疗的时间窗应较长.  相似文献   
5.
目的探讨CHA2DS2-VASc评分联合血浆脂蛋白相关磷脂酶A2水平(Lp-PLA2)对非瓣膜病心房颤动(NVAF)患者脑梗死风险的预测价值。方法入选广州医科大学附属惠州医院住院的242例NVAF患者,记录入院时血浆Lp-PLA2水平,计算CHA2DS2-VASc评分。出院后每3个月随访1次,随访期间发生缺血性脑卒中或随访满1a随访结束,根据随访结果分为脑梗死组和非脑脑梗死组。结果脑梗死组CHA2DS2-VASc评分、Lp-PLA2水平比非脑梗死组偏高。经Logistic回归分析证实,高CHA2DS2-VASc评分、高Lp-PLA2水平为NVAF患者发生脑梗死的危险因素。CHA2DS2-VASc评分、Lp-PLA2水平、CHA2DS2-VASc评分联合Lp-PLA2水平预测NVAF患者发生脑梗死的受试者工作特征(ROC)曲线下面积分别为0.815、0.796、0.879。结论 CHA2DS2-VASc评分联合Lp-PLA2水平可提高对NVAF患者发生脑梗死风险的预测价值。  相似文献   
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