伴有阻塞性睡眠呼吸暂停综合征的急性脑梗死患者血浆溶血磷脂含量的测定

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.

Changes of plasma lysophosphatidic levels in patients with obstructive sleep apnea syndrome-associated acute cerebral infarction

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.