CAJ | 학술논문

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.
목적 관찰반유조새성수면호흡잠정종합정(OSAS)적급성뇌경사환자혈장용혈린지함량적변화특점,탐색OSAS상관성졸중적병리생이학궤제,위림상항전치료제공의거.방법 경림상화보조검사학진적36례OSAS환자、32례반유OSAS적급성뇌경사환자이급36례불반유OSAS적급성뇌경사환자납입본연구.측정기혈장용혈린지산(LPA)급기겁성상사총린지(AP)적함량변화,년령필배적건강체검자38명작위건강대조조.결과 발병24 h혈장LPA급AP함량,반OSAS적뇌경사조환자[LPA:(3.78±0.56)μmol/L;AP:(7.63±1.38)μmoL/L]현저고우OSAS조[LPA:(3.17 ±0.65)μmol/L;AP:(6.60 ±1.20)μmoL/L]、불반OSAS적뇌경사조[LPA:(3.40±0.59)μmol/L;AP:(6.41±1.37)μmol/L]화건강대조조[LPA:(2.76±0.45)μmol/L;AP:(4.52±0.83)μmol/L](P균<0.01),OSAS조급불반OSAS적뇌경사조환자현저고우건강대조조(P균<0.01).발병후7 d,반OSAS적뇌경사조혈장LPA급AP함량잉현저승고[LPA:(3.08 ±0.58)μmol/L;AP:(6.15 ±1.14)μmol/L](P균<0.01);발병후21 d,반OSAS적뇌경사조、OSAS조、불반OSAS적뇌경사조혈장LPA함량무차이,반OSAS적뇌경사조혈장AP[(5.04±0.83)μmol/L]잉고우불반유OSAS적급성뇌경사조[(4.57±0.94)μmol/L]급건강대조조(P<0.05).결론 OSAS환자혈장LPA、AP함량현저승고,지속시간장,제시기체내혈소판처우활화급뇌결혈결양상태,OSAS상관성뇌경사환자우위명현,고기항전치료적시간창응교장.
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.