探讨血脂水平对急性脑梗死(ACI)后出血性转化(HT)及预后的影响。
ACI患者在1月1日之间症状发作后72小时内,2015年12月31日,2016年,进行回顾性分析。将患者分为A组(无HT)和B组(HT)。使用改良的Rankin量表(mRS)评估疾病发作3个月后的结果。mRS评分0-2分提示预后良好,mRS评分3-6分提示预后不良。
共有732名患者符合纳入标准,其中A组628例,B组104例,HT发生率14.2%,中位发病时间为2d(四分位距,1-7d)。B组梗死面积大、皮质受累的患者比例分别为80.8%和79.8%,分别,均明显高于A组(28.7%和33.4%,分别)。B组房颤发生率明显高于A组(39.4%vs.13.9%,P<0.001)。调整后的多变量分析结果显示,梗死面积较大,皮质受累和房颤是HT的独立危险因素,总胆固醇(TC)是HT的保护因素(OR=0.359,95%CI0.136~0.944,P=0.038)。正常TC水平每降低1mmol/L,HT的风险增加了64.1%。B组3个月时的死亡率和发病率(21.2%和76.7%,分别)均显著高于A组(8.0%和42.8%,分别)。调整后的多因素分析结果显示大梗死面积(OR=12.178,95%CI5.390~27.516,P<0.001)是长期不良结局的独立危险因素。低密度脂蛋白胆固醇(LDL-C)是保护因素(OR=0.538,95%CI0.300-0.964,P=0.037)。正常LDL-C水平每降低1mmol/L,不良结局的风险增加了46.2%.主要疗法,包括静脉注射重组人组织纤溶酶原激活剂(rTPA),强化降脂他汀类药物和抗血小板,与HT或长期没有显着相关,ACI后预后不良。
对于梗死面积较大的患者,尤其是那些有皮质受累的人,AF,或较低水平的TC,ACI后HT的风险可能会增加。这些患者长期不利结果的风险可能随着LDL-C的降低而增加。
To study the influence of blood lipid levels on hemorrhagic transformation (HT) and prognosis after acute cerebral infarction (ACI).
Patients with ACI within 72 h of symptoms onset between January 1st, 2015, and December 31st, 2016, were retrospectively analyzed. Patients were divided into group A (without HT) and group B (HT). The outcomes were assessed after 3 months of disease onset using the modified Rankin Scale (mRS). An mRS score of 0-2 points indicated excellent prognosis, and an mRS score of 3-6 points indicated poor prognosis.
A total of 732 patients conformed to the inclusion criteria, including 628 in group A and 104 in group B. The incidence of HT was 14.2%, and the median onset time was 2 d (interquartile range, 1-7 d). The percentages of patients with large infarct size and cortex involvement in group B were 80.8 and 79.8%, respectively, which were both significantly higher than those in group A (28.7 and 33.4%, respectively). The incidence rate of atrial fibrillation (AF) in group B was significantly higher than that in group A (39.4% vs. 13.9%, P < 0.001). The adjusted multivariate analysis results showed that large infarct size, cortex involvement and AF were independent risk factors of HT, while total cholesterol (TC) was a protective factor of HT (OR = 0.359, 95% CI 0.136-0.944, P = 0.038). With every 1 mmol/L reduction in normal TC levels, the risk of HT increased by 64.1%. The mortality and morbidity at 3 months in group B (21.2 and 76.7%, respectively) were both significantly higher than those in group A (8.0 and 42.8%, respectively). The adjusted multivariate analysis results showed that large infarct size (OR = 12.178, 95% CI 5.390-27.516, P < 0.001) was an independent risk factor of long-term unfavorable outcomes, whereas low-density lipoprotein cholesterol (LDL-C) was a protective factor (OR = 0.538, 95% CI 0.300-0.964, P = 0.037). With every 1 mmol/L reduction in normal LDL-C levels, the risk of an unfavorable outcome increased by 46.2%. Major therapies, including intravenous recombinant human tissue plasminogen activator (rTPA), intensive lipid-lowering statins and anti-platelets, were not significantly related to either HT or long-term, post-ACI poor prognosis.
For patients with large infarct sizes, especially those with cortex involvement, AF, or lower levels of TC, the risk of HT might increase after ACI. The risk of a long-term unfavorable outcome in these patients might increase with a reduction in LDL-C.