The Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China.
Department of Neurobiology, Beijing Institute of Geriatrics, Xuanwu Hospital of Capital Medical University, Beijing, China.
Curr Neurovasc Res. 2019;16(2):135-141. doi: 10.2174/1567202616666190412160451.
Gastrointestinal (GI) hemorrhage is serious during the acute phase and is reported to be related to an increased risk of death during the acute phase of acute ischemic stroke in particular. Our study was designed to investigate the relationship between GI hemorrhage and the mortality of acute ischemic stroke, assessing the influence of cerebrovascular risk factors, brain herniation and oral anticoagulation on the onset of GI hemorrhage. The identified risk factors for the occurrence of GI hemorrhage help to elucidate their respective roles in the mortality of acute ischemic stroke.
A total of 15993 consecutive patients with acute ischemic stroke, including 216 cases and 15777 controls, were enrolled in the study from October 2010 to December 2018. Basic clinical and examination data were collected at the time of study enrollment. GI hemorrhage was diagnosed according to the presence of clinical features and endoscopy. Chi-square test and multiple logistic regressions were conducted to explore the associations between the GI hemorrhage occurrence and known risk factors. Kaplan-Meier was used to assess the influence of GI hemorrhage on the age of mortality of acute ischemic stroke.
GI hemorrhage cases among patients with acute ischemic stroke accounted for 1.35%. Male patients with ischemic stroke were more likely to have GI hemorrhage than their female counterparts (odds ratio (OR): 1.79; P = 0.000). Patients with atrial fibrillation (AF) had a higher incidence of GI hemorrhage than their counterparts without AF (3.03% vs. 1.20%; P < 0.05). Use of oral anticoagulants was related to increased risk for GI hemorrhage (OR: 1.96; P = 0.00). After adjusting for age and sex, both AF and oral anticoagulant use maintained associations with increased risk for GI hemorrhage (2.59-times and 2.02-times risk respectively; P = 0.00). Patients with hyperlipidemia had a lower incidence of GI hemorrhage than their counterparts without hyperlipidemia (0.62% vs. 1.60%; P < 0.05). Hyperlipidemia was associated with a reduced risk of GI hemorrhage (OR: 0.38, 95% confidence interval (CI): 0.25-0.58; P = 0.00), even after adjusting for age and sex (OR: 0.41; P = 0.00). Patients with brain herniation had a 6.54-times increased risk for GI hemorrhage (P = 0.00). GI hemorrhage was associated with 10.98-fold risk for mortality of acute ischemic stroke (P = 0.00). There was an interaction between GI hemorrhage and brain herniation and increased 26.91-fold risk for the mortality after acute ischemic stroke (P = 0.00).
AF, oral anticoagulant use, brain herniation and male sex increase GI hemorrhage risk, while hyperlipidemia reduces risk. GI hemorrhage itself increases the risk for mortality of acute ischemic stroke. The interaction between GI hemorrhage and brain herniation increased the risk for the mortality after acute ischemic stroke.
胃肠道(GI)出血在急性期较为严重,据报道,其与急性缺血性脑卒中急性期的死亡风险增加有关。本研究旨在探讨 GI 出血与急性缺血性脑卒中死亡率之间的关系,评估脑血管危险因素、脑疝和口服抗凝剂对 GI 出血发生的影响。确定 GI 出血发生的危险因素有助于阐明它们在急性缺血性脑卒中死亡率中的各自作用。
本研究共纳入了 15993 例连续急性缺血性脑卒中患者,包括 216 例病例和 15777 例对照,这些患者于 2010 年 10 月至 2018 年 12 月期间入组。在研究入组时收集了基本的临床和检查数据。根据临床特征和内镜检查诊断 GI 出血。采用卡方检验和多因素逻辑回归分析探讨 GI 出血发生与已知危险因素之间的关系。采用 Kaplan-Meier 法评估 GI 出血对急性缺血性脑卒中患者死亡年龄的影响。
急性缺血性脑卒中患者中 GI 出血的发生率为 1.35%。与女性相比,男性缺血性脑卒中患者更易发生 GI 出血(优势比(OR):1.79;P = 0.000)。房颤(AF)患者的 GI 出血发生率高于无 AF 的患者(3.03%比 1.20%;P < 0.05)。使用口服抗凝剂与 GI 出血风险增加相关(OR:1.96;P = 0.00)。在调整年龄和性别后,AF 和口服抗凝剂的使用与 GI 出血风险增加均保持关联(分别为 2.59 倍和 2.02 倍;P = 0.00)。与无高脂血症的患者相比,高脂血症患者的 GI 出血发生率较低(0.62%比 1.60%;P < 0.05)。高脂血症与 GI 出血风险降低相关(OR:0.38,95%置信区间(CI):0.25-0.58;P = 0.00),即使在调整了年龄和性别后(OR:0.41;P = 0.00)。脑疝患者发生 GI 出血的风险增加 6.54 倍(P = 0.00)。GI 出血与急性缺血性脑卒中死亡率的风险增加 10.98 倍相关(P = 0.00)。GI 出血与脑疝之间存在交互作用,使急性缺血性脑卒中后死亡率增加 26.91 倍(P = 0.00)。
AF、口服抗凝剂使用、脑疝和男性会增加 GI 出血风险,而高脂血症会降低风险。GI 出血本身会增加急性缺血性脑卒中的死亡风险。GI 出血与脑疝之间的相互作用增加了急性缺血性脑卒中后死亡的风险。