Ischemic insular damage and stress ulcer in patients of acute ischemic stroke

Abstract

Background and aimsStress ulcer (SU) is a common complication in patients with acute ischemic stroke. The relationship of infarction location and the incidence of SU was unclear. Herein, we aim to investigate the association between ischemic insular damage and the development of SU.MethodsData were retrieved from the SPARK study (Effect of Cardiac Function on Short‐Term Functional Prognosis in Patients with Acute Ischemic Stroke). We included the patients who had experienced an ischemic stroke within 7 days. The diagnosis of SU was based on clinical manifestations, including hematemesis, bloody nasogastric tube aspirate, or hematochezia. Evaluation of ischemic insular damage was conducted through magnetic resonance imaging. Cyclo‐oxygenase regression analysis and Kaplan–Meier survival curves were used to assess the relationship between ischemic insular damage and the occurrence of SU.ResultsAmong the 1357 patients analyzed, 110 (8.1%) developed SUs during hospitalization, with 69 (6.7%) experiencing infarctions in the anterior circulation. After adjusting for potential confounders, patients with ischemic insular damage exhibited a 2.16‐fold higher risk of developing SUs compared to those without insular damage (p = .0206). Notably, among patients with infarctions in the anterior circulation, those with insular damage had a 2.21‐fold increased risk of SUs (p = .0387). Moreover, right insular damage was associated with a higher risk of SUs compared to left insular damage or no insular damage (p for trend = .0117). Kaplan–Meier curves demonstrated early separation among groups, persisting throughout the follow‐up period (all p < .0001).ConclusionsThis study identified a significant independent correlation between ischemic insular damage, particularly on the right side, and the development of SU during hospitalization, indicating the need to consider prophylactic acid‐suppressive treatment for patients with ischemic insular damage.