Relationship between hyperintensity on MRI-T1WI and hemorrhagic transformation after cerebral infarction and its influencing factors

This study aims to investigate the correlation between hyperintensity on Magnetic Resonance Imaging-T1 weighted imaging (MRI-T1WI) and post-infarction hemorrhagic transformation (HT) after cerebral infarction (CI) and analyze the influencing factors. This retrospective study comprised 115 patients diagnosed with cerebral infarction at our hospital. Their clinical data were collected, and they were then divided into a hyperintensity and a non-hyperintensity group based on their T1WI image characteristics. Comparative analysis was performed and the diagnostic value of T1WI hyperintensity for HT and influencing factors were assessed. Lesions in the 115 cerebral infarction patients were distributed as follows: 52 in the cerebral cortex, 37 in the basal ganglia, 14 in the cerebellum, 7 in the thalamus, and 5 in the subcortex. Hyperintensity on T1WI was observed in 4 cases before treatment, which increased to 27 cases after treatment, including 16 affecting the cerebral cortex. These hyperintense signals manifested as spotty, patchy or linear patterns along the gyri. In the basal ganglia, 10 cases exhibited spotty or patchy signals, surrounded by an annular hypointense shadow. Additionally, 3 cases involved the cerebellum, 1 the thalamus, and 1 the subcortex, all with spotty or patchy hyperintensities. HT occurred in 17 out of 115 patients (14.78%) one month after treatment. The diagnostic performance of T1WI hyperintensity for HT showed sensitivity, specificity, accuracy, positive predictive value, and negative predictive value of 94.12%, 84.69%, 86.09%, 51.61% and 98.81%, respectively, with a Kappa value of 0.588. Multivariate logistic regression analysis revealed that age, atherosclerosis, and infarct size were significant risk factors for T1WI hyperintensity in cerebral infarction (p < 0.05). Hyperintensity on T1WI in cerebral infarction primarily correlates with HT and could be a valuable diagnostic marker for HT, with age, atherosclerosis and infarct size identified as potential influencing factors.