Influences of blood lipids on the occurrence and prognosis of hemorrhagic transformation after acute cerebral infarction: a case-control study of 732 patients

Gang Lv, Guo-qiang Wang, Zhen-xi Xia, Hai-xia Wang, Nan Liu, Wei Wei, Yong-hua Huang, Wei-wei Zhang

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.