Hemorrhagic transformation (HT) of cerebral infarction is considered as one of the most serious complications. Increasing evidence show that statin use might reduce the neuroinflammation and even improve clinical prognosis of stroke patients. However, there is not enough evidence that premorbid statin use may affect the risk of hemorrhagic transformation in stroke patients. The aim of our study was to investigate the role of premorbid long-term statin use in HT after acute ischemic stroke.
We retrospectively analyzed ischemic stroke patients in Huashan Hospital from 1 January 2012 to 31 December 2022 based on hospital electronic case records. Since thrombolysis or thrombectomy might interfere with the effect of statin use we excluded patients who received thrombolysis or thrombectomy treatment. A matched case-control study was conducted for reducing the impact of various confounding factors. The independent roles of statin use and serum lipids in HT was evaluated by binary logistic regression analysis.
A total of 254 ischemic stroke patients met the inclusion criteria and have been matched at 1:1 ratio, according age (± 5 years), admission NIHSS (± 3 scores), prior antiplatelets and anticoagulation therapy and previous stroke history. The patients without HT were regarded as control group. The percentage of HT was significantly lower in patients with premorbid long-term statin use (22.1 % vs. 41.7 %, p = 0.001). The incidence rate of diabetes mellitus and symptomatic deterioration (NIHSS increase ≥ 4) was higher in patients with HT. There were 18 patients having intracerebral hemorrhage before any reperfusion treatment. They had lower level of LDL-C (1.76 (1.73, 2.26) vs 2.72 (2.28, 3.09), p < 0.001) and were prone to previously take statins (55.6 % vs 16.5 %,p < 0.001). However, ECASS classification and all the outcome scores did not present any statistical difference in our study. In logistic regression analysis DM (OR = 2.001, 95 %CI 1.124–3.563, p = 0.018), increased levels of LDC-C (OR = 0.334, 95 %CI 0.172–0.649), p = 0.001) and HDL-C (OR = 13.303, 95 %CI 2.050–86.328, p = 0.001) were independent risk factors in occurrence of HT in patients with ischemic stroke, while premorbid statin use (OR = 0.269, 95 %CI 0.117–0.615, p = 0.002) could still be regarded as a protective factor in preventing intracranial hemorrhage after cerebral infarction. Additionally, lower level of LDL-C was also an independent risk factor in spontaneous HT after cerebral infarction (OR = 45.45, 95 %CI 5.62–333.33, p < 0.001), regardless of statin use.
Premorbid long-term statin use plays a protective role in the HT after cerebral infarction. However, low serum LDL-C and high HDL-C might be independent risk factors in the occurrence of HT irrespective of statin use. The previous statin uses and serum lipid levels have no impact on prognosis of HT.
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