Abstract

Hemorrhagic transformation (HT) is a severe complication occurring in acute ischemic stroke (AIS) patients. We explored the association between low triiodothyronine (T3) syndrome and HT in AIS patients. A total of 208 consecutive participants with HT and 208 age- and sex-matched stroke patients without HT were enrolled in this study. HT was diagnosed by follow-up imaging assessment, and was radiologically classified as hemorrhagic infarction (HI) type 1 or 2 or parenchymal hematoma (PH) type 1 or 2. HT was also classified into asymptomatic or symptomatic. The incidence of low T3 syndrome was significantly higher among patients who developed HT than among those without HT. Moreover, the more severe the HT, the lower the detected T3 levels. Multivariate-adjusted binary logistic regression showed that low T3 syndrome was an independent risk factor for HT and symptomatic HT in AIS patients. Low T3 syndrome was also significantly associated with a higher risk of PH, but not with the risk of HI. Thus, low T3 syndrome was independently associated with the risk of HT, symptomatic HT, and severe HT (PH) in AIS patients, which suggests monitoring T3 could be a useful means of preventing HT in patients with ischemic stroke.

Highlights

  • Hemorrhagic transformation (HT) is a common complication among patients suffering from acute ischemic stroke (AIS) [1, 2], and has been shown to result in poor outcomes, including early mortality and disability [3,4,5]

  • Low T3 syndrome was independently associated with the risk of HT, symptomatic HT, and severe HT (PH) in AIS patients, which suggests monitoring T3 could be a useful means of preventing HT in patients with ischemic stroke

  • Consistent with earlier reports [15, 23,24,25,26], our results indicate that compared to AIS patients without HT, those with HT tend to have a history of atrial fibrillation, greater stroke severity, and higher inflammatory indices, including leukocyte counts and fibrinogen levels

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Summary

Introduction

Hemorrhagic transformation (HT) is a common complication among patients suffering from acute ischemic stroke (AIS) [1, 2], and has been shown to result in poor outcomes, including early mortality and disability [3,4,5]. Risk factors for HT previously identified in ischemic stroke patients include old age [6], atrial fibrillation [4], prolonged interval between stroke onset to treatment [5], elevated blood glucose [7], higher systolic blood pressure [8], thrombolysis [9], and symptom severity [10]. Given that disruption of vascular endothelial cells is a crucial mechanism related to the development of HT after cerebral ischemia [15], the presence of low thyroid hormone levels may indicate an increased risk of HT

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