Department of Medicine and Neurology, The Royal Melbourne Hospital, University of Melbourne, Parkville, Vic., Australia.
Cerebrovasc Dis. 2011;32(4):401-5. doi: 10.1159/000331467. Epub 2011 Oct 8.
Fluid-attenuated inversion recovery (FLAIR) hyperintensity within an acute cerebral infarct may reflect delayed onset time and increased risk of hemorrhage after thrombolysis. Given the important implications for clinical practice, we examined the prevalence of FLAIR hyperintensity in patients 3-6 h from stroke onset and its relationship to parenchymal hematoma (PH).
Baseline DWI and FLAIR imaging with subsequent hemorrhage detection (ECASS criteria) were prospectively obtained in patients 3-6 h after stroke onset from the pooled EPITHET and DEFUSE trials. FLAIR hyperintensity within the region of the acute DWI lesion was rated qualitatively (dichotomized as visually obvious or subtle (i.e. only visible after careful windowing)) and quantitatively (using relative signal intensity (RSI)). The association of FLAIR hyperintensity with hemorrhage was then tested alongside established predictors (very low cerebral blood volume (VLCBV) and diffusion (DWI) lesion volume) in logistic regression analysis.
There were 49 patients with pre-treatment FLAIR imaging (38 received tissue plasminogen activator (tPA), 5 developed PH). FLAIR hyperintensity within the region of acute DWI lesion occurred in 48/49 (98%) patients, was obvious in 18/49 (37%) and subtle in 30/49 (61%). Inter-rater agreement was 92% (κ = 0.82). The prevalence of obvious FLAIR hyperintensity did not differ between studies obtained in the 3-4.5 h and 4.5-6 h time periods (40% vs. 33%, p = 0.77). PH was poorly predicted by obvious FLAIR hyperintensity (sensitivity 40%, specificity 64%, positive predictive value 11%). In univariate logistic regression, VLCBV (p = 0.02) and DWI lesion volume (p = 0.03) predicted PH but FLAIR lesion volume (p = 0.87) and RSI (p = 0.11) did not. In ordinal logistic regression for hemorrhage grade adjusted for age and baseline stroke severity (NIHSS), increased VLCBV (p = 0.002) and DWI lesion volume (p = 0.003) were associated with hemorrhage but FLAIR lesion volume (p = 0.66) and RSI (p = 0.35) were not.
Visible FLAIR hyperintensity is almost universal 3-6 h after stroke onset and did not predict subsequent hemorrhage in this dataset. Our findings question the value of excluding patients with FLAIR hyperintensity from reperfusion therapies. Larger studies are required to clarify what implications FLAIR-positive lesions have for patient selection.
在急性脑梗死中,FLAIR 高信号可能反映溶栓后迟发性和出血风险增加。鉴于其对临床实践的重要意义,我们检查了发病后 3-6 小时的患者中 FLAIR 高信号的发生率及其与实质血肿(PH)的关系。
从 EPITHET 和 DEFUSE 试验的汇总数据中,前瞻性地获得了发病后 3-6 小时的患者的基线 DWI 和 FLAIR 成像,以及随后的出血检测(ECASS 标准)。急性 DWI 病变区域内的 FLAIR 高信号被定性评估(分为视觉明显或细微(即仅在仔细调整窗口后可见))和定量评估(使用相对信号强度(RSI))。然后,在逻辑回归分析中,将 FLAIR 高信号与出血与已建立的预测因素(极低脑血容量(VLCBV)和弥散(DWI)病变体积)一起进行测试。
共有 49 例患者接受了预处理 FLAIR 成像(38 例接受组织纤溶酶原激活剂(tPA)治疗,5 例发生 PH)。49 例患者中有 48 例(98%)在急性 DWI 病变区域出现 FLAIR 高信号,其中 18 例(37%)明显,30 例(61%)细微。两位评估者之间的一致性为 92%(κ=0.82)。在 3-4.5 小时和 4.5-6 小时时间段内,明显 FLAIR 高信号的发生率在研究中无差异(40%比 33%,p=0.77)。明显 FLAIR 高信号对 PH 的预测能力较差(敏感性 40%,特异性 64%,阳性预测值 11%)。在单变量逻辑回归中,VLCBV(p=0.02)和 DWI 病变体积(p=0.03)预测 PH,但 FLAIR 病变体积(p=0.87)和 RSI(p=0.11)则不能。在对年龄和基线卒中严重程度(NIHSS)进行调整的等级逻辑回归中,增加的 VLCBV(p=0.002)和 DWI 病变体积(p=0.003)与出血相关,但 FLAIR 病变体积(p=0.66)和 RSI(p=0.35)则不相关。
在发病后 3-6 小时,可见的 FLAIR 高信号几乎普遍存在,但在该数据集中并未预测随后的出血。我们的研究结果质疑将 FLAIR 高信号患者排除在再灌注治疗之外的价值。需要更大的研究来阐明 FLAIR 阳性病变对患者选择的影响。