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Ischemia‐modified albumin in acute aortic dissection

机译:缺血修饰的白蛋白用于急性主动脉夹层

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: Acute aortic dissection (AOD) is associated with high mortality and early diagnosis and treatment are essential. Ischemia‐modified albumin (IMA) is a marker of myocardial ischemia whereas cardiac enzymes are released when myocardial necrosis occurs. We investigated, for the first time, whether IMA increases in AOD either at presentation or after surgery. : We studied 46 consecutive patients with documented AOD; we also evaluated 13 consecutive patients with dilated ascending aortas scheduled for elective surgery and admitted for preoperative coronary angiography; 46 age‐matched normal subjects served as controls. Only patients with acute onset of symptoms were included. We evaluated IMA, cardiac enzymes, ‐terminal pro‐B‐type natriureticpeptide, albumin, C‐reactive protein (CRP), and D‐dimers on admission, 24 hr post‐operatively and 4 days post‐operatively. Duration from symptom onset to the first sample was 23±17 hr. : IMA did not differ between patients with AOD at presentation (93±19 U/ml), patients with chronic aneurysms (90±14 U/ml) and normal controls (91±9 U/ml). In addition, IMA did not change significantly after surgical repair. IMA, at baseline, however, correlated positively with time from symptom onset as well as CRP levels ( =0.05 and =0.007, respectively). : IMA is not elevated in AOD when blood sampling is performed within 23±17 hr after symptom onset nor increases after surgery. J. Clin. Lab. Anal. 24:399–402, 2010. © 2010 Wiley‐Liss, Inc.
机译::急性主动脉夹层(AOD)与高死亡率相关,早期诊断和治疗至关重要。缺血修饰的白蛋白(IMA)是心肌缺血的标志物,而心肌酶在发生心肌坏死时释放。我们首次调查了IMA在就诊时或手术后AOD是否增加。 :我们研究了46例连续的AOD患者;我们还评估了13例计划进行择期手术并接受术前冠状动脉造影的连续扩张主动脉扩张患者; 46名年龄匹配的正常受试者作为对照。仅包括症状急性发作的患者。我们评估了入院时,术后24小时和术后4天的IMA,心脏酶,终末pro B型钠尿肽,白蛋白,C反应蛋白(CRP)和D二聚体。从症状发作到第一个样本的持续时间为23±17 hr。 :IMA在出现AOD的患者(93±19 U / ml),患有慢性动脉瘤的患者(90±14mlU / ml)和正常对照组(91±9mlU / ml)之间没有差异。此外,手术修复后IMA没有明显改变。然而,基线时的IMA与症状发作的时间以及CRP水平呈正相关(分别为0.05和0.007)。 :在症状发作后23±17 hr内进行采血时,IMA的AOD不会升高,手术后也不会升高。 J.临床实验室肛门24:399–402,2010.©2010 Wiley-Liss,Inc.

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