TIME COURSE OF ALPHA-1-ACID GLYCOPROTEIN AND ITS RELATION TO MYOCARDIAL AFTER ACUTE MYOCARDIAL-INFARCTION

TIME COURSE OF ALPHA-1-ACID GLYCOPROTEIN AND ITS RELATION TO MYOCARDIAL AFTER ACUTE MYOCARDIAL-INFARCTION
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DOI:
10.1016/0002-9149(85)90846-x
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发表时间:
1985-01-01
影响因子:
2.8
通讯作者:
LOUIE, M
LOUIE, M
中科院分区:
医学3区
文献类型:
--
作者:
GIARDINA, EGV;RABY, K;LOUIE, M

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急性期反应物,α-1-酸性糖蛋白,与一些基本的抗心律失常药物结合,包括利多卡因、奎尼丁、心得安、丙咪嗪和异丙吡胺。与α-1-酸性糖蛋白的结合导致游离药物分数的减少,并可能改变药物的预期浓度:反应关系,特别是当α-1-酸性糖蛋白有不可预测的大小或快速变化时。为探讨急性心肌梗死(AMI)后1个月血中α1-酸性糖蛋白的变化规律及变化幅度,采集了27例急性心肌梗死(AMI)患者的血样,其中14例为急性心肌梗死患者,13例为无急性心肌梗死的胸痛综合征患者。急性心肌梗死患者α1-酸性糖蛋白在发病72小时后显著升高(平均153±35 mg/dl)(p<0.05),第7天最高(平均165±53 mg/dl)(p<0.05),28天恢复至基线水平。有胸痛但无急性心肌梗死的患者α1-酸性糖蛋白无明显变化。回归分析显示肌酸激酶(p<0.005)、乳酸脱氢酶(p<0.001)与α-1-酸性糖蛋白呈显著正相关,提示大面积急性心肌梗死患者的α-1-酸性糖蛋白浓度较高。急性心肌梗死患者在恢复期和出院时,由于α-1-酸性糖蛋白结合的改变,可能导致对总药物浓度的误解以及对抗心律失常药物的急性反应。
The acute phase reactant, alpha-1-acid glycoprotein, binds to a number of basic antiarrhythmic drugs, including lidocaine, quinidine, propranolol, imipramine and disopyramide. Binding to alpha-1-acid glycoprotein accounts for a decrease in free drug fraction and may alter the expected concentration: response relation of drugs particularly when there are unpredictably large or rapid changes in alpha-1-acid glycoprotein. To determine the time course and magnitude of alpha-1-acid glycoprotein for 1 month after acute myocardial infarction (AMI), blood samples were collected from 27 patients, 14 with AMI and 13 with a chest pain syndrome but no AMI. Patients with AMI had a significant increase in alpha-1-acid glycoprotein after 72 hours (mean 153 ± 35 mg/dl) (p < 0.05), and the maximum was observed on day 7 (mean 165 ± 53 mg/dl) (p < 0.05), returning to baseline by 28 days. There was no significant change in alpha-1-acid glycoprotein in patients with chest pain but no AMI. Regression analysis showed a significant relation between creatine kinase (p < 0.005) and lactic dehydrogenase (p < 0.001) vs alpha-1-acid glycoprotein indicating alpha-1-acid glycoprotein concentration is high in patients with large AMI. Changes in binding resulting from alpha-1-acid glycoprotein during AMI could account for misinterpretation of total drug concentration and response to antiarrhythmic drugs acutely, during convalescence and at discharge.