TY - JOUR
T1 - Time course of alpha-1-acid glycoprotein and its relation to myocardial enzymes after acute myocardial infarction
AU - Giardina, Elsa Grace V.
AU - Raby, Khether
AU - Freilich, David
AU - Vita, Joseph
AU - Brem, Rachel
AU - Louie, May
N1 - Funding Information:
From the Department of Medicine, Columbia University, New York, New York. This study was supported in part by a Grant-in-Aid from the American Heart Association, Dallas, Texas; Grant HL27206 from the National Heart, Lung, and Blood Institute; and Grant No. RR-00645 from the Research Resources Administration, Bethesda, Maryland. Manuscript received December 31, 1984; revised manuscript received April 1, 1985, accepted April 2, 1985.
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1985/8/1
Y1 - 1985/8/1
N2 - 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.
AB - 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.
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U2 - 10.1016/0002-9149(85)90846-X
DO - 10.1016/0002-9149(85)90846-X
M3 - Article
C2 - 4025163
AN - SCOPUS:0021829219
VL - 56
SP - 262
EP - 265
JO - American Journal of Cardiology
JF - American Journal of Cardiology
SN - 0002-9149
IS - 4
ER -