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Increased Alpha-1-Acid Glycoprotein and Lidocaine Disposition in Myocardial Infarction

PHILIP A. ROUTLEDGE, M.D.; WAYNE W. STARGEL, Pharm. D.; GALEN S. WAGNER, M.D.; and DAVID G. SHAND, M.B., Ph.D.
[+] Article and Author Information

Grant support: by U.S. Public Health Service Grant HL 23726. Dr. Routledge is a Merck International Fellow in Clinical Pharmacology and is in receipt of a Wellcome Research Travel Grant.

▸Requests for reprints should be addressed to David G. Shand, M.B.; Box 3813, Division of Clinical Pharmacology, Duke University Medical Center; Durham, NC 27710.


Durham, North Carolina


© 1980 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1980;93(5):701-704. doi:10.7326/0003-4819-93-5-701
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In 15 patients with confirmed myocardial infarction, alpha-1-acid glycoprotein rose significantly from 117 mg/dL at admission to 140 mg/dL at 36 hours (p <0.01), but not in 15 age- and sex-matched patients with chest pain only. Twelve patients were given prolonged infusions of lidocaine (2 mg/min). In patients with myocardial infarction, the rise in plasma α1-acid glycoprotein concentration was associated with increased lidocaine binding and a rise in total lidocaine concentrations between 12 and 48 hours (p < 0.05). Because of the binding changes, however, the rise in free drug concentration (31.2%) was significantly less than the 56.3% rise in total drug level (p < 0.05). No changes in α1-acid glycoprotein or lidocaine disposition were seen between 12 and 48 hours in the control subjects. Our results show that the rise in α1-acid glycoprotein after myocardial infarction is associated with lidocaine accumulation, but increased plasma binding attenuates the rise in free drug. This suggests that the toxicologic implications of lidocaine accumulation may have been exaggerated and therapeutic monitoring of total plasma levels may be misleading.

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