Procainamide
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| Systematic (IUPAC) name | |
| 4-amino-N-(2-diethylaminoethyl) benzamide | |
| Clinical data | |
| AHFS/Drugs.com | monograph |
| Pregnancy cat. | C (US) |
| Legal status | POM (UK) |
| Routes | IV, IM, oral |
| Pharmacokinetic data | |
| Bioavailability | 85% (oral) |
| Protein binding | 15 to 20% |
| Metabolism | Hepatic (CYP2D6-mediated) |
| Half-life | ~2.5 to 4.5 hours |
| Excretion | Renal |
| Identifiers | |
| CAS number | 51-06-9  |
| ATC code | C01BA02 |
| PubChem | CID 4913 |
| DrugBank | DB01035 |
| ChemSpider | 4744 |
| UNII | L39WTC366D |
| KEGG | D08421 |
| ChEBI | CHEBI:8428 |
| ChEMBL | CHEMBL640 |
| Chemical data | |
| Formula | C13H21N3O |
| Mol. mass | 235.325 g/mol |
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Procainamide INN (pron.: /proʊˈkeɪnəmaɪd/; trade names Pronestyl, Procan, Procanbid) is a pharmaceutical antiarrhythmic agent used for the medical treatment of cardiac arrhythmias, classified by the Vaughan Williams classification system as class Ia.
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History [edit]
Procainamide was approved by the US FDA on June 2, 1950, under the brand name Pronestyl.[1] It was launched by Bristol-Myers Squibb in 1951.[2]
Mechanism [edit]
It is a sodium channel blocker which blocks open sodium channels and prolongs the cardiac action potential (outward potassium (K+) currents may be blocked). This results in slowed conduction, and ultimately the decreased rate of rise of the action potential, which may result in widening of QRS on electrocardiogram.[3]
Uses [edit]
This drug is used for both supraventricular and ventricular arrhythmias. For example, it can be used to convert new-onset atrial fibrillation, though it is suboptimal for this purpose.[4] It can also be used to treat Wolff-Parkinson-White syndrome by prolonging the refractory period of the accessory pathway.[5]
Administration [edit]
Procainamide is administered intravenously or orally. When administered intravenously, a loading dose should first be given, though care should be taken not to cause hypotension.
Procainamide's major active metabolite is N-acetylprocainamide (NAPA), which is approximately equipotent with the parent drug as an antiarrhythmic agent.[6] NAPA has an elimination half-life about twice that of procainamide, and it can reach somewhat higher plasma levels during chronic procainamide administration.[7] The loading dose is 100 mg IV bolus given slowly over five minutes. The maximum dose is 17 mg/kg. Use is discontinued when dysrhythmia is suppressed, or if hypotension ensues, the QRS complex widens by 50% or more, or the maximum dose is achieved.
Side effects [edit]
Adverse effects include rash, myalgia, hypersensitivity reactions (fever, agranulocytosis), drug-induced lupus erythematosus[8] (particularly in slow-acetylators), and proarrhythmic effects (e.g., torsades de pointes). Treatment with procainamide can cause antibody production against cellular components, accounting for the systemic lupus erythematosus-like adverse reactions. The Systemic Lupus Erythematosus reaction may present months or years after the initiation of the drug. A positive anti-histone antibody blood test may be useful in determining whether an SLE presentation is drug induced. [9]
References [edit]
- ^ US Food and Drug Administration. "Drugs at FDA: FDA Approved Drug Products". USA: U.S. Food and Drug Administration (FDA). Retrieved 2012-8-13.
- ^ Hollman A (February 1992). "Procaine and procainamide". Br Heart J 67 (2): 143. doi:10.1136/hrt.67.2.143. PMC 1024743. PMID 18610401.
- ^ Zamponi, G. W.; Sui, X.; Codding, P. W.; French, R. J. (1993). "Dual actions of procainamide on batrachotoxin-activated sodium channels: Open channel block and prevention of inactivation". Biophysical Journal 65 (6): 2324–2334. doi:10.1016/S0006-3495(93)81291-8. PMC 1225974. PMID 8312472.
- ^ Fenster, P. E.; Comess, K. A.; Marsh, R.; Katzenberg, C.; Hager, W. D. (1983). "Conversion of atrial fibrillation to sinus rhythm by acute intravenous procainamide infusion". American Heart Journal 106 (3): 501–504. doi:10.1016/0002-8703(83)90692-0. PMID 6881022.
- ^ Sellers Jr, T. D.; Campbell, R. W.; Bashore, T. M.; Gallagher, J. J. (1977). "Effects of procainamide and quinidine sulfate in the Wolff-Parkinson-White syndrome". Circulation 55 (1): 15–22. PMID 830205.
- ^ Dutcher, JS; Strong, JM; Lucas, SV; Lee, WK; Atkinson Jr, AJ (1977). "Procainamide and N-acetylprocainamide kinetics investigated simultaneously with stable isotope methodology". Clinical pharmacology and therapeutics 22 (4): 447–57. PMID 902457.
- ^ Drayer, DE; Reidenberg, MM; Sevy, RW (1974). "N-acetylprocainamide: An active metabolite of procainamide". Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine 146 (2): 358–63. PMID 4834444.
- ^ Kameda H, Mimori T, Kaburaki J, et al. (November 1998). "Systemic sclerosis complicated by procainamide-induced lupus and antiphospholipid syndrome". Br. J. Rheumatol. 37 (11): 1236–9. doi:10.1093/rheumatology/37.11.1236. PMID 9851277.
- ^ Clinical Medicine for the MRCP Paces. Volume 1: Core Clinical Skills. Mehta and Iqbal. Oxford University Press.2010.
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