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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Prajmaline

Introduction

Overview

Overview

Prajmaline (Neo-gilurythmal)[1] is a class Ia antiarrhythmic agent[2] which has been available since the 1970s.[3] Class Ia drugs increase the time one action potential lasts in the heart.[4] Prajmaline is a semi-synthetic propyl derivative of ajmaline, with a higher bioavailability than its predecessor.[5] It acts to stop arrhythmias of the heart through a frequency-dependent block of cardiac sodium channels.[2]

Mechanism

Mechanism

Prajmaline causes a resting block in the heart.[6] A resting block is the depression of a person’s Vmax after a resting period. This effect is seen more in the atrium than the ventricle.[6] The effects of some Class I antiarrhythmics are only seen in a patient who has a normal heart rate (~1 Hz).[7] This is due to the effect of a phenomenon called reverse use dependence.[7] The higher the heart rate, the less effect Prajmaline will have.

Uses

Uses

The drug Prajmaline has been used to treat a number of cardiac disorders. These include: coronary artery disease,[8][9] angina,[8][9] paroxysmal tachycardia and Wolff–Parkinson–White syndrome.[1] Prajmaline has been indicated in the treatment of certain disorders where other antiarrhythmic drugs were not effective.[1]

Administration

Administration

Prajmaline can be administered orally,[9] parenterally[8] or intravenously.[8] Three days after the last dose, a limited effect has been observed. Therefore it has been suggested that treatment of arrhythmias with Prajmaline must be continuous to see acceptable results.[1]

Pharmacokinetics

Pharmacokinetics

The main metabolites of Prajmaline are: 21-carboxyprajmaline and hydroxyprajmaline. Twenty percent of the drug is excreted in the urine unchanged.

Daily therapeutic dose is 40–80 mg. Distribution half-life is 10 minutes. Plasma protein binding is 60%. Oral bioavailability is 80%. Elimination half-life is 6 hours. Volume of distribution is 4-5 L/kg. [3]

Side Effects

Side Effects

There are no significant adverse side-effects of Prajmaline when taken alone and with a proper dosage.[1][8][9] Patients who are taking other treatments for their symptoms (e.g. beta blockers and nifedipine) have developed minor transient conduction defects when given Prajmaline.[8]

Overdose

Overdose

An overdose of Prajmaline is possible. The range of symptoms seen during a Prajmaline overdose include: no symptoms, nausea/vomiting, bradycardia, tachycardia, hypotension, and death.[3]

Other Potential Uses

Other Potential Uses

Due to Prajmaline’s sodium channel-blocking properties, it has been shown to protect rat white matter from anoxia (82 +/- 15%).[10][11] The concentration used causes little suppression of the preanoxic response.[10][11]

References

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Janicki, K., J. Orski, and J. Kakol. “Antiarrhythmic Effects of Prajmaline (Neo-Gilurythmal) in Stable Angina Pectoris.” Przegl Lek 52.10 (1995): 485-91. PubMed. Web. 6 Feb. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/8834838>.
  2. ↑ 2.0 2.1 Weirich, J., and H. Antoni. “Differential Analysis of the Frequency-Dependent Effects of Class 1 Antiarrhythmic Drugs According to Periodical Ligand Binding.” Journal of Cardiovascular Pharmacology 15.6 (1990): 998-1009. PubMed. Web. 6 Feb. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/1694924>.
  3. ↑ 3.0 3.1 3.2 Koppel, Claus, Ursula Oberdisse, and Gerhard Heinemeyer. “Clinical Course and Outcome in Class IC Antiarrhythmic Overdose.” Clinical Toxicology 28.4 (1990): 433-44. Web. 6 Feb. 2011. <http://informahealthcare.com/doi/pdf/10.3109/15563659009038586>.
  4. ↑ Milne, J. R., K. J. Hellestrand, R. S. Bexton, P. J. Burnett, N. Debbas, and A. Camm. “Class 1 Antiarrhythmic Drugs — Characteristic Electrocardiographic Differences When Assessed by Atrial and Ventricular Pacing.” European Heart Journal 5 (1984): 99-107. Web. 6 Feb. 2011. <http://eurheartj.oxfordjournals.org/content/5/2/99.full.pdf>.
  5. ↑ Hinse, C., and J. Stöckigt. “The Structure of the Ring-opened N Beta-propyl-ajmaline (Neo-Gilurytmal) at Physiological PH Is Obviously Responsible for Its Better Absorption and Bioavailability When Compared with Ajmaline (Gilurytmal).” Pharmazie 55.7 (2000): 531-32. PubMed. Web. 6 Feb. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/10944783>.
  6. ↑ 6.0 6.1 Langenfeld, H., J. Weirich, C. Köhler, and K. Kochsiek. “Comparative Analysis of the Action of Class I Antiarrhythmic Drugs (Lidocaine, Quinidine, and Prajmaline) in Rabbit Atrial and Ventricular Myocardium.” Journal of Cardiovascular Pharmacology 15.2 (1990): 338-45. PubMed. Web. 6 Feb. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/1689432>.
  7. ↑ 7.0 7.1 Langenfeld, H., C. Köhler, J. Weirich, M. Kirstein, and K. Kochsiek. “Reverse Use Dependence of Antiarrhythmic Class Ia, Ib, and Ic: Effects of Drugs on the Action Potential Duration?” Pacing and Clinical Electrophysiology 2nd ser. 15.11 (1992): 2097-102. Web. 6 Feb. 2011. <http://onlinelibrary.wiley.com/doi/10.1111/j.1540-8159.1992.tb03028.x/pdf>.
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 Sowton, E., I. D. Sullivan, and J. C. P. Crick. “Acute Haemodynamic Effects of Ajmaline and Prajmaline in Patients with Coronary Heart Disease.” European Journal of Clinical Pharmacology 26.2 (1984): 147-50. PubMed. Web. 6 Feb. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/6723753>.
  9. ↑ 9.0 9.1 9.2 9.3 Handler, C. E., A. Kritikos, I. D. Sullivan, A. Charalambakis, and E. Sowton. “Effects of Oral Prajmaline Bitartrate on Exercise Test Responses in Patients with Coronary Artery Disease.” European Journal of Clinical Pharmacology 28.4 (1985): 371-74. PubMed. Web. 6 Feb. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/4029242>.
  10. ↑ 10.0 10.1 Stys, PK. “Protective Effects of Antiarrhythmic Agents against Anoxic Injury in CNS White Matter.” Journal of Cerebral Blood Flow & Metabolism 15.3 (1995): 425-32. PubMed. Web. 6 Feb. 2011. <http://www.ncbi.nlm.nih.gov/pubmed/7714000>.
  11. ↑ 11.0 11.1 Malek, S., J. Adorante, and P. Stys. “Differential Effects of Na-K-ATPase Pump Inhibition, Chemical Anoxia, and Glycolytic Blockade on Membrane Potential of Rat Optic Nerve.” Brain Research 1037.1-2 (2005): 171-79.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]