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American Heart Journal Oct 1989The effect of procainamide on intraventricular conduction and refractoriness, and the prevention of induction of ventricular tachycardia (VT) were studied in 29 patients...
The effect of procainamide on intraventricular conduction and refractoriness, and the prevention of induction of ventricular tachycardia (VT) were studied in 29 patients who had remote myocardial infarction and inducible sustained monomorphic VT. AFter intravenous administration of 15 mg/kg procainamide, induction of VT was suppressed in seven (24%) patients (responders), while in 22 (76%) VT was still inducible (nonresponders). The percent change in paced QRS duration at a cycle length (CL) of 400 msec produced by procainamide was significantly less in responders than in nonresponders: 29.8 +/- 3.9% versus 38.9 +/- 10.8% (p = 0.0020). The percent change in the right ventricular effective refractory period (ERP) at CLs of 600 and 400 msec was significantly greater in responders than in nonresponders: 14.6 +/- 6.9% versus 7.9 +/- 7.3% (p = 0.0414) for ERP at a CL of 600 msec and 15.1 +/- 7.0% versus 8.0 +/- 7.4% (p = 0.0386) for ERP at a CL of 400 msec. Stepwise discriminant analysis showed that greater percent increase in ERP at a CL of 400 msec and lesser percent increase in paced QRS duration at a CL of 400 msec were significantly independent markers for the responders. These findings suggest that lesser slowing of conduction and greater prolongation of refractoriness by procainamide tend to abolish reentry within the reentrant circuit. Greater slowing of conduction and lesser prolongation of refractoriness tend to stabilize a reentrant circuit, and promote the continued induction of VT.
Topics: Electrocardiography; Humans; Monitoring, Physiologic; Neural Conduction; Procainamide; Refractory Period, Electrophysiological; Stroke Volume; Tachycardia
PubMed: 2801477
DOI: 10.1016/0002-8703(89)90582-6 -
Clinical Pharmacology and Therapeutics Oct 1988The steady-state pharmacokinetics and pharmacodynamics of procainamide and its active N-acetyl metabolite (NAPA) were assessed alone and in combination with...
The steady-state pharmacokinetics and pharmacodynamics of procainamide and its active N-acetyl metabolite (NAPA) were assessed alone and in combination with trimethoprim. Eight healthy men received oral sustained-release procainamide, 500 mg every 6 hours for 3 days, alone and with oral trimethoprim, 200 mg daily for 4 days. Concomitant trimethoprim significantly increased the plasma AUC(0-12) of both procainamide and NAPA (63% and 52%, respectively), with concurrent decreases in their renal clearances (47% and 13%, respectively) and a 39% increase in the mean urinary recovery of NAPA (as percentage of procainamide and NAPA recovery). After trimethoprim coadministration, there was also a trend toward a decrease in the apparent acetylation clearance of procainamide (19%, p = 0.057). The change in procainamide and NAPA renal clearances after trimethoprim coadministration strongly correlated with their baseline renal clearances (r = 0.84 and r = 0.74, respectively, p less than 0.0001). There was small but significant increase in the corrected QT interval with procainamide administration, which increased further with trimethoprim coadministration. We conclude that trimethoprim increases the plasma concentrations of procainamide and NAPA by decreasing their renal clearances and allowing more conversion of procainamide to NAPA.
Topics: Acecainide; Acetylation; Adult; Creatinine; Drug Interactions; Humans; Hydrogen-Ion Concentration; Male; Metabolic Clearance Rate; Procainamide; Trimethoprim
PubMed: 2458879
DOI: 10.1038/clpt.1988.181 -
Anesthesiology Feb 1979The use of procainamide or procaine for treatment of malignant hyperthermia is commonly recommended. The skeletal muscle relaxant dantrolene has also been indicated for... (Comparative Study)
Comparative Study
The use of procainamide or procaine for treatment of malignant hyperthermia is commonly recommended. The skeletal muscle relaxant dantrolene has also been indicated for treatment of this complication during anesthesia. In the present study, effects of procainamide and dantrolene were compared in malignant hyperthemia-susceptible (MHS) pigs in vivo and on MHS muscle from human patients in vitro. The ED50 for dantrolene block of indirectly evoked twitch tension was 0.85 mg/kg in MHS pigs. A final cumulative dose of 2 mg/kg resulted in 68 per cent block of the twitch response. In contrast, procainamide at a final cumulative dose of 14 mg/kg had no effect on twitch response of the MHS pigs. Dantrolene, 3 micrometer, in vitro (approximately 0.8 mg/kg in vivo) was effective in preventing or reversing the abnormal halothane-induced contracture response of human MHS muscle strips. Procainamide, 0.11 mM, a dose approximating clinical levels (about 22 mg/kg), had no effect on basal twitch response or on the abnormal halothan-induced contracture of MHS human muscle. These results confirm the effectiveness of dantrolene and the lack of effectiveness of procainamide in the treatment of malignant hyperthemia.
Topics: Animals; Dantrolene; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Halothane; Hydantoins; Malignant Hyperthermia; Muscle Contraction; Muscles; Procainamide; Swine
PubMed: 434484
DOI: 10.1097/00000542-197902000-00008 -
Archives of Neurology Jun 1981Because procainamide hydrochloride (Pronestyl) may block neuromuscular transmission (NMT), this drug is contraindicated in cases of myasthenia gravis. Reduction of the...
Because procainamide hydrochloride (Pronestyl) may block neuromuscular transmission (NMT), this drug is contraindicated in cases of myasthenia gravis. Reduction of the safety factor of NMT is also seen in other conditions, including peripheral neuropathies. A patient with uremic peripheral neuropathy in whom myasthenia-like weakness developed during procainamide therapy is described. Procainamide should be given with caution in cases of peripheral neuropathies in which there may be a reduction of the safety factor of NMT.
Topics: Adult; Female; Humans; Muscular Diseases; Peripheral Nervous System Diseases; Procainamide
PubMed: 6263235
DOI: 10.1001/archneur.1981.00510060080016 -
The New England Journal of Medicine Dec 1969
Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Humans; Myocardial Infarction; Procainamide
PubMed: 5349809
DOI: 10.1056/NEJM196912042812313 -
Angiology Jul 1982
Topics: Arrhythmias, Cardiac; Digestive System; Drug Interactions; Heart; Humans; Lupus Erythematosus, Systemic; Procainamide; Quinidine
PubMed: 7091775
DOI: 10.1177/000331978203300705 -
Neuromuscular Disorders : NMD 1991The effects of procainamide administration were assessed in a 5-yr-old boy with Schwartz-Jampel syndrome (chondrodystrophic myotonia). Without procainamide the resting...
The effects of procainamide administration were assessed in a 5-yr-old boy with Schwartz-Jampel syndrome (chondrodystrophic myotonia). Without procainamide the resting metabolic rate was found to be significantly higher than in an age-matched control group. With a serum level of 3.8 mg l-1 procainamide a reduction of the resting metabolic rate of 22% was observed, and times needed to climb stairs and to re-open eyes after forceful contraction (blepharospasm) were significantly reduced.
Topics: Child, Preschool; Energy Metabolism; Follow-Up Studies; Humans; Male; Motor Activity; Muscles; Osteochondrodysplasias; Procainamide
PubMed: 1822347
DOI: 10.1016/0960-8966(91)90124-b -
Canadian Journal of Anaesthesia =... Nov 1987The in vitro effect of procainamide on plasma cholinesterase (PCHE) activity in the plasma of ten normal ASA physical status I patients was studied using a kinetic...
The in vitro effect of procainamide on plasma cholinesterase (PCHE) activity in the plasma of ten normal ASA physical status I patients was studied using a kinetic method. The mean plasma cholinesterase activity without procainamide (control) was 0.90 +/- 0.09 units.ml-1. The dibucaine numbers of all the samples were in the normal range of 78 to 86, indicating normal genotypes. The mean plasma cholinesterase activity, in the presence of procainamide in concentrations of 5.0, 10.0, 20.0 and 40.0 micrograms.ml-1, was reduced to 0.73 +/- 0.04, 0.61 +/- 0.03, 0.45 +/- 0.02, and 0.36 +/- 0.01 units.ml-1, respectively. At therapeutic concentrations of 4 to 12 micrograms.ml-1, procainamide inhibited cholinesterase activity 15 to 30 per cent. The authors also showed that the concentration of procainamide required to inhibit 50 per cent of plasma cholinesterase activity was 20 micrograms.ml-1 (I50). The authors conclude that procainamide when tested in vitro had a statistically significant depressant effect on plasma cholinesterase activity at all the concentrations studied.
Topics: Adult; Cholinesterase Inhibitors; Cholinesterases; Female; Humans; In Vitro Techniques; Kinetics; Male; Procainamide
PubMed: 3677282
DOI: 10.1007/BF03010515 -
The American Journal of Cardiology Feb 1991
Topics: Humans; Procainamide; Therapeutic Equivalency
PubMed: 1990818
DOI: 10.1016/0002-9149(91)90605-k -
The American Journal of Cardiology Oct 1973
Topics: Aged; Biotransformation; Depression, Chemical; Electrocardiography; Epinephrine; Heart Conduction System; Humans; Hydrogen-Ion Concentration; Hypotension; Isoproterenol; Male; Pacemaker, Artificial; Peritoneal Dialysis; Procainamide
PubMed: 4744699
DOI: 10.1016/s0002-9149(73)80070-0