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Procainamide

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21. Clinicopathological study of a patient with procainamide-induced systemic lupus erythematosus. (PubMed)

Clinicopathological study of a patient with procainamide-induced systemic lupus erythematosus. A patient who developed a multisystem involvement of systemic lupus erythematosus (SLE) after 9 years of procainamide therapy, during which time he ingested enormous amounts of the drug, is described. The patient first suffered from recurrent episodes of pleuritis and arthritis, after which he developed a characteristic SLE nephritis associated with a high level of antinative DNA antibodies and a low (...) level of complement. He finally died from a complication of a nonbacterial endocarditis. Autopsy showed polyserositis and typical deposits of electron-dense material on the glomerular basement membrane, and confirmed the clinical diagnosis of Libman-Sacks endocarditis. The possibility that procainamide-induced SLE might have all the clinical, immunological, and pathological features of spontaneous SLE, especially in patients exposed to large doses of the drug for many years, is discussed.

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1976 Annals of the Rheumatic Diseases

22. Antinuclear antibodies during procainamide treatment and drug acetylation. (PubMed)

Antinuclear antibodies during procainamide treatment and drug acetylation. Acetylator capacity was determined in two groups of patients who had received procainamide for more than three months. In seven patients antinuclear antibodies (A.N.A.) were detected during treatment, and these changes disappeared (in six patients) or were less pronounced (one patient) after withdrawal of the drug. These patients tended to have faster acetylation rates, and five were phenotypically "rapid" acetylators (...) . Five patients who did not develop A.N.A. during treatment had less rapid (P less than 0.05) rates of acetylation, and four were "slow" acetylators. We suggest that the immunological changes which may occur during procainamide treatment may be associated with the acetylated metabolite of procainamide rather than the parent compound and that it might be possible to identify patients at risk.

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1975 British medical journal

23. Sustained release procainamide in patients with myocardial infarction. (PubMed)

Sustained release procainamide in patients with myocardial infarction. Sustained release procainamide tablets were administered to 34 patients 48 hours after the onset of an acute myocardial infarct. Therapeutic blood levels of procainamide in the range of 4 to 8 mug/ml were consistently achieved using an 8-hourly maintenance dose of 1.5g after an initial loading dose of 2g. In contrast conventional procainamide capsules administered to 21 comparable patients repeatedly failed to produce plasma (...) concentrations in the therapeutic range, despite the administration of a maintenance dose of 375 mg 3 hourly, after a loading dose of 1g. It is suggested that when the oral administration of procainamide is indicated for the management of ventricular arrhythmias after myocardial infarction, a sustained release preparation should be used.

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1976 British Heart Journal

24. Lupus-like syndrome induced by procainamide. (PubMed)

Lupus-like syndrome induced by procainamide. 6039650 1967 10 31 2018 11 13 0007-1447 3 5568 1967 Sep 23 British medical journal Br Med J Lupus-like syndrome induced by procainamide. 780-1 McDevitt D G DG Glascow J F JF eng Case Reports Journal Article England Br Med J 0372673 0007-1447 9Y8NXQ24VQ Propranolol L39WTC366D Procainamide AIM IM Arrhythmias, Cardiac drug therapy Female Humans Lupus Erythematosus, Systemic chemically induced Middle Aged Procainamide adverse effects Propranolol

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1967 British medical journal

25. Adverse reactions to procainamide. (PubMed)

Adverse reactions to procainamide. 1 Data from a comprehensive drug surveillance programme are analysed to provide details of procainamide use and toxicity in medical wards of teaching hospitals in five countries. 2 Out of a total of 488 recipients 9.2% had one or more adverse effect attributed to the drug; common effects being arrhythmias, gastro-intestinal upsets and drug fever. Although occasionally of major severity, no patient died as a consequence of procainamide toxicity. 3 Toxicity

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1977 British journal of clinical pharmacology

26. Acetylator phenotype and the clinical pharmacology of slow-release procainamide (PubMed)

Acetylator phenotype and the clinical pharmacology of slow-release procainamide Slow-release procainamide given 8-hourly is shown to produce plasma levels generally accepted as giving effective prophylaxis against ventricular dysrhythmias occurring after recent myocardial infarction. Patients can be classified into 'slow' and 'fast' acetylators of procainamide. Knowledge of acetylator status is helpful in determining the dose of procainamide necessary to attain effective steady-state plasma (...) levels while avoiding toxic ones. Acetylator status cannot be assessed accurately using sulphadimidine when the patients are also taking procainamide.

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1976 British journal of clinical pharmacology

27. The ganglion blocking action of procainamide (PubMed)

The ganglion blocking action of procainamide In cats and rabbits procainamide (20 to 50 mg, intravenously) produced a fall of blood pressure of 20 to 50 mm Hg which reached a maximal effect within 1 min and lasted for about 5 min. Procainamide reduced the pressor responses to nicotine and to carotid arterial occlusion and reduced the depressor response to vagal stimulation, but did not antagonize the actions of adrenaline or noradrenaline on blood vessels. The contractions of the nictitating (...) membrane to stimulation of the preganglionic cervical sympathetic nerve were partially or completely blocked by 20 to 50 mg of procainamide given intravenously. The ganglion blocking effect was more abrupt in onset and more slow to recover than that due to hexamethonium and had about 1/250th of the activity of the latter. Procainamide (1 mg) reduced the acetylcholine output of the perfused superior cervical ganglion to below 30% of the control value and blocked transmission completely. Small doses (10

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1964 British journal of pharmacology and chemotherapy

28. Comparative effectiveness of lignocaine, quinidine, propranolol and procainamide as antifibrillatory agents. (PubMed)

Comparative effectiveness of lignocaine, quinidine, propranolol and procainamide as antifibrillatory agents. 5487011 1971 02 04 2014 11 20 0007-1188 40 1 1970 Sep British journal of pharmacology Br. J. Pharmacol. Comparative effectiveness of lignocaine, quinidine, propranolol and procainamide as antifibrillatory agents. 149P Murnaghan M F MF eng Comparative Study Journal Article England Br J Pharmacol 7502536 0007-1188 98PI200987 Lidocaine 9Y8NXQ24VQ Propranolol ITX08688JL Quinidine L39WTC366D (...) Procainamide IM Animals Depression, Chemical Electric Stimulation Heart drug effects Heart Rate drug effects In Vitro Techniques Lidocaine therapeutic use Muscle Contraction drug effects Procainamide therapeutic use Propranolol therapeutic use Quinidine therapeutic use Rabbits Ventricular Fibrillation prevention & control 1970 9 1 1970 9 1 0 1 1970 9 1 0 0 ppublish 5487011 PMC1702659

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1970 British journal of pharmacology

29. The effect of experimental cardiac arrhythmias of a new anticonvulsant agent, Kö 1173, and its comparison with phenytoin and procainamide. (PubMed)

The effect of experimental cardiac arrhythmias of a new anticonvulsant agent, Kö 1173, and its comparison with phenytoin and procainamide. 4192640 1970 07 29 2018 11 13 0007-1188 39 1 1970 May British journal of pharmacology Br. J. Pharmacol. The effect of experimental cardiac arrhythmias of a new anticonvulsant agent, Kö 1173, and its comparison with phenytoin and procainamide. 183P-184P Allen J D JD Kofi J M JM Shanks R G RG Zaidi S A SA eng Comparative Study Journal Article England Br J (...) Pharmacol 7502536 0007-1188 0 Anticonvulsants 5ACL011P69 Ouabain 6158TKW0C5 Phenytoin L39WTC366D Procainamide IM Animals Anticonvulsants administration & dosage Arrhythmias, Cardiac drug therapy Cardiac Complexes, Premature drug therapy Dogs Heart Rate drug effects Ouabain pharmacology Phenytoin administration & dosage Procainamide administration & dosage Tachycardia drug therapy 1970 5 1 1970 5 1 0 1 1970 5 1 0 0 ppublish 4192640 PMC1702975 Circ Res. 1968 Feb;22(2):221-36 5639040 JAMA. 1965 Mar 1;191

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1970 British journal of pharmacology

30. Procainamide-induced systemic lupus erythematosus. (PubMed)

Procainamide-induced systemic lupus erythematosus. 4194201 1970 09 11 2018 11 13 0003-4967 29 3 1970 May Annals of the rheumatic diseases Ann. Rheum. Dis. Procainamide-induced systemic lupus erythematosus. 236-43 Sheldon P J PJ Williams W R WR eng Journal Article England Ann Rheum Dis 0372355 0003-4967 0 Antibodies, Anti-Idiotypic 0 Antibodies, Antinuclear 0 Immunoglobulin G L39WTC366D Procainamide IM Aged Angina Pectoris drug therapy Antibodies, Anti-Idiotypic Antibodies, Antinuclear analysis (...) Arrhythmias, Cardiac drug therapy Blood Sedimentation Humans Immunoglobulin G Leukocyte Count Lupus Erythematosus, Systemic chemically induced Male Middle Aged Myocardial Infarction drug therapy Neutrophils Procainamide adverse effects 1970 5 1 1970 5 1 0 1 1970 5 1 0 0 ppublish 4194201 PMC1031257 J Tenn Med Assoc. 1965 Sep;58(9):287-9 4157556 JAMA. 1965 Oct 4;194(1):23-6 4157597 Arch Neurol. 1966 Mar;14(3):326-30 5905083 Arch Intern Med. 1966 May;117(5):620-6 5935016 Isr J Med Sci. 1966 May-Jun;2(3):354

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1970 Annals of the Rheumatic Diseases

31. Procainamide-induced systemic lupus erythematosus. (PubMed)

Procainamide-induced systemic lupus erythematosus. 4180268 1969 05 02 2018 11 13 0035-9157 62 2 1969 Feb Proceedings of the Royal Society of Medicine Proc. R. Soc. Med. Procainamide-induced systemic lupus erythematosus. 197-8 Atkins C J CJ Hamilton E B EB eng Journal Article England Proc R Soc Med 7505890 0035-9157 0 Antibodies, Antinuclear L39WTC366D Procainamide IM Antibodies, Antinuclear analysis Female Humans Lupus Erythematosus, Systemic chemically induced Middle Aged Neutrophils (...) Procainamide adverse effects 1969 2 1 1969 2 1 0 1 1969 2 1 0 0 ppublish 4180268 PMC1810776 Arch Intern Med. 1966 May;117(5):620-6 5935016 Lancet. 1966 Aug 27;2(7461):467-9 4161590 Am J Cardiol. 1967 Sep;20(3):367-73 4166916 Arthritis Rheum. 1964 Dec;7:684-6 14240626 Arthritis Rheum. 1967 Oct;10(5):407-15 6057644 N Engl J Med. 1962 Dec 27;267:1357-8 13927984 Br Med J. 1967 Sep 23;3(5568):780-1 6039650

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1969 Proceedings of the Royal Society of Medicine

32. Systemic lupus erythematosus during treatment with procainamide. (PubMed)

Systemic lupus erythematosus during treatment with procainamide. 5015024 1972 06 05 2018 11 13 0007-0769 34 3 1972 Mar British heart journal Br Heart J Systemic lupus erythematosus during treatment with procainamide. 284-8 Swarbrick E T ET Gray I R IR eng Journal Article England Br Heart J 0370634 0007-0769 0 Steroids L39WTC366D Procainamide AIM IM Adult Aged Arrhythmias, Cardiac drug therapy Female Humans Lupus Erythematosus, Systemic blood chemically induced Male Middle Aged Pericarditis (...) chemically induced Procainamide adverse effects Steroids therapeutic use 1972 3 1 1972 3 1 0 1 1972 3 1 0 0 ppublish 5015024 PMC458471 Br J Clin Pract. 1967 May;21(5):248-51 6046409 Proc R Soc Med. 1969 Feb;62(2):197-8 4180268 Medicine (Baltimore). 1969 May;48(3):217-28 5769742 Ann Rheum Dis. 1970 May;29(3):236-43 4194201 JAMA. 1965 May 10;192:444-7 14284842

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1972 British Heart Journal

33. Lupus-like syndrome, with persistent immunological abnormalities, related to procainamide therapy. (PubMed)

Lupus-like syndrome, with persistent immunological abnormalities, related to procainamide therapy. 4538330 1972 10 25 2018 11 13 0008-4409 107 4 1972 Aug 19 Canadian Medical Association journal Can Med Assoc J Lupus-like syndrome, with persistent immunological abnormalities, related to procainamide therapy. 312-5 Anastassiades T P TP Miliiken J A JA eng Journal Article Canada Can Med Assoc J 0414110 0008-4409 0 Antibodies, Antinuclear 0 Immunoglobulin G L39WTC366D Procainamide AIM IM Adult (...) Antibodies, Antinuclear analysis Blood Protein Electrophoresis Female Humans Immune System Diseases chemically induced Immunoglobulin G analysis Lupus Erythematosus, Systemic chemically induced Myotonic Dystrophy drug therapy Procainamide adverse effects Syndrome 1972 8 19 1972 8 19 0 1 1972 8 19 0 0 ppublish 4538330 PMC1940765 J Clin Invest. 1966 Mar;45(3):321-9 4159450 Arch Neurol. 1966 Mar;14(3):326-30 5905083 Dis Chest. 1967 Feb;51(2):172-6 6019120 Am J Cardiol. 1967 Sep;20(3):367-73 4166916 Clin Exp

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1972 Canadian Medical Association Journal

34. Procainamide-induced SLE and lymphoreticular disorders (PubMed)

Procainamide-induced SLE and lymphoreticular disorders A 56-year-old male patient diagnosed as a case of procainamide-induced systemic lupus erythematosus (SLE) was found to have a lymphoproliferative disorder at postmortem examination.Contrary to other immune disorders, the association of SLE with neoplasia is a rare occurrence. The present case raises the question of whether a relationship exists between the lupus diathesis and lymphoreticular neoplasia. The study of the incidence

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1974 Canadian Medical Association Journal

35. Use of plasma levels in evaluation of procainamide dosage. (PubMed)

Use of plasma levels in evaluation of procainamide dosage. 4132893 1974 06 25 2018 11 13 0007-0769 36 3 1974 Mar British heart journal Br Heart J Use of plasma levels in evaluation of procainamide dosage. 265-70 Shaw T R TR Kumana C R CR Royds R B RB Padgham C M CM Hamer J J eng Journal Article England Br Heart J 0370634 0007-0769 8W8T17847W Urea 98PI200987 Lidocaine L39WTC366D Procainamide AIM IM Administration, Oral Adult Aged Arrhythmias, Cardiac drug therapy Body Weight Cardiac Complexes (...) , Premature drug therapy Humans Lidocaine therapeutic use Middle Aged Myocardial Infarction complications Procainamide administration & dosage blood therapeutic use Spectrometry, Fluorescence Time Factors Urea blood Ventricular Fibrillation drug therapy 1974 3 1 1974 3 1 0 1 1974 3 1 0 0 ppublish 4132893 PMC458828 Lancet. 1968 Feb 24;1(7539):386-8 4169974 Br Med J. 1968 Jul 20;3(5611):143-6 5662545 N Engl J Med. 1969 Dec 4;281(23):1253-60 4900236 N Engl J Med. 1972 Aug 3;287(5):227-31 5037497 Ann Intern

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1974 British Heart Journal

36. Comparison of the therapeutic effectiveness of aprindine, procainamide and quinidine in chronic ventricular dysrhythmias (PubMed)

Comparison of the therapeutic effectiveness of aprindine, procainamide and quinidine in chronic ventricular dysrhythmias 1 A cross-over study with aprindine (100 mg daily after a loading dose of 200 mg), procainamide (4 × 1000 mg daily) and quinidine bisulphate (2 × 750 mg daily), all given orally, was performed in seventeen patients with stable chronic premature ventricular contractions following healed myocardial infarction. 2 The effectiveness of the treatment was evaluated during three (...) consecutive weeks by continuous ambulatory tape recording of the electrocardiogram and repeated determinations of plasma levels were done. 3 The results showed that aprindine was more effective than procainamide and quinidine. 4 For the three drugs the therapeutic plasma levels varied markedly from patient to patient, but for each patient taken individually, the therapeutic activity could be correlated with the plasma levels.

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1974 British journal of clinical pharmacology

37. Procainamide and phenytoin. Comparative study of their antiarrhythmic effects at apparent therapeutic plasma levels. (PubMed)

Procainamide and phenytoin. Comparative study of their antiarrhythmic effects at apparent therapeutic plasma levels. The antiarrhythmic effects of procainamide and phenytoin were studied in 81 patients admitted to the coronary care unit at the University Hospital in Linköping because of a suspected or proven diagnosis of acute myocardial infarction, and who developed ventricular arrhyhmias, requiring treatment, during the first 8 hours in hospital. Patients were randomly allocated (...) to a procainamide of phenytoin group. The drugs were given as intravenous and oral loading doses followed by oral maintenance therapy. Plasma levels of the two druge were frequently determined and the electrocardiogram was continuously recorded during the 24-hour trial and analysed minute by minute. A significantly higher frequency of therapeutic failure was found in the phenytoin group (23 of 35 patients)compared to the procainamide group(13 of 39 aptients) during the first 2 hours after initiation of therapy

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1975 British heart journal

38. Procainamide absorption studies to test the feasibility of using a sustained-release preparation. (PubMed)

Procainamide absorption studies to test the feasibility of using a sustained-release preparation. Using in vitro techniques it was confirmed that whilst the release of procainamide from the conventional formulation (Pronestyl) was rapid, that from the sustained-release preparation (Cardiorytmin Retard) occurred over a prolonged period. 2 The peak plasma procainamide concentrations after single doses of Cardiorytmin Retard were relatively lower and occurred later than those after single doses (...) of Pronestyl. Furthermore, after reaching a peak, the fall in plasma procainamide concentration was less rapid after the sustained-release preparation. Early urinary recovery of procainamide in patients and in healthy volunteers was greater after Pronestyl than after Cardiorytmin Retard, though overall recovery in urine was similar. These findings indicate that the absorption of the sustained-release preparation is slower, though the overall bioavailabilities of the two preparations are almost the same. 3

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1975 British journal of clinical pharmacology

39. Comparative evaluation of intravenous phenytoin, procainamide and practolol in the acute treatment of ventricular arrhythmias. (PubMed)

Comparative evaluation of intravenous phenytoin, procainamide and practolol in the acute treatment of ventricular arrhythmias. Ten patients with a persistent ventricular arrhythmia, but no other sign of heart disease, were studied by means of an exercise test performed 4 times with a fixed work load, over 30--40 min. No drug was given in the first exercise test and in the others phenytoin, procainamide or practolol were chosen at random for i.v. administration. Blood samples for determination (...) of plasma concentration were frequently collected. The ECG was recorded continuously during the exercise test and was analysed minute by minute. Despite plasma levels within the suggested therapeutic range, only procainamide showed a statistically significant antiarrhythmic effect in this group of patients.

1977 European journal of clinical pharmacology

40. A pharmacokinetic comparison of two sustained-release oral procainamide preparations. (PubMed)

A pharmacokinetic comparison of two sustained-release oral procainamide preparations. 1 The pharmacokinetics of two different sustained-release oral procainamide preparations were studied in ten hospital patients with normal blood ureas and no clinical evidence of heart failure. Each patient received either one or other preparation at 12 hourly intervals for four doses. Frequent blood sampling enabled close monitoring of blood levels. 2 Results showed that both preparations were essentially (...) similar in their pharmacokinetics. Both effectively double the half-life of conventional oral procainamide to 6.5 h and are suitable as prophylactic preparations. One patient developed toxic levels, thought to be related to her metabolic status of being a very slow acetylator. To avoid toxicity pre-therapy assessment of a patient's cardiac and renal function and acetylator status is advised.

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1979 British journal of clinical pharmacology

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