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PubMed1985

Usefulness of invasive and non-invasive electrophysiologic studies in the selection of antiarrhythmic drugs for the patients with paroxysmal supraventricular tachyarrhythmia.

A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachycardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or procainamide. In AV nodal re-entrant tachycardia, verapamil was the most effective for termination. In the manifest WPW syndrome, disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.

Administration, Oral↗

PubMed1991

Characteristics of electrocardiographic changes with some representative antiarrhythmic drugs in adult rats.

The characteristics of ECG changes with representative antiarrhythmic drugs; procainamide (PA) (class Ia), lidocaine (LC) (class Ib), propranolol (PN) (class II), and verapamil (VP) (class IV) were investigated in adult rats. Action potential (AP) was also recorded from myocardial cells during electrical stimuli with frequencies of 1-5 Hz. All the four drugs produced ECG abnormalities which contained AV and SA blocks at middle and high dose levels. Three drugs except VP induced a prolongation of QRS complex and notched QRS at low or middle dose level. As compared such effects with those in dogs and humans, some differences were noted as follows: (1) a dose-dependent prolongation of QT interval by LC and PN, and (2) a shortening of RR interval by VP at the dose of 0.6 mg/kg or less. LC and PN elongated the QT interval in the unipolar precordial chest lead ECGs at right anterior chest positions. These two drugs did not affect the duration of AP (APD90), whereas maximum upstroke velocity (Vmax) decreased. These results suggest that the prolongation of QT interval with LC and PN was due to a delay in local ventricular conduction time, especially on the right ventricle. The shortening of RR interval by VP was clearly blocked by the pretreatment with PN, indicating that this shortening reflected the sympathetic nervous reflex presumably due to the peripheral vasodilation effect of VP.

Action Potentials↗

PubMed1978

Drug-induced lupus erythematosus with in vivo lupus erythematosus cells in pleural fluid.

Pleural involvement in drug-induced lupus erythematosus is not uncommon. Lupus erythematosus cells were found in vivo in the pleural of an elderly patient who had received procainamide (Pronestyl) hydrochloride (2 gm daily) for nine months. Patients who initially have pleural effusions while receiving drugs capable of inducing lupus erythematosus should have the fluid analyzed for lupus erythematosus cells to help clarify the cause of the effusion.

Aged↗

PubMedDate not supplied

Pharmacokinetics in patients with cardiac failure.

Cardiac failure is often associated with disturbances in cardiac output, autonomic nervous system activity, central and systemic venous pressures, and sodium and water metabolism. These disturbances influence the extent and pattern of tissue perfusion, may lead to tissue hypoxia and visceral congestion, and may alter gastrointestinal motility. By these mechanisms, cardiac failure potentially affects absorption and disposition characteristics of drugs, which may necessitate adjustment in dosage regimen for optimum therapy. Lignocaine is the drug which has been studied most extensively in cardiac failure. Volumes of distribution and clearance are decreased. As a drug whose metabolism is largely limited by liver blood flow, decreased blood flow to the liver accounts for some of the change in clearance, but impaired hepatic metabolism appears also to play a role in some patients. Accumulation of active metabolites of lignocaine and procainamide in patients with cardiac failure can influence therapeutic and toxic effects. Theophylline metabolism, which is largely independent of blood flow, appears to be reduced significantly in patients with severe cardiac failure and necessitates reduction of dosage. In the presence of severe cardiac failure, digoxin clearance may be less than anticipated on the basis of estimates of renal function. Quinidine plasma levels may be higher after single doses due to reduced volume of distribution. Quinidine metabolites are believed not to be pharmacologically active but may create confusion with nonspecific assays. Specific assays are recommended in cardiac failure, especially complicated by renal insufficiency. Data are lacking relating pharmacokinetic alterations to haemodynamic measurements in patients with cardiac failure. Whereas the direction of change in pharmacokinetic parameters may be predicted, variability in the magnitude of change is so great that determination of drug concentration in blood remains as essential adjunct to therapy.

Absorption↗

PubMedDate not supplied

Pharmacologically active drug metabolites: therapeutic and toxic activities, plasma and urine data in man, accumulation in renal failure.

Drugs that are administered to man may be biotransformed to yield metabolites that are pharmacologically active. The therapeutic and toxic activities of drug metabolites and the species in which this activity was demonstrated are compiled for the metabolites of 58 drugs. The metabolite to parent drug ratio in the plasma of non-uraemic man and the percentage urinary excretion of the metabolite in non-uraemic man are also tabulated. Those active metabolites with significant pharmacological activity and high plasma levels, both relative to that of the parent drug, will probably contribute substantially to the pharmacological effect ascribed to the parent drug. Active metabolites may accumulate in patients with end stage renal disease if renal excretion is a major elimination pathway for the metabolite. This is true even if the active metabolite is a minor metabolite of the parent drug, as long as the minor metabolite is not further biotransformed and is mainly excreted in the urine. Minor metabolite accumulation may also occur if it is further biotransformed by a pathway inhibited in uraemia. Some clinical examples of the accumulation of active drug metabolites in patients with renal failure are: (a) The abolition of premature ventricular contractions and prevention of paroxysmal atrial tachycardia in some cardiac patients with poor renal function treated with procainamide are associated with high levels of N-acetylprocainamide. (b) The severe irritability and twitching seen in a uraemic patient treated with pethidine (meperidine) are associated with high levels of norpethidine. (c) The severe muscle weakness and tenderness seen in patients with renal failure receiving clofibrate are associated with excessive accumulation of the free acid metabolite of clofibrate. (d) Patients with severe renal insufficiency taking allopurinol appear to experience a higher incidence of side reactions, possibly due to the accumulation of oxipurinol. (e) Accumulation of free and acetylated sulphonamides in patients with renal failure is associated with an increase in toxic side-effects (severe nausea and vomiting, evanescent macular rash). (f) Peripheral neuritis seen after nitrofurantoin therapy in patients with impaired renal function is thought to be due to accumulation of a toxic metabolite. The high incidence of adverse drug reactions seen in patients with renal failure may for some drugs be explained in part, as the above examples illustrate, by the accumulation of active drug metabolites. Monitoring plasma levels of drugs can be an important guide to therapy. However, if a drug has an active metabolite, determination of parent drug alone may cause misleading interpretations of blood level measurements. The plasma level of the active metabolite should also be determined and its time-action characteristics taken into account in any clinical decisions based on drug level monitoring.

Acetaminophen↗

PubMedDate not supplied

Acetylator phenotype and lupus erythematosus.

There are several known therapeutic implications of acetylator phenotype; among them, the association of a higher incidence of procainamide- and hydralazine-induced lupus in slow acetylators. Presumably, this is because acetylation of the aromatic amine or hydrazine functional group leads to a non-toxic product. Several other drugs which have been implicated in drug-induced lupus also contain an aromatic amine or hydrazine group. The clinical and laboratory characteristics of drug-induced and idiopathic lupus are similar but the degree to which the pathophysiological mechanisms are related, if at all, is unknown. There is also evidence reported for an association between the slow acetylator phenotype and idiopathic lupus. If true, this relationship should provoke some new experimental approaches to investigation into the mechanism of idiopathic lupus.

Acetylation↗

PubMedDate not supplied

Reliability of antiarrhythmic drug plasma concentration monitoring.

Measurement of drug levels is becoming increasingly popular to optimise the dosage of various drugs. In the case of antiarrhythmic drugs, the narrow therapeutic margin of most of these agents and a direct relationship between their pharmacological effects and plasma concentrations would justify more widespread use of monitoring. Optimum plasma concentration ranges have been described for lignocaine (lidocaine), procainamide, quinidine and, more recently, also for disopyramide, mexiletine, tocainide and other new antiarrhythmics. A critical analysis of the original data shows, however, that therapeutic and toxic levels are not so well defined as often assumed: small numbers of patients, marked interindividual variability, sometimes inadequate documentation of arrhythmias and lack of standardised blood sampling characterise many of these studies. Uncertainty about the reliability of concentration-effect relationships also arises when active drug metabolites are identified or there are marked concentration-dependent changes of drug protein-binding. In addition, abolition of various types of arrhythmias might require different drug concentrations. Nevertheless, therapeutic monitoring can be of practical value in patients with life-threatening ventricular arrhythmias and can also greatly facilitate dosage adjustment in cases with renal hepatic or severe cardiac failure. For a correct interpretation of drug levels, the time of blood sampling, dosage regimen, duration of treatment, pharmacokinetic principles, and the clinical condition of the patient must be taken into account. Further studies are needed to define the optimum therapeutic range for several drugs and to evaluate the usefulness of plasma concentration measurements in routine antiarrhythmic treatment.

Amiodarone↗

PubMedDate not supplied

Drug interferences with plasma assays in therapeutic drug monitoring.

In this article, many of the reports which describe the various assay procedures for 8 of the most commonly monitored drugs in plasma (digoxin, gentamicin, phenobarbitone, phenytoin, procainamide, quinidine, salicylates and theophylline) are reviewed, together with studies dealing with interferences of other drugs with these assays. Factors which are evaluated include whether the interference was studied when the drug was taken by a patient or a volunteer or by adding it to serum in vitro, the concentration or dose of the interfering drug (when reported), and the clinical implications of the interference. Suggestions as to how to eliminate some of these potential sources of interference are made.

Anti-Bacterial Agents↗

PubMed1977

Drug-induced cardiovascular diseases.

A wide variety of drugs may be associated with serious cardiovascular toxicity. Toxicity due to drugs primarily used for treating cardiovascular toxicity. Toxicity due to drugs primarily used for treating cardiac disorders is the most extensively documented, especially the arrhythmias due to digitalis glycosides. Various arrhythmias are also caused by toxic levels of many antiarrhythmic agents including quinidine, procainamide and phenytotin. Myocardial depression and heart failure are serious side-effects of beta-adrenoceptor blocking agents and myocardial ischaemia due to sympathominetic amines may result from both direct and indirect mechanisms. The many toxic reactions in the cardiovascular system due to non-cardiac drugs are less widely known and for the most part less clearly understood. Many remain controversial at the current time; for example, the diathesis toward thromboembolism in women taking oral contraceptives. Potential cardiac toxicity due to drugs used in the rapidly expanding sphere of anti-neoplastic chemotherapy is exemplified by the cardiomyopathy-like toxicities of doxorubicin and daunorubicin. Many of the psychotherapeutic drugs including phenothiazine antipsychotics and tricyclic antidepressants have arrhythmogenic potential.

Adrenal Cortex Hormones↗

PubMed1985

Haemodynamic effects of class I antiarrhythmic agents.

In order to choose the most appropriate antiarrhythmic agent, the basic haemodynamic characteristics of class I antiarrhythmic agents must be known. Class Ia agents, quinidine and procainamide, have minor haemodynamic effects, while disopyramide causes serious left ventricular depression. Class Ib drugs are exceptionally well tolerated, and class Ic agents have the potential for adverse haemodynamic effects in patients with left ventricular dysfunction. In this article, haemodynamic effects of class I antiarrhythmic agents are described, with particular emphasis on their clinical implications.

Anti-Arrhythmia Agents↗

PubMed1985

Genetically determined variability in acetylation and oxidation. Therapeutic implications.

The clinical significance of two separate genetic polymorphisms which alter drug metabolism, acetylation and oxidation is discussed, and methods of phenotyping for both acetylator and polymorphic oxidation status are reviewed. Particular reference is made to the dapsone method, which provides a simple means of distinguishing fast and slow - and possibly intermediate - acetylators, and to the sparteine method which allows a clear separation of oxidation phenotypes. Although acetylation polymorphism has been known for some time, definite indications for phenotyping are few. It is doubtful whether acetylator phenotype makes a significant difference to the outcome in most isoniazid treatment regimens, and peripheral neuropathy from isoniazid in slow acetylators is easily overcome by pyridoxine administration. However, in comparison with rapid acetylators, slow acetylators receiving isoniazid have an increased susceptibility to phenytoin toxicity, and perhaps also to carbamazepine toxicity. It is also possible that rapid acetylators receiving isoniazid attain higher serum fluoride concentrations from enflurane and similar anaesthetics than do similarly treated slow acetylators. Thus, when drug interactions of these types are suspected, phenotyping for acetylator status may be advisable. If routine monitoring of serum procainamide and N-acetylprocainamide concentrations is practised, phenotyping of subjects prior to therapy with these agents should not be necessary. Although acetylator phenotype influences serum concentrations of hydralazine, when this drug is given in combination with other drugs acetylator phenotype has not been shown to influence the therapeutic response. Slow acetylator phenotype along with female gender and the presence of HLA-DR antigens appear to be risk factors in the development of hydralazine-induced systemic lupus erythematosus (SLE). Determination of acetylator phenotype may therefore help determine susceptibility to this adverse reaction. In the case of sulphasalazine, adult slow acetylators require a lower daily dose of the drug than fast acetylators in order to maintain ulcerative colitis in remission without significant side effects. It is therefore advisable to determine acetylator phenotype prior to sulphasalazine therapy. Work on the association of acetylation polymorphism with various disease states is also reviewed. It is possible that a higher incidence of bladder cancer is associated with slow acetylation phenotype - especially in individuals exposed to high levels of arylamines. The question as to whether idiopathic SLE is more common in slow acetylators remains unresolved. There appears to be no difference between fa

Acetylation↗

PubMed2005

Autosomal dominant polycystic kidney disease showing rupture of a lateral ventral hernia following paralytic ileus.

We report an 83-year-old Japanese male with autosomal dominant polycystic kidney disease (ADPKD), which was marked by unusually enlarged kidneys, and in whom ileus occurred after administration of procainamide. The bowels became swollen and ruptured the skin and appeared on the outside of the skin. Even after the ileus state was resolved, the projected intestinal tract was not restored due to a large defect of the skin, and ostomy was performed. Abdominal hernia including lateral ventral hernia due to enlarged kidneys may result in perforation of the abdominal wall as well as intestinal wall.

Aged↗

PubMed1983

Studies of autologous mixed lymphocyte reactions in patients with systemic lupus erythematosus.

The autologous mixed lymphocyte reaction (AMLR) measures the proliferative response of peripheral blood T cells to surface antigens of non T cells. The AMLR of SLE patients with active or inactive disease either with (13) or without (6) immunosuppressive treatment was low compared with age and sex-matched controls, confirming previous reports. Only one patient with inactive, untreated SLE and one with drug induced lupus (procainamide) showed normal AMLR. Autologous reactivity was also reduced in 2 patients without treatment who presented with clinically complex disease syndromes, including primary biliary cirrhosis, or polyarteritis nodosa, together with Sjögren's syndrome and serological evidence of lupus. The AMLR could not be increased by changing the ratio of responder to stimulator cells. Patients with decreased AMLR also showed a decreased response to phytohemagglutinin which suggested a general depression of T cells. There was no correlation between the decreased AMLR and age, clinical features or anti-DNA antibody levels of the patients. In allogeneic mixed lymphocyte reactions (MLR) it was shown that non-T cells from SLE patients were poorer stimulators of allogeneic T cells than normal cells, and T lymphocytes from SLE patients were poorer responders to allogeneic non-T cells than were normal T cells. Both effects were much more marked in patients with active disease than in those with inactive SLE. This suggests a defect in both responder and stimulating cell populations in SLE.

Adult↗

PubMed1990

Applicability of the popliteal lymph node assay in the Brown-Norway rat.

A number of drugs and chemicals can induce autoimmune disorders. Previous studies suggested the popliteal lymph node (PLN) assay might be a suitable and reliable model to detect such compounds in the mouse. The applicability of this assay has been examined in the Brown-Norway rat using a panel of positive as well as negative reference compounds. Popliteal lymph nodes were excised and weighed seven days after subcutaneous injection of 5 mg of each compound into one footpad. Interestingly, all negative reference compounds produced no significant increase in PLN weight index whereas four positive reference compounds were associated with PLN-weight indices greater than 2.3. However, no increase in PLN weight was noted in procainamide- and isoniazide-treated rats as previously reported in the mouse. This first set of experiments indicates that the PLN assay is applicable to Brown-Norway rats and warrants further investigation.

Animals↗

PubMed1987

Removal of toxic levels of N-acetylprocainamide with continuous arteriovenous hemofiltration or continuous arteriovenous hemodiafiltration.

Two patients with renal failure developed N-acetylprocainamide toxicity while receiving procainamide. Treatment consisted of continuous arteriovenous hemofiltration in one and hemodialysis followed by continuous arteriovenous hemodiafiltration in the other. The efficacy of these treatments was compared with the efficacy of three-times-weekly hemodialysis as used in two patients on chronic hemodialysis who had elevated N-acetylprocainamide levels. Continuous methods produced a more rapid reduction in N-acetylprocainamide levels than intermittent hemodialysis.

Acecainide↗

PubMed1983

Reactive hypoglycemia and insulin autoantibodies in drug-induced lupus erythematosus.

An 82-year-old woman developed symptomatic reactive hypoglycemia in the same year she developed a lupus-like syndrome, probably secondary to the administration of procainamide or hydralazine. Reactive hypoglycemia was confirmed by an oral glucose tolerance test, in which plasma glucose decreased from a fasting level of 87 mg/dL to 32 mg/dL at 3 hours and 23 mg/dL at 4 hours, the last value being associated with loss of consciousness. The patient awoke after the intravenous administration of dextrose. Sensitivity to exogenous insulin was normal or increased. Attempts to measure plasma insulin levels led to the finding of anti-insulin antibodies in the patient's serum; these antibodies were of relatively low titer, were IgG, and not associated with antibodies to the insulin receptor. The patient had no history of exogenous insulin use. Her reactive hypoglycemia appeared due to the autoimmune insulin syndrome, which developed in association with drug-induced lupus erythematosus.

Aged↗

PubMed1999

Doppler sonographic evaluation of left atrial function after cardioversion of atrial fibrillation.

Restoration of sinus rhythm is not always followed by immediate return of effective atrial contraction. Left atrial mechanical function can be assessed by Doppler echocardiography; in the present study we measured the atrial ejection force, which is a noninvasive Doppler-derived parameter that measures the strength of atrial contraction. The aim of the present study was to evaluate the influence of clinical and echocardiographic parameters: duration and cause of atrial fibrillation, different modality of cardioversion, and left atrial size with respect to the delay in the return of effective atrial contraction after cardioversion. Seventy patients were randomly chosen to undergo cardioversion by either direct current shock or intravenously administered procainamide hydrochloride. The 52 patients who had sinus rhythm restored underwent a complete Doppler echocardiographic examination 1 h after the restoration of sinus rhythm and after 1 day, 7 days, and 1 month. The relation between clinical variables and atrial ejection force was tested. Atrial ejection force was greater immediately and 24 h after cardioversion in patients who underwent pharmacologic therapy compared to patients treated with direct current shock (11.3+/-3 versus 5+/-2.9 dynes; P<0.001). In both groups atrial ejection force increased over time. The mode of cardioversion was significantly associated with recovery of left atrial mechanical function by day 1 in univariate and multivariate analysis (odds ratio, 0.14; 95% confidence interval, 0.02-1.2). The other variable associated with the delay in the recovery of atrial function was a dilated left atrium (odds ratio, 0.16; 95% confidence interval, 0.12-1.6). Atrial ejection force is a noninvasive parameter that can be easily measured after cardioversion and gives accurate information about the recovery of left atrial mechanical function. The recovery of left atrial function was influenced by the mode of cardioversion and left atrial size.

Aged↗

PubMed1976

Application of a vidicon spectrometer for simultaneous multicomponent drug determinations.

A rapid scanning vidicon spectrometer has been evaluated for the simultaneous determination of drugs in mixtures, without a separation step. Spectral data in the ultraviolet region are collected on-line with a small computer at repetition rates of 100 scans per second. Absorbance data at several wavelengths are processed by matrix equations to resolve them into the concentration of each component in each mixture. Results are reported for two-component mixtures of procainamide and N-acetylprocainamide in serum, for two-component aqueous mixtures of butabarbital and seconbarbital, and for seven-component aqueous mixtures of phenobarbital, diphenylhydantoin, aminophylline, acetaminophen, salicylamide, phenylbutazone, and secobarbital. We conclude that the computer-inter-faced vidicon spectrometer is a viable tool for simultaneous multicomponent determinations.

Acetaminophen↗