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PubMed1989

Hypoglycemia associated with renal failure.

Hypoglycemia associated with renal failure is more common than generally thought. Its occurrence is often a marker of multisystem failure and has an ominous prognostic implication. Its pathogenesis is frequently complex and involves one or several mechanisms. In the evaluation of uremic hypoglycemia, the first step should be the exclusion of obvious causes such as insulin, oral hypoglycemic agent therapy, and the use of drugs known to cause hypoglycemia. Propranolol, salicylates, and disopyramide are among the most commonly implicated agents. Additional triggering events are alcohol consumption, sepsis, chronic malnutrition, acute caloric deprivation, concomitant liver disease, congestive heart failure, and an associated endocrine deficiency. When no obvious cause can be demonstrated, the hypoglycemia is referred to as spontaneous. Spontaneous uremic hypoglycemia has been attributed to deficiency of precursors of gluconeogenesis, that is, alanine, deficient gluconeogenesis, impaired glycogenolysis, diminished renal gluconeogenesis and impaired renal insulin degradation and clearance, poor nutrition, and, in a few cases, deficiency in an immediate counterregulatory hormone such as catecholamine and glucagon. However, the mechanism(s) seems to differ from one patient to the other. Dialysis also predisposes to hypoglycemia in uremia, possibly because of the chronic state of malnutrition. Postdialysis hypoglycemia is secondary to glucose-induced hyperinsulinemia, which is caused by the high glucose content in the dialysate. In uremic hypoglycemia, neuroglycopenic manifestations predominate because of frequent autonomic nervous system dysfunction and lack of catecholamine release in response to hypoglycemia. Its severity and duration are variable. Hypoglycemia should be suspected in any patient with renal failure who exhibits any change in mental or neurologic status. Detection of hypoglycemia should rely on frequent and careful glucose determinations in any patient with uremia.

Acute Kidney Injury↗

PubMed1989

Drug-induced hypoglycemia. A review of 1418 cases.

The present review catalogues 1418 reported cases of drug-induced hypoglycemia. The main findings are that sulfonylureas (especially chlorpropamide and glyburide), either alone or with a second hypoglycemic or potentiating agent, still account for 63% of all cases; that alcohol, propranolol, and salicylate, either singly or with another hypoglycemic drug, are the next most frequent offenders (19% of the total); and that one older drug (quinine) and three new ones (pentamidine, ritodrine, and disopyramide) have caused an additional 7% of all episodes of severe hypoglycemia. The clinical factors that set the stage for drug-induced hypoglycemia are still restricted food intake, age, hepatic disease, and renal disease, both individually and even more so in combination. Drug-induced hypoglycemia continues to be so common that virtually every unconscious patient should be considered hypoglycemic until immediate estimation of the blood sugar level rules it in or out. If ruled in, the clinician should promptly start 10% intravenous glucose and plan to maintain it uninterruptedly for 1 or more days, with added glucagon, hydrocortisone, and diazoxide administration if necessary, until sustained hyperglycemia guarantees that all drug effects have worn off.

Adolescent↗

PubMed1989

The actions and role of calcium entry blockers in hypertension: cardiac considerations.

The calcium antagonists, although initially restricted to the treatment of angina pectoris, are now finding widespread application as safe and effective therapy for hypertension. These drugs reduce systemic vascular resistance and thus address the usual primary physiologic defect in high blood pressure. Reduction of blood pressure with these agents appears to lead to the concomitant reduction of hypertension-induced ventricular hypertrophy and improvement of ventricular function. Unlike other vasodilators, calcium antagonists do not secondarily lead to sodium retention or stimulation of the renin-angiotensin-aldosterone and sympathoadrenal systems. They are effective in the treatment of angina pectoris and may inhibit the onset or progression of atherosclerosis. As calcium antagonists primarily block voltage-operated, as opposed to receptor-operated, sarcolemmal calcium channels, they may be rationally and effectively combined with agents such as converting enzyme inhibitors and adrenergic antagonists. Calcium antagonists have important interactions with drugs relevant to the treatment of cardiac disease. The combination of verapamil and beta blockers or disopyramide and diltiazem with amiodarone should be avoided; caution is advised in the concomitant use of calcium antagonists and digoxin or the major antiarrhythmic agents.

Calcium Channel Blockers↗

PubMed1988

Determinants of stereospecific binding of type I antiarrhythmic drugs to cardiac sodium channels.

The determinants of stereospecific binding of type I antiarrhythmic drugs to specific sites associated with the sodium channel were assessed using rat cardiac myocytes. The asymmetric carbon atoms of stereoisomers may be located at two sites within type I drugs. The structure of these drugs can be schematically illustrated as Aromatic-C1-link-C2-Amine, where C1 and C2 represent potentially asymmetric carbon atoms. We used enantiomeric pairs with either C1 or C2 asymmetric carbon atoms to assess the importance of conformation at these sites to drug binding. The affinities of enantiomers of seven sodium channel blockers were measured with a radioligand binding assay using [3H]batrachotoxinin benzoate [( 3H]BTXB) and freshly isolated cardiac myocytes. The enantiomers inhibited [3H]BTXB binding in a dose-dependent manner, with a mean Hill number of 1.0 +/- 0.1. The ratios of affinities [IC50 of (+)-isomer/IC50 of (-)-isomer] were, for the C1 pairs: quinidine, 0.29; cinchonidine, 0.55; disopyramide, 1.11; RAC 109, 5.33; and for C2 pairs: flecainide, 1.03; mexiletine, 2.15; tocainide, 3.01. The stereospecific differences in drug binding suggest that the orientations of both the aromatic and the amine groups to the rest of the drug molecule are important determinants of drug binding to the cardiac sodium channel. This also suggests the presence of at least two stereospecific domains within the binding sites for type I antiarrhythmic drugs.

Animals↗

PubMed1986

Basic cardiac electrophysiology and mechanisms of antiarrhythmic agents.

Basic cardiac electrophysiology and how it applies to antiarrhythmic drug therapy are reviewed. Normal impulse propagation through the heart proceeds in sequence from the sinoatrial (SA) node, through the atrial specialized conducting system, the atrioventricular (AV) node, the His-Pur-kinje system, and into the ventricles. The cardiac cell maintains a resting membrane potential until an electrical stimulus depolarizes the cell and generates an action potential. The action potential is composed of five phases that represent the changing ionic fluxes and membrane potentials of the cardiac cell. The heart contains two types of cardiac conducting fibers. The fast- and slow-current action potentials generated by these fiber types exhibit distinctly different electrophysiologic properties. Cardiac arrhythmias generally result from an abnormality in the rate, rhythm, or conduction of an electrical impulse in the heart. They may be described as disturbances in normal impulse initiation (automaticity), impulse conduction, or both. Various portions of the conduction system are under the control of the autonomic nervous system, which depends on the balance between the activity of the parasympathetic and sympathetic nervous systems. Intracellular and extracellular concentrations of potassium, calcium, and magnesium have important effects on the electrophysiology of the heart. These changes can be critical in the production of various arrhythmias or may affect the efficacy or toxicity of various antiarrhythmic agents. The electrophysiology of quinidine, procainamide, disopyramide, lidocaine, tocainide, phenytoin, flecainide, amiodarone, and bretylium tosylate is discussed to detail the relationship between drug action and antiarrhythmic efficacy. The electrophysiologic effects of beta-blocking agents and calcium-channel antagonists are also presented. This basic primer on cardiac electrophysiology should provide the practitioner with an improved understanding of the effects, indications, and limitations of antiarrhythmic drugs.

Action Potentials↗

PubMed1986

New perspectives in cardiology: pharmacodynamic classification of antiarrhythmic drugs.

Recent advancements in cardiac pharmacology and physiology have led to the identification of many new antiarrhythmic drugs and a better understanding of basic arrhythmogenic mechanisms. These parallel developments prompted a new nomenclature system for classifying the clinically important antiarrhythmic drugs according to their predominant electrophysiologic actions in cardiac cells. Antiarrhythmic drugs are now grouped into 4 main classes: classes I through IV. Class I agents comprise the standard membrane-stabilizing drugs such as lidocaine, quinidine, and procainamide; newer class I agents include disopyramide, aprindine, tocainide, and flecainide. Class II agents decrease sympathoadrenal excitation of the heart, and the clinically relevant members of this type act through blockade of the cardiac beta 1-adrenergic receptors; propranolol is the prototype. Class III agents selectively prolong the cardiac action potential and refractory period, and bretylium and amiodarone represent this group. Class IV agents are the calcium entry blocking drugs such as verapamil. An understanding of this classification system is essential to the internist and cardiologist who are beset with an emerging array of new antiarrhythmic drugs and affiliated pharmacodynamic terminologies.

Action Potentials↗

PubMed1986

New perspectives in cardiology: recent advances in antiarrhythmic drug therapy.

During the past decade, advances in basic and applied cardiology have led to the introduction of several new antiarrhythmic drugs that have distinct clinical advantages over their older counterparts. These therapeutic advantages comprise either a more favorable pharmacokinetic disposition in the patient or new and perhaps novel mechanisms of antiarrhythmic actions. The class IV agent verapamil, for example, selectively blocks the slow inward Ca++ current in excitable tissues and this action is proving to be quite effective in controlling supraventricular tachyarrhythmias. Tocainide is a newly approved class I agent that exerts lidocaine-like effectiveness in treating serious ventricular arrhythmias. Unlike lidocaine, however, tocainide is not restricted to intensive care because it is effective after oral administration and has comparatively longer duration of antiarrhythmic action. Other recently approved or investigational agents include bretylium and amiodarone (class III), and aprindine, mexiletine, and disopyramide (class I). Along with clinical advantages, however, each drug has a characteristic pharmacologic-toxicologic profile and resulting spectrum of therapeutic application for only particular cardiac dysrhythmias. The advantages and disadvantages of each compound should be weighed equally when the new antiarrhythmic drugs are assessed as therapeutic alternatives for the older ones.

Adrenergic beta-Antagonists↗

PubMed1988

Combination drug therapy for ventricular arrhythmias.

The role of drug combinations for the treatment of patients with ventricular arrhythmias is reviewed. The use of single drugs to suppress ventricular arrhythmias is often unsatisfactory; a drug may be ineffective or cause intolerable adverse effects. Simultaneous use of antiarrhythmic agents with different but compatible electrophysiologic effects may control arrhythmias refractory to single-drug therapy. Patients may tolerate combination therapy fairly well because dosages in combination therapy are often lower than those employed when either drug is used alone. Although comparison of drug trials is hampered by nonuniformity among study protocols, the data suggest that drug combinations can be effective in treating some patients. Pairs of drugs showing the most promise have been a class IA drug (procainamide, quinidine, or disopyramide) with a class IB drug (usually mexiletine), and a class IA drug with a beta blocker. Amiodarone should be combined with a class I drug only as a last resort. There is little evidence to support the simultaneous use of two class IA drugs. Selection of a drug combination should be guided by consideration of the patient's medical history, concurrent disease states, and risk of sudden cardiac death. The efficacy of combination therapy should be evaluated by electrophysiologic testing or ambulatory electrocardiography. Combination antiarrhythmic therapy should be reserved for patients in whom single-drug therapy has been ineffective or poorly tolerated. More studies are needed to further define the efficacy, safety, and role of drug combinations in the treatment of ventricular arrhythmias.

Arrhythmias, Cardiac↗

PubMed1988

[Hemodynamics in ventricular arrhythmias and in their treatment].

The hemodynamic consequences of ventricular tachyarrhythmias are influenced by age, underlying cardiac disease, left ventricular ejection fraction, and possibly by atrial natriuretic peptide. Severity and frequency of the rhythm disorder play, of course, a major role, e.g., monomorphic or polymorphic ventricular premature complexes (VPC), rare or frequent VPC, ventricular tachycardia, ventricular flutter or fibrillation, torsade de pointes, and tachycardia, etc. The therapeutic approach with antiarrhythmic drugs or cardiac pacemakers in cases of conduction disturbances have an additional impact on cardiac performance. Compared to ventricular pacing, a significant higher cardiac output was observed during AV sequential (so called "physiological") pacing evaluated by radionuclide ventriculography. Especially in patients with a reduced left ventricular ejection fraction, the negative inotropic effects of antiarrhythmic drugs are of major importance. A decrease of cardiac output may occur under beta-blocking agents, propafenone, flecainide and particularly disopyramide. On the other hand, amiodarone does not impair cardiac output significantly during acute high dose loading and longterm therapy. In general, negative inotropic effects of antiarrhythmic substances are overestimated; they may even be neglected as long as the antiarrhythmic agent leads to effective suppression of the symptomatic ventricular tachyarrhythmia.

Amiodarone↗

PubMed1988

Clinical pharmacology and pharmacokinetics of pirmenol.

Pirmenol hydrochloride is a promising antiarrhythmic agent with quinidine-like (Class Ia) properties presently undergoing evaluation. It's clinical pharmacology and pharmacokinetics are reviewed. The author outlines the effects of pirmenol on the sinus node, atrial tissue, A-V node, and ventricular tissue and describes its antiarrhythmic efficacy in clinical studies to date, including his own study in 21 patients with a history of sustained ventricular tachycardia. The author summarizes the hemodynamic and pharmacokinetic studies of pirmenol noting that its effects are relatively independent of potassium concentration. The drug's side effects profile is presented, and it is concluded that pirmenol is well tolerated. Hypotension has not been a significant problem with intravenous pirmenol. Precipitation or worsening of clinical heart failure appears to occur only rarely. The favorable pharmacokinetics of pirmenol permit dosage at less frequent intervals than with procainamide, quinidine, disopyramide. Pirmenol has shown efficacy for ventricular arrhythmias even in some patients refractory to Class Ia agents. Antiarrhythmic effects appear to be correlated with plasma levels, and a well-defined therapeutic minimum has been determined.

Administration, Oral↗

PubMedDate not supplied

Frequency-dependent effects of class I, III and IV antiarrhythmic drugs on the conduction and excitability in rabbit ventricular muscle.

The frequency-dependent effect of 11 antiarrhythmic drugs on the impulse conduction time and excitability threshold was studied in isolated rabbit right ventricular muscle. Before drug application, conduction time and excitability threshold were independent of the stimulation cycle length (200-2000 msec). Quinidine, tocainide, lidocaine, disopyramide, procainamide, flecainide, lorcainide and mexiletine increased conduction time and excitability threshold in a frequency-dependent manner (use-dependency) while verapamil, clofilium and bretylium did not significantly alter conduction and excitability at any applied stimulation frequency. It was concluded that the use-dependent effect which was described earlier with most Class I antiarrhythmic drugs on the rate of rise of the action potential can be also demonstrated in extracellular electrophysiological experiments and this must be considered during routine pharmacological screenings.

Animals↗

PubMed1986

[Latent Wolff-Parkinson-White syndrome as the electrophysiological and morphological basis of supraventricular tachycardia].

The concealed Wolff-Parkinson-White (WPW) syndrome, the electrophysiologic and morphologic basis of cardiac arrhythmias, was shown to be a cause of the attacks of supraventricular tachycardia. The latter is rooted in the concealed WPW syndrome in about 30% of patients showing no electrocardiographic signs of pre-excitation. Electrophysiologic criteria of the diagnosis of supraventricular tachycardias due to the concealed WPW syndrome are listed. Concealed Kent's bundle was most commonly found on the left side. As regards antiarrhythmic therapy, disopyramide is one of the most effective drugs for patients with supraventricular tachycardias due to the concealed WPW syndrome.

Action Potentials↗

PubMed1985

[Antiarrhythmic action of 3-carbethoxyamino-5-dimethylaminoacetyl-iminodibenzyl hydrochloride (Bonnecor, AWD 19-166, GS -15) on experimental arrhythmia induced by aconitin, ouabain, calcium chloride and barium chloride].

In comparison with detajmium, prajmalium, ajmaline, quinidine, lidocaine, disopyramide, propranolol, and Ethmozin the substance GS 015 is tested on the aconitin-induced arrhythmia of the rat, the auricular fibrillation by aconitin of the dog, the ventricular arrhythmia induced by ouabaine of the dog, the arrhythmia caused by calcium chloride of the rat, and the arrhythmia induced by barium chloride of the rabbit. The particular qualities of effect in the special forms of arrhythmia are discussed in connection with the study of the antiarrhythmic action in case of coronary occlusion, with the increase of the electric fibrillatory threshold, and with the electrophysiologic tests.

Aconitine↗

PubMed1985

[Paroxysmal junctional reciprocal tachycardia and fetoplacental anasarca].

Foeto-placental anasarca was diagnosed at 34 weeks gestation in a patient with acute hydramnios. Foetal tachycardia at 300 bpm was recorded. This obstetrical problem led to the birth of a premature baby with generalised oedema, for which the only apparent cause was the tachycardia. This was identified as a paroxysmal junctional reciprocating tachycardia, initiating on atrial extrasystolic echos, terminating on R waves, with lengthening of the PR interval at the onset of tachycardia, without acceleration of the sinus rate and P'R = RP'. Paroxysmal junctional reciprocating tachycardia in utero was responsible for congestive cardiac failure and foeto-placental anasarca. The cardiac failure was treated by foetal delivery, artificial respiration and digoxin. The association of digoxin-disopyramide reduces the frequency of attacks of tachycardia and treatment may be stopped after one year's follow-up.

Edema↗

PubMed1979

Control of refractory cardiac arrhythmias with amiodarone.

Amiodarone hydrochloride was used to treat 19 patients with symptomatic arrhythmias refractory to quinidine sulfate, procainamide hydrochloride, disopyramide phosphate, antazoline hydrochloride, lidocaine hydrochloride, bretylium tosylate, propranolol hydrochloride, phenytoin sodium, and practotol acetanilide given to the limit of tolerance. In 17 patients, attacks were completely controlled. Arrhythmias treated successfully included recurrent supraventricular tachycardias, recurrent supraventricular tachycardias with Wolff-Parkinson-White syndrome, and refractory ventricular arrhythmias including recurrent ventricular tachycardia and ventricular fibrillation complicating acute coronary heart disease. Control was confirmed by continuous ECG monitoring both in the hospital and when ambulatory and was maintained for up to four years. Attacks of supraventricular tachycardia were reduced from 7.9/mo to one attack every 53.5 months on amiodarone. Hospital admissions for arrhythmias were reduced from 34 the year before treatment to none the year after. Therefore, amiodarone is an excellent drug for control of many refractory arrhythmias, but two patients with recurrent atrial fibrillation were refractory to this treatment.

Adult↗

PubMed1980

[Electrocardiographical changes and rhythm disorders in Barlow's syndrome].

Mitral valve prolapse ( MVP ) , responsible for most of the symptoms which had previously been interpreted as being due to neurocirculatory disorders or cardiac neurosis , is being recognised more often and has an incidence of about 6-8 % in an unselected population . Although this condition was considered for a long time to be a benign auscultatory abnormality , it may be the cause of serious cardiac complication . Arrhythmias predominate with an incidence of 60 to 80 % on continuous electrocardiography . In a series of 245 patients with mitral valve prolapse confirmed on echocardiography , 52 patients chosen at random were studied to determine the incidence pf ST changes , disturbances of heart rate , QT interval , changes of QRS , arrhythmias with resting , exercise and continuous ECG over 24 hours ( HMS = Holter Monitoring System ) . Abnormalities of ventricular repolarisation , especially flattening of the T wave and , less commonly , St depression were observed in about one third of the patients . These changes were more common in the inferior but were also found in the left precordial leads . 73 % of the 52 patients had a heart rate of 75/mn and their QT intervals showed the following changes : 30.7 % Had a duration greater than the 120 th percentile ; 19.2 % had a duration greater than the upper limit of normal . The other 50 % had a QT interval of around the 100 th percentile . None had a duration of less than the 90 th percentile . In 22.5 % patients , QRS changes due to conduction defects were recorded ( 15 % right bundle branch block - RBBB - , 7.5 % incomplete RBBB ) . HMS is the method of choice for detection of arrhythmias . Resting ECG only showed premature ventricular contractions ( PVCs ) in 12.5 % , compared to 32.5 % on exercise ECG and 62.5 % on HMS . 50 % PVCs were monomorphic , 5 % polymorphic , 7.5 % in salvos and 7.4 % supraventricular in origin . The circadian variation of PVC was striking with a high incidence during periods of activity . There was no statistical correlation between the incidence of PVCs , age , sex , type of MVP and the symptoms and auscultatory findings . The theories on the pathogenesis of the arrhythmias are divided between that based on an underlying cardiomyopathy ( confirmed by the presence of degenerated myocytes on electron microscopy ) and the mechanical hypothesis ( chordae tendinae irritating the endocardium or traction on the papillary muscle with resulting ischaemia ) which provide a better explanation of the clear predominance of monomorphic PVCs . The treatment of Barlow's syndrome is discussed . In our opininon , therapy is only required for ventricular arrhythmias detected by a sufficiently sensitive method such as HMS . Most authors use beta blockers , eventually in association with quinidine Therapeutic successes have also been observed with mexiletine , amiodarone , aprindine and less commonly with disopyramide .

Adolescent↗

PubMed1984

[Effect of anti-arrhythmia agents and nitroglycerin on enzyme activities of the liver].

In a prospective multicenter study the phenomenon of an anicteric reaction with increasing enzyme activities is tested with the antiarrhythmics prajmalin, propafenone, disopyramide and sparteine and additionally with nitroglycerine. Transaminases, alkaline phosphatase and gamma-GT increased with all five substances up to three times of the normal, concerning one, two or three and in a few cases four parameters. The bilirubin was always normal and no clinic symptoms were registered. Increased enzyme levels were found on the fourth day after exposition, the maximum on the 10th-16th day and normalisation on about the 25th day under continuing the same medication. No relation to age or sex was found. The results are discussed in comparison with the literature.

Adult↗

PubMed1983

[Flecainide: a new antiarrhythmic agent].

The authors report their clinical experience with flecainide, a new Class I antiarrhythmic drug, in 44 patients classified into three groups. The first group (7 cases) comprised patients with a wide range of arrhythmias sensitive to the usual antiarrhythmic agents. The second (17 cases) were atrial arrhythmias resistant to the usual antiarrhythmic agents and were mainly vagal atrial arrhythmias. The last group (20 cases) comprised patients with resistant VT, 14 of whom had underlying cardiac disease (8 chronic infarcts). The results obtained were analysed by a score test because of the wide range of arrhythmias and the wide variations in their spontaneous recurrent rate. The antiarrhythmic effect was checked by repeated Holter monitoring correlated with the results of interrogation. Provocative pacing studies were performed in 5 cases of inducible VT under therapy. The results with flecainide were compared with those obtained with reference Class I antiarrhythmics: quinidine, 700 to 1100 mg/day or disopyramide, 600 mg/day. Amiodarone was often associated with each Class I antiarrhythmic because of the resistant nature of these arrhythmias. In group I the results with flecainide were equivalent to those of quinidine. In the other two groups the results were significantly better than those of the reference antiarrhythmic: mean scores: group II 3,20 +/- 0,5 compared to 1,9 +/- 0,4 (p less than 0,01); group III 3,70 +/- 0,37 compared to 1,85 +/- 0,22 (p less than 0,001). Tolerance was good apart from neurosensory side effects (loss of accomodation, vertigo) which were dose dependent and which led to the withdrawal of therapy in only 4 cases. Four types of cardiac side effects were observed: aggravation of existing sinoatrial block (1 case); aggravation of existing intraventricular block (2 cases); aggravation of contractile function which was very poor before therapy (2 cases); and sudden death during therapy in patients with ischemic heart disease in cardiac failure and with incessant resistant VT (2 cases). In these instances the role of the drug cannot be confirmed. These complications were observed with doses of more than 5 mg/kg/day and in patients with cardiac failure. Two of these patients had serum flecainide levels which were very high. It may therefore be possible to reduce the incidence of these complications by adapting dosage to the patient's clinical state and to the serum drug levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗