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In patients without established cardiac disease, the occurrence of premature ventricular complexes without sustained ventricular tachycardia is more an annoyance than a medical risk, and treatment is not required. In contrast, patients with established heart disease and premature ventricular complexes have a higher likelihood of developing ventricular tachycardia or fibrillation. These patients should be treated with a beta blocker or class I antiarrhythmic drug. Treatment of arrhythmias in pregnant women is rarely needed. When treatment is required, amiodarone should be avoided, and beta blockers should be used with caution, because these agents have been associated with fetal growth retardation. The most important rhythm abnormality in athletes is ventricular tachycardia associated with hypertrophic cardiomyopathy. If the presence of the disease is confirmed by echocardiography, beta-blocker therapy is necessary, and these patients should be limited to participation in nonstrenuous sports. Acute arrhythmias in children with Wolff-Parkinson-White syndrome can be treated with adenosine. Radiofrequency ablation of the accessory pathway can provide long-term control.
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A protocol for programmed ventricular stimulation is described in which the effect of increasing stimulation current on ventricular refractoriness and arrhythmia induction was specifically examined. The protocol was evaluated prospectively in 70 patients undergoing electrophysiological study for documented or suspected ventricular arrhythmias. Programmed electrical stimulation was performed at the right ventricular apex and outflow tract using single and double extrastimuli and burst pacing. Stimulation currents of 2, 5, 10, and 20 mA were used in ascending order. The initial (lowest) current was never less than twice diastolic threshold and was maintained during each stimulation run until refractoriness was reached. The current was then increased to the next level to facilitate premature capture until refractoriness was encountered at 20 mA or a sustained arrhythmia occurred. Ventricular arrhythmias were induced in 34 patients, 31 of whom had presented with a sustained ventricular arrhythmia. The incidence of induced arrhythmias was low in those patients who had presented with symptoms alone, a non-sustained arrhythmia, or a sustained arrhythmia in association with a predisposing clinical event. Only one patient with a negative result had further ventricular arrhythmias during the mean follow up period of 15 months. Although each increase in stimulation current caused a decrease in measured ventricular refractoriness, this resulted in only four arrhythmias. Only one arrhythmia was induced above 5 mA. These results suggest that this simple protocol using two extrastimuli and a single stimulation current of 5 mA will reliably identify most patients who have symptomatic ventricular arrhythmias.
Antiarrhythmic effects of three new drugs, propafenone, tocainide, and SUN 1165, were examined using three canine ventricular arrhythmia models, i.e., digitalis, adrenaline and two-stage coronary ligation arrhythmias. The effects of procainamide, disopyramide, lidocaine, and phenytoin, class 1 antiarrhythmic drugs, on digitalis arrhythmia were also examined. The minimum effective plasma concentrations of all these drugs for each arrhythmia model were determined for a quantitative comparison. Propafenone and tocainide suppressed all the arrhythmias, while SUN 1165 suppressed digitalis and coronary ligation arrhythmias. The minimum effective plasma concentrations of propafenone for digitalis, adrenaline, 24-h coronary ligation, and 48-h coronary ligation arrhythmias were 1.8 +/- 0.7, 0.58 +/- 0.20, 3.5 +/- 0.3, and 3.6 +/- 0.9 micrograms/ml, respectively, and those of tocainide were 6.2 +/- 2.1, 23.7 +/- 9.0, 11.4 +/- 0.5, and 8.6 +/- 2.9 micrograms/ml, respectively (mean +/- standard deviation, n = 6-7). The minimum effective concentrations of SUN 1165 for digitalis, 24-h coronary ligation, and 48-h coronary ligation arrhythmias were 0.92 +/- 0.19, 2.5 +/- 0.4, and 1.2 +/- 0.4 micrograms/ml. The minimum effective concentrations for digitalis arrhythmias were 1.7 +/- 0.4 micrograms/ml for disopyramide, 10.1 +/- 2.4 micrograms/ml for procainamide, 3.5 +/- 1.6 micrograms/ml for lidocaine, and 11.3 +/- 3.0 micrograms/ml for phenytoin. Digitalis arrhythmia seems to be a useful model for detecting class 1 drugs, as it was suppressed by all the class 1 Na-channel blocking antiarrhythmic drugs, while class 2 beta adrenergic blockers and class 4 Ca-channel blockers had no effect. Also, not all the class 1 drugs suppressed coronary ligation and adrenaline arrhythmias.
BACKGROUND: Intravenous dobutamine is an acceptable pharmacologic stress agent for evaluation of myocardial ischemia, but it has the undesirable side effect of precipitating cardiac arrhythmias. All patients are susceptible to the arrhythmogenic potential of dobutamine. However, the presence of a baseline arrhythmia creates additional concern about proceeding with a pharmacologic dobutamine stress test. The purpose of this study was to evaluate cardiac arrhythmias during dobutamine stress as they relate to the presence or absence of baseline arrhythmias in patients undergoing radionuclide myocardial perfusion imaging. METHODS AND RESULTS: Data from 486 consecutive dobutamine stress tests in nuclear cardiology were reviewed retrospectively. Baseline and stress electrocardiographic monitoring and 12-lead electrocardiograms were used for classification of arrhythmias. For patients without baseline arrhythmias, the estimated probability of having nonsustained ventricular tachycardia with dobutamine stress was 4.0% (16 of 403), as compared with 15.7% (13 of 83) for patients with baseline arrhythmias (p < 0.001). Three of the 403 patients (0.7%) and 2 of the 83 patients (2.4%) had their study terminated because of ventricular tachycardia (p > 0.05). CONCLUSIONS: The probability of having nonsustained ventricular tachycardia with dobutamine stress testing was significantly greater in patients who had baseline arrhythmias than in those who had no arrhythmias at baseline. Although termination of the study because of ventricular tachycardia was not statistically significant between these two groups, patients with baseline cardiac arrhythmias should be considered at higher risk for the development of nonsustained ventricular tachycardia during dobutamine stress testing than patients who have no baseline arrhythmia.
In patients with malignant ventricular arrhythmia, the utility of exercise testing for exposing arrhythmias and guiding antiarrhythmic drug selection and dosage is not yet generally accepted. A major reservation relates to the issue of reproducibility of arrhythmia provocation. This prospective study comprised 28 patients referred for evaluation of ventricular arrhythmia. In half of these subjects the clinical arrhythmia was sustained ventricular tachycardia or ventricular fibrillation. Maximal exercise testing adhering to a Bruce protocol was performed on 2 separate days. No antiarrhythmic drugs were administered at the time of testing. Of the 28 patients, 27 had an increase in arrhythmia with exercise. The prevalence rates of arrhythmia were greater than 80% and did not significantly differ between test 1 and test 2. Excluding infrequent single ventricular premature complexes, the reproducibility of a test with positive outcome was 76%. Similarly, test-retest agreement, a bidirectional measure of reproducibility, was greater than 74%. Kappa coefficients ranged from 0.26 to 0.36 for all grades of arrhythmia, indicating that reproducibility was consistently greater than by chance alone. Linear regression analysis of arrhythmia frequency in the 2 tests yielded R values of 0.76 to 0.96 and slopes of 0.82 to 1.2. No patient had enough spontaneous variability in repetitive forms to suggest spurious efficacy or aggravation. For ventricular premature complexes there was an 8 to 14% incidence of spurious efficacy and a 4 to 7% incidence of spurious aggravation. These results suggest that exercise-induced ventricular arrhythmia is sufficiently reproducible to serve as an adjunct method in the evaluation and management of patients with potentially life-threatening ventricular arrhythmias.
OBJECTIVES: We studied the relations between heart failure, ejection fraction, arrhythmia suppression and mortality. BACKGROUND: Both left ventricular ejection fraction and functional class of heart failure are strongly associated with mortality after acute myocardial infarction. Both are also related to the presence of ventricular arrhythmias and have been identified as factors related to the ability to suppress ventricular arrhythmias. Little has been reported about the relations between these two factors and arrhythmia suppression or mortality. METHODS: Baseline data from the Cardiac Arrhythmia Suppression Trial were used to define several categories of heart failure and to relate both the resulting categories and ejection fraction to arrhythmia suppression and mortality using logistic and survival regression analytic methodologies. RESULTS: Regardless of the prospective baseline definition of heart failure used, the data consistently showed that heart failure was a more powerful predictor of subsequent congestive heart failure events and arrhythmia suppression and was equally powerful in predicting death. However, each variable provided incremental information when included in the prediction model. Heart failure and ejection fraction appeared to be independent predictors of death. Interactions were observed: A low ejection fraction was more predictive of failure of arrhythmia suppression in patients with than without evidence of heart failure before or at baseline; a low ejection fraction was more predictive of subsequent congestive heart failure events in patients without than with evidence of heart failure before or at baseline. CONCLUSIONS: Although heart failure as a prognostic feature appears to be somewhat superior to ejection fraction, both are powerful predictors of arrhythmia suppression and cardiac events in patients with ventricular arrhythmia after myocardial infarction. Each provides incremental prediction.
OBJECTIVE: The aim was to compare the binding characteristics of a highly purified digoxin specific antigen binding fragment (digoxin immune Fab: DIGIBIND) with digoxin and with two commonly used derivatives of digoxin, beta methyl digoxin and beta acetyl digoxin, and to assess its ability to abolish the arrhythmogenic effects of these digitalis glycosides. METHODS: The binding characteristics of DIGIBIND with digoxin, beta methyl digoxin, and beta acetyl digoxin were assessed in vitro by measuring their ability to inhibit the binding of DIGIBIND to 3H-digoxin. From these studies the affinities of the interactions between DIGIBIND and these glycosides, and the binding capacity of DIGIBIND for each of these glycosides, could be measured. The ability of DIGIBIND to abolish the arrhythmogenic effects of digoxin, beta methyl digoxin, and beta acetyl digoxin was assessed using an in vivo anaesthetised guinea pig model (n = 36, weight 300-400 g), in which these glycosides were infused intravenously (50 micrograms.kg-1 x min-1) until the onset of ventricular arrhythmias, at which point the total amount of glycoside given was calculated. A single bolus dose of either vehicle or DIGIBIND was then given intravenously, and the time to restoration of normal cardiac rhythm noted. After the administration of DIGIBIND, a second infusion of the same glycoside was given to reinitiate the ventricular arrhythmias. The time to onset of the arrhythmias was noted, and the additional amount of glycoside given calculated. RESULTS: In vitro studies showed the binding of DIGIBIND to 3H-digoxin to be inhibited by digoxin and by the two derivatives. The affinities of these interactions with DIGIBIND were significantly different, that for digoxin being some twofold greater than that for beta methyl digoxin and beta acetyl digoxin. The ED50 concentrations were 14.1 (95% CI 12.2, 15.2), 29.2(26.1, 32.7), and 36.2(33.0, 39.8) nM, respectively. However, there were no significant differences between these glycosides in their binding capacities. The in vivo studies showed that intravenous infusion of digoxin, beta methyl digoxin, or beta acetyl digoxin induced similar ventricular arrhythmias. The onset of the arrhythmias was clearly discernible, and required a significantly lower dose of digoxin compared with that of beta methyl digoxin and beta acetyl digoxin. These doses were 667(SEM 55), 868(33), and 854(40) nmol.kg-1, respectively. Termination of the infusion had no effect on the arrhythmias, and in those animals which received a bolus intravenous injection of saline there was no return to normal cardiac rhythm. By contrast, in animals which received a bolus intravenous injection of DIGIBIND, there was complete abolition of the arrhythmias within 4-6 min. Although the dose of DIGIBIND given to abolish digoxin induced arrhythmias was approximately 25% less than that given to abolish beta methyl digoxin and beta acetyl digoxin induced arrhythmias (p < 0.05), the time to restoration of normal cardiac rhythm after DIGIBIND was not significantly different for digoxin compared with beta methyl digoxin and beta acetyl digoxin, at 4.6(0.9), 4.9(0.8), and 5.7(0.8) min, respectively. To reinitiate the arrhythmias in those animals which had received DIGIBIND, a dose of glycoside was required which was not significantly different from that given prior to the DIGIBIND. This observation therefore confirmed the stoichiometric relationship between DIGIBIND and each of the glycosides in respect of the neutralising action of DIGIBIND in abolishing the arrhythmogenic effects of these agents. CONCLUSIONS: Although there is some small difference in the affinities of the binding interactions, there is no difference in the binding capacities of DIGIBIND for digoxin, beta methyl digoxin, or beta acetyl digoxin in vitro. These binding interactions are manifest as the ability of DIGIBIND to abolish the arrhythmogenic effects of digoxin and the two derivatives in vivo.
A continuous ECG recording has been made in 31 myocardial infarction patients during the first 24 hours after admission to hospital. The number and severity of ventricular arrhythmias were recorded in great detail. Before discharge from hospital the patients were submitted to 20 hours of ECG tape recording, an exercise test on a bicycle ergometer and a static work test (handgrip). Another exercise test was performed one month after discharge. During the first day in the Coronary Care Unit (CCU) all 31 patients had ventricular arrhythmias and in 27 of them the arrhythmia was classified as major (calling for treatment according to Lown's criteria). At the exercise tests 23 patients showed ventricular arrhythmias, 12 of them considered as major. No antiarrhythmic therapy was given during the investigation. No correlation was found between the degree of arrhythmia during the first day in the CCU and during the exercise tests. Tape-recorded ECG's appeared to be inferior to dynamic exercise tests in the ability to disclose a latent tendency to ventricular arrhythmia. Static work did not provoke any ventricular arrhythmias. At a 2-year follow-up 5 patients had died, 4 of them suddenly. Examination of additional material on 11 patients with ventricular tachycardia or ventricular fibrillation during the CCU stay, showed that 2 had died, but only one suddenly. Frequency and severity of arrhythmias during the first day after the infarction seemed to correlate poorly to a persistent tendency to arrhythmias during the first day after the infarction seemed to correlate poorly to a persistent tendency to arrhythmias or to the risk of sudden death during the following 2 years. A dynamic exercise test performed before discharge would appear to be more effective in selecting patients in need of long-term prophylaxis. However, very few patients seem to need such a specific antiarrhythmic prophylaxis.
An increasing number of premature ventricular stimuli are being used during programmed stimulation of the heart in the investigation of patients with documented or suspected ventricular arrhythmias. To analyze the significance of the different types of ventricular arrhythmias that are initiated, we evaluated in a prospective study the effect of from one to four ventricular premature stimuli in 52 patients without (non-VT group) and 50 patients with (prior-VT group) documented ventricular tachycardia or ventricular fibrillation. More than half of the patients in the prior-VT group had coronary heart disease. In the majority of patients of the non-VT group the heart was normal. In 44 of the 50 patients in the prior-VT group the clinically documented ventricular arrhythmia was initiated by programmed ventricular stimulation of the heart. In 88% of these 44 patients, one or two ventricular premature beats were required to initiate the clinical arrhythmia. A ventricular arrhythmia could be initiated in 31 of the 52 patients in the non-VT group. The ventricular arrhythmias included nonsustained monomorphic ventricular tachycardia (two patients), six to 25 complexes of sustained polymorphic ventricular tachycardia (24 patients), and ventricular fibrillation (five patients). In 70% of patients in the non-VT group three or four ventricular premature beats were required to initiate the ventricular arrhythmia. Our results indicate that not only the number of extrastimuli required to initiate ventricular arrhythmias but also the type of ventricular arrhythmia initiated differed between the two groups of patients. Nonsustained polymorphic ventricular tachycardia and ventricular fibrillation are nonspecific responses to aggressive stimulation protocols.
We compared face immersion and exercise stress testing by diving and swimming as screening methods for arrhythmias induced by immersion in water. The subjects were 64 children with various arrhythmias who were tested using 5 methods: diving, swimming, face immersion in 25 degrees C water, face immersion in 6 degrees C water, and a treadmill exercise test. Significant arrhythmias occurred during diving or swimming in 51 children, with 44 developing arrhythmias while diving. Both tachyarrhythmias and bradyarrhythmias were seen during diving, but 17 children who also showed significant arrhythmias while swimming mostly had tachyarrhythmias. A comparison with the incidence of arrhythmias produced by diving showed that face immersion in cold water had a sensitivity of 88.6%, a specificity of 85.0%, a predictive value of 92.9%, and an accuracy of 87.5%. Arrhythmias were alleviated in 12.5%, unchanged in 79.7%, and aggravated in 7.8% of the subjects. Face immersion thus appeared to be a useful and adequate screening substitute for diving. Exercise testing was also compared with swimming (sensitivity, 52.9%; specificity, 100%; predictive value, 100%; and accuracy, 87.5%). Arrhythmias were alleviated in 12.5% and unchanged in 87.5% of patients. Although exercise testing produced many false-negatives, all of the severe arrhythmias were reproduced.
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To define the practice habits of United States cardiologists and the treatment of ventricular arrhythmias, a random sample of 1,000 of 12,000 cardiologists was sent a pretested questionnaire. After follow-up procedures, 252 responded, of which 18% were academically-based, 29% were hospital-based and 53% were office-based. Attitudes about antiarrhythmic drug therapy for the treatment of ventricular arrhythmias were influenced by the presence and severity of cardiac disease, the presence and severity of cardiac disease, the presence of symptoms and the type of ventricular arrhythmias. In this survey, only 1% of cardiologists treated patients with asymptomatic ventricular premature complexes and no heart disease, but 17% treated such patients if unsustained ventricular tachycardia was present. The treatment rate among cardiologists increased to 38% when coronary artery disease with left ventricular dysfunction was present in patients with asymptomatic ventricular premature complexes. The presence of any cardiac disease and symptomatic ventricular arrhythmias increased the treatment rate to 80 to 100%. Approximately 50% of responding physicians treated patients comparable to the Cardiac Arrhythmia Suppression Trial study population with antiarrhythmic drugs. Beta blockers were the most common antiarrhythmic drug class chosen as the most appropriate initial therapy in new patients with ventricular arrhythmias. Whereas no cardiologists thought that amiodarone was appropriate to initiate in new patients with benign or potentially malignant ventricular arrhythmias, as many as 33 to 43% of cardiologists would use amiodarone for refractory patients with such arrhythmias, a response contradictory to the approved labeling for this drug. Less than one half of cardiologists recognize the high potential organ toxicity for quinidine, procainamide and tocainide.(ABSTRACT TRUNCATED AT 250 WORDS)
UNLABELLED: The results of serial electrophysiologic testing in patients with sustained ventricular tachycardia or ventricular fibrillation indicate that if the arrhythmia is suppressible with antiarrhythmic drugs, the prognosis is better than when arrhythmias continue to be inducible despite antiarrhythmic drug treatment. Whether electrophysiologically guided antiarrhythmic drug therapy improves outcome or merely selects groups of patients with good and bad prognosis, is not known. To answer this question, a prospective randomized trial was conducted with 166 patients (sustained ventricular tachycardia n = 84; primary ventricular fibrillation n = 46; syncope n = 36). When the arrhythmia was inducible by programmed stimulation during control, patients were allocated to receive either electrophysiologically guided antiarrhythmic drug therapy (group I), or metoprolol (daily dose up to 200 mg) without invasive testing (group II). Patients with non-inducible arrhythmias were also treated with metoprolol (group III). RESULTS: During a follow-up of 10 +/- 8 (SD) months, there were arrhythmia recurrences in 30 patients, and sudden cardiac death in 17. Follow-up did not differ between group I (n = 59) and group II (n = 53). There was a tendency for the outcome to be better in patients of group III (n = 54) than in those of group II (Log-rank test p = 0.057). In group I, patients whose arrhythmias became suppressed did much better during follow-up than those with still inducible arrhythmias (p less than 0.0001). Thus, while invasive testing is a good predictor of outcome, electrophysiologically guided antiarrhythmic drug therapy is not better than a beta blocker in patients with sustained ventricular tachyarrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: We sought to determine the yield of in-hospital monitoring for detection of significant arrhythmia complications in patients starting sotalol therapy for atrial arrhythmias and to identify factors that might predict safe outpatient initiation. BACKGROUND: The need for hospital admission during initiation of antiarrhythmic therapy has been questioned, particularly for sotalol, with which proarrhythmia may be dose related. METHODS: The records of 120 patients admitted to the hospital for initiation of sotalol therapy were retrospectively reviewed to determine the incidence of significant arrhythmia complications, defined as new or increased ventricular arrhythmias, significant bradycardia or excessive corrected QT (QTc) interval prolongation. RESULTS: Twenty-five patients (20.8%) experienced 35 complications, triggering therapy changes during the hospital period in 21 (17.5%). New or increased ventricular arrhythmias developed in 7 patients (5.8%) (torsade de pointes in 2), significant bradycardia in 20 (16.7%) (rate <40 beats/min in 13, pause >3.0 s in 4, third-degree atrioventricular block in 1, permanent pacemaker implantation in 3) and excessively prolonged QTc intervals in 8 (6.7%) (dosage reduced or discontinued in 6). Time to the earliest detection of complications was 2.1 +/- 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for complications within 3 days of monitoring. Baseline electrocardiographic intervals or absence of heart disease failed to distinguish a low risk group. Multivariate analysis identified absence of a pacemaker as the only significant predictor of arrhythmia complications (p = 0.022). CONCLUSIONS: Because clinically significant complications can be detected with in-hospital monitoring in one of five patients starting sotalol therapy, hospital admission is warranted for initiation of sotalol. Patients without pacemakers are at higher risk for these complications.
The results of the Cardiac Arrhythmia Suppression Trial (CAST) have not finished modifying the methodology and strategy of development of new antiarrhythmic agents for the treatment of ventricular arrhythmias. The demonstration of a dissociation between a proved antiarrhythmic effect and increased mortality in coronary patients treated with encainide or flecainide, means that, in this situation, antiarrhythmic efficacy cannot be considered to be a substitute criterion of therapeutic benefit. The consequences of these results are as follows: in phase II, the dose-effect relationships should be studied in patients with chronic ventricular extrasystole without ischemic heart disease. This model is sufficiently predictive for the selection of the dosage to be tested in phase III; in phase III, studies of benign ventricular arrhythmias, antiarrhythmic efficacy is demonstrated by ambulatory ECG recordings. If these studies include patients with ischemic heart disease, the patients must be placed on betablocker therapy and the benefits in terms of reduction of mortality have to be shown by controlled trials versus placebo. In malignant life-threatening arrhythmias, open clinical trials may be performed using provocative electrophysiological studies. The inclusion of patients with implanted automatic defibrillator devices could constitute control groups for the placebo group. The future of antiarrhythmic agents for the treatment of ventricular arrhythmias greatly depends on the search for criteria of severity of arrhythmias and the validation of intermediate criteria of efficacy.