Ventricular Premature Depolarizations Research Articles

Pharmacologic Therapy in Patients with Ventricular Tachyarrhythmias

Table 5 can be used as framework for a summary of the previous discussion on pharmacologic therapy for ventricular tachyarrhythmias. The system for grading the severity of symptoms of ventricular tachyarrhythmias, previously presented in Table 3, is arranged vertically along the left side of Table 5. Horizontally across the top, patients are grouped according to the presence or absence of structural heart disease, and those with structural heart disease are further dichotomized according to left ventricular ejection fraction. As can be seen, patients with class I symptoms should not be treated whenever possible, although in patients with reduced left ventricular function (especially coronary heart disease), an argument can be made for empirical treatment with beta-adrenoceptor blocking agents whenever possible. Patients with class II symptoms can be treated empirically with beta-adrenoceptor blocking agents. Other antiarrhythmic agents may be safer when there is no underlying structural heart disease, but this has not been proved. The use of antiarrhythmic agents other than beta-adrenoceptor blocking agents in patients with class II symptoms should probably be guided and monitored by ambulatory electrocardiographic recording and exercise tolerance testing. In the patient with hemodynamically stable ventricular tachycardia, electrophysiologic-guided therapy is probably preferable whenever possible. Encainide, flecainide, and similar drugs should be avoided when there is a possibility of residual ventricular premature depolarizations of three or more per hour. Some uncertainty remains concerning the treatment of patients with class III and class IV symptoms and no structural heart disease. Some patients may fall into a specific group that is very responsive to drug therapy. These patients should probably be treated like other patients with class III and class IV symptoms. Electrophysiologic testing may be helpful. When such patients have a reproducibly induced sustained ventricular tachyarrhythmia, it is likely that antiarrhythmic drug therapy will render the arrhythmia noninducible, and that they will do well while receiving long-term pharmacologic therapy. When such patients do not have a reproducibly induced sustained ventricular tachyarrhythmia, the main controversy is whether therapy is needed. If it is decided that such a patient needs therapy, the choice is usually between empiric amiodarone and an ICD, although catheter ablation may be helpful in selected instances. Patients with class III and class IV symptoms who have structural heart disease require therapy. Although this continues to be an evolving area of investigation, for many of these patients, the initial attempt at therapy should be pharmacologic.(ABSTRACT TRUNCATED AT 400 WORDS)

Automated interpretation of cardiac arrhythmias: Design and evaluation of a computerized model

Historically, the development of computerized models that utilize the deductive methods used by clinicians for the interpretation of cardiac arrhythmias have been limited by the absence of a consistently reliable means of detecting atrial activation. In this study, a theoretical model was developed with a hierarchical organization of problem-solving strategies utilizing automated analysis of atrial activation from a commercially available esophageal pill electrode and ventricular activation from a simultaneously recorded surface electrocardiographic lead. The theoretical model was then tested in 21 patients with 1 or more or 28 distinct supraventricular and ventricular arrhythmias. Of the 641 individual cardiac cycles analyzed, 636 (99.2%) were correctly identified. The accuracy of a contextual, that is, more comprehensive, interpretation of consecutive cardiac cycles was 638 641 (99.5%). The following cardiac arrhythmias were identified: sinus rhythm, sinus bradycardia, atrial premature depolarizations, atrial flutter, and supraventricular tachycardias with normal and aberrant ventricular conduction, first-degree and second-degree heart block; junctional escape, junctional rhythm, idioventricular rhythm, ventricular premature depolarization, and ventricular tachycardia with and without retrograde activation; atrial bigeminy, atrial trigeminy, atrial couplets, ventricular bigeminy, ventricular trigeminy, and ventricular couplets. This study represents the first computerized model ever developed to incorporate the morphology and timing of atrial activation with the morphology and timing of ventricular activation for arrhythmia diagnosis. Such modeling appears to be capable of achieving accurate interpretation of spontaneous, complex clinical cardiac arrhythmias and atrioventricular relationships.

Post myocardial infarction stratification and the signal-averaged electrocardiogram

T HE CAUSE OF DEATH in patients who are discharged from the hospital following myocardial infarction (MI) is attributable to three factors: (1) reinfarction resulting in heart failure or a fatal arrhythmia, (2) cardiac rupture, and (3) primary ventricular tachyarrhythmia. Several studies’-” have demonstrated that the majority of patients who die suddenly have a sustained ventricular tachycardia that degenerates into ventricular fibrillation, and a minority have a bradyarrhythmia. Factors that precipitate the arrhythmic event remain poorly understood but likely include ischemia, drugs, premature ventricular depolarizations, and the presence of a substrate with slow conduction characteristics.” Mortality in patients with MI has decreased significantly in the last few years. This decrease has been shown for both early and late mortality. The significant decline in mortality is related to several factors.l’-‘” Among these are (1) the institution of coronary care units, (2) reduction in arrhythmic deaths resulting from ventricular fibrillation, (3) the use of intravenous and oral P-blocking agents, and (4) the use of thrombolytic agents. Whereas in 1966 the l-year mortality was 14% and the 6-year mortality was 42% for patients discharged from the hospital, today in the era of thrombolytic therapy the mortality is in the range of 3% to 5% for 1 year and likely 11% to 13% for 6 years” accounting for a 60% to 75% reduction in mortality. It is likely that mortality will remain high in patients who do not undergo thrombolysis, who are more than 70 years of age, who have multiple infarctions, and who have severe left ventricular dysfunction as well as ventricular arrhythmias. Thus, risk stratification assumes importance so that one can identify low-risk patients who require no intervention and highrisk patients who may require interventional therapy. A variety of tests have been used for risk stratification of patients post-MI. These tests have included exercise electrocardiogram (ECG), 24-hour Holter monitoring, radionuclear angiography, coronary angiography, and programmed ventricular stimulation.z”-3” In recent years the technique of signal averaging in association with high gain amplification has been used to detect late potentials,“‘-3y which are high frequency low amplitude signals that occur in the terminal part of the QRS complex and/or the ST segment. These late potentials have been postulated to be noninvasive markers of the arrhythmic substrate, which is characterized by slow inhomogenous propagation of conduction.l” The purpose of this article is to review the role of the signal-averaged ECG in risk stratification of patients post-MI..

Effect of xylazine on the arrhythmogenic dose of epinephrine in thiamylal/halothane-anesthetized horses

Summary The effect of xylazine on the arrhythmogenic dose of epinephrine (ade) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, iv) followed by thiamylal (4 to 6 mg/kg, iv) and was maintained at 1 minimal alveolar concentration (mac) of halothane (0.89%). Base apex ecg and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 µg/kg/min) for a maximum of 10 minutes. The ade was defined as the lowest epinephrine infusion rate to the nearest 0.25 µg/kg/min at which at least 4 premature ventricular depolarizations occurred in a 15- second period. Xylazine (1.1 mg/kg, iv) was administered after the control ade was determined. Xylazine did not significantly alter the ade (control, 1.12 ± 0.38 µg/kg/ min; xylazine, 1.21 ± 0.46 µg/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ade determinations. Significant differences in pH, Pao2, Paco2, or base excess were not observed between baseline and ade in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ade determinations.

Moricizine increased short-term mortality in survivors of myocardial infarction with low ejection fractions and ventricular premature depolarizations

Source Citation The Cardiac Arrhythmia Suppression Trial II Investigators. Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. N Engl J Med. 1992 Jul 23;327:227-33

Ventricular arrhythmias in horses: 21 cases (1984-1989)

Summary Ventricular premature depolarizations (vpd) were identified in 21 horses in which unexplained tachycardia or an arrhythmia was detected on auscultation. Horses were categorized into 3 groups on the basis of ecg findings. Seven horses had uniform isolated vpd (group 1); 7 horses had repetitive uniform vpd at a rate <100 vpd/min (group 2); and 7 horses had either multiform vpd, R-on-T, or ≥ 100 vpd/min (group 3). Concurrent systemic disease was identified in 12 horses, 7 of which had gastrointestinal tract disorders. Serum cardiac isoenzyme activities were high in 6 (2 from each group) of 13 horses in which they were measured. Serum electrolyte concentrations were normal in all but 1 of 11 horses in which they were measured. Antiarrhythmic drugs were given to 9 horses (all of which were in group 2 or group 3), 6 of which converted to sinus rhythm. Two horses that had R-on-T in the ECG died shortly after initiation of antiarrhythmic treatment. An accelerated idioventricular rhythm persisted in 1 horse for at least 8 months and failed to respond to antiarrhythmic drugs. Ventricular premature depolarizations resolved or decreased considerably in frequency in 11 horses without the administration of antiarrhythmic agents. Treatment in these horses included therapy for any underlying systemic disease, corticosteroids, nonsteroidal antiinflammatory drugs, or stall rest. The remaining horse was euthanatized several hours after hospitalization. Five horses died or were euthanatized either during hospitalization or several months after being discharged. Myocardial lesions were identified at necropsy in 2 horses.

Prognostic significance of ventricular premature depolarizations measured 1 year after myocardial infraction in patient with early postinfarction asymptomatic ventricular arrhythmia

Objectives. The objective of this study was to examine the relation between death and the frequency of premature ventricular depolarizations measured approximately 1 year after myocardial infarction.Background. The reported association between premature ventricular depolarizations and death in the weeks after myocardial infarction is in part the basis for the use of antiarrhythmic drugs. Such an association has not been reported on for observations obtained at a much greater interval after myocardial infarction.Methods. We examined the association between mortality and premature ventricular depolarization rates measured 1 year after myocardial infarction in patients with asymptomatic ventricular arrhythmia early (between 6 and 90 days, median 28) after infarction, as measured by 24-h ambulatory electrocardiographic recording. The study group consisted of 502 patients enrolled in the Cardiac Arrhythmia Pilot Study during 1983 to 1985. They were followed up during the course of the study and subsequently by a National Death Index search (average follow-up interval 1,080 days).Results. Death was recorded for 87 patients through 1987. Because patients were admitted to the Cardiac Arrhythmia Pilot Study only if they had ≥10 ventricular premature depolarizations/h, the arrhythmia rate measured at baseline (that is, early after infarction) was not expected to, and did not, predict mortality. In 360 patients ventricular premature depolarization rates were measured approximately 1 year from their index myocardial infarction while they were not receiving antiarrhythmic therapy. In these patients, who had survived 1 year after the index infarction, the rate of ventricular premature depolarizations/h measured 1 year after infarction was highly predictive of subsequent death (p < 0.001). Recent heart failure and a history of diabetes mellitus were also strongly predictive of death.Conclusion. The prognostic value of ventricular premature depolarizations observed 1 year after a myocardial infarction may be significant even in a sample selected for frequent ventricular premature depolarizations observed early after the event.

Long Term ECG Recording with Hotter Monitoring in Clinically Healthy Horses

The electrocardiogram of 9 horses was continuously recorded for 24 h with Holter monitoring to examine the variations in heart rate and rhythm during daily routine procedures and at night. Three horses had transient sinus bradycardia, and 3 had periods of sinus tachycardia. Heart blocks were detected in 3 horses, and all horses had periods of sinus arrhythmia. These changes in the heart rate and rhythm were apparently caused by variations in autonomic nervous system tone and they are probably "normal" findings in resting, undisturbed horses. Ventricular premature depolarisations were not observed in any horse, but some single supraventricular premature contractions were detected. There was preliminary evidence that in order to register the real resting heart rate and rhythm of a horse the ECG should be recorded over a long period, and also at night and without the presence of the investigator.

Cocaine-enhanced arrhythmogenesis: neural and nonneural mechanisms.

Cocaine abuse increases the susceptibility to cardiovascular complications and sudden cardiac death in man. We used programmed electrical stimulation of the heart to examine the arrhythmogenic influence of cocaine. Twenty-three pentobarbital-anesthetized adult dogs underwent programmed electrical stimulation using one to four extrastimuli before and during cocaine infusion. Autonomic decentralization was performed prior to the protocol in eight dogs. Induced ventricular arrhythmias included single premature ventricular depolarizations, doublets, triplets, ventricular tachycardia, and ventricular fibrillation. Intravenous cocaine, and subsequent adrenergic and muscarinic receptor blockade, or calcium channel blockade were evaluated for their influence on arrhythmogenesis. The incidence of induced ventricular arrhythmias was significantly elevated following cocaine and was reduced following propranolol and atropine. Verapamil, however, did not reduce the incidence of induced arrhythmias. In addition, cocaine significantly increased arrhythmia induction in decentralized animals, but propranolol, atropine, and phentolamine failed to reduce the proarrhythmic effects of cocaine in these animals. Thus, cocaine has a proarrhythmic effect on the heart with multiple mechanisms. The adrenergic mechanism appears to be a result of neurotransmitter uptake blockade, whereas the likely ionic mechanism is a neurally independent, direct effect on the heart.

Moricizine: pharmacodynamic, pharmacokinetic, and therapeutic profile of a new antiarrhythmic.

Moricizine (Ethmozine) is a phenothiazine derivative recently approved in the United States for the treatment of malignant ventricular arrhythmias. Moricizine closely resembles group IA antiarrhythmic agents in the intensity of its effect on the sodium channel, but it differs from the IA subclass in that it shortens the action potential duration in ventricular tissue. Moricizine suppresses frequent ventricular premature depolarizations and nonsustained ventricular tachycardia in 60% to 70% of patients, and it suppresses induced ventricular tachycardia in 15% to 25% of patients. It is well tolerated, with a low incidence of adverse effects. The suggested dosage is 600 to 900 mg per day in three divided doses. Treatment of arrhythmias with prognostic significance should be initiated in the hospital, and monitored with electrophysiologic studies. Additional clinical experience is needed to better define moricizine's role in antiarrhythmic therapy.

Enhanced induction of ventricular arrhythmias during sympathetic stimulation before and during coronary artery occlusion

We used programmed electrical stimulation to examine the arrhythmogenic influence of the sympathetic nervous system before and during coronary artery occlusion. In 29 anesthetized dogs the left and/or right stellate ganglia were stimulated at 2–8 hertz. Program-induced ventricular arrhythmias included single premature ventricular depolarizations, doublets, triplets, ventricular tachycardia and ventricular fibrillation. Both the number of extrastimuli and the duration of coronary occlusion significantly influenced ventricular arrhythmia induction. After pooling the number of extrastimuli, type of artery occluded, and the duration of occlusion, the influences of unilateral and bilateral stellate stimulations were evaluated. The incidence of induced ventricular arrhythmias was 54% during control conditions (prior to sympathetic stimulation). Right stellate stimulation had no influence on arrhythmogenesis, causing ventricular arrhythmia induction in 52% (NS) of the trials. Left stellate stimulation resulted in increased ventricular arrhythmias (68%; P < 0.05) in response to programmed electrical stimulation. Bilateral stellate stimulation elevated program-induced ventricular arrhythmias (63%; P < 0.05). The effects of the stellate stimulations on arrhythmia induction were similar during and up to 180 minutes of coronary occlusion. Thus, the arrhythmogenic influence of sympathetic stimulation was present before and during coronary artery occlusion.

Events in the cardiac arrhythmia suppression trial: Baseline predictors of mortality in placebo-treated patients

Patients randomized to placebo in the encainide and flecainide arms of the Cardiac Arrhythmia Suppression Trial (CAST) have been found to have a relatively low 1-year mortality rate of 3.9% in comparison with previous studies of patients in the postmyocardial infarction period. To determine the comparability of CAST with previous studies, baseline variables were examined in the 743 patients randomized to placebo in the flecainide and encainide arms of CAST. Twenty-three baseline characteristics were correlated with major outcome events: arrhythmic death (16 events), total mortality (26 events) and congestive heart failure (51 events).On multivariate analysis the risk of new or worsening congestive heart failure was significantly associated with diuretic use, diabetes, high New York Heart Association functional class, age, prolonged QRS duration and low ejection fraction. The risk of arrhythmic death or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, history of heart failure, use of digitalis, diabetes and prolonged QRS duration. Total mortality or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, diabetes, ST segment depression, high functional class, prolonged QRS duration and low ejection fraction.The variables at baseline associated with mortality from all causes or arrhythmic death or resuscitated cardiac arrest and heart failure in the CAST placebo-treated patients are similar to those identified in previous postmyocardial infarction studies. Thus, the observation of increased mortality in CAST associated with the administration of encainide and flecainide for suppression of ventricular premature depolarizations is probably applicable to any comparably defined group of patients in the postmyocardial infarction period.

Post-myocardial infarction mortality in patients with ventricular premature depolarizations. Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Pilot Study.

Among survivors of acute myocardial infarction, frequent and repetitive ventricular premature depolarizations (VPDs) detected on ambulatory monitoring contribute independently to the risk of all-cause mortality and sudden death. Apart from the beta-blockers, no antiarrhythmic drug has been reliably demonstrated to reduce mortality among patients with VPDs. A pilot study was undertaken to gather data to aid in the design of a multicenter trial of amiodarone for the reduction of mortality from cardiac arrhythmias in such patients. Seventy-seven patients with acute myocardial infarction within the previous 6-30 days and 10 or more VPDs/hr or one or more runs of ventricular tachycardia on 24-hour electrocardiographic recording were randomized in a double-blind fashion in a 2:1 amiodarone-to-placebo ratio. The loading dose was 10 mg/kg/day for 3 weeks. The maintenance dose was 300-400 mg/day with reductions at 4-month intervals in response to VPD suppression, excessive plasma levels, or toxicity. VPD suppression at 1 week and 2 weeks was 63% and 85%, respectively, on amiodarone and 17% and 27%, respectively, on placebo. Apart from thyroid-stimulating hormone elevation and skin reactions, no side effects occurred more frequently with amiodarone. The study drug was stopped for side effects or noncompliance in 35% of amiodarone patients and 34% of placebo patients. Patients were followed for a maximum of 2 years (mean, 20 months). Arrhythmic death or resuscitated ventricular fibrillation occurred in two of 48 amiodarone patients (6%) and four of 29 placebo patients (14%), whereas the rates of all-cause mortality were five of 48 (10%) and six of 29 (21%), respectively. Amiodarone, in moderate loading and maintenance dosages with adjustments in response to plasma levels, VPD suppression, and side effects, results in effective VPD suppression and acceptable levels of toxicity.

Paced Beats Following Single Nonsensed Complexes in a “Codependent” Cardioverter Defibrillator and Bradycardia Pacing System: Potential for Ventricular Tachycardia Induction

Patients with implantable defibrillators often require bradycardia pacemakers. Adverse interactions between separate defibrillator and bradycardia pacing units have occurred, including failure to detect ventricular fibrillation due to persistent bradycardia pacing during the arrhythmia. A device with combined bradycardia pacing and antitachycardia therapy capability may obviate adverse device interactions. We describe a previously unrecognized phenomenon that may occur in a combined device when the algorithms for sensing bradycardia and tachycardia are "codependent"; that is, the circuitry for brady- and tachyarrhythmia detection relies on the same automatic gain sense amplifier. Three of 37 patients in whom the device was implanted had ventricular tachycardia initiated when bradycardia pacing stimuli were delivered by the device after probable nonsensed sinus beats. In each case, nonsensed beats appeared to have a markedly diminished amplitude, occurred after ventricular premature depolarizations that produced large amplitude electrograms, and had an electrogram morphology that matched that of sinus rhythm. In each case, the bradycardia pacing interval was at least 1,200 msec (range 1,200 to 1,714 msec). In two of the three patients, large amplitude ventricular premature depolarizations or nonsustained ventricular tachycardia caused an adjustment of the gain control that potentiated the failure to sense the subsequent lower amplitude signal. In all three patients, the induced arrhythmia was rapidly terminated by pacing or cardioversion. Decreasing the bradycardia pacing interval by 110-514 msec has prevented recurrence during short-term follow-up. Our findings suggest that codependent bradycardia and antitachycardia devices may have their own unique potential difficulties in adapting to rapid changes in rate and signal amplitude.

Events in the cardiac arrhythmia suppression trial (CAST): Mortality in patients surviving open label titration but not randomized to double-blind therapy

The patient characteristics and outcomes were studied in the 318 patients who survived open label drug titration in the Cardiac Arrhythmia Suppression Trial (CAST) and who were not randomized to double-blind therapy and in 942 patients, who were randomized to double-blind placebo therapy. The patients randomized to placebo therapy had a lower total mortality or resuscitated cardiac arrest rate (4% vs. 8.5%). However, at baseline, nonrandomized patients were dissimilar from patients randomized to placebo in the following ways: older; lower left ventricular ejection fraction; greater use of digitalis, diuretic drugs and antihypertensive agents; lesser use of beta-adrenoceptor blocking agents and more frequent prior cardiac problems, including runs of ventricular tachycardia and left bundle branch block. A matched comparison that took these inequities into account showed no significant differences in mortality or rate of resuscitation from cardiac arrest between nonrandomized patients and clinically equivalent patients randomized to placebo. Cox regression analysis indicated that two factors significantly increased the hazard ratio for arrhythmic death or resuscitated cardiac arrest in the nonrandomized patients: female gender (4.7, p less than 0.05) and electrocardiographic events (ventricular tachycardia, proarrhythmia, widened QRS complex, heart block, bradycardia) during open label titration (7.0, p less than 0.005). However, some potentially important differences between men and women were not included in the Cox regression model. Of the nonrandomized patients, approximately 70% were not randomized because of lack of suppression of ventricular premature depolarizations or adverse events, or both, and the remaining 30% because of patient or private physician request with no indication of another reason.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term evaluation of cardiac function in obese patients treated with a very-low-calorie diet: a controlled clinical study of patients without underlying cardiac disease

Twenty obese women were randomly assigned to consume (for 16 wk) either a 420-kcal/d liquid diet (n = 12) or a 1200-kcal/d balanced diet (n = 8). Thereafter, patients in both conditions were prescribed a 1200-kcal/d diet for the remainder of treatment (week 45). Six obese nondieters served as control subjects. Ambulatory electrocardiographic (Holter) monitor readings were obtained on all patients at baseline and weeks 3, 9, 13, 17, 19, and 45 of the study and were analyzed for ventricular premature depolarizations (VPDs) per hour, paired forms, and runs of ventricular tachycardia. There were no statistically significant changes in VPDs in any condition during treatment. Similarly, there were no significant changes in the PR, QRS, and corrected QT intervals. The results indicate that under appropriate medical supervision, very-low-calorie diets can be used safely for up to 16 wk by significantly obese patients free of pre-existing cardiac disease.

Ventricular septal summit stimulation in atrlo-ventricular nodal reentry tachycardia

In all, 18 consecutive patients with atdoventricuiar nodal reentry tachycardia (AVNRT) underwent right ventricular (RV) stimulation duling AVNRT from either the RV apex or summit. Stimulation from the RV apex advanced the tachycardia with the same atrial sequence in 8 of 18 patients (33%), hut never concl@vely excluded the m ence of a low atrial tachycardia. RV summit stimulation resulted in direct stimulation of the low septal rim atrium in 8 patients. RV summit stim ulaticn advanced the tachycardia in 4 patients, de layed it in 2 and terminated R in 3 without an atrial electrogram. The latter 2 fmdings exclude the presence of a low atrial tachycardia. Thus, in ps tients with AVNRT, application of extrastimuli closer to the putative reentrant site enables greater efficacy in tachycardia resetting and in excluding a low septal atrial tachycardia. (AmJCardiol1993,72:1299-1273) trioventricular nodal reentrant tachycatdia (AVNRT) A is 1 of the most common causes of supraventricular tachycardia.’ AVNRT remains a diagnosis of exclusion, and the differentiation of AVNRT from other forms of tachycardia, particularly low atrial tachycardia, can be difficult. The effect of programmed ventricular premature depolarizations during tachycardia has been shown to be critical in helping to establish diagnosis.2 Ventricular premature depolarizations inserted during AVERT, which either terminate the tachycardia without retrograde atrial activation or result in delay of the succeeding atrial impulse, exclude the diagnosis of atria1 tachycardia. Furthermore, a ventricular premature depolarization that advances the tachycardia without change in the atrial activation sequence strongly suggests AVNRT However, because of the short excitable gap and refractoriness of intervening tissue, ventricular premature depolarizations inserted from the right ventricular apex frequently do not enter the tachycardia circuit in patients with AVNRT. We hypothesized that activation closer to the putative reentrant circuit by stimulation near the His bundle would facilitate access into the circuit. Therefore in this study, we compared stimulation of the right ventricular (RV) apex with that of the RV summit in patients with AVNRT.

Avoiding interpretive pitfalls when assessing arrhythmia suppression after myocardial infarction: Insights from the long-term observations of the placebo-treated patients in the Cardiac Arrhythmia Pilot Study (CAPS)

The Cardiac Arrhythmia Pilot Study (CAPS) was a 1 year trial that analyzed the safety and effectiveness of arrhythmia suppression in 502 patients surviving acute myocardial infarction who had ≥10 ventricular premature depolarizations/h or ≥5 runs of ventricular tachycardia on a Holter recording obtained 6 to 60 days after the acute infarction. Because 100 of these patients received placebo in a double-blind fashion for 1 year, a comprehensive objective analysis was performed of spontaneous arrhythmia changes based on real data rather than statistical estimates.In the CAPS placebo group, 19% developed some serious clinical event in 1 year (death, heart failure, proarrhythmia) that could likely be attributable to antiarrhythmic drug toxicity. A significant reduction in the frequency of ventricular premature depolarizations (p = 0.004) occurred in the first few weeks of “therapy,” with a further significant (p < 0.04) decrease between 3 to 12 months. After initiation of placebo antiarrhythmic therapy, 27% had “apparent ventricular premature depolarization suppression” (70% reduction) after one Holter recording evaluation and nearly half (48%) after six Holter recordings to assess suppression were performed.It is concluded that 1) setting a higher percent suppression goal or obtaining multiple baseline Holter recordings decreases the chance of mistaking suppression for spontaneous variability: 2) obtaining frequent individual Holter recordings over the course of drug therapy actually increases the chance of sampling during one extreme variability period, the result of which is to incorrectly infer “suppression” or “proarrhythmia”: and 3) runs of ventricular tachycardia occur in the CAPS study group infrequently, are of low density and exhibit extreme variability such that a primary suppression goal focused on runs of ventricular tachycardia is not a reliable end point for assessing antiarrhythmic therapy.

Return Ventricular Rhythm: New Mechanism for Tachyarrhythmia

A case study is presented in which the electrocardiographic patterns during tachycardia showed ventricular premature depolarizations with retrograde conduction to the atria probably using a left-sided anomalous pathway and reentry to the ventricles with normal ventricular activation and duplication of the heart rate. This type of tachycardia is being labeled "return ventricular rhythm" and, as far as it is known, this is the first description of its mechanism.

The Cardiac Arrhythmia Suppression Trial: How Has it Impacted on Contemporary Arrhythmia Management?

Implications of the Cardiac Arrhythmia Suppression Trial. A most important issue in cardiology practice has been when and how to treat asymptomatic patients with ventricular arrhythmia. This is a particularly thorny problem, since the presence of complex ventricular ectopy is an independent risk variable in patients with a variety of forms of heart disease. The Cardiac Arrhythmia Suppression Trial (CAST) was designed to answer the question of whether or not abolition of ventricular premature depolarizations, in those who had had a myocardial infarction, would confer any substantial benefit, especially in terms of a mortality reduction. Unfortunately, that question has not yet been answered, but the preliminary results of the CAST has had a major impact on physicians, patients, the scientific community, industry, and regulatory agencies. This article reviews the implications of the CAST and describe how it has affected the contemporary management of patients with cardiac arrhythmia. (J Cardiovasc Electrophysiol, Vol. 1, pp. 457–463, October 1990)