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Biomedical subjects

M E Josephson

Publications and source records attributed to M E Josephson.

At least 91 records · Page 5Linked to original sources
PubMed1993

Polymorphic ventricular tachycardia induced by programmed stimulation: response to procainamide.

OBJECTIVES: This study was designed to evaluate the effects of procainamide on polymorphic ventricular tachycardia induced by programmed stimulation and to correlate the responses with heart disease, left ventricular endocardial activation abnormalities and the signal-averaged electrocardiogram (ECG). BACKGROUND: Polymorphic ventricular tachycardia is induced frequently during electrophysiologic studies. In many patients this response is an artifact of programmed stimulation; in others, it appears to be clinically relevant. Previous observations have suggested that in some patients type IA antiarrhythmic agents can change the response to programmed stimulation from polymorphic to uniform ventricular tachycardia. METHODS: Programmed right ventricular stimulation was performed in the absence of antiarrhythmic drugs and after procainamide. Signal-averaged ECGs and left ventricular maps were performed during sinus rhythm in the absence of antiarrhythmic drugs. RESULTS: We evaluated 79 consecutive patients undergoing clinical electrophysiologic studies, in whom polymorphic ventricular tachycardia was the only arrhythmia induced in the absence of antiarrhythmic drugs. After procainamide administration, uniform monomorphic ventricular tachycardia was induced in 24 patients (Group 1), inducible polymorphic ventricular tachycardia persisted in 30 patients (Group 2) and no ventricular tachycardia could be induced in the remaining 25 patients (Group 3). Twenty-three (96%) of 24 patients developing uniform ventricular tachycardia after procainamide administration had coronary artery disease compared with 63% of Group 2 and 48% of Group 3 patients (p = 0.003). Left ventricular aneurysms were also found more frequently (46%) in the patients developing uniform ventricular tachycardia after procainamide than in either Group 2 or Group 3 (13% and 0%, respectively, p < 0.008). Abnormalities of the signal-averaged ECG typically seen in patients with spontaneous reentrant sustained ventricular tachycardia were significantly more frequent in patients who developed inducible uniform ventricular tachycardia after procainamide than in those who did not. Similarly, patients developing uniform ventricular tachycardia after procainamide had more extensive abnormalities of left ventricular endocardial activation revealed by catheter maps during sinus rhythm. CONCLUSIONS: The conversion of inducible polymorphic ventricular tachycardia to uniform ventricular tachycardia after procainamide administration occurs almost exclusively in patients with coronary disease, previous myocardial infarction and abnormal left ventricular function. This response may permit activation mapping of tachycardias, allowing the application of surgical or catheter ablation techniques that would otherwise not be possible in such patients.

Cardiac Pacing, Artificial↗
PubMed1993

Atrioventricular nodal reentry: evidence supporting an intranodal location.

The exact site of the reentrant circuit in AV nodal reentry remains controversial. While recent ablative techniques have yielded information, the interpretation of which suggests that the atrium is required, other explanations for these interpretations are available. Prior pathophysiological studies with three-dimensional reconstruction of the node suggest that it is a highly anisotropic structure and extends through Koch's Triangle. Data from humans suggesting the atria are not necessary include the presence of AV dissociation during supraventricular tachycardia (SVT), depolarization of atrial tissue surrounding the node without affecting SVT, pacing induced AH intervals exceeding those during SVT, and site dependency of a critical AH interval (exceeding atrial refractoriness) that is required for initiation of AV nodal reentry.

Animals↗
PubMed1993

Myocardial electrical impedance mapping of ischemic sheep hearts and healing aneurysms.

BACKGROUND: This study was designed to examine the bulk electrical properties of myocardium and their variation with the evolution of infarction after coronary occlusion. These properties may be useful in distinguishing between normal, ischemic, and infarcted tissue on the basis of electrophysiological parameters. METHODS AND RESULTS: The electrical impedance of myocardial tissue was studied in a sheep model of infarction. The animal model involved a one-stage ligation of the left anterior descending and second diagonal arteries at a point 40% of the distance from the apex to the base. By use of a four-electrode probe, an epicardial mapping system was developed that allowed for cardiac cycle gated and signal-averaged measurements. Subthreshold current (15 microA) was injected through two of the electrodes at frequencies of 1, 5, and 15 kHz and the induced potential measured with the other two electrodes. Epicardial maps of the left ventricle were obtained during acute infarction and at 1-, 2-, and 6-week intervals after occlusion. Results showed the average specific impedance of the myocardium before infarction to be 158 +/- 26 omega-cm independent of location on the epicardium. By 60 minutes after coronary occlusion, the specific impedance had increased by 199% (p < 0.005, n = 9); it remained elevated for up to 4 hours. One week after infarction, the specific impedance decreased to 59% of the control value (p < 0.025, n = 8). Six weeks after occlusion, the specific impedance remained low at 57% of that of the noninfarcted tissue (p < 0.005, n = 9). The phase angle of the complex impedance was also measured and revealed similar changes. The hydroxyproline content of the tissue was assayed to assess infarct healing. CONCLUSIONS: In this animal model, impedance is a bulk electrical property of tissue that varies with the evolution of myocardial infarction. Impedance mapping revealed significantly different values for normal, ischemic, and infarcted tissue and may prove useful in better defining the electrophysiological characteristics of such tissue.

Animals↗
PubMed1993

Comparison of resetting and entrainment of uniform sustained ventricular tachycardia. Further insights into the characteristics of the excitable gap.

BACKGROUND: Resetting and entrainment have both been used to characterize the electrophysiological properties of the reentrant circuit in ventricular tachycardia. Several entrainment studies have suggested that the circuit has decremental properties, because the return cycle increases at faster pacing rates. Resetting, however, demonstrates a fully excitable gap in the majority of tachycardias. METHODS AND RESULTS: The response to resetting and overdrive pacing was analyzed in 18 ventricular tachycardias. Resetting demonstrated some duration of a fully excitable gap in 14 of 18 tachycardias. Overdrive pacing was performed at several cycle lengths with an incremental number of stimuli (1-15 beats) such that the first beat that interacted with the tachycardia (the nth beat) could be identified. The return cycles measured during resetting and the nth beat of pacing were identical (r = 0.99). At relatively long paced cycle lengths, paced beats after the nth beat resulted in a constant return cycle in most tachycardias with a fully excitable gap. At rapid paced cycle lengths, an increase in the return cycle from the nth to the nth + 1 beat was associated with progressive prolongation in the return cycle with each incremental paced beat until a longer equilibrium return cycle was reached or the tachycardia terminated in response to pacing. CONCLUSIONS: We propose that the responses to resetting and overdrive pacing with or without entrainment appear to provide conflicting information about the characteristics of the circuit because they in fact measure entirely different electrophysiological parameters. The nth beat of pacing foreshortens the excitable gap to the extent that it arrives prematurely. Subsequent paced beats interact with an altered tachycardia circuit that has had less time to recover excitability. Resetting is the interaction of a single paced beat with the tachycardia and, as such, provides a more accurate assessment of the characteristics of the unaltered tachycardia circuit.

Aged↗
PubMed1992

Frequency and implications of resetting and entrainment with right atrial stimulation in atrial flutter.

Thirty-three patients (24 with typical and 9 with atypical flutter-wave morphology) were studied to evaluate the incidence and implications of resetting and entrainment of atrial flutter with right atrial stimulation. Resetting with single extrastimulus was present in 23 cases (group A) and absent in 10 (group B). Most cases of reset flutter were typical (20 of 23). Fixed fusion indicative of entrainment was observed in all 29 cases with pacing trains. Groups A and B did not differ significantly in flutter cycle length (230 +/- 20 vs 223 +/- 19 ms), atrial functional refractory period (165 +/- 18 vs 167 +/- 22 ms) or longest paced cycle length producing entrainment (213 +/- 19 vs 210 +/- 19 ms). In contrast, the return cycle after the longest paced cycle length producing entrainment was significantly shorter in group A (228 +/- 27 vs 284 +/- 56 ms; p = 0.001). The return cycle in group A was virtually identical to the flutter cycle length, whereas in group B it was greater (p = 0.002 compared with group A). Resetting was more frequent in typical than atypical flutter (20 of 24 vs 3 of 9; p = 0.01). Both typical and atypical flutter can be transiently entrained by right atrial pacing. Lack of resetting and longer return cycle, suggesting a longer conduction time between the reentrant circuit and the stimulation site, were mostly observed in atypical flutter. The data suggest a different location for both types of flutter, and may have implications for ablation techniques. A more cautious approach, with more extensive mapping, appears appropriate for ablation attempts of atypical flutter.

Adult↗
PubMed1992

Effect of high-current stimulation in patients with sustained ventricular tachycardia rendered noninducible by antiarrhythmic drugs.

Successful antiarrhythmic drug therapy for sustained ventricular tachycardia (VT) is presumed to be related to effects on myocardium within the re-entrant circuit. To test the hypothesis that prevention of VT induction may be related to effects on myocardium other than that directly involved in the tachycardia circuit, high-current stimulation was used to achieve shorter coupling intervals in 22 patients with sustained uniform VT that was rendered noninducible by antiarrhythmic agents during stimulation at twice threshold. Sustained uniform VT was induced in 10 patients in response to high-current stimulation (group 1), including 4 tachycardias with the same morphology observed in the baseline study. There were no inducible arrhythmias in 12 patients (group 2). Patients were receiving several different antiarrhythmic regimens, but there was no particular drug associated with the induction of VT using high-current stimulation. There was no statistically significant difference between groups 1 and 2 in baseline VT cycle length (247 +/- 41 vs 253 +/- 44 ms), drug-induced increase in effective refractory period (20 +/- 15 vs 16 +/- 7%), QRS duration (25 +/- 10 vs 20 +/- 17%) or maximal current strength delivered (10.9 +/- 5.3 vs 9.3 +/- 4.0 mA). There was no significant difference in local activation with high-current stimulation between groups 1 and 2. In conclusion, sustained uniform VT was induced in 45% (10 of 22) of patients whose arrhythmias were rendered noninducible by antiarrhythmic agents during programmed stimulation at twice threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1992

Rate-dependent failure of ventricular capture in patients treated with oral propafenone.

The effects of propafenone on ventricular excitability were studied in 18 patients after 9 +/- 6 days on oral propafenone (900 mg/day). Late diastolic double threshold right ventricular stimulation was performed at variable rates. In five patients (28%, group I) an intermittent, rate-dependent failure of ventricular capture was reproducibly observed during stimulation at rates above the sinus rhythm but not exceeding 150 beats min-1. In four patients loss of capture was preceded by gradual prolongation of the interval between the stimulus artifact and the local right ventricular bipolar electrogram. Such findings were not observed in the remaining 13 patients (group II) on propafenone nor in 28 studies in the same patients on different antiarrhythmic agents. Group I vs group II patients were older (72 +/- 4 vs 53 +/- 18 years, P = 0.002), had longer right ventricular effective refractory periods on the baseline (P = 0.004) and on propafenone (P = 0.0003), and had longer QRS duration on propafenone. The increase produced by propafenone in sinus rhythm QRS duration, paced QRS duration and ventricular effective refractory period was greater in group I than in group II: 42 +/- 36 vs 14 +/- 12 ms, P = 0.01, 94 +/- 43 vs 34 +/- 26 ms, P = 0.0002, 88 +/- 64 vs 22 +/- 37 ms, P = 0.025, respectively. Thus propafenone can produce rate-dependent failure of ventricular capture which is associated with marked prolongation of refractoriness and QRS duration suggesting a marked use-dependent drug effect in selected patients.

Administration, Oral↗
PubMed1992

Failure of defibrillator paddle as mimic for subcutaneous patch lead during nonthoracotomy implantable cardioverter defibrillator lead configuration assessment.

It is a common, although virtually unsubstantiated, practice to assess the efficacy of nonthoracotomy lead systems for implantable cardioverter defibrillators using a defibrillator paddle as mimic for the subcutaneous patch lead. We report a case in which an adequate defibrillation threshold was documented with the nonthoracotomy lead system using a defibrillator paddle but not following implantation of the true subcutaneous patch lead. This case suggests that the substitution of a defibrillator paddle for the subcutaneous patch lead during nonthoracotomy lead system evaluation may have significant limitations in assessing lead configuration efficacy.

Adult↗
PubMed1992

Results of electrophysiological testing and long-term follow-up in patients sustaining cardiac arrest only while receiving type IA antiarrhythmic agents.

UNLABELLED: Therapeutic management of patients sustaining a cardiac arrest while receiving antiarrhythmic agents can be difficult since the role of the drug in possibly facilitating the arrhythmia is often difficult to define. To determine if the response to programmed stimulation could give insight into which patients may have experienced a drug-induced cardiac arrest, we studied 29 patients (61 +/- 9 years) with no prior history of sustained ventricular tachyarrhythmias (VT) who suffered a cardiac arrest only while receiving type Ia antiarrhythmic agents. Patients with documented myocardial infarction, acute ischemia, electrolyte abnormalities, or torsade de pointes were excluded from the study. Twenty-four patients had coronary artery disease with prior myocardial infarction (ejection fraction 28% +/- 9%) and five patients had idiopathic dilated cardiomyopathy (ejection fraction 31% +/- 6%). During baseline electrophysiological testing, 19 patients (66%) had inducible sustained ventricular arrhythmias: uniform VT, n = 14 (group I), polymorphic VT or ventricular fibrillation, n = 5 (group II). Ten patients (group III) had no inducible sustained ventricular arrhythmias. To determine if rechallenge with a type Ia agent could facilitate induction of a sustained ventricular arrhythmia in group III, eight patients underwent ten electrophysiological studies during therapy with either procainamide or quinidine. Only two patients developed sustained VT in response to programmed stimulation. Patients in groups I and II received therapy guided by electrophysiological testing, including antiarrhythmic agents alone (n = 8), subendocardial resection (n = 4), or an implantable cardioverter defibrillator (n = 7). Patients in group III received antiarrhythmic agents empirically (n = 3), or for treatment of atrial tachyarrhythmias (n = 2) or nonsustained VT (n = 1). In addition, four patients in group III received an implantable cardioverter defibrillator. During a mean follow-up of 28 +/- 27 months (range: 1 day-84 months) 13 patients died suddenly or received a defibrillator shock preceded by syncope or presyncope: group I: n = 5; group II: n = 2; group III: n = 6. IN CONCLUSION: (1) most patients sustaining a cardiac arrest only in the presence of type Ia antiarrhythmic agents have inducible sustained VT in the absence of antiarrhythmic agents, and (2) the risk of recurrent VT persists in patients without inducible sustained arrhythmias in the drug-free state, regardless of whether they manifest inducible arrhythmias after rechallenge with a type Ia agent.

Aged↗
PubMed1992

Sudden cardiac death in patients with chronic coronary heart disease.

Sudden cardiac death (SCD) is responsible for 300,000-400,000 deaths per year with a recurrence rate of up to 40% in survivors within the first 2 years. SCD often occurs in patients with chronic coronary artery disease, which is manifested by myocardial infarction and left ventricular dysfunction but is infrequently associated with acute infarction. SCD may be the initial symptom of coronary artery disease. Primary or rapid ventricular tachycardia are the most common arrhythmic causes of SCD. Endocardial mapping studies during electrophysiological study have shown areas of slowed conduction with abnormal endocardial electrograms in SCD patients with moderately damaged ventricles. SCD increases with age and occurs more frequently in men with coronary artery disease as a significant risk factor. Complex ventricular ectopy, once thought of as an independent risk factor, is not as good a predictor as poor left ventricular function for recurrence of SCD. While signal-averaged electrocardiograms can identify patients with slowed conduction, their positive predictive value for SCD is poor. Initial evaluation should be aimed at the identification of ischemia, since those patients with SCD and acute myocardial infarction do well when treated for their ischemia. The arrhythmias that are inducible during electrophysiological study are rapid and poorly tolerated. Patients with inducible ventricular tachycardia who are rendered noninducible pharmacologically have a good prognosis, whereas those who are still inducible or have no inducible arrhythmias have a high recurrence rate of SCD and should be considered for subendocardial resection when appropriate or for placement of an implantable defibrillator.

Arrhythmias, Cardiac↗
PubMed1991

Usefulness of the delta HA interval to accurately distinguish atrioventricular nodal reentry from orthodromic septal bypass tract tachycardias.

Surface electrocardiographic criteria may be inadequate to distinguish some cases of atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) from those with orthodromic SVT incorporating a posterior septal bypass tract (orthodromic SVT) because of similarities in P-wave morphology and timing during SVT. Invasive electrophysiologic studies may occasionally leave uncertainty in the correct diagnosis, using currently accepted criteria. A new criterion for distinguishing these 2 forms of SVT was therefore devised and tested based on differences in the sequence of activation of the His bundle and atrium during SVT and ventricular pacing. Eighty-four patients underwent invasive electrophysiologic studies (60 with proved AV nodal SVT, 24 with proved orthodromic SVT), during which His to atrial (HA) intervals were measured during SVT as well as ventricular pacing at the same rate. The newly devised criterion, the delta HA interval (HApace-HAsvt) was found to accurately distinguish AV nodal SVT (delta HA greater than 0 ms) from orthodromic SVT (delta HA less than -27 ms). An intermediate value of delta HA = -10 ms was chosen which had a 100% sensitivity, specificity and predictive accuracy in differentiating the 2 forms of SVT. A clear retrograde His potential during ventricular pacing, which is essential for application of this criterion, was present in 78 of 84 (93%) cases. In summary, patients with delta HA intervals greater than -10 ms separate AV nodal reentry from orthodromic SVT incorporating a septal bypass tract, and no overlap exists between the 2 groups. This criterion may be useful in differentiating the mechanism of SVT in cases in which distinction is not possible by other methods.

Adolescent↗
PubMed1991

Usefulness of the electrophysiology laboratory for evaluation of proarrhythmic drug response in coronary artery disease.

Two potential manifestations of proarrhythmic responses to type IA antiarrhythmic agents in the electrophysiology laboratory were evaluated in 122 patients with chronic coronary artery disease and previous myocardial infarction: (1) conversion of uniform nonsustained ventricular tachycardia (VT) into sustained VT after drug administration, and (2) induction of sustained VT by fewer extrastimuli after drug administration. Forty-two patients were evaluated for nonsustained VT. Eighty patients were evaluated for sustained VT: 30 of these had spontaneous sustained VT only while receiving empiric therapy with quinidine or procainamide, whereas the remaining 50 developed spontaneous VT in the absence of antiarrhythmic drugs. All patients underwent programmed stimulation in the baseline state and after procainamide. Four patients had conversion of induced uniform nonsustained VT into the same morphology, but sustained VT after procainamide administration. These responses only occurred in patients evaluated for nonsustained VT. Over 90% of patients presenting with sustained VT had uniform sustained VT induced at the baseline study and after procainamide, regardless of whether the spontaneous arrhythmia occurred only in the presence or absence of antiarrhythmic drugs. There was no significant difference in the change in mode of induction from baseline to procainamide study, regardless of whether patients had developed spontaneous VT only in the presence or absence of antiarrhythmic drugs. One patient with no inducible VT at the baseline study had inducible uniform sustained VT after procainamide administration, and 1 patient with inducible VT at baseline developed spontaneous sustained uniform VT after procainamide administration. Both patients had developed spontaneous sustained VT only while receiving therapy with type IA agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Complexes, Premature↗
PubMed1991

ACC policy statement. Recommended guidelines for training in adult clinical cardiac electrophysiology. Electrophysiology/ Electrocardiography Subcommittee, American College of Cardiology.

Training in clinical cardiac electrophysiology should take place in an Accreditation Council for Graduate Medical Education accredited cardiology program, and the electrophysiology training program itself should be accredited by the Council. Each trainee must be eligible for board certification in Internal Medicine and either eligible for certification in Cardiovascular Diseases or in a program leading to eligibility. Training faculty should be certified in clinical cardiac electrophysiology or demonstrate equivalent credentials. At least two training faculty members are preferred. The faculty must be dedicated to teaching, active in performing or promoting research and must spend a substantial portion of their time in research, teaching and practice of clinical electrophysiology. A curriculum of training should be established. Faculty experts in the related basic sciences should be available and involved in teaching. The institution should have a fully equipped clinical electrophysiology laboratory and complete noninvasive capabilities. A close working relation with a cardiac surgery faculty member skilled in surgical treatment of arrhythmias is required. Training in application of pharmacologic and all current nonpharmacologic therapies, in the outpatient and inpatient setting, is necessary. The clinical exposure must include all facets of arrhythmia diagnosis and treatment and must be quantitatively sufficient to allow the trainee to develop proficiency. The period of training should not be less than one year in addition to the period of cardiology fellowship required by the ABIM for board eligibility. A continuous period of training is preferred.

Anti-Arrhythmia Agents↗
PubMed1991

The mechanism of propafenone-induced slowing of ventricular tachycardia in man as defined by analysis of resetting response patterns.

The major finding in this study was that all VTs in patients treated with propafenone had a fully excitable gap. As only well tolerated, uniform VT in patients with chronic coronary artery disease was included for study, this result may not apply for ventricular arrhythmias in other patient populations. This is incompatible with the hypothesis that propafenone slows VT by increasing refractoriness within the VT circuit. Instead, the drug-mediated prolongation in VT cycle length is caused by effects on conduction velocity in fully recovered tissue and/or a change in the barriers of the circuit.

Aged↗
PubMed1991

Differences in electrophysiological substrate in patients with coronary artery disease and cardiac arrest or ventricular tachycardia. Insights from endocardial mapping and signal-averaged electrocardiography.

BACKGROUND: Many studies have combined patients with hemodynamically well-tolerated ventricular tachycardia (VT) and those with cardiac arrest (CA) as a single, homogenous group. Recent studies suggest that these two groups have different electrophysiological substrates and responses to therapy. Most of these studies, however, enrolled patients with a variety of cardiac diagnoses. METHODS AND RESULTS: We used signal-averaged electrocardiography (SAECG) and endocardial catheter mapping to define the electrophysiological substrate in patients with coronary artery disease and VT or CA and correlate the results of the two methods. We also examined the usefulness of SAECG in CA patients to differentiate those with inducible arrhythmias from those who are noninducible. VT patients were more likely to have had a prior myocardial infarction (p = 0.0005) and to have inducible arrhythmias (p = 0.0001) than were CA patients. The induced arrhythmias in patients who presented with VT was VT in more than 90% of cases, whereas in CA patients, polymorphic ventricular tachycardia (PMVT) accounted for one third of induced arrhythmias. Mean filtered QRS duration was longer (135 versus 120 msec) and the terminal QRS voltage was smaller (20 versus 34 microV) in VT than in CA patients (p less than 0.01). Sixty-three percent of CA patients and 87% of VT patients had abnormal SAECG (p = 0.001). VT patients had more extensive endocardial abnormalities and more abnormal (53% versus 40%, p = 0.002), fractionated (8% versus 3%, p = 0.02), late (17% versus 8%, p = 0.0003), and late abnormal or fractionated (14% versus 4%, p = 0.0001) sites than CA patients. VT patients had a greater duration of the longest electrogram (129 versus 109 msec, p = 0.0006) and total endocardial activation time (68 versus 54 msec, p = 0.009). Among CA patients, those with induced VT had more extensive substrate than did those with induced PMVT and were similar to VT patients with induced VT. Among CA patients, the trend for more patients with inducible VT (77%) or PMVT (55%) than noninducible patients (47%) to have an abnormal SAECG did not reach statistical significance (p = 0.14). The positive and negative predictive values of an abnormal SAECG were 77% and 44%, respectively. CONCLUSIONS: VT patients have more extensive endocardial substrate than CA patients, which translates into greater and more frequent SAECG abnormalities. Among CA patients, there are significant differences in substrate between patients with induced VT and those with induced PMVT. SAECG is not useful in differentiating CA patients who have inducible VT or PMVT from those who do not.

Coronary Disease↗
PubMed1990

Cycle-length response of ventricular tachycardia associated with coronary artery disease to procainamide and amiodarone.

We undertook this study to determine if the cycle-length response of ventricular tachycardia (VT) to procainamide and amiodarone is similar in the individual patient. We enrolled 40 patients with uniform, monomorphic VT at a baseline, drug-free electrophysiologic study, after procainamide infusion and during oral amiodarone therapy. We found a significant correlation (p less than 0.01) between VT cycle-lengths on the 2 agents as well as the percent change in cycle length from baseline. Only 60% of the patients exhibited VT rates within 10% between the 2 agents. Importantly, less than 20% of patients had further slowing of the VT rate (greater than 10% slowing) during amiodarone therapy as compared to procainamide. Thus, although the cycle-length response of VT to procainamide correlates with the cycle-length response to amiodarone, 40% of patients have a disparate response (greater than 10% difference in cycle length) to the 2 agents; additional slowing of VT rates in response to amiodarone beyond that seen with procainamide is unlikely. These results have important implications regarding the institution of amiodarone therapy and the need for repeat electrophysiologic testing during amiodarone therapy.

Amiodarone↗