Hoshiar Abdollah

Significance of ventricular arrhythmias initiated by programmed ventricular stimulation: the importance of the type of ventricular arrhythmia induced and the number of premature stimuli required.

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.

Canadian Trial of Physiological Pacing Effects of Physiological Pacing During Long-Term Follow-Up

Background—The Canadian Trial of Physiological Pacing (CTOPP) reported that the risk of stroke or cardiovascular death was similar between patients receiving ventricular versus physiological pacemakers at the end of the original follow-up period of 3 years. However, the occurrence of atrial fibrillation was significantly less frequent with physiological pacemakers. To assess a potential delayed benefit of physiological pacing, follow-up of patients in this study was extended to 6 years. Methods and Results—A total of 1474 patients requiring a pacemaker for symptomatic bradycardia were randomized to receive ventricular and 1094 to physiological pacemakers. The primary outcome was stroke or cardiovascular death. The study was completed in July 1998, and follow-up was extended to July 2001. At a mean follow-up of 6.4 years, there was no difference between treatment groups in the primary outcome of cardiovascular death or stroke. There was no significant difference in total mortality or stroke between groups. There was a significantly lower rate of development of atrial fibrillation in the physiological group, with a relative risk reduction of 20.1% (CI, 5.4 to 32.5; P =0.009). Conclusions—The CTOPP extended study does not show a difference in cardiovascular death or stroke, or in total mortality, or in stroke between patients implanted with ventricular or physiological pacemakers over a mean follow-up of >6 years. However, there is a persistent significant reduction in the development of atrial fibrillation with physiological pacing.

Results of a ventricular stimulation protocol using a maximum of 4 premature stimuli in patients without documented or suspected ventricular arrhythmias.

A prospective study was undertaken to assess the results of an aggressive ventricular stimulation protocol in 52 nonmedicated patients without a documented or suspected ventricular arrhythmia (VA). Thirty-five patients had no structural heart disease, 8 coronary artery disease, 6 hypertrophic cardiomyopathy, 2 mitral valve disease and 1 patient had congestive cardiomyopathy. The patients were 12 to 72 years old. One to 4 ventricular premature beats (twice diastolic threshold, 2 ms in duration) were given during sinus rhythm and during ventricular pacing at 100 beats/min at the right ventricular apex. End points were initiation of 6 or more beats of VA or every extrastimulus brought to its refractory period. In 31 of 52 patients (60%), a VA was initiated (nonsustained polymorphic ventricular tachycardia in 24 patients, nonsustained monomorphic ventricular tachycardia in 2 and ventricular fibrillation requiring countershock in 5). Repetitive ventricular responses (RVR) (1 to 5 beats) were initiated in 46 patients. In 15 patients only RVRs were initiated. In 6 patients RVRs or VA were not initiated. At the end of the follow-up period (mean 14 months), no patient had spontaneous VA and all were alive. This study shows that ventricular stimulation can result in initiation of VA in patients without clinical VA. Interpretation of results of programmed ventricular stimulation in patients without clinically documented VA should be made with caution.

A comparison of the electrophysiologic effects of intravenous and oral amiodarone in the same patient.

In 12 patients (nine with Wolff-Parkinson-White syndrome and three with ventricular tachycardia) the electrophysiologic effects of intravenous (5 mg/kg body weight in 1 min) and oral (total dose 9800 to 11,200 mg) amiodarone were studied with programmed stimulation of the heart. Intravenous and oral amiodarone had a similar (p less than .05) effect of lengthening on the effective refractory period of the atrioventricular node. Only intravenous amiodarone prolonged (p less than .05) the AH interval. Oral amiodarone was more effective than intravenous amiodarone in lengthening the anterograde effective refractory period of the accessory atrioventricular pathway. Only oral amiodarone prolonged the effective refractory period of atrium and ventricle and the HV interval, all significantly (p less than .05). Intravenous amiodarone slowed (p less than .05) the rate of circus-movement tachycardia in patients with Wolff-Parkinson-White syndrome, and further slowing was observed after oral amiodarone. Termination of tachycardia by intravenous amiodarone predicted prevention of reinitiation of tachycardia during oral amiodarone. These data indicate that intravenous and oral amiodarone do not have the same electrophysiologic effects. It is not clear whether cumulative effects, active metabolites, or both are responsible for these differences.

Relationship Between Pacemaker Dependency and the Effect of Pacing Mode on Cardiovascular Outcomes

Background—A recently completed trial, the Canadian Trial of Physiological Pacing (CTOPP), showed that physiological pacing did not significantly reduce mortality, stroke, or heart failure hospitalization, but it did show that atrial fibrillation occurred less frequently in patients with physiological pacing. Many pacemaker patients experience only transient bradyarrhythmias with an adequate unpaced heart rate (UHR) and are not pacemaker-dependent. The purpose of the present analysis was to determine if pacemaker-dependent patients have an increased benefit from physiological pacing compared with non–pacemaker-dependent patients. Methods and Results—Of 2568 patients included in the CTOPP trial, 2244 patients had a pacemaker dependency test performed at the first follow-up visit. The yearly event rate of cardiovascular death or stroke steadily increased with decreasing UHR in the ventricular pacing group, but it remained constant in the physiological pacing group. When the patients were subdivided to UHR ≤60 bpm or >60 bpm, there was an interaction between pacing mode treatment and UHR subgroup. The Kaplan-Meier plot confirmed a physiological pacing advantage only in the UHR ≤60 bpm subgroup. This differential effect was also present for the outcomes of cardiovascular death and total mortality. Conclusions—This study demonstrated that UHR at first follow-up has an important influence on how pacing mode selection affects cardiovascular death and total mortality. Pacemaker-dependent patients with low UHR will probably be paced frequently and will likely benefit from physiological pacing. In contrast, non–pacemaker-dependent patients will likely be paced infrequently and may not benefit from physiological pacing.

Value of QRS alteration in determining the site of origin of narrow QRS supraventricular tachycardia.

To determine the value of alternation of QRS morphology in determining the site of origin of sustained narrow QRS supraventricular tachycardia (SVT), we retrospectively studied 163 distinct tachycardias in 161 patients (ages 4 to 91 years) in whom the site of origin of SVT was proven by intracardiac electrophysiologic study. Sustained SVT was defined as lasting longer than 30 sec. Narrow QRS was defined as QRS width less than 0.12 sec. Atrial fibrillation and flutter were excluded. The presence or absence of QRS alternation was judged at least 10 sec after initiation of SVT. Circus movement tachycardia with anterograde AV node conduction and a retrograde accessory AV pathway was seen in 89 patients (58 with Wolff-Parkinson-White syndrome, 31 with concealed accessory pathway); intra-AV nodal reentrant tachycardia (AVNT) was present in 57 cases, and 17 tachycardias were atrial in origin. QRS alternation was present in 36 of 163 cases (22%). In only eight of these 36 did RR interval length alternation accompany alternation in QRS morphology. Thirty-three of 36 (92%) tachycardias with QRS alternation were circus movement tachycardias. Two were atrial in origin and one was AVNT. We conclude that the presence of QRS alternation during sustained narrow QRS SVT is highly indicative of a retrograde accessory AV pathway in the tachycardia circuit.

Effect of amiodarone in paroxysmal supraventricular tachycardia with or without Wolff-Parkinson-White syndrome

In Wolff-Parkinson-White (WPW) syndrome, the two most commonly occurring arrhythmias are circus movement tachycardia (CMT) and atrial fibrillation (AF). In 70% of patients with clinically documented CMT in whom the arrhythmia could be initiated by programmed electrical stimulation of the heart, the same CMT could still be initiated after long-term oral amiodarone administration. Spontaneous clinical recurrence of the arrhythmia was, however, observed in only 10% of patients. This finding suggests that the beneficial effect of amiodarone on CMT is primarily based on the prevention of the CMT-initiating premature beat. This may also apply to atrioventricular nodal reentrant tachycardia, in which amiodarone is also extremely effective in preventing relapses. The role of amiodarone in other forms of reentrant, or ectopic, supraventricular tachycardias is less well defined. During AF in WPW syndrome, the ventricular rate is related to the duration of the anterograde refractory period of the accessory pathway. Amiodarone prolongs this value, resulting in the reduction of ventricular rate during AF. Unfortunately, in the presence of a short anterograde refractory period of the accessory pathway, amiodarone results in only a small amount of lengthening of this value. In these patients the beneficial effect of amiodarone may primarily be related to the prevention of episodes of AF. We also found that the effect of oral amiodarone on the duration of the anterograde refractory period of the accessory pathway can (1) be abolished by sympathetic stimulation with isoproterenol and (2) be predicted from the effect of ajmaline or procainamide given intravenously. These observations clearly have practical clinical implications.

Electrocardiography Pitfalls and Artifacts: The 10 Commandments

Artifacts are common in patients who require ECG monitoring. Artifacts can simulate arrhythmias such as atrial flutter and ventricular tachycardia and lead to inappropriate treatment. Electrode and lead misplacements are another common pitfall and can lead to ECG changes that may be interpreted as ischemic in origin and can mimic serious arrhythmias. A simplified algorithm (REVERSE is the mnemonic) may help clinicians correctly identify both suspected electrode misplacements and artifacts.

Continuous electrical activity during sustained monomorphic ventricular tachycardia: Observations on its dynamic behavior during the arrhythmia

Catheter mapping was performed during sinus rhythm and monomorphic ventricular tachycardia (VT) in 56 consecutive patients with sustained, monomorphic VT. Forty-two patients had an old myocardial infarction (VT-old MI group), 6 patients had right ventricular dysplasia (VT-RV dysplasia group), and 8 patients had idiopathic VT (idiopathic-VT group). Continuous electrical activity was recorded in 15 of 42 patients of the VT-old MI group (36%), 5 of 6 of the VT-RV dysplasia group (83%), and in 0 of 8 patients in the idiopathic VT group (0%). In 17 of 20 patients with continuous electrical activity during VT, observations on the dynamic behavior of continuous electrical activity during VT revealed at least 1 of the following characteristics: spontaneous disappearance and reappearance of continuous electrical activity without changes in rate, morphologic pattern or axis of VT; pacing-induced transient termination of continuous electrical activity without termination of VT; spontaneous disappearance of continuous electrical activity during VT as a rate-dependent phenomenon; Wenckebach-like conduction to other areas resulting in transient and periodic continuous electrical activity; dependence of continuous electrical activity on ventricular activation pattern during VT; pacing-induced change from a noncontinuous electrogram into continuous electrical activity without prevention of termination of VT; and termination of continuous electrical activity after antiarrhythmic drugs without termination of VT. Continuous electrical activity was always recorded in the aneurysm and never over normal heart areas. At the sites where continuous electrical activity was recorded during VT, potentials recorded during sinus rhythm were abnormal. Our observations suggest that several electrophysiologic phenomena can simulate continuous electrical activity during monomorphic VT. Transient, continuous electrical activity is a frequent phenomenon that represents electrical activity from abnormal areas not necessarily required to perpetuate VT.

Echo-wave termination of ventricular tachycardia. A common mechanism of termination of reentrant arrhythmias by various pharmacological interventions.

BackgroundBased on epicardial mapping, different mechanisms of termination of reentrant ventricular tachycardia by various pharmacological interventions are described. Methods and ResultsIn 40 Langendorff-perfused rabbit hearts, rings of anisotropic left ventricular epicardium were made by a cryoprocedure. Sustained monomorphic ventricular tachycardia based on continuous circus movement of the impulse around the ring was induced by programmed stimulation. Increasing doses of heptanol (n = 10), potassium (n = 10), tetrodotoxin (n = 6), RP62719 (a new class III drug) (n = 4), flecainide (n = 5), and propafenone (n = 5) were administered to terminate ventricular tachycardia. Epicardial mapping (248 points) was used to study the mechanism of termination of ventricular tachycardia. In 28 of 40 hearts, ventricular tachycardia terminated because the drugs produced complete conduction block of the impulse in a segment of the reentrant pathway. In the remaining 12 hearts (heptanol, n = 2; potassium, n = 3; tetrodotoxin, n = 2; RP62719, n = 2; flecainide, n = 1; and propafenone, n = 2), termination of ventricular tachycardia occurred by collision of the circulating impulse with a spontaneous antidromic wave front reflected within the circuit. This phenomenon occurred when the circulating impulse encountered an arc of functional conduction block that did not extend along the whole width of the ring. As a result, the impulse dissociated into a continuing orthodromic circulating wave and a returning antidromic echo-wave caused by microreentry within the ring. ConclusionsIndependent of their mechanisms of action, sodium channel blockers, electrical uncouplers, and class III drugs terminate reentrant ventricular tachycardia either by complete conduction block or by collision of the impulse with an echo-wave.