Jesse C. Davis

Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity.

To define the role of verapamil in the treatment of ventricular tachycardia (VT), we studied 21 patients with chronic recurrent VT. Electrophysiologic studies were performed before and during intravenous infusion of verapamil (0.15 mg/kg followed by 0.005 mg/kg per min). On the basis of the mode of VT initiation and termination, we identified three groups of patients: (a) 11 patients had VT suggestive of reentry, as VT could be initiated with ventricular extrastimulation and terminated with overdrive ventricular pacing. Verapamil did not affect the inducibility and cycle length of VT. (b) 7 patients had VT suggestive of catecholamine-sensitive automaticity as VT could not be initiated with programmed electrical stimulation but could be provoked by isoproterenol infusion. Moreover, the VT could not be converted to a sustained sinus rhythm with overdrive ventricular pacing and it resolved only with discontinuing isoproterenol infusion. Verapamil exerted no effects on VT. (c) 3 patients had VT with electrophysiologic characteristics suggestive of triggered activity related to delayed afterdepolarizations. Characteristically, after attaining a range of cycle lengths, the sinus, atrial or ventricular paced rhythm could initiate VT without ventricular extrastimulation. The first beat of VT invariably occurred late in the cardiac cycle with a premature coupling interval 0-80 ms shorter than the preceding QRS cycle length; the premature coupling interval gradually decreased as the sinus, atrial or ventricular paced cycle length progressively shortened. Of note, verapamil completely suppressed VT inducibility in these three patients. These observations lead us to suggest that verapamil does not affect VT caused by reentry and catecholamine-sensitive automaticity but is effective in suppressing VT caused by triggered activity related to delayed afterdepolarizations in humans.

Clinical features and prognosis of patients with out of hospital cardiac arrest and a normal electrophysiologic study

Nineteen patients survived a cardiac arrest not associated with an acute myocardial infarction, and had a normal electrophysiologic study with no inducible ventricular tachycardia despite programmed stimulation with one to three extrastimuli at two or more ventricular sites. Among 14 patients who had obstructive coronary artery disease, cardiac arrest occurred during exertion or an episode of angina pectoris in 11; 24 hour ambulatory electrocardiographic recordings demonstrated infrequent or no premature ventricular complexes in 10 and an ischemic response occurred during stage I or II (Bruce protocol) in 6 of 9 patients who underwent exercise testing. Treatment of these patients consisted of myocardial revascularization (eight patients) or antianginal medications (six patients). Only three patients were also treated with an antiarrhythmic drug. Over a follow-up period of 26 +/- 15 months (mean +/- standard deviation), only one patient died suddenly. Two patients who had coronary artery spasm were treated with coronary vasodilator medications and had no recurrence of cardiac arrest over 7 and 36 months of follow-up, respectively. Three patients who had cardiomyopathy or no identifiable structural heart disease were treated with nadolol or amiodarone and had no recurrence of cardiac arrest over 3 to 27 months of follow-up. Among patients who survive a cardiac arrest and have a normal electrophysiologic study, those with obstructive coronary artery disease or coronary artery spasm generally have an excellent prognosis with treatment directed primarily at the underlying heart disease. The clinical features of these patients suggest that cardiac arrest was related to ischemia rather than a primary arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac arrest and sudden death in patients treated with amiodarone for sustained ventricular tachycardia or ventricular fibrillation: Risk stratification based on clinical variables

Multivariate analysis of 11 clinical variables was performed in 104 patients with sustained, symptomatic ventricular tachycardia (VT) or ventricular fibrillation treated with amiodarone to determine variables predictive of subsequent cardiac arrest or sudden death. Twenty-five patients (24%) had fatal or nonfatal cardiac arrest after 7.3 +/- 6.2 months (mean +/- standard deviation) of therapy. Multivariate analysis identified an ejection fraction of less than 0.40, syncope or cardiac arrest before amiodarone therapy, and VT (3 or more consecutive ventricular premature complexes) during predischarge ambulatory electrocardiographic monitoring as variables associated with a high risk of subsequent fatal or nonfatal cardiac arrest (p less than 0.03). Patients who had these 3 clinical variables had a much higher predicted incidence of cardiac arrest at 6 months (62%) and 12 months (76%) than did patients with an ejection fraction greater than 0.40, without syncope or cardiac arrest before amiodarone therapy, and without VT during predischarge ambulatory electrocardiographic monitoring (2% and 5%, respectively) (p less than 0.02). Risk stratification using clinical variables can predict which patients are at high risk of recurrent cardiac arrest or sudden death during amiodarone therapy.

The scintigraphic characteristics of ventricular pre-excitation through Mahaim fibers with the use of phase analysis.

The phase image pattern of blood pool scintigrams was blindly assessed in 11 patients exhibiting conduction through Mahaim pathways, including 6 nodoventricular and 5 fasciculoventricular. These patterns were compared with the phase image findings in normal subjects, patients with left and right bundle branch block in the absence of pre-excitation and patients with pre-excitation through atrioventricular (AV) connections. In all patients with a Mahaim pathway, the site of earliest phase angle was septal or paraseptal. Phase progression was asymmetric and the pre-excited ventricle demonstrated the earliest mean ventricular phase angle in 10 of 11 patients. This pattern, and the associated ventricular phase difference, appeared to vary from that in normal subjects and in those with a septal AV connection, in whom phase progression is generally symmetric. Scintigraphic phase analysis provided localizing information and presented patterns consistent with Mahaim pathways. Although not able to differentiate among Mahaim pathway subtypes, these phase patterns differed from those in normal subjects, those with right and left lateral free wall pathways and most patients with a septal AV pathway. However, the phase pattern of patients with a Mahaim pathway may not differ from that of patients with a septal AV connection displaying an asymmetric pattern of phase progression, or those with left and right bundle branch block in the absence of pre-excitation. Objective, yet imperfect phase measurements supported these differences. Such image findings may complement the often complex electrophysiologic evaluation of patients presenting with pre-excitation.

Coexistent posteroseptal and right-sided atrioventricular bypass tracts

Twelve patients with a posteroseptal accessory pathway underwent complete electrophysiologic studies, and four were found to have a second atrioventricular (AV) bypass tract that was right anterior, right anteromedial or right anterolateral in location. In two of these four patients, the presence of the right-sided AV bypass tract was confirmed by intraoperative epicardial mapping or after catheter-induced abolition of retrograde conduction through the posteroseptal bypass tract. In three of the four patients with a dual AV bypass tract, the delta wave pattern was clearly atypical of the pattern seen with an isolated posteroseptal accessory pathway. Instead of a transition from an isoelectric or slightly positive delta wave in lead V1 to markedly positive delta waves in leads V2 to V6, the delta waves were negative or only slightly positive in leads V2 to V5. However, in a fourth patient with dual AV bypass tracts, the only atypical electrocardiographic finding was an intermittently positive delta wave in lead II; at times this patients electrocardiogram was consistent with an isolated posteroseptal bypass tract, with negative delta waves in the inferior leads. There appears to be an association between posteroseptal and right-sided accessory pathways. In patients with a posteroseptal accessory pathway who are candidates for catheter or surgical bypass tract ablation, a complete mapping study of the tricuspid anulus is mandatory, even when the electrocardiogram is typical of an isolated posteroseptal bypass tract.

Effects of catheter-delivered electrical discharges near the tricuspid anulus in dogs

The possibility of using electrical discharges to ablate right free wall accessory pathways by delivering a series of catheter shocks near the tricuspid anulus was assessed in a canine model. Before the shock, the amplitudes of the atrial and ventricular electrograms recorded from the distal electrodes were compared (A/V ratio), and the atrial pacing threshold was determined. To assess effects on function and arrhythmogenicity, right heart pressures were measured and programmed ventricular stimulation was performed before the shock and prior to sacrifice 7 to 10 days after the shock. Nine dogs received a total of 24 discharges at varying energies (50 to 400 J). Nonsustained ventricular tachycardia occurred with 13 shocks (62%) and transient atrioventricular block with 9 shocks (43%). There was no worsening in cardiac or valvular function as determined by right heart pressure measurements or right ventriculography. Programmed ventricular stimulation performed before the shocks and repeated before sacrifice failed to induce ventricular arrhythmias. The endocardial lesion produced by the shock was roughly circular and its area correlated with both the magnitude of the shock as well as the atrial pacing threshold. Transmural necrosis always occurred at the anulus when the A/V ratio was between 1.00 and 1.50 and preshock atrial pacing threshold suggested adequate wall contact (less than 1.5 mA). There was mild inflammation of the adventitia of the right coronary artery near two discharge sites (both 200 J) and inflammation of the media near one discharge site (400 J); no intimal involvement was seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Localization of Ventricular Tachycardia Exit Site and Subsequent Contraction Sequence and Functional Effects With Bedside Radionuclide Angiography

OBJECTIVES In an effort to better understand the clinical effects of ventricular tachycardia (VT), we sought to characterize function and conduction during VT in patients. BACKGROUND The image evaluation of VT has been limited by the lack of technical tools and its often-dramatic hemodynamic effect. Objective bedside imaging of VT-induced changes in contraction pattern, synchrony, and volumes has never been performed but could aid in the understanding of rhythm tolerance. METHODS Equilibrium radionuclide angiography (ERNA) with phase analysis was performed during the course of 32 VT rhythms. Left ventricular ejection fraction, wall motion, synchrony, relative volumes, and exit sites were compared in 13 patients tolerant to VT (Group I) and 9 intolerant to VT (Group II). RESULTS The ERNA VT exit site agreed with the results of electrocardiogram in 26 of 32 (81%) cases and with electrophysiologic study in 16 of 19 (84%) cases (both p < 0.05). A greater rate (157 vs. 130, p < 0.0001) accompanied VT intolerance, but the exit site in 4 patients with multiple VT patterns also appeared important to tolerance. Left ventricular ejection fraction, similar in both groups in sinus rhythm, decreased with VT in Groups I (28 to 19) and II (31 to 15), both p<0.03, with a greater relative decrease in LV ejection fraction, LV stroke volume (65% vs. 45%, p < 0.01), cardiac output (30% vs. 2%), and LV end-diastolic volume (36% vs. 27%, both p < 0.001), in Group II. The standard deviation of LV phase angle (Ø) was the only parameter which differed between Groups I and II (35 vs. 45, p < 0.01) in sinus rhythm. With VT, wall motion deteriorated generally, but with greater standard deviation LVØ, p < 0.05, and dyssynchrony in Group II. Ventricular tachycardia induced 14 functional aneurysms, often adjacent to VT exit sites. CONCLUSIONS A challenging bedside imaging protocol evaluated VT-induced changes. We found that the use of ERNA demonstrated function, synchrony, and volume differences between tolerant and intolerant VT rhythms, delineated the contraction pattern, and localized exit sites.

Dissociation of atrial electrograms by right and left atrial pacing in patients with atrioventricular reciprocating tachycardia

Seventeen patients had atrioventricular (AV) reciprocating tachycardia incorporating an AV bypass tract as the retrograde limb of the tachycardia circuit. High right atrial pacing during tachycardia dissociated the low septal right atrial electrogram in four of seven patients with a left free wall bypass tract, neither of two patients with a right free wall bypass tract, four of six patients with a posteroseptal bypass tract and both patients with an anteroseptal bypass tract. Pacing from the coronary sinus during tachycardia dissociated the atrial electrogram recorded at the os of the coronary sinus in no patient with a left free wall bypass tract, both patients with a right free wall bypass tract, two patients with a posteroseptal bypass tract and one patient with an anteroseptal bypass tract. These findings suggest two distinct inputs to the AV node, with the left-sided input being part of the tachycardia circuit in patients with a left free wall bypass tract and the right-sided input being part of the tachycardia circuit in patients with a right free wall bypass tract. However, in some patients with a septal bypass tract, neither the right- nor the left-sided atrial input appears to be a necessary link in the tachycardia circuit.

Catheter Atrioventricular Junctional Ablation in Patients with Accessory Pathways

Seven patients with accessory pathway and symptomatic alrioventricular reciprocating tachycardia underwent catheter ablution of the atrioventricular junction (AVJ). Four patients had the Wolff‐Park inson White syndrome, two had concealed left free‐wall accessory pathways, and one patient had a nodoventriculor connection. All patients failed multiple antiarrhythmic drugs and one failed attempted surgical ablation of a posteroseptal accessory pathway. Chronic interruption of atrioventricular node‐His conduction was achieved in all patients. Over a mean follow‐up period of 21 ± 14 months, four patients remained asymptomatic without antiarrhythmic therapy. One patient developed atrial fibrillation after magnet application to her VVI pacemaker, another developed atrial gutter, and a third had nonparoxysmal sinus or atrial tachycardia. Two patients required chronic quinidine therapy. Two patients with concealed accessory pathways had pacemaker‐mediated tachycardia which was controlled by pacemaker reprogramming. Atrioventricular junctional ablation in patients with accessory pathways proved elective in that all are currently controlled without need for surgical intervention. On follow‐up, a relatively high incidence of atrial arrhythmias requiring antiarrhythmic therapy was found.

Procainamide-induced incessant supraventricular tachycardia in the Wolff-Parkinson-White syndrome.

A patient with the Wolff‐Parkinson‐While syndrome presented with incessant orthodromic atrioventricular tachycardia following initiation of procainamide therapy. This finding was repeatedly documented both clinically as well as during electrophysiologic testing. Escape atrial complexes, which occurred following junctional premature complexes, failed to initiate tachycardia in the control state but tachycardia was always reinitiated by an identical escape sequence after procainamide. In addition, the tachycardia persisted and was repeatedly spontaneously reinitiated for prolonged periods after procainamide. The pro‐arrhythmic effects of procainamide may be explained on the basis of both its vagolytic action on the atrioventricular node as well as by prolongation of refractoriness in the accessory pathway. These observations add to the literature on pro‐arrhythmic effects of commonly used antiarrhythmic drugs.