Michael J. Griffith

ADENOSINE IN THE DIAGNOSIS OF BROAD COMPLEX TACHYCARDIA

Adenosine, in incremental bolus doses up to 0.25 mg/kg, was given during regular broad complex tachycardia in 26 patients examined in an electrophysiological laboratory. In 8 of 9 cases of broad complex supraventricular tachycardia (SVT) the arrhythmia was terminated, converted into a narrow complex SVT, or atrioventricular block was induced. In all 9 cases of narrow complex SVT, the arrhythmia was stopped, or atrioventricular block was induced. The arrhythmia was stopped in only 1 of 17 cases of ventricular tachycardia. 6 patients with atrial fibrillation and ventricular pre-excitation were given adenosine, with no effect on mean ventricular rate (averaged over 3 s), although a significant, but short-lived, reduction in minimum RR interval was observed (from 242 ms, SD 45, to 217 ms, SD 39). The mean dose of adenosine required to stop the arrhythmia or to induce atrioventricular block in broad complex SVT (0.14 mg/kg, SD 0.04) was higher than in narrow complex SVT (0.11 mg/kg, SD 0.04). No adverse haemodynamic effects were observed in any patient, and large doses were tolerated by the patients with ventricular tachycardia. The data show that adenosine has a useful role in the diagnosis and treatment of regular broad complex tachycardia.

Comparison of adenosine and verapamil for termination of paroxysmal junctional tachycardia

The effects of intravenous adenosine and intravenous verapamil on paroxysmal junctional tachycardia were compared in 20 patients undergoing invasive cardiac electrophysiologic study. In 13 patients the diagnosis was of a reentrant tachycardia using an extranodal accessory connection (atrioventricular [AV] reentrant tachycardia); 5 of these patients had overt preexcitation in sinus rhythm, 4 had concealed accessory connections and 4 had latent or intermittent preexcitation. In 7 patients the diagnosis was of an AV nodal reentrant tachycardia. Administration of adenosine resulted in termination of tachycardia in all 20 patients at a mean dose of 0.125 mg/kg (range 0.05 to 0.20). Although termination of tachycardia was frequently accompanied by atrial and ventricular premature complexes, no significant arrhythmias were observed after conversion. Administration of verapamil (0.145 mg/kg) resulted in termination of tachycardia in 19 of 20 patients but was followed by symptomatic arrhythmias in 2: preexcited atrial flutter in 1 patient and preexcited atrial tachycardia in another. Latent or intermittent preexcitation was unmasked in 4 of 4 patients immediately after termination of tachycardia by adenosine. Termination of tachycardia by verapamil revealed preexcitation in only 1 of these 4 patients. Analysis of results in terms of successful termination of tachycardia, absence of significant arrhythmias after conversion and unmasking of latent or intermittent preexcitation reveals that adenosine therapy was satisfactory in all 20 patients, whereas verapamil was satisfactory in only 14 of the 20 patients (p less than 0.05). All 6 of the patients with unsatisfactory responses to verapamil had AV reentrant tachycardia. These results suggest that adenosine has particular advantages over verapamil as acute treatment for patients presenting with an AV reentrant tachycardia.

Use of intravenous adenosine in sinus rhythm as a diagnostic test for latent preexcitation

In a proportion of patients with left free wall accessory connections, preexcitation is apparent only during atrial arrhythmias or atrial pacing (latent preexcitation). These patients may be at risk of a rapid ventricular response to atrial fibrillation despite the absence of preexcitation in sinus rhythm. The ability of intravenous adenosine to unmask latent preexcitation was evaluated in 22 patients with a history of documented supraventricular tachycardia and a normal electrocardiogram during sinus rhythm. Preexcitation was unmasked in response to adenosine in 4 patients: all 4 were shown to have latent preexcitation at electrophysiologic study. In 12 patients atrioventricular (AV) nodal conduction delay or block was induced without preexcitation after adenosine (first-degree AV block in 8, second-degree block in 4): at subsequent electrophysiologic study none of these patients was found to have latent preexcitation. Five patients had little or no PR prolongation in response to adenosine: of these, 2 were shown to have latent preexcitation at electrophysiologic study. Atrial fibrillation was induced in 1 patient and a narrow complex regular tachycardia in another after intravenous adenosine. Intravenous adenosine during sinus rhythm is capable of producing AV nodal conduction delay or block in 73% of patients with a history of supraventricular tachycardia: in these patients adenosine provides a diagnostic test that is both 100% sensitive and 100% specific for latent preexcitation. In those patients in whom adenosine does not produce AV conduction delay or block, further investigation is required to establish or refute the diagnosis of latent preexcitation.

Transesophageal contrast echocardiography and color flow mapping: methods of choice for the detection of shunts at the atrial level?

The detection of shunts at the atrial level is important, and a reliable means of diagnosis is required. Precordial contrast echocardiography is usually performed to detect such shunts. To investigate the advantages of transesophageal echocardiographic techniques, we studied 167 consecutive patients with both precordial and transesophageal echocardiography, using two-dimensional imaging with contrast techniques (with and without a Valsalva maneuver) and color flow mapping. A patent foramen ovale was diagnosed in 31 patients, an atrial septal defect in 11 (7 with bidirectional shunts), and a pulmonary arteriovenous fistula in 3 patients. All right-to-left shunts were detected with transesophageal contrast echocardiography. With these results used as the gold standard, the sensitivity of combined precordial techniques was 37% and that of transesophageal color flow mapping 46%. All left-to-right shunts were detected by transesophageal color flow mapping. With these results used as the gold standard, the sensitivities of both precordial color flow mapping and a transesophageal negative right atrial contrast study were 27%. We conclude that transesophageal contrast echocardiography is the echocardiographic method of choice for the detection of a right-to-left shunt at the atrial level, which cannot be excluded by negative results on precordial study or on transesophageal color flow map study. A left-to-right shunt at this level is best detected by transesophageal color flow mapping.

Effects of intravenous adenosine on antegrade refractoriness of accessory atrioventricular connections.

Background Several groups have suggested the use of intravenous adenosine or adenosine triphosphate in the diagnosis of regular broad complex tachycardias. However, the short half-life of these agents has precluded assessment of their effects on refractoriness of accessory connections, and their safety in preexcited arrhythmias has not been demonstrated. Methods and Results We examined the effects of intravenous adenosine on accessory atrioventricular (AV) connections in 30 patients with the Wolff-Parkinson-White syndrome. Intravenous adenosine (12 mg, rapid bolus) was administered to 14 patients (group 1) during continuous atrial pacing at a cycle length 20 msec below that required to cause 2:1 conduction block in the accessory connection (mean pacing cycle length 261+41 msec). After adenosine, transient 1:1 conduction occurred via the accessory connection in 12 of 14 patients, indicating a shortening of antegrade refractoriness. In three of seven patients, this effect was abolished after intravenous propranolol (0.2 mg/kg). Nineteen patients (group 2) received adenosine (0.17 ± 0.04 mg/kg) during induced, preexcited atrial arrhythmias. The minimum RR interval during preexcited atrial fibrillation transiently decreased (252 ± 44 msec to 224 ± 35 msec, p< 0.01) after adenosine, but no change in average RR interval was observed (360 ± 59 msec to 357 ± 60 msec, NS). The preexcited ventricular response to atrial flutter was transiently accelerated in five of eight patients (415 ± 21 msec to 360 ± 49 msec, p< 0.05) due to shortening of flutter cycle length (207 ± 10 msec to 180 ± 24 msec, p< 0.05). However, 2:1 accessory connection conduction was maintained in all eight patients. All effects were short lived, with the decrease in RR interval during atrial fibrillation occurring for a maximum of two RR intervals only. No patient suffered ventricular arrhythmias or hemodynamic deterioration. Conclusions Adenosine shortens antegrade refractoriness of accessory AV connections, and in some patients this action is mediated by f3-adrenergic stimulation. Adenosine may cause acceleration of preexcited atrial arrhythmias, but these effects are transient and should not discourage the use of adenosine as a diagnostic agent in broad complex, regular tachycardias of uncertain origin.

Multivariate analysis to simplify the differential diagnosis of broad complex tachycardia.

Univariate analysis has identified several criteria that aid the differential diagnosis of broad complex tachycardia. In this study of 102 consecutive patients multivariate analysis was performed to identify which of 15 clinical and 11 electrocardiographic variables were independent predictors of ventricular tachycardia. These were shown to be a history of myocardial infarction, the QRS waveforms in leads aVF and V1, and a change in axis from sinus rhythm to tachycardia of more than 40 degrees. If none of the criteria was met, the diagnosis was almost certainly supraventricular tachycardia. If one criterion was met the diagnosis was probably supraventricular tachycardia. If two criteria were met then the diagnosis was probably ventricular tachycardia. If three or four criteria were met, the diagnosis was almost certainly ventricular tachycardia. The predictive accuracy was 93%. This was increased to 95% by including two other criteria--definite independent P wave activity and ventricular extrasystoles with the same QRS configuration as that in tachycardia. These criteria were not included in the multivariate analysis because though they were 100% specific they were seldom seen. These four criteria can be used as simple rules in determining the origin of a broad complex tachycardia.

Relative efficacy and safety of intravenous drugs for termination of sustained ventricular tachycardia

The relative safety and efficacy of intravenous administration of adenosine, lignocaine, disopyramide, flecainide, and sotalol for termination of stable, induced ventricular tachycardia was assessed in serial trials. Ventricular tachycardia was terminated by pacing if it persisted 10-15 min after the end of drug administration. 24 patients with recurrent ventricular tachycardia were studied. Ventricular tachycardia was terminated by a drug in 35 of 105 trials. In 6 patients no drug terminated the arrhythmia. Adenosine did not terminate tachycardia or have any serious adverse effect in any patient; both flecainide and disopyramide were significantly more effective than lignocaine, but flecainide had significantly more severe adverse effects than lignocaine. Lignocaine was the safest drug and should continue to be used as first-line drug therapy for stable ventricular tachycardia. Disopyramide should be considered as second-line treatment. DC cardioversion is necessary for unstable ventricular tachycardia, and its availability must be ensured before attempted pharmacological intervention.

A prospective study of the efficacy and safety of adjuvant metoprolol and xamoterol in combination with amiodarone for resistant ventricular tachycardia associated with impaired left ventricular function

Combination antiarrhythmic drug therapy may be more effective than treatment with a single agent for control of refractory cases of sustained ventricular tachycardia (VT). In a prospective randomized crossover study of 20 patients with impaired left ventricular function (ejection fraction of 28% +/- 8%) and recurrent VT in spite of treatment with amiodarone, we compared the efficacy and safety of adjuvant therapy with metoprolol, 50 mg two times daily and xamoterol, 200 mg two times daily. Metoprolol caused hemodynamic deterioration in five patients, and only one also experienced intolerance to xamoterol. Sustained VT was inducible in all 20 patients who were receiving amiodarone alone but was suppressed or rendered nonsustained in 8 of 20 patients during treatment with amiodarone plus xamoterol and in 6 of 17 patients during treatment with amiodarone plus metoprolol. Addition of xamoterol restored sinus rhythm in four patients who presented with incessant VT, and metoprolol was effective for three of them. Neither beta-blocker significantly altered tachycardia cycle length or any electrophysiologic parameter other than the slowing of the sinus rate. Both beta-blockers suppressed exercise-induced VT in 3 of 4 patients, and addition of xamoterol significantly increased treadmill exercise duration (7.1 +/- 1.8 min) compared with administration of amiodarone alone (3.8 +/- 1.5 min; p < 0.01). Fourteen patients were discharged with prescriptions for amiodarone-beta-blocker combinations. During a mean follow-up period of 13 months (range, 2 to 24 months), there were three cases of recurrent VT (in all patients VT remained inducible) and no sudden deaths.(ABSTRACT TRUNCATED AT 250 WORDS)

ADJUVANT XAMOTEROL OR METOPROLOL IN PATIENTS WITH MALIGNANT VENTRICULAR ARRHYTHMIA RESISTANT TO AMIODARONE

In a randomised cross-over study, six patients with recurrent sustained ventricular tachycardia (VT) were treated with 3 regimens--amiodarone, amiodarone plus metoprolol, and amiodarone plus xamoterol. All patients had poor left ventricular function and were resistant to multiple drugs. Xamoterol (a partial beta-agonist) was more effective than metoprolol as adjuvant therapy to amiodarone in the control of recurrent sustained ventricular arrhythmias and was not associated with any clinical deterioration of ventricular function. Xamoterol was also more effective than metoprolol for suppression of VT at programmed stimulation and as effective as metoprolol for suppression of VT on exercise. Exercise tolerance was significantly greater during treatment with xamoterol/amiodarone than during treatment with metoprolol/amiodarone or with amiodarone alone.

Ventricular Wenckebach after intravenous therapy with Class I antiarrhythmic agents

Two unusual cases of Wenckebach-like conduction block in the infranodal tissues which developed after an intravenous dose of a Class I antiarrhythmic drug are presented. The first case shows infra-Hisian Wenckebach during sustained atrioventricular nodal reentrant tachycardia. The second case demonstrates rate-dependent Wenckebach-like exit block between the pacing catheter and the right ventricular tissues during pacing.