Potentially fatal interaction between azithromycin and disopyramide.

A patient on disopyramide developed disopyramide toxicity when treated concurrently with azithromycin. Evidence of toxicity included an elevated serum disopyramide level and ventricular tachycardia requiring cardioversion. The azalide antibiotic presumably inhibited dealkylation of disopyramide to its major metabolite, mono-N-dealkyldisopyramide. Physicians should avoid using azithromycin in patients on disopyramide. If this drug combination is unavoidable, disopyramide levels must be closely monitored.

Effects of adenosine on local stimulus-response latency and induction of atrial fibrillation by premature stimuli.

Premature atrial stimuli delivered during the relative refractory or "vulnerable" period exhibit increased local stimulus-response latency and may occasionally induce atrial arrhythmias. The use of adenosine to treat supraventricular tachycardias may also provoke atrial arrhythmias. In this study we investigated the effects of adenosine on the latency of premature complexes in relation to repolarization and induction of atrial arrhythmias in 14 patients without structural heart disease. A monophasic action potential catheter was used for recording in the right atrium and introducing premature stimuli (S2) at twice diastolic threshold after eight paced (S1) complexes. At short coupling intervals, S2 latency increased relative to S1 latency. S2 was delivered repeatedly at a fixed coupling interval (producing maximal local response latency) and adenosine (6 mg) was given intravenously. Adenosine decreased S2 latency significantly (23+/-5 to 11+/-3 ms, P<0.01), to values similar to S, latency. However, despite the decrease in S2 latency, the combination of adenosine and S2 more often resulted in transient atrial arrhythmias (11 of 14 patients vs 2 of 14 patients without adenosine, P<0.05). Adenosine had no effect on S, latency (9+/-2 vs. 9+/-2 ms) but decreased monophasic action potential duration from 202+/-37 to 158+/-38 ms (P<0.01). Adenosine was also given to 10 patients with S2 introduced at a coupling interval 40-50 ms less than the baseline effective refractory period. This resulted in a decrease in atrial refractoriness and capture of S2 in all cases. Latency for S2 was significantly greater than Si latency (21+/-12 vs. 9+/-2 ms, P<0.01) and transient atrial arrhythmias were induced in 9 of 10 patients. We conclude that for a given S2 coupling interval, adenosine decreases local stimulus-response latency but increases atrial vulnerability to transient atrial arrhythmias. Decreased latency may be related to a shift in the zone of relative refractoriness associated with an adenosine-mediated decrease in monophasic action potential duration. Induction of atrial arrhythmias in the presence of adenosine occurs independently of increased latency and is therefore not dependent on S2 falling within the relative refractory period at the site of stimulation.

Complications of dual chamber pacemaker implantation in the elderly. Pacemaker Selection in the Elderly (PASE) Investigators.

Pacemakers are frequently implanted, yet accurate prospective data on implant complications are limited. Elderly patients may be at increased risk of implant complications and are increasingly being referred for pacemaker implantation. The purpose of the present analysis was to define the incidence and possible predictors of serious complications of dual chamber permanent pacemaker implantation in the elderly. Therefore, we sought to prospectively identify the incidence and predictors of pacemaker implant complications in a large multicenter trial involving patients receiving a dual chamber pacemaker. The Pacemaker Selection in the Elderly (PASE) study was a prospective trial designed to evaluate quality of life in dual chamber pacemaker recipients age 65 years or older randomized to DDDR versus VVIR programming. In addition to being age 65 years or older, patients enrolled in this study were in normal sinus rhythm, and had standard indications for permanent pacemaker implantation. All patients received dual chamber pacemakers and were randomized to DDDR versus VVIR pacing. Pacemaker implant complications were collected on standardized forms which were completed at pacemaker implantation and during follow-up appointments. In this study of 407 patients, there were 26 complications occurring in 25 patients (6.1%). The most frequent complication was lead dislodgment which occurred in 9 patients. This was followed by pneumothorax (8 patients) and cardiac perforations (4 patients). In 18 patients (4.4%) repeat surgical procedures (including chest tubes) were required. Complications were noted prior to discharge in only 18 patients. There were no significant predictors of overall complications. Pneumothorax was more frequent in patients > or = 75 years old, and was observed only in patients with subclavian venous access. In conclusion, complications from pacemaker implantation in the elderly are seen in 6.1% of patients and 4.4% of patients require a repeat surgical procedure. Other than advanced age and lower weight predicting for pneumothorax, there are no significant clinical predictors of complications.

Effects of adenosine on retrograde refractoriness of accessory atrioventricular connections.

Ventricular premature stimuli were used to demonstrate adenosine-mediated decreases in the retrograde refractoriness of accessory atrioventricular connections. This response is consistent with the concept that accessory atrioventricular connections have electrophysiologic properties that are similar to those of atrial myocardium.

Commotio cordis: cardiovascular manifestations of a rare survivor.

Death due to low-energy chest wall trauma, commotio cordis, may occur in young athletes. Death is sudden and usually refractory to even immediate resuscitation efforts. Herein are described the clinical, angiographic, and hemodynamic data of a rare survivor. These observations suggest that commotio cordis not only may be secondary to ventricular fibrillation, but also may be associated with coronary vasospasm or segmental changes in myocardial contractility.

Effects of adenosine on wavelength of premature atrial complexes in patients without structural heart disease.

Intravenous adenosine produced slight decreases in conduction times for premature atrial complexes but proportionally greater shortening of the functional refractory period. Decreased wavelength may provide a basis for transient atrial fibrillation, which is sometimes observed after adenosine administration.

Comparison of decremental and burst overdrive pacing as treatment for ventricular tachycardia associated with coronary artery disease.

Several forms of antitachycardia pacing have been used successfully for terminating cardiac arrhythmias, and implantable devices now incorporate a tier of overdrive pacing for treating of ventricular tachycardia (VT). No consensus exists regarding the optimal mode of pacing therapy. Accordingly, a prospective, randomized, crossover study of antitachycardia pacing was performed to analyze the effects of 2 decremental forms (10 and 5 ms) and a synchronized burst overdrive pacing mode on episodes of VT. Overdrive antitachycardia pacing was an effective therapy (78%) for terminating VT. Burst overdrive pacing and an autodecremental pacing protocol, incorporating a 10 ms decrement, were found to be effective and comparable forms of therapy. Both of these pacing methods were superior in terminating VT when compared with a pacing scheme using a 5 ms coupling decrement (p less than 0.01). Tachycardia acceleration occurred in 6.4% of the episodes of VT. None of the pacing methods displayed a specific propensity for tachycardia acceleration, and no measure of tachycardia segments identified a predilection for pace terminability. Antitachycardia pacing is an effective therapy for VT and different pacing formulas have variable effects. Further, these effects appear to be independent of tachycardia cycle length and variability.

Adenosine: a clinical experience and comparison with verapamil for the termination of supraventricular tachycardias.

The efficacy and side-effects of adenosine for treatment of supraventricular arrhythmias were compared to verapamil therapy in patients presenting to the emergency room. Clinical variables and the time interval from the initiation of treatment to the termination of the supraventricular tachycardia, as well as the time from the initial effective dose of medication to the termination of supraventricular tachycardia were compared for adenosine and verapamil. Adenosine was given to a total of 44 patients, 16 patients in the electrophysiology laboratory, and 28 patients in the emergency room for evaluation and termination of their tachycardia. In the electrophysiology laboratory, 7 patients had AV node reentry, 5 had Wolff-Parkinson-White syndrome, 2 of whom had atrial flutter and fibrillation but no bypass tract reentry, 1 had concealed bypass tract reentry, 1 had Lown-Ganong-Levine syndrome, 1 had intraatrial reentry, and 1 had an automatic atrial tachycardia. Twenty-five patients received adenosine in the emergency room and 3 patients in the hospital for 31 episodes of supraventricular arrhythmias. In the emergency room, 11 patients had supraventricular tachycardia due to AV node reentry, 3 had Wolff-Parkinson-White syndrome, 6 had atrial flutter or intra-atrial re-entry, 2 had ventricular tachycardia, and 3 had sinus tachycardia. In the hospital, 2 patients had atrial flutter and one had sinus tachycardia. The group of 14 patients with supraventricular tachycardia due to Wolff-Parkinson-White syndrome or AV node reentry presenting in the emergency room were compared in a retrospective manner to the patients treated with standard verapamil therapy with respect to time from initiation of therapy to termination of supraventricular tachycardia and time from effective dose of medication to the termination of supraventricular tachycardia, as well as side-effects. There was no significant difference between the two groups with respect to clinical variables. Adenosine converted 18 of 18 episodes of supraventricular tachycardia in 14 patients 24.6 +/- 9.6 seconds from the administration of the effective dose (0.104 +/- 0.024 mg/kg) and a mean of 4.4 +/- 2.0 minutes from the initiation of therapy. Verapamil converted 29 of 32 episodes of supraventricular tachycardia in 20 patients, 10.9 +/- 7 minutes from the administration of the effective dose, and a mean of 16.8 +/- 20 minutes from the initiation of therapy using a mean of 8.4 +/- 3.4 mg of IV verapamil.(ABSTRACT TRUNCATED AT 400 WORDS)