James B. Kirchhoffer

Complications of Dual Chamber Pacemaker Implantation in the Elderly

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 ≤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

Predictors and Clinical Impact of Atrial Fibrillation After Pacemaker Implantation in Elderly Patients Treated with Dual Chamber Versus Ventricular Pacing

The Pacemaker Selection in the Elderly (PASE) trial was a prospective, multicenter, single blind, randomized comparison of single chamber, rate adaptive, ventricular pacing (VVIR) with dual chamber, rate adaptive pacing (DDDR) in 407 patients aged ≥65 years (mean 76 ± 7 years, 60% male) with standard bradycardia indications for dual chamber pacemaker implantation. The incidence, predictors, and clinical consequences of atrial fibrillation (AF) developing after pacemaker implantation in the PASE trial were studied prospectively. During a median follow‐up of 18 months, AF developed in 73 (18%) patients. Kaplan‐Meier estimated cumulative incidences of AF in patients with sinus node dysfunction (n = 176) at 18 months were 28% in the VVIR and 16% in the DDDR groups (P = 0.08). After adjustment for other clinical variables using a Cox multivariate regression model, randomization to VVIR compared with DDDR pacing mode among patients with sinus node dysfunction was independently associated with a 2.6‐fold increased relative risk (RR) of developing AF after pacemaker implantation (P = 0.01). Other independent clinical risk factors for development of postimplant AF included a preimplant history of hypertension (P = 0.02) or supraventricular tachyarrhythmias (P < 0.04). Patients who developed AF had similar health related quality of life scores and cardiovascular functional status after 18 months of pacing as patients who remained free of AF. The RR of death, stroke, or heart failure hospitalization was not increased in patients who developed AF. Thus, in the elderly patients with sinus node dysfunction requiring permanent pacing, DDDR pacing mode protected against the development of AF. However, development of AF after pacemaker implantation in this population was not associated with a significant impact on quality‐of‐life, functional status, or other clinical endpoints during 18 months of follow‐up. (PACE 2003; 26:2000–2007)

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 disopvramide. If this drug combination is unavoidable, disopyramide levels must be closely monitored.

Pacemaker lead infection: Detection by multiplane transesophageal echocardiography

Because a myocardial biopsy was not performed, we cannot rule out the possibility of myocarditis with intermittent exacerbations as an explanation for the patients symptoms and creatinine kinase elevations. However, the severity and sudden onset of the symptoms suggest that the process is acute myocardial infarction. In conclusion; we report a case of recurrent non-Q-wave myocardial infarction and cardiomyopathy associated with toluene abuse. Because of the increasing use of solvents as recreational drugs, toluene toxicity should be included in the differential diagnosis of myocardial infarction with normal coronary anatomic condition.

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.

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.

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 S1 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 S1 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 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 S1 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.

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.

Treatment of a Patient with an Adenosine‐Sensitive Ventricular Tachycardia Using Digoxin

Digitalis and Ventricular Tachycardia. Digoxin was used to treat a patient with an adenosine‐sensitive ventricular arrhythmia. The patient had an exercise‐induced ventricular tachycardia that was evaluated electrophysiologically and displayed characteristics of a triggered arrhythmia. The tachycardia was terminated reproducibly with 12 mg of intravenous adenosine. After treatment with digoxin (serum level = 1.7 ng/mL), the arrhythmia could no longer be initiated with programmed electrical stimulation or exercise treadmill testing. The patient has since remained symptom free for 10 months. The autonomic effects of digitalis are proposed to mediate drug efficacy in this form of ventricular tachycardia.