Rapid cardioversion of new onset atrial fibrillation with ibutilide in the emergency department.

People with atrial fibrillation commonly present to the emergency department. Ibutilide is an anti arrhythmic indicated for the cardioversion of atrial fibrillation and flutter where the onset is less than 48 hours.

Atrial fibrillation: defining potential curative ablation targets.

The concept that atrial fibrillation (or at least certain forms of the arrhythmia) may be amenable to reversal or amelioration by transcatheter ablation techniques has become increasingly accepted in recent years. As yet, however, the techniques being studied for ablation of atrial fibrillation address neither known critical anatomic elements nor well defined electrophysiologic markers. The approaches, although essentially empirical, are conceptually based on the 'multiple wavelet' or 'focal origin' hypotheses. To date, addressing 'focal origin' atrial fibrillation by transcatheter ablation has been the more encouraging. However, as technology evolves, both in terms of catheter design and possibly endocardial mapping techniques, approaches to wavelet or rotor mechanisms may become similarly effective. This communication examines concepts regarding the manner in which atrial fibrillation is initiated and maintained. The goals are to better understand the encouraging success of empirical ablation methods, and possibly derive insights which may help refine ablation targeting in the future.

Pharmacotherapy of neurally mediated syncope.

A wide variety of pharmacological agents are currently used for prevention of recurrent neurally mediated syncope, especially the vasovagal faint. None, however, have unequivocally proven long-term effectiveness based on adequate randomized clinical trials. At the present time, beta-adrenergic receptor blockade, along with agents that increase central volume (eg, fludrocortisone, electrolyte-containing beverages), appear to be favored treatment options. The antiarrhythmic agent disopyramide and various serotonin reuptake blockers have also been reported to be beneficial. Finally, vasoconstrictor agents such as midodrine offer promise and remain the subject of clinical study. Ultimately, though, detailed study of the pathophysiology of these syncopal disorders and more aggressive pursuit of carefully designed placebo-controlled treatment studies are essential if pharmacological prevention of recurrent neurally mediated syncope is to be placed on a firm foundation.

Implantable cardioverter-defibrillators.

Implantable defibrillators have become the dominant therapeutic modality for patients with life-threatening ventricular arrhythmias. Current defibrillators are small (<60 mL) and implanted with techniques similar to standard pacemakers. They provide high-energy shocks for ventricular fibrillation and rapid ventricular tachycardia, antitachycardia pacing for monomorphic ventricular tachycardia, as well as antibradycardia pacing. Newer devices incorporating an atrial lead allow dual-chamber pacing and better discrimination between ventricular and supraventricular tachyarrhythmias. Randomized controlled trials have shown superior survival with implantable defibrillators than with antiarrhythmic drugs in survivors of life-threatening ventricular tachyarrhythmias and in high-risk patients with coronary artery disease. Complications associated with implantable defibrillator therapy include infection, lead failure, and spurious shocks for supraventricular tachyarrhythmias. Most patients adapt well to living with an implantable defibrillator, although driving often has to be restricted. Limited evidence suggests that implantable defibrillator therapy is cost-effective when compared with other widely accepted treatments. The use of implantable defibrillators is likely to continue to expand in the future. Ongoing clinical trials will define further prophylactic indications of the implantable defibrillator and clarify its cost-effectiveness ratio in different clinical settings.

Resumption of motor vehicle operation in vasovagal fainters.

This study surveyed current practice patterns with respect to the manner by which cardiac arrhythmia specialists advise patients with vasovagal syncope regarding resumption of motor vehicle operation. Among 66 physician-respondents from 9 countries, 98% indicated that they rely on tilt-table testing to establish a diagnosis, and, if an effective treatment is found based on serial tilt-table testing, they recommend a 6- to 7-week symptom-free waiting period before advising return to driving.

Prehospital discharge defibrillation testing in ICD recipients: a prospective study based on cost analysis.

Prehospital discharge defibrillation testing is often performed to verify the function of newly implanted cardioverter defibrillators (ICDs). To determine whether elimination of predischarge testing could reduce costs without placing patients at additional risk, 31 patients were randomized in this prospective clinical evaluation to either receive or not receive a predischarge ICD defibrillation test. Expenses associated with postimplant care was the primary endpoint. All patients underwent induction of ventricular fibrillation after 6 months to evaluate ICD function. The groups were well matched in terms of patient characteristics, initial lead implant parameters, and defibrillation thresholds. Elimination of prehospital discharge testing resulted in a savings of $1,800/patient after 6 months, with no difference between groups in terms of ICD complication rates or unanticipated hospital admissions. Further studies are needed to better define the most appropriate time to assess defibrillation thresholds in the first year after implantation.

Submuscular versus subcutaneous pectoral implantation of cardioverter-defibrillators: effect on high voltage pathway impedance and defibrillation efficacy.

Implantable cardioverter-defibrillator (ICD) pulse generators are now routinely positioned in a pectoral location, either submuscularly (under the pectoralis muscles) or subcutaneously (over the pectoralis muscles). Furthermore, in current ICDs, the generator shield usually participates in the defibrillation energy pathway ("hot can"). Consequently, the precise generator location could affect defibrillation system efficacy. To assess this issue, we compared high voltage pathway impedance and defibrillation threshold (DFT) in 20 patients undergoing submuscular and 46 patients undergoing subcutaneous pectoral implantation of an Angeion Sentinel ICD and an AngeFlex dual-coil defibrillation lead. Measurements were performed at time of ICD implant, pre-hospital discharge, and 1, 3 and/or 6 months later. Following induction of ventricular fibrillation, 569 biphasic waveform shocks were delivered between the generator shield and either the distal defibrillation coil (RV/can configuration) or both proximal and distal coils (RV/SVC/can configuration). Impedance differences between submuscular and subcutaneous implants were approximately 3-4 Ohms (p value of 0.132 to < 0.001 depending on time of follow-up and lead configuration). A significant increase in impedance over time was noted independent of implant location and lead configuration. The DFT at implant or pre-discharge was assessed in 27 individuals, and was 9.9 +/- 3.8 J in 8 patients in the submuscular group, and 7.4 +/- 3.3 J in 19 patients in the subcutaneous group (p = 0.057). In conclusion, anatomic location of a "hot can" ICD generator (submuscular versus subcutaneous) influences impedance to defibrillation current, but the impact is of small magnitude and does not appear to result in clinically important differences in DFT.

Physiologic cardiac pacing in patients with contemporary implantable cardioverter-defibrillators.

Contemporary implantable cardioverter-defibrillators (ICD) incorporate single-chamber ventricular pacing capability. However, because poor ventricular function and/or congestive heart failure is common in the ICD population, the provision of more "physiologic" pacing modes has been receiving increased attention. To evaluate the potential impact of ICDs with physiologic pacing features, we assessed the frequency with which atrial-based pacing modes with or without rate responsiveness are currently used in ICD recipients. Further, we characterized those clinical variables at initial ICD implant that tended to be associated with subsequent need for physiologic pacing. Clinical findings were reviewed in 250 consecutive patients who received ICDs with VVI pacing capability at the University of Minnesota Cardiac Arrhythmia Center between January 1991 and February 1997. Adjunctive physiologic pacing was undertaken in 35 patients (14%): 13 before or at the same time as their ICD, and 22 within a mean of 2.5 years after initial ICD surgery. A history of atrial tachyarrhythmia before ICD implantation (p <0.0001) and treatment with antiarrhythmic drugs at the time of ICD surgery (p <0.05) were predictors of subsequent need for physiologic pacing. The type of presenting ventricular tachyarrhythmia and electrophysiologic parameters (such as the HV interval and the shortest atrial pacing cycle length associated with 1:1 anterograde atrioventricular conduction) were not associated with a subsequent decision to implant a physiologic pacing system. Thus, we conclude that despite the need to implant a second device, physiologic pacing is currently used in an important subset of ICD recipients. Further, certain clinical features at time of ICD implant appear to characterize these patients and may prove helpful in patient selection for the next generation "dual-chamber" ICD.

Comparison of right atrial and peripheral procainamide infusion levels in patients with spontaneous or induced atrial fibrillation.

As part of a new effort to develop an implantable drug infusion/pacing system to treat atrial fibrillation, this study examined the effects of rapid intracardiac procainamide infusion in humans with pacing-induced atrial fibrillation. Twenty patients with atrial fibrillation for > 5 minutes during an EP study received 500 mg of procainamide either via a peripheral venous infusion (n = 5) or directly in the right atrium (n = 15). Peak coronary sinus and femoral vein procainamide blood levels (mean +/- SEM) during 10, 5, and 3.3 minute central infusions were 17.0 +/- 4.1, 25.1 +/- 4.5, 45.6 +/- 5.1 and 11.3 +/- 3.2, 17.1 +/- 6.4, 18.7 +/- 5.0, respectively. In contrast, peak coronary sinus and femoral procainamide levels following the 5 minute intravenous infusion were 17.7 +/- 5.1 and 9.3 +/- 2.1. Changes in QT, QTc, QRS, and RI intervals were similar at each infusion rate. Systolic blood pressures (BP) decreased more with higher procainamide infusion rates but similar when comparing intravenous versus central drug administration at the same rate. The mean +/- SEM decreases in blood pressure with the 10, 5, and 3.3 min procainamide infusions were 12f5, 20f11, and 39f14, respectively. Conversion to sinus rhythm was not a primary endpoint given the often transient nature of acute atrial fibrillation in this setting. We conclude that significantly higher femoral vein and coronary sinus procainamide levels can be achieved by central rather than peripheral drug infusion. These data support that concept that rapid central infusion of anti-arrhythmic therapy can result in high intracardiac levels of antifibrillatory agents for the treatment of paroxysmal atrial fibrillation.

Mechanism of atrioventricular nodal facilitation in rabbit heart: role of proximal AV node.

The phenomenon of atrioventricular (AV) nodal "facilitation," described in traditional "black box"-functional studies, implies enhanced AV nodal dromotropic function. We investigated the role of atrial prematurities in the modulation of the nodal cellular responses in the mechanism of AV nodal facilitation. Atrial and His (H) bundle electrograms and microelectrode recordings from proximal AV nodal cells were analyzed in 15 superfused rabbit AV node preparations. The pacing protocol consisted of 30 basic beats (S1; coupling interval S1-S1 = 300 ms) followed by a facilitating prematurity (S2; coupling intervals S1-S2 of 300, 200, 150, and 130 ms) followed by the test beat (S3; coupling interval S2-S3 scanned in 5-ms steps). Conduction curves (S2-H2 vs. S1-S2, S3-H3 vs. S2-S3, and S3-H3 vs. H2-S3) were constructed. Facilitation (i.e., shortening of S3-H3 when S1-S2 was shortened) was demonstrated in all preparations using the H2-S3 (P < 0.001) but not the S2-S3 format. Microelectrode recordings revealed a causal relationship between the improved proximal AV nodal cellular responses in facilitation and the prolonged S2-S3 interval. There was no evidence for enhanced nodal dromotropic function directly resulting from the introduction of the facilitating beats. Thus facilitation is based on inherent cycle-length-dependent properties of the AV node during application of a complex pacing protocol and primarily reflects the uncontrolled modulation of the proximal cellular response.

Nonpharmacologic treatment of atrial fibrillation: current and evolving strategies.

Atrial fibrillation is the most common cardiac arrhythmia requiring treatment. Limitations of medical treatment have prompted development of nonpharmacologic therapies for this arrhythmia. These are aimed at ventricular rate control during atrial fibrillation, termination of the arrhythmia, and/or prevention of recurrences. Ventricular rate control can be achieved with transcatheter ablation or modification of the atrioventricular node. The MAZE operation is effective in preventing arrhythmia recurrence, but because it requires cardiac surgery, its appeal is limited. Development of the technique for direct transcatheter ablation of atrial fibrillation is eagerly anticipated and may represent the standard curative treatment of the future. In appropriately selected patients, implantable device therapy may play an important role in the treatment of paroxysmal atrial fibrillation.

Mechanism of atrioventricular nodal facilitation in the rabbit heart: role of the distal AV node.

We investigated whether atrioventricular (AV) nodal facilitation is the result of distal AV nodal action potential shortening. Atrial and bundle of His (H) electrograms and microelectrode recordings from proximal and distal AV nodal cells were analyzed in eight superfused rabbit AV node preparations in response to two pacing protocols. In the facilitation protocol, an atrial extrastimulus (A3) was preceded by an atrial impulse (A2) introduced 300, 200, 150, or 125 ms after 30 basic beats (A1). The preexcitation protocol differed from the facilitation protocol by the addition of a premature His depolarization (h2) such that the H1-h2 interval was shorter than the H1-H2 interval. Conduction curves (A3-H3 vs. H2-A3, h2-A3, and A2-A3 intervals) were constructed. Facilitation was demonstrated in all preparations when H2-A3 was used (P = 0.02) but not in the A2-A3 format. Compared with facilitation at the same A1-A2 intervals, preexcitation, despite shortening the distal cellular action potential duration, resulted in longer A3-H3 delays (P = 0.002), shorter A2-A3 intervals, and depression of the proximal nodal cellular response. Thus facilitation does not result from altered distal AV nodal characteristics and instead is a manifestation of an uncontrolled pacing protocol-dependent modulation of proximal AV nodal function.

High-resolution fluorescent imaging does not reveal a distinct atrioventricular nodal anterior input channel (fast pathway) in the rabbit heart during sinus rhythm.

INTRODUCTION: We sought to determine the precise pathways of engagement of the AV node during sinus rhythm. METHODS AND RESULTS: Langendorff-perfused rabbit hearts were stained with 20 microM of the voltage-sensitive dye di-4-ANEPPS. Preparations containing the right atrium, sinoatrial (SA) and AV nodes, and interatrial septum were subsequently dissected and mapped in vitro using a 16 X 16 photodiode array with an adjustable resolution of 150 to 750 microns per diode. Motion artifacts were eliminated by using 15 mM 2,3-butanedione monoxime (BDM). Activation time-points were defined as (-dF/dt)max' where F = fluorescence. Isochronal maps of activation were plotted using the triangulation method. In all preparations, spontaneous activation began at the SA node, rapidly spread along the crista terminalis (CrT), entered the AV nodal region via the posterior "slow" pathway, and retrogradely spread to the septal region with a smaller conduction velocity compared to that along the CrT. Collision of anterograde and retrograde wavefronts was frequently observed in the mid-septum. Notably, there was no evidence for the presence of a distinct anterior entrance into the AV node. CONCLUSIONS: Fast pathway conduction during sinus rhythm results from a broad posterior wavefront that envelops the AV node with subsequent retrograde atrial septal activation.

Clinical presentation of endocardial pacing lead malfunction.

This study highlights the wide spectrum of manifestation of pacing lead malfunction. Patients judged to be pacer dependent or in whom ventricular lead malfunction is suspected, and patients with severe symptoms before pacemaker implantation, should be considered at high risk for the development of hemodynamic compromise; prompt hospital admission and pacing lead replacement should be performed.

Pacing strategies to prevent atrial fibrillation.

The role of cardiac pacing in preventing atrial fibrillation in patients at risk for this arrhythmia is a relatively new concept. This article discusses the influence of the pacing mode, rate, atrial pacing site, and novel pacing algorithms on the prevention of atrial fibrillation.

Hospital readmission in patients treated with tiered-therapy implantable defibrillators.

BACKGROUND: We wished to determine the incidence, reasons, costs, and predictors of cardiac-related hospital readmission in patients with tiered-therapy implantable defibrillators. Hospital readmission in patients with defibrillators reduces their quality of life and increases the cost associated with such therapy. METHODS AND RESULTS: We retrospectively studied 65 consecutive local patients (median age, 67 years; median ejection fraction, 0.34) who underwent tiered-therapy defibrillator implantation at this institution. Patients were followed for a median of 19 months (interquartile range, 10 to 27 months). The cause, duration, costs, and predictors of cardiac-related rehospitalizations were analyzed. There were 76 cardiac admissions for 34 patients. The rate of cardiac-related hospital readmission was 0.72 per patient-year of follow-up. Arrhythmia-related admissions accounted for 43 of such admissions in 24 patients. Actuarial freedom from cardiac-related admissions was 0.57 and 0.40 at 1 and 2 years, respectively. The median length of stay for hospital readmissions was 5 days (interquartile range, 3 to 8 days). The median cost per admission was $5842 (interquartile range, $3549 to $12 170). The time to first readmission and the total rehospitalization time per year of follow-up were associated with a poor preimplant New York Heart Association functional class. Readmission for cardiac arrhythmias was not predicted by clinical parameters. CONCLUSIONS: Rehospitalization for cardiac reasons is common in patients receiving implantable defibrillators and is responsible for substantial resource consumption. The need for readmission for arrhythmia-related reasons cannot be predicted by clinical parameters at the time of device implantation.

Plasma atrial natriuretic peptide is elevated in patients with hypertrophic cardiomyopathy.

STUDY OBJECTIVES: To determine if plasma levels of atrial natriuretic peptide are elevated in patients with hypertrophic cardiomyopathy and to determine the relationship of atrial natriuretic peptide to symptoms and echocardiographic indices of left ventricular structure and diastolic function in these patients. DESIGN: A prospective study in which atrial natriuretic peptide was measured in peripheral venous plasma in 14 patients (age 44 +/- 14 years) with hypertrophic cardiomyopathy and 17 healthy controls. Echocardiography was performed in all cases and 30 controls to examine indices of left heart structure and function. All patients underwent clinical evaluation. RESULTS: The concentration of atrial natriuretic peptide was significantly higher in patients with hypertrophic cardiomyopathy than controls, (17.86 +/- 8.72 vs. 6.22 +/- 3.26 pmol/l, P = 0.0001). Diastolic dysfunction was observed in 11 of 14 patients with hypertrophic cardiomyopathy. No correlation was demonstrated between atrial natriuretic peptide levels and the degree of diastolic dysfunction, septal or free wall thickness, left atrial size, degree of mitral regurgitation or New York Heart Association functional class. CONCLUSIONS: Plasma levels of atrial natriuretic peptide are elevated in patients with hypertrophic cardiomyopathy but do not correlate with symptoms or echocardiographically-derived indices of left ventricular structure or diastolic function.

Natural history of isolated bundle branch block.

The purpose of this study was to determine the long-term outcome of patients with bundle branch block (BBB) who have no clinical evidence of cardiovascular disease. Among 110,000 participants in a screening program, 310 subjects with BBB without apparent of suspected heart disease were identified. Their outcome after a mean follow-up of 9.5 years was compared with that of 310 similarly screened age- and sex-matched controls. Among the screened population, isolated right BBB was more prevalent than isolated left BBB (0.18% vs 0.1%, respectively; p<0.001), and the prevalence of each abnormality increased with age (p<0.001). Total actuarial survival was no different for those with left BBB or right BBB and their respective controls. Cardiac mortality, however, was increased in the left BBB group when compared with their controls (p=0.01, log rank test). Left BBB, but not right BBB, was associated with an increased prevalence of cardiovascular disease at the follow-up (21% vs 11%; p=0.04). In the absence of clinically overt cardiac disease, the presence of left BBB or right BB is not associated with increased overall mortality. Isolated left BBB is associated with an increased risk of developing overt cardiovascular disease and increased cardiac mortality.