Usefulness of pindolol in neurocardiogenic syncope.

We prospectively studied the efficacy of pindolol, a beta-adrenergic blocker with intrinsic sympathomimetic activity (ISA), for the prevention of syncope recurrences in 31 patients with recurrent neurocardiogenic syncope. Pindolol proved to be an effective treatment, even in patients who had previously failed treatment with conventional beta blockers, suggesting a clinical benefit from addition of ISA to beta blockade in this setting.

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.

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.

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.

Review article: heart rate and blood pressure control in vasovagal syncope.

Vasovagal syncope is characterized by transient failure of usually reliable physiologic mechanisms responsible for maintaining both systemic arterial pressure and cerebral blood flow. Two circulatory phenomena are almost universally present: systemic arterial vasodilation and bradycardia. A third phenomenon, cerebrovascular constriction, has also been described but its contribution to the faint is less well established. The neural reflex pathways responsible for triggering the circulatory changes in the vasovagal faint are incompletely understood, but have recently been the subject of renewed interest. In part, this interest probably stems from the frequency with which vasovagal symptoms are now recognized to be the cause of fainting spells. Additionally, however, there is an increasingly recognized need to develop treatment strategies for those affected patients in whom recurrent vasovagal symptoms are particularly troublesome. It is the goal of this discussion to focus on those aspects of circulatory control, and in particular on potential interactions among certain neural and humoral systems, which may contribute to the inappropriate physiologic responses associated with the vasovagal faint.

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.

Recurrent supine syncope: an unusual manifestation of the neurally mediated faint.

INTRODUCTION: Syncope occasionally may occur in the supine patient due to severe brady- or tachyarrhythmia. However, recurrent syncope upon assumption of the supine position as a result of a neurally mediated reflex mechanism has not been reported previously. METHODS AND RESULTS: Two young patients, both of whom had significant systemic illnesses, experienced recurrent episodes of presyncope and/or syncope shortly after assuming the supine position. During ambulatory ECG monitoring, symptoms were provoked only by lying down and were associated with transient bradycardia. Head-up tilt table testing was undertaken as part of the syncope evaluation and was nondiagnostic in both cases. However, both patients exhibited a transient cardioinhibitory response with reproduction of typical symptoms upon return of the table to the supine position ("reverse tilt"). During follow-up (8 and 14 months), both patients improved with pharmacologic treatment (disopyramide in one case and midodrine in the other). CONCLUSION: Presyncope or syncope upon lying down can be an unusual manifestation of the neurally mediated faint.

Termination of implantable pacemaker therapy: experience in five patients.

BACKGROUND: Established guidelines direct the initial implantation of permanent pacemakers. Elective replacement of these devices is common. However, no guidelines exist for the removal of permanent pacemakers and the termination of long-term cardiac pacing. OBJECTIVE: To describe the feasibility and safety of terminating cardiac pacing in carefully selected patients. DESIGN: Case series. SETTING: University hospital. PATIENTS: Five adults with permanent pacemakers who were referred for pacemaker replacement or a complication related to cardiac pacing. All patients showed alleviation or reversal of the electric disturbance that originally led to the implantation of the device. The patients had received a pacemaker for a class I or II indication (that is, symptomatic bradycardia or asymptomatic, persistent third-degree atrioventricular block at the level of the atrioventricular node). INTERVENTION: After an appropriate natural rhythm was documented, pacemakers were removed from all patients. MEASUREMENTS: Time without recurrence of symptomatic bradycardia. RESULTS: No patient had recurrent symptomatic bradycardia after 18 to 48 months of clinical follow-up. CONCLUSIONS: The presence of a permanent pacemaker does not necessarily imply a permanent need for cardiac pacing. Discontinuation of cardiac pacing may be considered in certain patients. Establishing consensus criteria about the potential indications, methods, and timing of the termination of cardiac pacing seems appropriate.

Syncope in pharmacologically unmasked Brugada syndrome: indication for an implantable defibrillator or an unresolved dilemma?

A 30-year-old Caucasian male was referred for evaluation of a 2-year history of recurrent post-exertion lightheadedness and near syncopal spells in the setting of a family history of unexplained sudden cardiac death. Cardiac evaluation demonstrated normal heart structure, but the 12-lead surface ECG was suggestive of but not diagnostic of Brugada syndrome. An exercise stress test reproduced the patient's usual symptoms during the recovery period, and was consistent with a typical vasovagal faint. The same symptoms were observed during a head-up tilt table test. However, given the family history and ECG, pharmacological testing with procainamide, isoprenaline and metoprolol, as well as programmed ventricular stimulation, were undertaken. Pharmacological provocation further supported a diagnosis of Brugada syndrome, whereas programmed ventricular stimulation was considered non-diagnostic regarding ventricular tachyarrhythmia susceptibility. Consequently, despite ECG and pharmacological findings suggestive of Brugada syndrome, there appeared to be sufficient evidence to believe that this patient's symptoms were the result of neurally mediated syncope and not due to ventricular tachyarrhythmias. The patient was treated with midodrine, and has remained symptom-free for 16 months. Thus, given the frequency with which vasovagal syncope occurs in young patients, its occurrence is not unexpected in individuals with concomitant diagnoses such as Brugada syndrome. In as much as current recommendations favour implantable defibrillators in symptomatic Brugada syndrome, the identification of other causes of syncope in such patients poses an uncomfortable, and currently unsettled dilemma.

"Sagging heart syndrome": a cause of acute lead dislodgment in two patients.

Acute passive fixation atrial lead dislodgment occurred due to an unexpected and marked postural descent of the heart after permanent pacemaker implantation in two patients. Sagging of the heart in these two individuals may have been related to a history of morbid obesity followed by weight loss of over 100 pounds. Lead replacement with active fixation leads was required in both cases. The term "sagging heart syndrome" is proposed to describe this clinical entity. In certain adult populations, such as in patients with a history of significant weight loss, the "sagging heart syndrome" may represent a previously unrecognized cause of acute lead dislodgment.

Effect of parenteral d-sotalol on transvenous atrial defibrillation threshold in a canine model of atrial fibrillation.

In an effort to reduce energy requirements for atrial defibrillation to a level low enough to perform painless electrical cardioversion with an implantable atrial defibrillator, we tested the hypothesis that drug therapy with the class III agent d-sotalol, when used concurrently with a low-energy shock, reduces atrial defibrillation threshold. In a nonthoracotomy canine model of atrial fibrillation, intracardiac shocks were delivered between the distal coronary sinus and the mid-right atrium. Based on a step-up energy delivery protocol the atrial defibrillation threshold was defined as the least amount of energy that resulted in a >10% and <90% rate of successful defibrillation. At a dose associated with class III antiarrhythmic effects (5 mg/kg), d-sotalol significantly reduced atrial defibrillation threshold from 1.72 +/- 1.12 J to 0.59 +/- 0.60 J (p < 0.01). These results support the feasibility of using antiarrhythmic drug therapy with d-sotalol to minimize energy requirements for intracardiac electrical cardioversion of atrial fibrillation.

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.

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.