Sports participation in patients with implantable cardioverter-defibrillators.

The safety of sports participation for patients with implantable cardioverter-defibrillators (ICDs) is not yet defined, and current recommendations in both Europe and the US restrict these patients from competative sports more vigorous than golf or bowling. Postulated risks include increased frequency of arrhythmias, inability of the ICD to terminate ventricular arrhythmias during the metabolic changes accompanying extreme exercise, injury to the patient, or damage to the ICD system. However, survey data suggest that many ICD patients do participate in sports, and risks may be fewer than postulated. Ongoing research will better delineate the risks of sports for patients with ICDs.

Implantable Cardioverter Defibrillators: Uses; Abuses; Gains and Complications

Sudden cardiac death (SCD) due to a ventricular arrhythmia is one of the most common causes of death; yet its management continues to be a challenge. Controlled clinical trials have provided evidence that implantable cardioverter defibrillators (ICDs) are effective in reducing the risk of SCD in selected patients with ischaemic or non-ischaemic cardiomyopathy and/or ventricular arrhythmias. As increasing numbers of patients become eligible for ICDs; deciding whom should receive these becomes more complex; especially in patients with borderline risk factors and those with co-morbidities in whom the risk of death from nonarrhythmic cardiovascular cause is higher. What type of ICD a patient should receive remains a challenge. While ICD shocks themselves can affect outcomes adversely; no other therapy has proven more effective to date. Risks of implantation include infection; lead dislodgement and perforation. An ongoing challenge which also needs to be addressed includes whom will be footing the bill for device implants. More data is required to determine which patient population will benefit the most from ICD implants

Bolus isoproterenol infusions provide a reliable method for assessing interoceptive awareness.

Interoception, defined as the perception of internal body states, plays a central role in classic and contemporary theories of emotion. In particular, deviations from baseline body states have been hypothesized to be integral to the experience of emotion and feeling. Consequently, reliable measurement of interoception is critical to the testing of emotion theories. Heartbeat perception tasks have been considered the standard method for assessing interoceptive awareness, primarily due to their non-invasive nature and technical feasibility. However, these tasks are limited by the fact that above chance group performance rates on heartbeat detection (or the frequency of 'good detectors') are rarely higher than 40%, meaning that such tasks (as they are typically utilized) do not obtain a measure of interoceptive awareness in the majority of individuals. Here we describe a novel protocol for inducing and assessing a range of deviations in body states via bolus infusions of isoproterenol, a non-selective beta adrenergic agonist. Using a randomized, double-blinded, and placebo-controlled experimental design, we found that bolus isoproterenol infusions elicited rapid and transient increases in heart rate and concomitant ratings of heartbeat and breathing sensations, in a dose-dependent manner. Our protocol revealed changes in interoceptive awareness in all 15 participants tested, thus overcoming a major limitation of heartbeat detection tasks. These findings indicate that bolus isoproterenol infusions provide a reliable method for assessing interoceptive awareness, which sets a foundation for further investigation of the role of interoceptive sensations in the experience of emotion.

Report of the NASPE policy conference on arrhythmias and the athlete.

INTRODUCTION: This consensus statement summarizes the proceedings of The Expert Consensus Conference on Arrhythmias in the Athlete of the North American Society of Pacing and Electrophysiology (NASPE) on detecting, evaluating, and treating athletes with cardiovascular disorders that predispose to cardiac arrhythmias. METHODS AND RESULTS: The participants in the open policy conference were selected by the codirectors (Drs. Estes and Olshansky) based on expertise and contributions to the literature. All participants provided a referenced summary of their presentation. The writing group used the information from all published scientific studies, clinical trials, registries, clinical experience, and expert opinion to make recommendations regarding screening, evaluation, management, eligibility for competition, and a range of other medical, social, and legal issues regarding the recreational and competitive athlete. The codirectors of the symposium synthesized the participants' reports for this and made revisions according to suggestions of all members of the writing committee. The manuscript was reviewed by four independent reviewers assigned by the NASPE Committee for the Development of Position Statements and NASPE Board of Trustees. CONCLUSION: Despite considerable advances in knowledge regarding the diagnosis, therapy, and mechanisms of arrhythmias in the athlete, much remains unknown. Continued basic, clinical, and epidemiologic research is needed. Current screening techniques to detect athletes lack sensitivity and specificity. Evaluation of standardized screening programs with tracking of long-term outcomes is needed. Officials from athletic, academic, medical, and legal institutions need to form strategic partnerships to develop policy related to assessment of risk and assumption of responsibility for athletic activities.

Ventricular tachycardia with QRS configuration similar to that in sinus rhythm and a myocardial origin: differential diagnosis with bundle branch reentry.

INTRODUCTION: Tachycardia with a QRS configuration which resembles that in sinus rhythm is usually thought to be supraventricular. Ventricular tachycardia, with a similar QRS configuration to that in sinus rhythm on the 12-lead ECG, can occur. The mechanisms of this form of ventricular tachycardia have not been previously reported. METHODS AND RESULTS: The mechanism of ventricular tachycardia was defined during electrophysiological study in five patients. During sinus rhythm, all patients had a wide QRS complex (>0.12 s) on the 12-lead ECG. The morphology remained grossly unchanged during spontaneous, symptomatic tachycardia. Four of the five patients had coronary artery disease and left ventricular dysfunction. The remaining patient had idiopathic dilated cardiomyopathy. The relationship between the His bundle, deflection, the right bundle branch and the QRS complex was evaluated during tachycardia. Atrial and ventricular pacing, and ventricular activation mapping were performed during tachycardia to define the tachycardia mechanism. The tachycardia induced at electrophysiological testing, which was similar to the clinical tachycardia, was proven to be ventricular tachycardia in each patient. The morphology of ventricular tachycardia was right bundle branch block in two patients and left bundle branch block in three patients. The median tachycardia cycle length was 300 ms (range: 260-480 ms). His bundle activation occurred in a 1:1 relationship with ventricular activation during tachycardia in all patients at least intermittently. The tachycardias were thought initially to be bundle branch reentry tachycardia. With further intervention and continued observation, it became clear that His bundle activation was passive and was not required for the tachycardia to sustain. During tachycardia, His bundle activation appeared to precede the local ventricular activation. Instead, the His bundle was activated slowly from the previous ventricular beat causing a long ventricular-His (VH) interval. This was shown by: (1) activation patterns, (2) response to pacing, (3) intermittent VH dissociation, and (4) termination of ventricular tachycardia. CONCLUSION: A unique form of ventricular tachycardia is described. The QRS complex morphology on the 12-lead ECG during tachycardia was grossly similar to that during sinus rhythm. The His bundle activation was passive and occurred with a long activation time from the ventricle to the His bundle. Although it mimics usual bundle branch reentry, this form of ventricular tachycardia appears to be due to a different mechanism in which the His bundle is not obligatory for the continuation of the reentrant phenomenon.

Implantable cardioverter defibrillator practices and costs at an academic medical center.

This study addresses current costs of implanting implantable cardioverter defibrillators (ICDs) at one large medical center and documents actual costs using two methodologies. To determine the actual cost of ICD therapy, we studied all ICD implants performed in the procedure room (similar to an electrophysiology laboratory) who met accepted secondary prevention (AVID) indications for a 1-year period at Loyola University Medical Center. The study period coincided with the facility's shift of this procedure out of the operating room to a procedure room. Costs were analyzed two ways: a cost-based analysis and a cost-to-charge ratio analysis based on the facility's Medicare Cost Report. Twenty-four patients (14 inpatients and 10 outpatients) met the study inclusion criteria. Length of stay averaged 5.8 days for inpatients and 1.1 days for outpatients. In the cost-based analysis, the mean costs of the ICD implant (device, implant procedure, and preimplant and postimplant stay) were $33,509 for inpatient and $28,078 for outpatient implants. In the cost-to-charge ratio analysis, the mean costs for the inpatient hospitalization were $35,623. This is one of the first studies to document cost of ICD therapy and may serve as a benchmark for other facilities.

Apparent bidirectional conduction block following radiofrequency catheter ablation of typical atrial flutter.

OBJECTIVE: The purpose of this study is to determine the reliability of activation sequence mapping in assessing the presence of bidirectional conduction block (BCB) in typical atrial flutter (AFL) ablation. INTRODUCTION: Radiofrequency ablation (RFA) can cure typical AFL by creating BCB across the right atrial isthmus. Effective conduction block across this region can prevent AFL recurrence, but accurate assessment of isthmus conduction may be flawed. METHODS: BCB was measured before and after RFA by pacing at multiple rates on both sides of the isthmus during sinus rhythm. Pacing was performed from a low lateral tricuspid annulus site (proximal to the isthmus) and a coronary sinus Os site (distal to the isthmus), while recording simultaneously from 8-10 right atrial sites bordering the isthmus (4-5 free wall sites; 4-5 septal sites) as well as from an isthmus site. After ablation reinduction of atrial flutter was attempted from both sides of the block with rapid atrial pacing after BCB was established in all patients. In some patients lines of conduction block were evident at the isthmus (using the ablation catheter to map). RESULTS: Of 65 patients undergoing RFA of AFL, 59 had typical AFL. In all 59 patients, BCB was demonstrated at all pacing cycle lengths 30 min after RFA applications. In 6 of these 59, AFL was inducible with atrial pacing despite apparent BCB. Further RFA resulted in non inducibility in all 6 patients. In the remaining 53/59 patients, BCB was associated with noninducibility at 30 min. A total of 8 recurrences were seen during a mean 19.3 +/- 8.3 (SD) month follow-up. CONCLUSION: Apparent BCB as determined by activation sequence mapping outside of the isthmus is an excellent marker, but, as measured, may be a misleading method of assessing the presence or absence of conduction through the isthmus. It is necessary to attempt reinduction of AFL after apparent success. Elimination of typical AFL does not preclude other AFLs.

Apoptosis in the genesis of cardiac rhythm disorders.

Programmed cell death has provided a potential pathogenetic mechanism that could play a role in several diseases of the cardiac conduction system and the myocardium that are clinically expressed as disorders of the cardiac rhythm (Fig. 4). Most of these studies have been descriptive. The exact nature of the triggers for apoptotic cell death is not well understood and is a subject of current investigation. Alterations in the architecture of the myocardium play an important role in the pathogenesis of ventricular arrhythmias that are responsible for a large proportion of sudden cardiac deaths. Although apoptosis is essential for normal development, excessive apoptosis resulting from pathological triggers may result in destruction of tissues and in the development of heart disease in which a fatal arrhythmic event may be a final common pathway. At present, the triggers for programmed cell death in disorders of the cardiac rhythm are not understood completely. Because diverse conditions trigger apoptosis, treatment strategies may have to be directed toward attenuating such triggers and, in some instances, toward modifying the process itself. If future therapies that can favorably modulate the apoptotic process in conditions such as dilated cardiomyopathy and postmyocardial infarction are developed, they will have the potential to prevent the pathologic alteration of myocardial architecture that is conducive to arrhythmogenesis.

Case 4: a patient with symptomatic bradycardia.

Both the clinical and electrocardiographic presentations of sick sinus syndrome are highly variable. As illustrated by this month's case of Interactive Grand Rounds, the initial challenge to the clinician is to establish the correct diagnosis in the patient who has symptomatic bradyarrhythmias.

Location of death (in-hospital or out-of-hospital) and type of death (arrhythmic, nonarrhythmic, noncardiac) after inducible sustained ventricular tachyarrhythmias after syncope, sustained ventricular tachycardia, or nonfatal cardiac arrest (the ESVEM trial).

The ESVEM Trial evaluated methods to guide antiarrhythmic drug use in patients with spontaneous, inducible sustained tachyarrhythmias at electrophysiologic testing and frequent ventricular premature complexes (VPCs) per hour (>/=10). We assessed the relation between location (in-hospital or out-of-hospital) and classification of death (arrhythmic, nonarrhythmic, cardiac and/or noncardiac) for 486 randomized patients. Deaths were classified as out-of-hospital arrhythmic deaths if arrhythmic death occurred out-of-hospital, or if an arrhythmia preceded hospital admission and directly caused death. Of the 486 randomized patients, 188 (39%) died during 6 years of follow-up. The location and type of death could be determined clearly in 171 patients (91%). Ninety-one deaths were in-hospital (53%); 80 were out-of-hospital (47%). Arrhythmic deaths occurred in 85% out-of-hospital patients and in 30% in-hospital patients (p <0.001). Baseline characteristics were comparable for patients with out-of-hospital and in-hospital arrhythmic deaths. Twenty-seven of 95 arrhythmic deaths occurred in-hospital (28%); 72% occurred out-of-hospital. Out-of-hospital arrhythmic death accounted for 40% of deaths for which location and type of information were available. The 1- and 4-year actuarial out-of-hospital arrhythmic death rates were 9% and 18%, respectively. Of nonarrhythmic cardiac deaths, 91% were in-hospital and 9% were out-of-hospital. Of noncardiac deaths, 74% were in-hospital and 26% were out-of-hospital. Similar results were seen in the 296 patients for whom a drug was considered to be effective. Thus, over half the deaths in the ESVEM trial occurred in-hospital. The long-term actuarial risk of out-of-hospital arrhythmic death in ESVEM was unexpectedly low.