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.

Recurrence of symptomatic ventricular arrhythmias in patients with implantable cardioverter defibrillator after the first device therapy: implications for antiarrhythmic therapy and driving restrictions. CARE Group.

OBJECTIVES: The purpose of this study was to investigate whether clinical or electrophysiologic characteristics could predict initial and subsequent implantable cardioverter defibrillator (ICD) therapy. BACKGROUND: Identification of markers to predict subsequent ICD therapy and symptoms after the first event could affect patient management. METHODS: We analyzed baseline and follow-up data on 125 ICD patients followed for 408+/-321 days. Medications and ICD programming were not changed after first ICD therapy. RESULTS: Implantable cardioverter defibrillator therapy occurred in 58 patients (46%). Clinical features were as follows: mean left ventricular ejection fraction (LVEF) 29%+/-15%; coronary artery disease 84%; presenting arrhythmia with sustained monomorphic ventricular tachycardia (SMVT) in 68%. In a multivariate analysis the relative risk for ICD therapy in patients presenting with SMVT versus cardiac arrest (CA) was 2.57 (range, 1.32 to 5.01), and for patients with LVEF < or =25%, 1.95 (1.11 to 3.45), respectively (p < 0.05). Implantable cardioverter defibrillator therapy was not predicted by any other variable. Forty-six patients had second ICD therapy. Mean time to second ICD therapy was only 66+/-93 days compared with 138+/-168 days for first ICD therapy (p < 0.05). No predictor for second ICD therapy was found. Regarding symptoms, impaired consciousness during initial ICD therapy was predicted only by SMVT cycle length <250 ms at electrophysiologic testing. In contrast, symptoms were similar between first and second ICD therapy (p = 0.0001). Of note, ventricular tachycardia cycle length preceding first and second ICD therapy was similar (r = 0.76, p = 0.001). CONCLUSIONS: First ICD therapy tends to occur in patients presenting with SMVT and LVEF < or =25%. Subsequent therapy occurs sooner and is unpredictable, suggesting that antiarrhythmic drug therapy should be considered after the first symptomatic ICD therapy. Symptoms during first ICD therapy predict subsequent symptoms, and patients presenting with SMVT and asymptomatic first ICD therapy are at very low risk for future syncopal ICD therapy.

Late occurrence of heart block after radiofrequency catheter ablation of the septal region: clinical follow-up and outcome.

INTRODUCTION: There are few data regarding the occurrence of delayed heart block at least 24 hours after radiofrequency catheter ablation (RFCA) of AV nodal reentry or posteroseptal accessory pathways (APs). We investigated the late occurrence of heart block in this population, the clinical outcome, and whether findings at electrophysiologic study could have predicted its development. METHODS AND RESULTS: Two of 418 patients with AV nodal reentry undergoing RFCA using a posterior approach and 1 of 54 patients with RFCA of a posteroseptal AP developed late heart block. Anterograde and retrograde AV nodal conduction before and after RFCA were normal. Patients received 12, 15, and 32 RFCA lesions, respectively, using a mean maximum power of 44 W. The RFCA sites were the posterior septum for posteroseptal AP and the posterior and mid-septum for patients with AV nodal reentry, with no His electrogram ever recorded at the ablation site. During RFCA, junctional tachycardia occurred with 1:1 VA conduction in the patient with a posteroseptal AP, but occasional intermittent single retrograde blocked complexes were present in both patients with AV nodal reentry. No rapid junctional tachycardia or >1 consecutive retrograde blocked complex was ever observed during RFCA. Persistent high-degree AV block with junctional escape developed 2 days after RFCA in the posteroseptal AP patient. A permanent pacemaker was implanted, and normal conduction was noted 16 days after RFCA. Both patients with AV nodal reentry complained of fatigue, mainly on exertion, 3 to 4 days after RFCA, and ECG-documented exercise-induced variable AV block was obtained. Because heart block resolved in our initial patient, a prolonged monitoring period was allowed. Symptoms disappeared at 13 and 8 days, and a follow-up treadmill test showed normal PR interval and no heart block. No recurrence of heart block has been seen in any of these three patients. CONCLUSION: Late unexpected heart block after RFCA of AV nodal reentry and posteroseptal AP is rare, often resolves uneventfully in 1 to 2 weeks, and no specific electrophysiologic findings predicted its occurrence. Prolonged clinical observation is preferable to immediate pacemaker implantation in such patients.

Primary and secondary prevention of sudden cardiac death: the role of the implantable cardioverter defibrillator.

Sudden cardiac death (SCD) affects nearly 300,000 people each year in the U.S., and out-of-hospital rates for survival range from only 2% to 25%. A substantial reduction in SCD requires primary prevention through risk-stratification and secondary prevention of sustained ventricular tachycardia (VT-S) and ventricular fibrillation (VF). Because frequent premature ventricular complexes (PVCs) appeared to be associated with an increased risk for SCD in patients with significant ventricular dysfunction, it was thought that suppression of PVCs would prevent SCD. The implantable cardioverter defibrillator (ICD) electrically treats life-threatening VT-S and VF, and it can be implanted readily in the pectoral area. Two randomized, prospective, controlled trials demonstrated conclusively that the ICD is the treatment of choice in the primary prevention of SCD in patients with a previous MI. In addition, three randomized, controlled trials found the ICD to be superior to antiarrhythmic drugs in the secondary prevention of SCD. Physicians should learn to recognize patients who are candidates for the ICD and refer them to an electrophysiologist so that they can get this life-saving therapy.

Hyperventilation facilitates induction of supraventricular tachycardia: a novel method and the possible mechanism.

INTRODUCTION: Hyperventilation has been demonstrated to alter autonomic function. Sympathomimetic drugs (isoproterenol) and parasympatholytic drugs (atropine) may be needed to facilitate induction of supraventricular tachycardia (SVT). The aim of this study was to test the clinical utility and mechanisms of hyperventilation to facilitate SVT initiation. METHODS AND RESULTS: Fourteen patients with clinically documented SVT (9 AV nodal reentrant tachycardia and 5 AV reciprocating tachycardia) but noninducible during baseline electrophysiologic study were included. Immediately after hyperventilation test (at least 30 respirations/min) for 2 minutes, systolic blood pressure, sinus cycle length, anterograde and retrograde 1:1 conduction, and induced SVT were measured. Arterial blood gas, pH, and heart rate variability before and after hyperventilation were measured. Seven of nine patients with AV nodal reentrant tachycardia and 3 of 5 patients with AV reciprocating tachycardia could be induced immediately after the hyperventilation test. After hyperventilation, anterograde AV and retrograde VA 1:1 conduction were improved, sinus cycle length was decreased, and heart rate variability were decreased in both groups. CONCLUSION: Hyperventilation can facilitate induction of SVT. Improvement of conduction properties and changes of autonomic function are the possible mechanisms.

Prophylactic implantable cardioverter defibrillator trials: MUSTT, MADIT, and beyond. Multicenter Unsustained Tachycardia Trial. Multicenter Automatic Defibrillator Implantation Trial.

MUSTT and MADIT have clearly shown the survival benefit of an implantable cardioverter defibrillator (ICD) in patients with previous myocardial infarction, left ventricular ejection fraction < or = 0.40, and nonsustained ventricular tachycardia (VT), and who have had sustained VT induced at electrophysiology study. Progress in primary prevention of sudden cardiac death (SCD) depends on a concerted effort by clinicians to identify and appropriately treat MUSTT/MADIT-type patients; further research to more precisely define patient subgroups at risk for SCD and the willingness of industry to develop a lower priced ICD for prophylactic use are needed.

Screening and therapy for patients with nonsustained ventricular tachycardia.

Patients with coronary artery disease, nonsustained ventricular tachycardia (VT), and left ventricular dysfunction have an increased risk for sudden cardiac death. Two randomized prospective trials, the Multicenter Unsustained Tachycardia Trial (MUSTT) and the Multicenter Automatic Defibrillator Implantation Trial (MADIT), employed electrophysiologic testing for risk stratification in these types of patients. Individuals with inducible sustained VT were randomized to receive implantable cardioverter defibrillators (ICDs) or "conventional" therapy in MADIT, or were given no specific antiarrhythmic treatment vs electrophysiologically guided therapy in MUSTT. Both trials showed that overall mortality was reduced by approximately 50% with ICD therapy. In MUSTT, patients received no survival benefit with electrophysiologically guided drug treatment. MUSTT also demonstrated that untreated patients with inducible sustained VT had a worse prognosis than patients in whom sustained VT could not be initiated at electrophysiologic study. Even so, the data suggest that electrophysiologic testing alone may not be sensitive enough to identify broader groups of patients at risk for sudden death. In conclusion, patients with nonsustained VT who have coronary artery disease and a left ventricular ejection fraction <0.40 should undergo electrophysiologic testing, and if sustained VT is induced, ICD therapy should be prescribed.

Management of malignant ventricular arrhythmias and cardiac arrest.

Sudden cardiac death continues to be a major health problem in the United States, accounting for approximately 400,000 deaths per year. The last 10 yrs have seen major advances in the primary and secondary prevention of this problem. In patients who have survived an episode of cardiac arrest, the AVID study conclusively established the superiority of the implantable cardioverter defibrillator over empiric amiodarone. For patients with recurrent hemodynamically destabilizing ventricular tachycardia and ventricular fibrillation, intravenous amiodarone has emerged as a potent therapeutic agent, especially when other agents such as lidocaine and procainamide have not been effective. Finally, recent work has focused on the risk stratification of patients for sudden cardiac death. Both the MADIT and MUSTT studies suggest that patients with coronary artery disease, reduced ejection fraction, and nonsustained ventricular tachycardia who are inducible to a sustained ventricular arrhythmia at electrophysiology testing have improved survival with an implantable cardioverter defibrillator.

Electrophysiologic testing to identify patients with coronary artery disease who are at risk for sudden death. Multicenter Unsustained Tachycardia Trial Investigators.

BACKGROUND: The mortality rate among patients with coronary artery disease, abnormal ventricular function, and unsustained ventricular tachycardia is high. The usefulness of electrophysiologic testing for risk stratification in these patients is unclear. METHODS: We performed electrophysiologic testing in patients who had coronary artery disease, a left ventricular ejection fraction of 40 percent or less, and asymptomatic, unsustained ventricular tachycardia. Patients in whom sustained ventricular tachyarrhythmias could be induced were randomly assigned to receive either antiarrhythmic therapy guided by electrophysiologic testing or no antiarrhythmic therapy. The primary end point was cardiac arrest or death from arrhythmia. Patients without inducible tachyarrhythmias were followed in a registry. We compared the outcomes of 1397 patients in the registry with those of 353 patients with inducible tachyarrhythmias who were randomly assigned to receive no antiarrhythmic therapy in order to assess the prognostic value of electrophysiologic testing. RESULTS: Patients were followed for a median of 39 months. In a Kaplan-Meier analysis, two-year and five-year rates of cardiac arrest or death due to arrhythmia were 12 and 24 percent, respectively, among the patients in the registry, as compared with 18 and 32 percent among the patients with inducible tachyarrhythmias who were assigned to no antiarrhythmic therapy (adjusted P<0.001). Overall mortality after five years was 48 percent among the patients with inducible tachyarrhythmias, as compared with 44 percent among the patients in the registry (adjusted P=0.005). Deaths among patients without inducible tachyarrhythmias were less likely to be classified as due to arrhythmia than those among patients with inducible tachyarrhythmias (45 and 54 percent, respectively; P=0.06). CONCLUSIONS: Patients with coronary artery disease, left ventricular dysfunction, and asymptomatic, unsustained ventricular tachycardia in whom sustained ventricular tachyarrhythmias cannot be induced have a significantly lower risk of sudden death or cardiac arrest and lower overall mortality than similar patients with inducible sustained tachyarrhythmias.

Management of atrial fibrillation: therapeutic options and clinical decisions.

Atrial fibrillation (AF) is the most common, sustained tachyarrhythmia seen in clinical practice. Although it is not immediately life threatening, AF can cause troublesome symptoms and poses a risk of stroke. The patient's clinical status is often complicated by the presence of other cardiovascular or concomitant diseases. As a result, management of the patient with AF involves many questions and choices, all of which must be individualized. There are 3 general strategies for the management of patients with AF, including (1) restoration and maintenance of sinus rhythm, (2) control of ventricular rate, and (3) prevention of stroke. More than 1 strategy may be appropriate in some patients. Furthermore, either pharmacologic or nonpharmacologic options can be chosen in certain situations. Although some data from randomized clinical trials are available to aid in clinical decision-making, only the benefits of anticoagulation are supported by substantial evidence. This article explores practical approaches to several management issues and scenarios for which there are limited relevant clinical data. These include: (1) patient selection for ventricular rate control and assessment of treatment, (2) choice of antiarrhythmic drug for maintenance of sinus rhythm, (3) inpatient versus outpatient initiation of therapy, (4) definition of antiarrhythmic drug success, (5) methods of transthoracic direct cardioversion, and (6) prediction and prevention of AF after cardiac surgery.

Long-term follow-up of patients requiring intravenous amiodarone to suppress hemodynamically destabilizing ventricular arrhythmias.

BACKGROUND: Intravenous amiodarone is effective for the acute suppression of recurrent hemodynamically destabilizing ventricular arrhythmias. There are no follow-up data on patients undergoing long-term therapy with intravenous amiodarone. The objective of this investigation was to evaluate long-term outcome. METHODS AND RESULTS: We reviewed the clinical courses of 245 patients given intravenous amiodarone for sustained ventricular tachyarrhythmias. Of the 107 survivors (84% men; mean age 64 years) released from the hospital taking oral amiodarone, 41 were discharged with an empiric prescription for oral amiodarone. For 64 patients a decision regarding further therapy was based on results of an electrophysiologic study. Two patients were treated empirically with oral amiodarone and an implantable cardioverter defibrillator. Clinical variables and survival curves were the same for the empirically treated group and the group whose treatment was based on electrophysiologic findings (P =.89). Survival at 6, 12, and 18 months was 88%, 81% and 71%, respectively, for empirically treated patients, and 83%, 80% and 73%, respectively, for patients whose therapy was directed with an electrophysiologic study. Of the 64 patients who underwent electrophysiologic studies, 33 received an implantable cardioverter defibrillator. The Kaplan-Meier survival curves for patients with and patients without an implantable cardioverter defibrillator were similar (P =.46). CONCLUSIONS: Patients for whom recurrent ventricular tachycardia and fibrillation are suppressed with intravenous amiodarone and who are discharged receiving oral amiodarone have an 80% 1-year survival rate. Although not randomized, our data suggested that among such patients, electrophysiologic testing, implantation of a cardioverter defibrillator, or both may not be necessary. Ascertaining the best management strategy for these patients will require a prospective randomized trial.

A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators.

BACKGROUND: Empirical antiarrhythmic therapy has not reduced mortality among patients with coronary artery disease and asymptomatic ventricular arrhythmias. Previous studies have suggested that antiarrhythmic therapy guided by electrophysiologic testing might reduce the risk of sudden death. METHODS: We conducted a randomized, controlled trial to test the hypothesis that electrophysiologically guided antiarrhythmic therapy would reduce the risk of sudden death among patients with coronary artery disease, a left ventricular ejection fraction of 40 percent or less, and asymptomatic, unsustained ventricular tachycardia. Patients in whom sustained ventricular tachyarrhythmias were induced by programmed stimulation were randomly assigned to receive either antiarrhythmic therapy, including drugs and implantable defibrillators, as indicated by the results of electrophysiologic testing, or no antiarrhythmic therapy. Angiotensin-converting-enzyme inhibitors and beta-adrenergic-blocking agents were administered if the patients could tolerate them. RESULTS: A total of 704 patients with inducible, sustained ventricular tachyarrhythmias were randomly assigned to treatment groups. Five-year Kaplan-Meier estimates of the incidence of the primary end point of cardiac arrest or death from arrhythmia were 25 percent among those receiving electrophysiologically guided therapy and 32 percent among the patients assigned to no antiarrhythmic therapy (relative risk, 0.73; 95 percent confidence interval, 0.53 to 0.99), representing a reduction in risk of 27 percent). The five-year estimates of overall mortality were 42 percent and 48 percent, respectively (relative risk, 0.80; 95 percent confidence interval, 0.64 to 1.01). The risk of cardiac arrest or death from arrhythmia among the patients who received treatment with defibrillators was significantly lower than that among the patients discharged without receiving defibrillator treatment (relative risk, 0.24; 95 percent confidence interval, 0.13 to 0.45; P<0.001). Neither the rate of cardiac arrest or death from arrhythmia nor the overall mortality rate was lower among the patients assigned to electrophysiologically guided therapy and treated with antiarrhythmic drugs than among the patients assigned to no antiarrhythmic therapy. CONCLUSIONS: Electrophysiologically guided antiarrhythmic therapy with implantable defibrillators, but not with antiarrhythmic drugs, reduces the risk of sudden death in high-risk patients with coronary disease.

Implantable defibrillator event rates in patients with unexplained syncope and inducible sustained ventricular tachyarrhythmias: a comparison with patients known to have sustained ventricular tachycardia.

OBJECTIVES: To assess the clinical significance of inducible ventricular tachyarrhythmias among patients with unexplained syncope. BACKGROUND: Induction of sustained ventricular arrhythmias at electrophysiology study in patients with unexplained syncope and structural heart disease is usually assigned diagnostic significance. However, the true frequency of subsequent spontaneous ventricular tachyarrhythmias in the absence of antiarrhythmic medications is unknown. METHODS: In a retrospective case-control study, the incidence of implantable cardiac defibrillator (ICD) therapies for sustained ventricular arrhythmias among patients with unexplained syncope or near syncope (syncope group, n = 22) was compared with that of a control group of patients (n = 32) with clinically documented sustained ventricular tachycardia (VT). Sustained ventricular arrhythmias were inducible in both groups and neither group received antiarrhythmic medications. All ICDs had stored electrograms or RR intervals. Clinical variables were similar between groups except that congestive cardiac failure was more common in the syncope group. RESULTS: Kaplan-Meier analysis of the time to first appropriate ICD therapy for syncope and control groups produced overlapping curves (p = 0.9), with 57 +/- 11% and 50 +/- 9%, respectively, receiving ICD therapy by one year. In both groups, the induced arrhythmia was significantly faster than spontaneous arrhythmias, but the cycle lengths of induced and spontaneous arrhythmias were positively correlated (R = 0.6, p < 0.0001). During follow-up, three cardiac transplantations and seven deaths occurred in the syncope group, and two transplantations and five deaths occurred in the control group (36-month survival without transplant 52 +/- 11% and 83 +/- 7%, respectively, p = 0.03). CONCLUSIONS: In patients with unexplained syncope, structural heart disease and inducible sustained ventricular arrhythmias, spontaneous sustained ventricular arrhythmias occur commonly and at a similar rate to patients with documented sustained VT. Thus, electrophysiologic testing in unexplained syncope can identify those at risk of potentially life-threatening tachyarrhythmias, and aggressive treatment of these patients is warranted.

Relation of atrial refractoriness to upper and lower limits of vulnerability for atrial fibrillation/flutter following implantable ventricular defibrillator shocks.

BACKGROUND: Implantable ventricular cardioverter defibrillator (ICD) shocks can cause atrial fibrillation/flutter (AF). This study investigated the pathogenesis of AF after ICD shocks in a canine model. METHODS AND RESULTS: The study was conducted in 8 dogs. In 5 dogs (group 1), truncated exponential (8 ms, 78% tilt) monophasic and biphasic shocks were delivered through a bipolar epicardial (patch) or endocardial lead. After the last S1 of atrial pacing at a cycle length of 350 ms, shocks of 0.1 to 7.6 A (0.005 to 27.7 J) were delivered, timed to the atrial effective refractory period (AERP). Ventricular defibrillation thresholds were also determined. In 3 dogs (group 2), the effect of the open versus closed chest technique on AF induction was tested in the endocardial biphasic shock configuration. AF was induced in all 8 dogs and in all waveforms and configurations. Mean AF duration was 11.5+/-6 s, with a mean ventricular rate of 184+/-37 bpm. Ventricular shocks could induce AF only if they were timed between an AERP of -60 to 40 ms, -40 to 60 ms, -40 to 60 ms, and -20 to 60 ms in the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively. The mean+/-SD of the upper limit of vulnerability (ULV) for AF induction (in J) was 5. 2+/-0.6, 3.5+/-0.4, 5.2+/-1.2, and 2.5+/-0.1 for the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively (P<0.05). The lower limit of vulnerability (LLV) was 0.8+/-0.1, 0.8+/-0.1, 0.9+/-0, and 0.6+/-0 for the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively (P=NS). The ventricular defibrillation threshold (in J) for all wave forms and configurations was higher than the ULV (P<0. 05). CONCLUSIONS: (1) An atrial LLV and ULV exist for ventricular ICD shock-induced AF; (2) the shock-induced AF is related to both shock intensity and its timing to AERP; and (3) avoiding this atrial window of vulnerability may minimize the risk of post-ICD shock AF.