Adenosine-insensitive right ventricular tachycardia: novel variant of idiopathic outflow tract tachycardia.

BACKGROUND: A hallmark of idiopathic right ventricular outflow tract (RVOT) tachycardia is its sensitivity to adenosine (ADO), which is consistent with a triggered mechanism. We have identified a novel group of patients with ADO-insensitive, non-reentrant RVOT tachycardia. OBJECTIVE: This study aimed to identify the clinical and electrophysiologic characteristics of ADO-insensitive RVOT tachycardia. METHODS: The response of ventricular tachycardia (VT) to ADO was evaluated in 46 consecutive patients with inducible sustained idiopathic RVOT tachycardia. The clinical and electrophysiologic characteristics of patients with ADO-insensitive RVOT tachycardia were compared with patients with ADO-sensitive VT and arrhythmogenic right ventricular cardiomyopathy (ARVC) VT. RESULTS: Sustained RVOT tachycardia terminated with ADO in 41 patients (89%), while 5 patients (11%) had ADO-insensitive VT. The electrophysiology study findings of patients with ADO-sensitive and ADO-insensitive RVOT tachycardia were similar. Compared with a group of 10 patients with ARVC, patients with ADO-insensitive RVOT tachycardia had no ARVC-associated electrocardiographic or right ventricular morphologic findings, as well as fewer inducible VT morphologies. Analysis of myocardial biopsies at VT origin sites from 3 of 5 patients with ADO-insensitive RVOT tachycardia demonstrated somatic mutations in the A1 ADO receptor (R296C) in 1 patient and in the inhibitory G protein (F200L) in another patient, as described previously. These mutations were not identified at remote myocardial sites. Over a median follow-up period of 4.8 years, no patients insensitive to ADO developed an ARVC phenotype. CONCLUSION: Although most forms of idiopathic RVOT tachycardia are characterized by ADO sensitivity, we described a variant of ADO-insensitive VT that, in some cases, can be linked to somatic myocardial mutations involving the A1 ADO receptor-associated cyclic adenosine monophosphate-mediated pathway.

The prognostic impact of pre-implantation hyponatremia on morbidity and mortality among patients with left ventricular dysfunction and implantable cardioverter-defibrillators.

AIMS: Hyponatremia is commonly observed among patients with left ventricular (LV) dysfunction and is a marker for adverse outcomes. We aimed to determine the prognostic significance of pre-implant hyponatremia on the outcomes of death, acute decompensated heart failure (ADHF) and appropriate implantable cardioverter-defibrillator (ICD) therapy for ventricular arrhythmias among patients with ICDs. METHODS AND RESULTS: The study population consisted of patients with an ejection fraction ≤40% undergoing ICD implantation (n = 911) for the primary or secondary prevention of sudden cardiac death from 1997 to 2007. The predictive value of the severity of pre-implantation hyponatremia stratified into mild hyponatremia (n = 268, sodium 134-136 mmol/L), moderate hyponatremia (n = 105, sodium 131-133 mmol/L), and severe hyponatremia (n = 31, sodium ≤130 mmol/L) on the risk of death, ADHF, and appropriate ICD therapy for ventricular arrhythmias as compared with patients a normal serum sodium (n = 507, sodium ≥ 137 mmol/L), was calculated using multivariable Cox proportional hazards analyses. During a mean follow-up of 775 ± 750 days as the severity of hyponatremia (from a normal sodium to severe hyponatremia) increased an incremental incidence of death (25% to 61%, P < 0.001) and ADHF (11% to 26%, P = 0.004) was observed with a reduced incidence of ICD therapy for ventricular tachycardia/ventricular fibrillation (37-29%, P = 0.037). Compared with the normal sodium cohort, patients with severe hyponatremia demonstrated an increased risk of death [adjusted hazard ratio (AHR) 2.69 (95% confidence interval, CI 1.57-4.59), P = 0.004] and ADHF [AHR 2.98 (95% CI 1.41-6.30), P = 0.004], with a lower probability of appropriate ICD therapy [AHR 0.68 (95% CI 0.27-0.88), P = 0.031]. CONCLUSION: Hyponatremia is commonly observed among ICD recipients with LV dysfunction. Patients with an increasing severity of hyponatremia are at increased risk of death and HF related morbidity with a reduced incidence of appropriate ICD therapy particularly among patients with severe hyponatremia.

Evaluation of the Charlson comorbidity index to predict early mortality in implantable cardioverter defibrillator patients.

BACKGROUND: Current guidelines consider the implantation of an implantable cardioverter defibrillator (ICD) a class III indication in patients with a life expectancy of <1 year. An evaluation of concomitant noncardiac conditions may identify patients whom may not derive benefit with ICD therapy. We sought to evaluate the association of the Charlson comorbidity index (CCI) on the prediction of early mortality (EM), death <1 year after ICD implant. METHODS: The study population consisted of patients (n = 1062) undergoing ICD implantation for the primary or secondary prevention of sudden cardiac death from 1997 to 2007. The predictive value of the CCI on the risk of EM and appropriate shock therapy for ventricular arrhythmias as compared to patients without EM after ICD implant was calculated using multivariable Cox proportional hazards and receiver operator analyses. RESULTS: Patients experiencing EM (n = 110) demonstrated higher CCI scores (mean 2.8 ± 1.3 vs 1.5 ± 1.2, P < 0.001) as compared to individuals without EM (n = 963). Among patients with a CCI of 0, 1, 2, 3, 4, and ≥5, the incidence of EM increased from 5% to 78%. The CCI was an independent predictor of EM (AHR 1.4 [95% CI 1.2-1.6], P < 0.001, per single score increase). Patients who experienced EM demonstrated a decreased incidence of appropriate ICD therapy when compared to patients without EM (AHR 0.4 [95% CI 0.2-0.7], P = 0.001). CONCLUSION: Noncardiac conditions are commonly observed among patients undergoing ICD implantation. Guidelines must incorporate a comprehensive assessment of concomitant comorbidities to minimize the risk of EM and to maximize the survival benefit with ICD therapy.

The gender-paradox among patients with implantable cardioverter-defibrillators: a propensity-matched study.

BACKGROUND: Several meta-analyses of the implantable cardioverter-defibrillator (ICD) clinical trials have demonstrated that while men derived a mortality reduction with prophylactic ICD implantation, women did not. These trials also observed that women receive less appropriate ICD shock therapy compared to men. We aimed to investigate this "gender-paradox" among a heterogeneous community cohort of patients receiving ICDs. METHODS: We identified 1,445 consecutive patients undergoing ICD implantation from 1997 to 2007. The study population consisted of 582 patients, of whom 291 were women who could be propensity matched to 291 men, based on age, ejection fraction, implantation indication (primary or secondary), etiology of cardiomyopathy (ischemic or nonischemic), and the presence of a cardiac resynchronization therapy-defibrillator (CRT-D) device. The impact of gender difference on the probability of death and appropriate ICD shocks for ventricular arrhythmias was calculated using multivariable Cox proportional hazards analyses. RESULTS: During a mean follow-up of 909 ± 901 days, compared to men, women demonstrated a similar risk of death (25% vs 25%, adjusted hazard ratio [AHR] 1.05 [95% confidence interval (CI) 0.81-1.35], P = 0.74). In contrast, women demonstrated a decreased probability of appropriate ICD-shock therapy (14% vs 19%, AHR 0.80 [95% CI 0.59-0.88], P = 0.03) compared to men, and among cohorts with a nonischemic cardiomyopathy (10% vs 20%, P < 0.001) and CRT-D devices (7% vs 19%, P = 0.01). CONCLUSION: Among a community cohort with ICDs, women have a similar mortality compared to men while experiencing less appropriate ICD therapy. These results support the findings of a lower arrhythmic mortality among women.

The prognostic impact of shocks for clinical and induced arrhythmias on morbidity and mortality among patients with implantable cardioverter-defibrillators.

BACKGROUND: Recent investigations have demonstrated that the occurrence of implantable cardioverter-defibrillator (ICD) shocks is associated with adverse long-term outcomes. These studies have emphasized that the risk is most reasonably due to arrhythmias rather than to the shock itself. We sought to compare the impact of shock delivery for induced ventricular arrhythmias during implantation defibrillation threshold testing and noninvasive electrophysiology study (NIPS) to clinical shocks on long-term outcomes among patients with ICDs. METHODS: This was a cohort evaluation of 1,372 patients undergoing ICD implantation at a tertiary hospital from December 1997 to January 2007. The probability of all-cause mortality and hospitalization for acute decompensated heart failure (ADHF) was evaluated based upon the type of ICD shock received using multivariable Cox proportional analyses. The four shock types analyzed were implantation shocks only (n = 694), additional NIPS shocks only (n = 319), additional appropriate shocks only (n = 128), or additional inappropriate shocks only (n = 104). RESULTS: The risk of death (adjusted hazard ratio [AHR] 0.91 [95% confidence interval (CI) 0.69-1.20]; P = .491) or ADHF (AHR 0.71 [95% CI 0.46-1.16]; P = .277) were similar between recipients of NIPS shocks and recipients of implantation shocks. Receiving an appropriate ICD shock increased the risk of death (AHR 2.09 [95% CI 1.38-2.69]; P <.001) and ADHF (AHR 2.40 [95% CI 1.51-3.81]; P <.002) as compared with implantation shocks and also increased the risk of death (AHR 2.61 [95% CI 1.86-3.67]; P <.001) and ADHF (AHR 2.29 [95% CI 1.33-3.97]; P = .003) as compared with NIPS shocks. CONCLUSIONS: ICD shocks delivered during induced ventricular arrhythmias at the time of NIPS testing does not increase the risk of death or ADHF as compared with recipients of appropriate ICD shocks. The occurrence of spontaneous arrhythmias in vulnerable substrates may explain the increased risk.

Comparison of single and double vein approaches for His bundle ablation and pacemaker placement for symptomatic rapid atrial fibrillation.

BACKGROUND: His Bundle ablation (HBA) with permanent pacemaker (PPM) implantation is an effective strategy for controlling heart rate in symptomatic patients with rapid atrial fibrillation (AF), resistant to pharmacologic therapy. The standard double vein (DV) approach involves mapping and HBA from a femoral approach to achieve complete heart block (CHB), while single chamber (SC), dual chamber (DC), or biventricular (BiV) PPM is then placed via a subclavian approach. METHODS: We compared 7 patients with drug-resistant rapid AF who underwent the standard DV approach to 8 patients who underwent a single vein (SV) approach, in which HBA and PPM implantation were performed through the subclavian vein. The two groups were compared for acute success in creating CHB, total procedure and fluoroscopy times and patient discomfort. Results are expressed as mean +/- standard error (SEM). RESULTS: The procedure times for the SV versus DV were 70.4 +/- 11.4 v 100.0 +/- 19.2 min, and the fluoroscopy times, 13.9 +/- 3.1 (SV) v 13.0 +/- 2.9 (DV). All patients were discharged in stable condition with CHB and SC, DC pacemaker or BiV/Implantable Cardioverter Defibrillator (ICD). CHB with symptomatic improvement was maintained in all patients over a mean follow-up period of 22.6 months (SV), and 9.6 months (DV). CONCLUSION: The SV approach for HBA combined with PPM implantation was at least as effective and may be more efficient than the classic DV approach, and should be considered as an alternative to DV technique to reduce procedural time and patient discomfort.

Impact of magnesium sulfate on serum magnesium concentrations and intracellular electrolyte concentrations among patients undergoing radio frequency catheter ablation.

BACKGROUND: We evaluated the impact of intravenous magnesium on intracellular magnesium (iMg) and serum magnesium (sMg) in patients undergoing radio frequency catheter ablation (RFCA) for atrial fibrillation (AF). METHOD: Patients with AF received 4g intravenous magnesium sulfate or normal saline in a randomized, double-blinded fashion. Venous blood and buccal cells were collected for evaluation of sMg and iMg at baseline, postinfusion, at the end of ablation procedure and six-hours posttherapy. RESULTS: All subjects (n = 18) had baseline sMg within normal range but iMg concentrations below normal in 89% of subjects. Baseline sMg and iMg concentrations were similar between groups. After infusion, the magnesium group had significantly higher sMg concentration than the placebo group over the six hours. In contrast, iMg concentrations were significantly higher than placebo immediately after the infusion (P = 0.007) but not at the end of RFCA or six-hours postinfusion (P = 0.187 and P = 0.267). CONCLUSION: iMg deficiencies exist despite normal sMg concentrations in patients undergoing RFCA. Intravenous magnesium sulfate corrects iMg deficiencies immediately postinfusion.

Association between statin therapy and reductions in atrial fibrillation or flutter and inappropriate shock therapy.

AIMS: In patients without implantable cardioverter defibrillators (ICDs), statins have been shown to reduce the incidence of atrial fibrillation and atrial flutter (AF/AFL). We sought to determine if statin therapy could reduce the occurrence of AF/AFL with rapid ventricular rates with and without inappropriate shock therapy among a large heterogeneous ICD cohort. METHODS AND RESULTS: We prospectively followed 1445 consecutive patients receiving an ICD for the primary (n = 833) or secondary (n = 612) prevention from December 1997 through January 2007. Outcome measures include incidence of AF/AFL that initiated ICD therapy or was detected during ICD interrogation. Cox hazard regression analyses were conducted to determine the predictors of AF/AFL with and without inappropriate shock delivery and did not include inappropriate shocks resulting from lead dysfunction or other exogenous factors. Patients in this study (n = 1445) were followed over a mean follow-up period of (mean +/- SD) 874 +/- 805 days. There were 563 episodes of AF/AFL detected, with 200 episodes resulting in inappropriate shock therapy. Overall, 745 patients received statin therapy and 700 did not. The use of statin therapy was associated with an adjusted hazard ratio of 0.472 [95% confidence interval (CI), 0.349-0.638, P < 0.001] for the development of AF/AFL with shock therapy and 0.613 (95% CI, 0.496-0.758, P < 0.001) without shock therapy when compared with the group without statin use. CONCLUSION: Among a cohort with ICDs at high risk for cardiac arrhythmias, statin therapy was associated with a reduction in AF/AFL tachyarrhythmia detection and inappropriate shock therapy.

Association between statin use and mortality in patients with implantable cardioverter-defibrillators and left ventricular systolic dysfunction.

BACKGROUND: A few previous nested cohort trials have evaluated the use of statins on survival and the occurrence of ventricular tachycardia or fibrillation (VT/VF). While the studies generally agreed on the survival effects, they disagreed on the magnitude of the mortality benefit and on the effect on VT/VF. OBJECTIVE: The purpose of this study was to determine in a large, long-term follow-up cohort whether statin therapy could reduce mortality and the occurrence of VT/VF in a mixed population receiving an implantable cardioverter-defibrillator (ICD) for primary or secondary prevention and either ischemic or nonischemic cardiomyopathy. METHODS: Cohort evaluation of all patients undergoing implantation of an ICD with a left ventricular ejection fraction <40% at an urban U.S. teaching hospital from December 1997 through January 2007. Multivariable analysis of predictors of mortality and VT/VF were conducted. RESULTS: There were 314 deaths among the 1204 patients (26.1%). The use of statin therapy (n = 642) was associated with an adjusted hazard ratio of 0.67 (95% confidence interval [CI] 0.53-0.85; P<.001) for mortality as compared with the no-statin group (n = 562). The use of statin therapy was not associated with a reduction in the adjusted hazard ratio for VT/VF (0.85; 95% CI 0.68-1.06; P = .14). CONCLUSIONS: Statin therapy is associated with a reduction in overall mortality in patients with ischemic or nonischemic cardiomyopathy with an ICD implanted for either primary or secondary prevention. The magnitude of survival benefit might have been underestimated given our inability to use statin as a time-dependent covariate.

Electromagnetic Interference (EMI) and arrhythmic events in ICD patients undergoing gastrointestinal procedures.

BACKGROUND: The objective was to determine the effect of electromagnetic interference (EMI) in patients undergoing gastrointestinal endoscopy. The implantable cardioverter-defibrillator (ICD) is the primary therapeutic modality for patients at risk for sudden cardiac death. One potential problem with ICDs is interactions with electrical devices and medical procedures causing EMI or triggering arrhythmic events. Endoscopy frequently employs electrocautery (EC) for diagnosis and treatment of gastrointestinal diseases. Current guidelines advise inactivating ICDs before any surgical procedure. There is limited information on management of ICDs during endoscopy with or without EC. We prospectively evaluated patients with ICDs undergoing endoscopic procedures at our institution. METHODS AND RESULTS: Forty-one ICD patients underwent 52 gastrointestinal endoscopies over 17 months. The mean age of the population was 66 years (51-83). There were 28 men and 13 women. Thirteen patients had single chamber devices, 25 had dual chamber devices, and 2 had biventricular ICDs. The mean tachyarrhythmia detection rate programmed was 164.7 bpm (125-188). Eighteen procedures (43.9%) required biopsy, coagulation, or polypectomy. Of these, 10 (55%) required the use of EC. Only unipolar EC with mean current 19.6 mA was used. All ICDs were programmed to detection-only with therapies off. Sensitivity was left at nominal programmed settings. Post procedure interrogation showed no detection of EMI or tachyarrhythmic events. CONCLUSIONS: Our study shows no EMI or arrhythmic events triggered during endoscopic procedures in patients with pectorally implanted transvenous ICDs. Routine practice of programming ICDs off for gastrointestinal procedures may not be necessary. However, larger studies are needed before change in current recommendations.

The use of protamine after radiofrequency catheter ablation: a pilot study.

OBJECTIVE: Evaluate the effect of administering intravenous protamine immediately post-radiofrequency catheter ablation (RFCA) on thrombotic and bleeding complications in heparinized patients. METHODS: Heparinized patients that had RFCA for atrial or ventricular arrhythmias at our institution between January 2001 and March 2006 and had a complete data set were included in this cohort evaluation. Patients receiving at least one dose of protamine within 15 min of RFCA were deemed the prophylactic group while those not receiving protamine within 15 min were the control group. Thrombotic (cerebrovascular event, transient ischemic attack, pulmonary embolism, deep vein thrombosis, or myocardial infarction) and bleeding events (blood loss requiring transfusion, hematoma requiring intervention, or intracranial hemorrhage) were compared between groups. RESULTS: Overall, 158 patients (74% male, 55 +/- 13.5) met inclusion criteria. Of these, 73.4% received prophylactic protamine (average dose = 39 mg +/- 17). Only one patient (0.9%) in the prophylactic protamine group and zero patients in the control group experienced a thrombotic event (p > 0.99). Only two patients (1.7%) in the protamine group (n = 2 blood transfusions) and zero patients in the control group experienced bleeding events (p = 0.839). CONCLUSIONS: Administering prophylactic intravenous protamine to allow for quicker catheter removal following RFCA in heparinized patients did not markedly impact thrombotic or bleeding complication rates in our population. The perceived benefit in our institution to protamine administration in this population is a reduction in postoperative patient immobilization and discomfort, reduced PACU nursing care, and earlier time to discharge. Given the low rate of thrombotic and bleeding events, a study of several thousand patients would be needed to fully evaluate the impact on these events.

Right and left ventricular outflow tract tachycardias: evidence for a common electrophysiologic mechanism.

INTRODUCTION: "Idiopathic" ventricular arrhythmias most often arise from the right ventricular outflow tract (RVOT), although arrhythmias from the left ventricular outflow tract (LVOT) are also observed. While previous work has elucidated the mechanism and electropharmacologic profile of RVOT arrhythmias, it is unclear whether those from the LVOT share these properties. The purpose of this study was to characterize the electropharmacologic properties of RVOT and LVOT arrhythmias. METHODS AND RESULTS: One hundred twenty-two consecutive patients (61 male; 50.9 +/- 15.2 years) with outflow tract arrhythmias comprise this series, 100 (82%) with an RVOT origin, and 22 (18%) with an LVOT origin. The index arrhythmia was similar: sustained ventricular tachycardia (VT) (RVOT = 28%, LVOT = 36%), nonsustained VT (RVOT = 40%, LVOT = 23%), and premature ventricular complexes (RVOT = 32%, LVOT = 41%) (P = 0.32). Cardiac magnetic resonance imaging and microvolt T-wave alternans results (normal/indeterminate) were also comparable. In addition, 41% with RVOT foci and 50% with LVOT foci were inducible for sustained VT (P = 0.48), and induction of VT was catecholamine dependent in a majority of patients in both groups (66% and 73%; RVOT and LVOT, respectively; P = 1.0). VT was sensitive to adenosine (88% and 78% in the RVOT and LVOT groups, respectively, P = 0.59) as well as blockade of the slow-inward calcium current (RVOT = 70%, LVOT = 80%; P = 1.00) in both groups. CONCLUSIONS: Electrophysiologic and pharmacologic properties, including sensitivity to adenosine, are similar for RVOT and LVOT arrhythmias. Despite disparate sites of origin, these data suggest a common arrhythmogenic mechanism, consistent with cyclic AMP-mediated triggered activity. Based on these similarities, these arrhythmias should be considered as a single entity, and classified together as "outflow tract arrhythmias."

Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract.

BACKGROUND: Tachycardia-induced cardiomyopathy caused by ventricular tachycardia is a well-defined clinical entity. Less well appreciated is whether simple ventricular ectopy can result in cardiomyopathy. We sought to examine a potential causal relationship between repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract and cardiomyopathy and the role of ablation in reversing this process. METHODS AND RESULTS: The study consisted of 27 patients (11 men; age, 47+/-15 years) with repetitive monomorphic ventricular ectopy, including 8 patients (30%) with depressed ventricular function (ejection fraction < or =45%). All patients underwent assessment of cardiac structure and function. The burden of ectopy was quantified through 24-hour Holter monitoring. Patients then underwent ablation guided by 3D mapping. After ablation, patients underwent repeated Holter monitoring and reassessment of cardiac function. Patients with depressed ventricular function were more likely to be older than patients with normal function (58+/-14 versus 42+/-18 years; P=0.013). However, the burden of ventricular ectopy was similar in patients with (17,859+/-13,488 ectopic beats per 24 hours) and without (17,541+/-11,479 ectopic beats per 24 hours; P=0.800) preserved ventricular function. Successful ablation was performed in 23 patients (85%), including 7 of 8 patients with depressed ventricular function. In this latter group, ventricular function improved in all patients (from 39+/-6% to 62+/-6%; P=0.017). CONCLUSIONS: Repetitive monomorphic ventricular ectopy (in the absence of sustained ventricular tachycardia) originating from the right ventricular outflow tract is an underappreciated cause of unexplained cardiomyopathy. Successful ablation of the focal source of ventricular ectopy results in normalization of left ventricular function. Patients with ectopy-induced cardiomyopathy are significantly older than patients with preserved ventricular function, which suggests either that older patients are more susceptible to the development of a cardiomyopathy or that the cardiomyopathy has had a longer period of time in which to evolve.

Usefulness of prolonged QRS duration to identify high-risk ischemic cardiomyopathy patients with syncope and inducible ventricular tachycardia.

We evaluated 61 consecutive patients who had coronary artery disease, decreased left ventricular function, and syncope and underwent implantation of a cardioverter-defibrillator because sustained ventricular tachycardia was inducible at electrophysiologic testing. During a follow-up of 3.0 +/- 1.8 years, 23 patients (38%) developed ventricular tachycardia. Prolonged QRS duration (>/=120 ms) was the only significant predictor of arrhythmia. The 1- and 2-year rates without ventricular arrhythmia were 82% and 77%, respectively, in patients whose QRS duration was <120 ms. In contrast, 1- and 2-year rates without ventricular arrhythmia were only 64% and 51%, respectively, in patients whose QRS duration was >/=120 ms (risk ratio 3.7, 95% confidence interval 1.4 to 9.8, p = 0.0092).

Significance of adenosine-induced atrioventricular block in patients with unexplained syncope.

OBJECTIVES: The purpose of this study was to test whether a prolonged (>/=6 seconds) period of AV block in response to adenosine triphosphate (ATP) identifies additional patients at risk for bradycardia who may benefit from pacemaker implantation. BACKGROUND: Bradycardia is a common etiology for syncope in patients without underlying structural heart disease. Conventional testing using electrophysiologic and tilt table studies often fail to identify patients prone to episodes of symptomatic bradycardia. METHODS: Adenosine testing was performed in 92 consecutive patients (64 women, age 55 +/- 21 years) with syncope of uncertain origin referred for tilt table testing. The adenosine test measured the maximal R-R interval after bolus administration of intravenous adenosine 150 mug/kg to upright patients. A positive adenosine AV block response was defined as a maximal R-R interval > or =6 seconds. RESULTS: A total of 21 patients (23%) had a positive response. During mean follow-up of 14.3 +/- 5.9 months, 14 patients (16%) had recurrent syncope. Among patients with a positive adenosine response, 3 patients (14%) had recurrent syncope. In comparison, 11 of 69 patients (16%) without adenosine-induced AV block had recurrent syncope (P = 1.00). CONCLUSIONS: Prolonged adenosine-induced AV block in patients with unexplained syncope failed to predict recurrent syncopal episodes. These data do not support therapeutic interventions (e.g., pacemaker implantation) based on a positive adenosine AV block response alone.