Subclinical atrial fibrillation detection with a floating atrial sensing dipole in single lead implantable cardioverter-defibrillator systems: Results of the SENSE trial.

INTRODUCTION: Subclinical atrial fibrillation (AF), in the form of cardiac implantable device-detected atrial high rate episodes (AHREs), has been associated with increased thromboembolism. An implantable cardioverter-defibrillator (ICD) lead with a floating atrial dipole may permit a single lead (DX) ICD system to detect AHREs. We sought to assess the utility of the DX ICD system for subclinical AF detection in patients, with a prospective multicenter, cohort-controlled trial. METHODS AND RESULTS: One hundred fifty patients without prior history of AF (age 59 ± 13 years; 108 [72%] male) were enrolled into the DX cohort and implanted with a Biotronik DX ICD system at eight centers. Age-, sex-, and left ventricular ejection fraction-matched single- and dual-chamber ICD cohorts were derived from a Cornell database and from the IMPACT trial, respectively. The primary endpoint were AHRE detection at 12 months. During median 12 months follow-up, AHREs were detected in 19 (13%) patients in the DX, 8 (5.3%) in the single-chamber, and 19 (13%) in the dual-chamber cohorts. The rate of AHRE detection was significantly higher in the DX cohort compared to the single-chamber cohort (P = .026), but not significantly different compared to the dual-chamber cohort. There were no inappropriate ICD therapies in the DX cohort. At 12 months, only 3.0% of patients in the DX cohort had sensed atrial amplitudes less than 1.0 mV. CONCLUSION: Use of a DX ICD lead allows subclinical AF detection with a single lead DX system that is superior to that of a conventional single-chamber ICD system.

Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia.

BACKGROUND: Distinguishing between junctional tachycardia (JT) and atrioventricular nodal reentrant tachycardia (AVNRT) is essential to minimize unnecessary catheter ablation and the risk of heart block during treatment of AVNRT. OBJECTIVE: The purpose of this study was to investigate whether the tachycardia response to atrial overdrive pacing at a cycle length (CL) slightly shorter than tachycardia CL can differentiate between JT and AVNRT. We hypothesized that atrial overdrive pacing would transiently suppress JT but would entrain AVNRT. METHODS: Twenty-one patients in whom AVNRT was induced and atrial overdrive pacing during either AVNRT or JT was attempted were included in the study. We predicted that, upon cessation of atrial overdrive pacing, an atrial-His-His-atrial (AHHA) response would identify JT and an atrial-His-atrial (AHA) response would identify AVNRT. RESULTS: A total of 8 JT and 21 typical AVNRT were induced. Atrial overdrive pacing was attempted in all cases of JT and in 16 cases of AVNRT. An AHHA response was observed in 100% (8/8) of JT cases. In 2 cases of AVNRT, atrial overdrive pacing repetitively terminated the tachycardia. In the remaining patients with AVNRT, an AHA response was observed in 100% (14/14) of cases. When a response was able to be elicited, atrial overdrive pacing was 100% sensitive and 100% specific for differentiating JT from AVNRT. CONCLUSION: Atrial overdrive pacing during tachycardia can rapidly differentiate JT from AVNRT, which can improve the safety and efficiency of catheter ablation of these arrhythmias.

Predictive value of microvolt T-wave alternans in patients with left ventricular dysfunction.

OBJECTIVES: The purpose of this study was to prospectively evaluate the utility of microvolt T-wave alternans (TWA) in predicting arrhythmia-free survival and total mortality in patients with left ventricular (LV) dysfunction. BACKGROUND: Microvolt TWA has been proposed as a useful tool in identifying patients unlikely to benefit from prophylaxis with implantable cardioverter-defibrillator (ICD) prophylaxis. METHODS: We evaluated 286 patients with an LV ejection fraction

Effect of bundle branch block on microvolt T-wave alternans and electrophysiologic testing in patients with ischemic cardiomyopathy.

BACKGROUND: T-wave alternans (TWA) and electrophysiology study (EPS) are used for risk stratification for sudden death. OBJECTIVE: The purpose of the study was to determine the effect of bundle branch block or intraventricular conduction delay on TWA and EPS. METHODS: 386 patients with coronary artery disease, nonsustained ventricular tachycardia, and left ventricular ejection fraction < or =40% underwent TWA and EPS, and were followed for 40 +/- 19 months. RESULTS: Patients with wide QRS were more likely than narrow QRS patients to have nonnegative TWA (77% vs 63%, P <.01) or positive EPS (60% vs 48%, P = .03). Nonnegative TWA predicted the combined endpoint of ventricular tachyarrhythmia or death in narrow QRS (HR = 1.64, P = .04) but not wide QRS patients (HR = 1.04, P = .91). Similarly, positive EPS predicted the combined endpoint in narrow QRS (HR = 2.28, P <.001) but not wide QRS patients (HR = 0.94, P = .84). In multivariate analysis, QRS width and TWA, as well as QRS width and EPS, were independent predictors of events. There was no TWA- or EPS-based difference in arrhythmia-free survival within any specific wide QRS morphology. CONCLUSION: TWA and EPS are more often abnormal in patients with a wide QRS than in those with a narrow QRS. In patients with narrow QRS, both TWA and EPS stratify patients according to their risk of ventricular tachyarrhythmia or death. However, among patients with a wide QRS, regardless of specific QRS morphology, the risk is high and comparable regardless of TWA or EPS results. Therefore, the only truly low-risk group consists of those patients with negative test results and a narrow QRS.

Clinical and electrophysiological spectrum of idiopathic ventricular outflow tract arrhythmias.

OBJECTIVES: This study sought to compare and contrast the clinical and electrophysiological characteristics of outflow tract arrhythmias. BACKGROUND: Idiopathic ventricular outflow tract arrhythmias manifest clinically in 3 forms: 1) paroxysmal sustained monomorphic ventricular tachycardia (SMVT), 2) repetitive nonsustained ventricular tachycardia (NSVT), or 3) premature ventricular contractions (PVCs). Although these arrhythmias have a similar site of origin, it is unknown whether they share a common mechanism or similar clinical features. METHODS: A total of 127 patients (63 female [50%], mean age 51 +/- 15 years) were evaluated for outflow tract arrhythmias. RESULTS: A total of 36 (28%) presented with the index clinical arrhythmia of SMVT, 46 (36%) with NSVT, and 45 (35%) with PVCs. The sites of origin of the arrhythmias were similar among the 3 groups, occurring in the right ventricular outflow tract in 82%. Sustained ventricular tachycardia was more likely to be induced during exercise in the SMVT (10 of 15 patients [67%]) than NSVT or PVCs groups (p < 0.01). Sustained outflow tract ventricular tachycardia was induced at electrophysiology study in 78% of SMVT patients, 48% of NSVT patients, and 4% of PVCs patients. Adenosine was similarly effective in all 3 groups (p = NS). CONCLUSIONS: Patients with outflow tract arrhythmias can be differentiated based on the subtype of arrhythmia. However, the observation that approximately 50% of patients with NSVT and approximately 5% of patients with PVCs have inducible sustained ventricular tachycardia that behaves in an identically unique manner to those who present with sustained ventricular tachycardia (e.g., adenosine-sensitive) suggests that rather than representing distinct entities, outflow arrhythmias may be considered a continuum of a single mechanism.

Effect of oral beta-blocker therapy on microvolt T-wave alternans and electrophysiology testing in patients with ischemic cardiomyopathy.

BACKGROUND: Prior investigation has shown that intravenous beta-blockers decrease T-wave alternans (TWA) positivity in patients undergoing electrophysiology study (EPS). The present study examined whether oral beta-blocker use within 24 hours of TWA influences yield and predictive value of TWA and EPS. METHODS: We prospectively evaluated 387 patients (312 [81%] men, mean age 67 +/- 11 years) with coronary artery disease, left ventricular ejection fraction < or = 40%, and nonsustained ventricular tachycardia who underwent EPS and were followed for a mean of 2.8 +/- 1.4 years. T-Wave alternans was performed using an atrial pacing protocol and interpreted using standard criteria. Beta-blocker status was determined based on oral beta-blocker use in the 24 hours preceding the test: beta-blocker (-) (n = 62), beta-blocker (+) (n = 325). Follow-up for ventricular tachycardia, ventricular fibrillation, and death was obtained from chart review, device interrogation, and the Social Security Death Index. Estimated sensitivity and specificity of TWA and EPS stratified by beta-blocker use were calculated based on event-free 2-year survival. RESULTS: There was no difference in EPS (31 [50%] inducible off beta-blockers vs 166 [51%] on beta-blockers [P = .89]) or TWA (26 [42%] positive, 17 [27%] indeterminate off beta-blockers vs 136 [42%] positive, 81 [25%] indeterminate on beta-blockers [P = .89]). Beta-blocker use within 24 hours of testing did not affect the predictive value of TWA or EPS for overall or 2-year event-free survival. CONCLUSIONS: Oral beta-blocker therapy appears to have no effect on yield or predictive value of EPS or TWA in patients with coronary artery disease, diminished left ventricular function, and a history of nonsustained ventricular tachycardia.

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).

Response to adenosine differentiates focal from macroreentrant atrial tachycardia: validation using three-dimensional electroanatomic mapping.

BACKGROUND: We previously proposed that adenosine has mechanism-specific effects on atrial tachycardia (AT), such that adenosine terminates AT attributable to triggered activity, transiently suppresses automatic rhythms, and has no effect on macroreentrant AT. This, however, remains controversial, because other studies have reported that adenosine terminates reentrant AT. To clarify this issue, we used 3D electroanatomic mapping to delineate the tachycardia circuit and thereby determine whether the response to adenosine differentiates focal from macroreentrant AT. METHODS AND RESULTS: We examined the effect of adenosine on 43 ATs in 42 consecutive patients (59+/-15 years of age; 26 female) who received adenosine during tachycardia and whose mechanism of AT was characterized by pharmacological perturbation, entrainment, 3D electroanatomic mapping, and results of radiofrequency ablation. Eight tachycardias were macroreentrant (noncavotricuspid isthmus-dependent), and 35 ATs were focal (either triggered or automatic). Adenosine administered during AT (at doses sufficient to result in AV block) terminated or transiently suppressed focal AT in 33 of 35 cases, whereas 8 of 8 macroreentrant ATs were adenosine insensitive (P<0.001). Twenty-eight of 35 focal ATs were located along the crista terminalis or tricuspid annulus. CONCLUSIONS: The response of AT to adenosine can immediately differentiate atrial tachycardia arising from a focal source from that attributable to macroreentry. This finding can be exploited to facilitate developing a focused, strategic ablative approach at the onset of a procedure.

Lesional tachycardias related to mitral valve surgery.

OBJECTIVES: The purpose of this study was to define the anatomic distribution of electrically abnormal atrial tissue and mechanisms of atrial tachycardia (AT) after mitral valve (MV) surgery. BACKGROUND: Atrial tachycardia is a well-recognized long-term complication of MV surgery. Because atrial incisions from repair of congenital heart defects provide a substrate for re-entrant arrhythmias in the late postoperative setting, we hypothesized that atriotomies or cannulation sites during MV surgery also contributed to postoperative arrhythmias. METHODS: In 10 patients with prior MV surgery, electroanatomic maps were constructed of 11 tachycardias (6 right atrium [RA], 4 left atrium [LA] and 1 biatrial). Activation and voltage maps were used to identify areas of low voltage, double potentials and conduction block. RESULTS: Lesions were present in the lateral wall of the RA (six of seven maps) and in the LA along the septum adjacent to the right pulmonary veins (four of five maps). In 8 of 10 patients, these findings corresponded to atrial incisions or cannulation sites. Arrhythmia mechanisms were identified for 9 of 11 tachycardias. A macro-re-entrant circuit was mapped in six cases, three involving lesions in the lateral wall of the RA and three involving the LA septum and right pulmonary veins. In three of these cases figure-of-eight re-entry was demonstrated, and in the other three a single macro-re-entrant circuit was observed. In three other cases, a focal origin was identified adjacent to abnormal tissue in the RA (two cases) or within a pulmonary vein (one case). CONCLUSIONS: Surgical incisions for MV surgery provide a substrate for atrial arrhythmias. Both macro-re-entrant and focal mechanisms contribute to AT after MV surgery.