Mechanism and interpretation of two-for-one response to premature atrial complexes during atrioventricular node re-entry tachycardia.

AIMS: The response to premature atrial complexes (PACs) during tachycardia has been shown to differentiate atrioventricular nodal re-entrant tachycardia (AVNRT) from focal junctional tachycardia (JT). His refractory PAC (HrPACs) perturbing the next His (resetting with fusion) is diagnostic of AVNRT and such a late PAC fusing with the native beat cannot reset the focal source of JT. Early PAC advancing the immediate His with continuation of tachycardia suggests JT but can also occur in AVNRT due to simultaneous conduction through the AV nodal fast and slow pathways [two-for-one response (TFOR)]. The objective of this study was to evaluate the incidence and mechanism of TFOR after early premature atrial complexes (ePACs) during AVNRT and to differentiate it from the known response to ePACs during JT. METHODS AND RESULTS: Typical AVNRT cases were diagnosed using standard criteria. We evaluated the responses to scanning PACs delivered during tachycardia in 100 patients undergoing AV node slow pathway modification for AVNRT. The responses to HrPACs and ePACs delivered from coronary sinus os or high right atrium were retrospectively reviewed. In 10 patients, ePACs advanced the immediate His with continuation of tachycardia. In all 10 cases, HrPACs advanced the next His, confirming AVNRT as the mechanism, and indicating a TFOR. CONCLUSION: A TFOR can occur in a small number of patients during AVNRT and is therefore not diagnostic of JT. However, HrPACs always perturbed the next His in these cases, confirming the diagnosis of AVNRT and allowing for differentiation from JT.

Single-center experience of the FIRM technique to ablate paroxysmal and persistent atrial fibrillation.

INTRODUCTION: Focal impulse and rotor modulation (FIRM)-guided ablation has had mixed results of published success, and most studies have had a follow-up for a year or less. We aimed to study a consecutive group of patients followed for at least 1.5 years, subgrouped into those with an initial FIRM ablation and those with a previous, failed ablation who now received a FIRM guided one, to evaluate for success in each group and factors that might affect success. METHODS: Of 181 patients, 167 were available for analysis. Group 1 (n = 122) had a first or primary ablation (paroxysmal atrial fibrillation [PAF] 51; persistent atrial fibrillation [PeAF] 71) and group 2 (n = 45) had a redo ablation (PAF 18; PeAF 27). All patients were done under general anesthesia. FIRM mapping was done in the right atrium first and then the left, and only rotors consistently seen on multiple epochs were ablated, using 15 to 30 W. Rotor ablation was discontinued when remapping showed elimination of rotational activity at the site. Wide area catheter ablation was done for pulmonary vein isolation (PVI). Routine follow-up was at 3, 6, and 12 months of the first year, with a Holter monitor at 6 months, and then every 6 months thereafter. Event recorders were given to patients with potential arrhythmic symptoms. RESULTS: Mean follow-up was 16 months. Nearly 40% of patients had obstructive sleep apnea; mean body mass index was 32; and average left atrial size was 39.7 mm and 46.2 mm for PAF and PeAF patients, respectively. Freedom from atrial arrhythmia recurrence was: in group 1 patients, 82.4% for PAF and 67.6% for PeAF patients; in group 2 patients, 83.3% for PAF, but only 40.7% for PeAF patients. Comparing outcomes for the first 10 patients studied to the next 20 or more done by three operators showed no difference, suggesting no learning curve affecting the ablation results. Furthermore, the univariate analysis did not show any demographic factor to have an independent significance for ablation success or failure. Spontaneous termination during rotor ablation occurred in 76.8% of PAF and 27.6% of PeAF patients but did not affect the long-term outcomes for maintenance of sinus rhythm. CONCLUSIONS: FIRM-guided atrial ablation plus PVI in our patient population resulted in good success from a recurrence of atrial arrhythmias in patients undergoing an initial ablation procedure. For those with persistent AF undergoing a second procedure now using FIRM guidance plus PVI, the results are lower. Further research is needed to define better the appropriate population for FIRM-guided ablation and the degree of ablation needed for success in these patients.

Electrocardiographic features and prevalence of bilateral bundle-branch delay.

BACKGROUND: Definitive diagnosis of bilateral bundle-branch delay/block may be made when catheter-induced right bundle-branch block (RBBB) develops in patients with baseline left bundle-branch (LBB) block. We hypothesized that a RBBB pattern with absent S waves in leads I and aVL will identify bilateral bundle-branch delay/block. METHODS AND RESULTS: Fifty patients developing transient RBBB pattern in lead V1 during right heart catheterization were studied. Patients were grouped according to whether the baseline ECG demonstrated a normal QRS, left fascicular blocks, or LBB block pattern. The RBBB morphologies in each group were compared. The prevalence of bilateral bundle-branch delay/block pattern was examined in our hospital ECG database. All patients with baseline normal QRS complexes (n=30) or left fascicular blocks (4 anterior, 5 posterior) developed a typical RBBB pattern. Among the 11 patients with a baseline LBB block pattern, 7 developed an atypical RBBB pattern with absent S waves in leads I and aVL and the remaining 4 demonstrated a typical RBBB. The absence of S waves in leads I and aVL during RBBB was 100% specific and 64% sensitive for the presence of pre-existing LBB block. Among the consecutive 2253 hospitalized patients with RBBB, 34 (1.5%) had the bilateral bundle-branch delay/block pattern. CONCLUSIONS: An ECG pattern of RBBB in lead V1 with absent S wave in leads I and aVL indicates concomitant LBB delay. Pure RBBB and bifascicular blocks are associated with S waves in leads I and aVL.

The surface electrocardiogram predicts risk of heart block during right heart catheterization in patients with preexisting left bundle branch block: implications for the definition of complete left bundle branch block.

BACKGROUND: Patients with left bundle branch block (LBBB) undergoing right heart catheterization can develop complete heart block (CHB) or right bundle branch block (RBBB) in response to right bundle branch (RBB) trauma. We hypothesized that LBBB patients with an initial r wave (>or=1 mm) in lead V1 have intact left to right ventricular septal (VS) activation suggesting persistent conduction over the left bundle branch. Trauma to the RBB should result in RBBB pattern rather than CHB in such patients. METHODS: Between January 2002 and February 2007, we prospectively evaluated 27 consecutive patients with LBBB developing either CHB or RBBB during right heart catheterization. The prevalence of an r wave >or=1 mm in lead V1 was determined using 118 serial LBBB electrocardiographs (ECGs) from our hospital database. RESULTS: Catheter trauma to the RBB resulted in CHB in 18 patients and RBBB in 9 patients. All 6 patients with >or=1 mm r wave in V1 developed RBBB. Among these 6 patients q wave in lead I, V5, or V6 were present in 3. Four patients (3 in CHB group and 1 in RBBB group) developed spontaneous CHB during a median follow-up of 61 months. V1 q wave >or=1 mm was present in 28% of hospitalized complete LBBB patients. CONCLUSIONS: An initial r wave of >or=1 mm in lead V1 suggests intact left to right VS activation and identifies LBBB patients at low risk of CHB during right heart catheterization. These preliminary findings indicate that an initial r wave of >or=1 mm in lead V1, present in approximately 28% of ECGs with classically defined LBBB, may constitute a new exclusion criterion when defining complete LBBB.

Differentiating junctional tachycardia and atrioventricular node re-entry tachycardia based on response to atrial extrastimulus pacing.

OBJECTIVES: The purpose of this study was to differentiate non-re-entrant junctional tachycardia (JT) and typical atrioventricular node re-entry tachycardia (AVNRT). BACKGROUND: JT may mimic AVNRT. Ablation of JT is associated with a lower success rate and a higher incidence of heart block. Electrophysiologic differentiation of these tachycardias is often difficult. METHODS: We hypothesized that JT can be distinguished from AVNRT based on specific responses to premature atrial complexes (PACs) delivered at different phases of the tachycardia cycle: when a PAC is timed to His refractoriness, any perturbation of the subsequent His indicates that anterograde slow pathway conduction is involved and confirms a diagnosis of AVNRT. A PAC that advances the His potential immediately after it without terminating tachycardia indicates that retrograde fast pathway is not essential for the circuit and confirms a diagnosis of JT. This protocol was tested in 39 patients with 44 tachycardias suggesting either JT or AVNRT based on a short ventriculo-atrial interval and apparent AV node dependence. Tachycardias were divided into 3 groups: clinically obvious AVNRT, clinically obvious JT, and clinically indeterminate rhythm. RESULTS: In the 26 cases of clinically obvious AVNRT, the sensitivity and specificity of the test were 61% and 100%, respectively. In the 9 cases of clinically obvious JT, the sensitivity and specificity were 100% and 100%, respectively. In the 9 cases of clinically indeterminate rhythm, the technique indicated AVNRT in 1 patient and JT in 7 patients, and the test was indeterminate in 1 patient. CONCLUSIONS: The response to PACs during tachycardia can distinguish JT and AVNRT with 100% specificity in adult patients.