Change In Atrial Activation Sequence Research Articles

Postmitral Valve Replacement Biatrial, Septal Macroreentrant Atrial Tachycardia Developing After Perimitral Flutter Ablation

Atypical macroreentrant atrial tachycardias are frequently encountered in patients after cardiac surgery, correction of congenital heart disease, or atrial fibrillation ablation. Ablation of one circuit can produce an abrupt change in atrial activation sequence giving rise to another macroreentrant circuit. In this report, we present a unique case of a biatrial septal macroreentrant atrial tachycardia, which developed after perimitral flutter ablation in a patient with mitral valve replacement. Editor’s Perspective see p 175 A 59-year-old man with a mitral valve replacement (bioprosthesis) in 1983 for a rheumatic mitral stenosis and a rereplacement in 1999 (right-sided approach with a vertical incision of the interatrial septum) with a mechanical prosthesis attributable to the degeneration of the former prosthesis was referred for the ablation of a sustained atrial tachycardia with a stable cycle length of 260 ms. The echocardiogram demonstrated a left ventricular ejection fraction of 45% to 50%, a moderately dilated right atrium (RA) as well as left atrium (LA) without signs of a prosthetic malfunction. The baseline surface 12-lead ECG showed an atypical atrial flutter with a regular, monomorphic atrial activity and an irregular atrioventricular conduction (Figure 1A). With broad positive flutter waves in unipolar lead V1 and inferior limb leads II, III and avF but negative flutter waves in limb leads I and avL, the ECG morphology suggested LA localization. Any significant 12-lead isoelectric interval was absent. Endocardial activation mapping with a quadripolar catheter in the RA and a steerable octapolar catheter in the coronary sinus (CS; Bard Medical, Covington, GA) demonstrated a distal to proximal activation sequence in the CS with a baseline cycle length of 260 ms, suggestive of a lateral to septal activation of the LA posterior wall (Figure 1B). An irrigated tip ablation catheter (Navistar Thermocool, Biosense Webster, Diamond Bar) was advanced into the LA via …

Change in atrial activation sequence during orthodromic reciprocating tachycardia: What is the mechanism?

Change in atrial activation sequence during orthodromic reciprocating tachycardia: What is the mechanism?

Para-Hisian pacing: Useful clinical technique to differentiate retrograde conduction between accessory atrioventricular pathways and atrioventricular nodal pathways

Para-Hisian pacing is a useful tool to differentiate between retrograde conduction over an accessory pathway and retrograde conduction over the fast or slow atrioventricular (AV) nodal pathways. 1-3 Para-Hisian pacing uses right ventricular (RV) pacing close to the His bundle or proximal right bundle branch (RBB). As the position of the ventricular pacing catheter changes subtly during respiration (or by changing pacing output), the pacing stimulus changes capture among (1) basal anteroseptal RV plus His bundle or proximal RBB (His bundle-RBB capture); (2) capture of basal anteroseptal RV alone; and (3) His bundle-RBB capture alone. These changes in pacing capture result in abrupt changes in the timing of His bundle activation relative to the timing of ventricular activation. The presence or absence of a change in atrial activation sequence, stimulus-atrial (SA) intervals, and His bundle-atrial (HA) interval identifies whether retrograde conduction is dependent on ventricular activation (retrograde conduction over an accessory pathway) or His bundle activation (retrograde conduction over the AV node) or both (accessory pathway and AV node; Figures 1 and 2). The loss of His bundle-RBB capture is usually identified by the widening of the QRS complex, indicating that some of the ventricular myocardium (farthest from the RV basal septal pacing site) is activated by the His-Purkinje system during both RV and His bundle-RBB capture. Our preferred approach is to position the RV pacing catheter toward the RV outflow tract, 1‐2 cm superior to the His bundle catheter. While pacing at moderate output (5‐10 mA and 2 ms pulse width), the RV catheter is slowly withdrawn toward the His bundle catheter (proximal RBB) until intermittent His bundle-RBB capture occurs because of changes in catheter position during respiration. As the pacing catheter is moved closer to the His bundle, the ventricular potential in the His bundle electrogram becomes earlier and the retrograde His bundle potential becomes later, providing greater separation between the local ventricular and His bundle potentials. The use of closely spaced electrodes (1 mm edge-to-edge) on the His bundle catheter shortens the duration of the local ventricular potential in the His bundle electrogram, preventing the masking of the His bundle potential by the local ventricular potential. Closely spaced electrodes on the pacing catheter may provide a smaller pacing field, facilitating intermittent loss of His bundle-RBB capture with small changes in catheter position during respiration. A deflectable RV pacing catheter is positioned more easily for para-Hisian pacing and subsequent positioning of the pacing catheter close to the location of an accessory pathway (Figure 3A). In patients with proximal RBB block (such as resulting from previous ablation), His bundle-RBB capture requires pacing proximal to the RBB block site and may not be achieved from the RV. Other approaches include changing pacing output to achieve intermittent His bundle-RBB capture and use of the distal electrodes on the His bundle catheter for pacing. 4

Intra-atrial conduction block along the mitral valve annulus during accessory pathway ablation: evidence for a left atrial "isthmus".

We observed a change in the atrial activation sequence during radiofrequency (RF) energy application in patients undergoing left accessory pathway (AP) ablation. This occurred without damage to the AP and in the absence of a second AP or alternative arrhythmia mechanism. We hypothesized that block in a left atrial "isthmus" of tissue between the mitral annulus and a left inferior pulmonary vein was responsible for these findings. Electrophysiologic studies of 159 patients who underwent RF ablation of a left free-wall AP from 1995 to 1999 were reviewed. All studies with intra-atrial conduction block resulting from RF energy delivery were identified. Fluoroscopic catheter positions were reviewed. Intra-atrial conduction block was observed following RF delivery in 11 cases (6.9%). This was evidenced by a sudden change in retrograde left atrial activation sequence despite persistent and unaffected pathway conduction. In six patients, reversal of eccentric atrial excitation during orthodromic reciprocating tachycardia falsely suggested the presence of a second (septal) AP. A multipolar coronary sinus catheter in two patients directly demonstrated conduction block along the mitral annulus during tachycardia. An isthmus of conductive tissue is present in the low lateral left atrium of some individuals. Awareness of this structure may avoid misinterpretation of the electrogram during left AP ablation and may be useful in future therapies of atypical atrial flutter and fibrillation.

Electrophysiologic effects of adenosine in patients with supraventricular tachycardia.

We correlated the electrophysiologic (EP) effects of adenosine with tachycardia mechanisms in patients with supraventricular tachycardias (SVT). Adenosine was administered to 229 patients with SVTs during EP study: atrioventricular (AV) reentry (AVRT; n=59), typical atrioventricular node reentry (AVNRT; n=82), atypical AVNRT (n=13), permanent junctional reciprocating tachycardia (PJRT; n=12), atrial tachycardia (AT; n=53), and inappropriate sinus tachycardia (IST; n=10). There was no difference in incidence of tachycardia termination at the AV node in AVRT (85%) versus AVNRT (86%) after adenosine, but patients with AVRT showed increases in the ventriculoatrial (VA) intervals (13%) compared with typical AVNRT (0%), P<0.005. Changes in atrial, AV, or VA intervals after adenosine did not predict the mode of termination of long R-P tachycardias. For patients with AT, there was no correlation with location of the atrial focus and adenosine response. AV block after adenosine was only observed in AT patients (27%) or IST (30%). Patients with IST showed atrial cycle length increases after adenosine (P<0.05) with little change in activation sequence. The incidence of atrial fibrillation after adenosine was higher for those with AVRT (15%) compared with typical AVNRT (0%) P<0.001, or atypical AVNRT (0%) but similar to those with AT (11%) and PJRT (17%). The EP response to adenosine proved of limited value to identify the location of AT or SVT mechanisms. Features favoring AT were the presence of AV block or marked shortening of atrial cycle length before tachycardia suppression. Atrial fibrillation was more common after adenosine in patients with AVRT, PJRT, or AT. Patients with IST showed increases in cycle length with little change in atrial activation sequence after adenosine.

Para-Hisian pacing. A new method for differentiating retrograde conduction over an accessory AV pathway from conduction over the AV node.

Differentiation between ventriculoatrial (VA) conduction over an accessory AV pathway (AP) and the AV node (AVN) may be difficult, especially in patients with a septal AP. A new pacing method, para-Hisian pacing, was tested in 149 patients with AP and 53 patients without AP who had AV nodal reentrant tachycardia (AVNRT). Ventricular pacing was performed adjacent to the His bundle and proximal right bundle branch (HB-RB), initially at high output to capture both RV and HB-RB. The output was then decreased to lose HB-RB capture. The change in timing and sequence of retrograde atrial activation between HB-RB capture and noncapture was examined. Loss of HB-RB capture without change in stimulus-atrial (S-A) interval or atrial activation sequence indicated exclusive retrograde AP conduction. An increase in S-A interval without change in His bundle-atrial interval or atrial activation sequence indicated exclusive retrograde AVN conduction. A change in atrial activation sequence indicated the presence of both retrograde AP and AVN conduction. Para-Hisian pacing correctly identified retrograde AP conduction in 132 of 147 AP patients, including all septal and right free wall APs. Retrograde AVN conduction masked AP conduction in 9 of 34 patients with a left free wall AP and 6 of 9 patients with the permanent form of junctional reciprocating tachycardia. Para-Hisian pacing correctly excluded AP conduction in all 53 patients with AVNRT. Para-Hisian pacing reliably identifies retrograde conduction over septal and right free wall APs, but AVN conduction may mask APs located far from the pacing site or with a long retrograde conduction time.