Rate-dependent block in the sinus venosa of the swine heart during transverse right atrial activation: correlation between electrophysiologic and anatomic findings.

UNLABELLED: Rate-dependent block in the sinus venosa. INTRODUCTION: Whether the crista terminalis or the sinus venosa result in rate-dependent block during transverse activation of the right atrial activation remains unknown. In the present study, right atrial activation at different cycle lengths was studied in the swine heart using high-resolution noncontact mapping (Endocardial Solutions). The location of the block was tagged and correlated with postmortem anatomical findings. METHODS AND RESULTS: Eight pigs were studied using noncontact mapping to obtain right atrial geometry and detailed sequence of activation using noncontact endocardial mapping. During sinus rhythm, activation proceeded uninterrupted craniocaudally along the sinus venosa and crista terminalis with similar conduction velocities (1.08+/-0.17 and 1.17+/-0.14 m/sec, respectively). Proximal coronary sinus stimulation was used to create transverse activation of the posterior right atrial wall. A rate-dependent decrease in conduction velocity occurred in the sinus venosa region (0.93+/-0.21, 0.82+/-0.14, and 0.52+/-0.09 m/sec at 500, 400, and 300 ms, respectively; P<0.05). The line of block verified by isopotential mapping and double potentials was obtained at cycle lengths of 240+/-30 ms. This line of the block was tagged with radiofrequency current lesions. Postmortem, all lesions were located in the sinus venosa region, 9.8+/-4.1 mm from the posteromedial edge of the crista terminalis. This region showed abrupt changes in muscle fiber thickness and orientation as well as in collagen content. CONCLUSIONS: The sinus venosa and not the crista terminalis results in a rate-dependent line of block during transverse right atrial activation. The morphologic characteristics of the sinus venosa appear to facilitate block in this region.

Left atrial tachycardia originating from the mitral annulus-aorta junction.

BACKGROUND: At the mitral annulus-aorta (MA-Ao) junction, the left atrium is continuous through the subaortic curtain with the musculature of the anterior mitral leaflet. Under experimental conditions, this region can generate abnormal electrical activity. In patients with left atrial tachycardia, we investigated whether this region could be the source of this arrhythmia. METHODS AND RESULTS: In 10 (28%) of 35 consecutive patients with left atrial tachycardia, the arrhythmia originated from the MA-Ao junction. Sustained, self-limited episodes of atrial tachycardia (cycle length, 340+/-56 ms; duration, 125+/-69 seconds) were repeatedly induced. Prematurity of the extrastimulus and time to first atrial tachycardia complex were directly correlated (R=0.66; P<0.001). During tachycardia, bipolar electrograms at the earliest site preceded onset of the P wave by 44+/-14 ms and were of longer duration and lower amplitude than those recorded from nearby left atrial sites (52+/-8 versus 24+/-4 ms, P<0.001; and 0.53+/-0.08 versus 3.45+/-0.96 mV, respectively; P<0.001). Ablation eliminated the tachycardia with no recurrence after a mean follow-up of 24+/-19 months. A comparative study in mouse embryos demonstrated the presence of the developing specialized conduction system in the MA-Ao region starting at embryonic age 11.5. CONCLUSIONS: The MA-Ao junction can be a frequent source of left atrial tachycardia. This previously unrecognized site of origin may explain why catheter ablation has been less successful in eliminating left versus right atrial tachycardias. Remnants of the developing specialized conduction system could be the underlying substrate of this arrhythmia.

Demonstration of a left atrial input to the atrioventricular node in humans.

BACKGROUND: During right atrial stimulation, the anterior and posterior approaches provide inputs to the atrioventricular (AV) node. The purpose of the present study was to determine how activation proceeding from the left atrium reaches the AV node. METHODS AND RESULTS: We studied AV nodal conduction during right and left atrial (coronary sinus) stimulation in 46 patients (27 women and 19 men; mean age, 46+/-4 years) who had structurally normal hearts. At an identical cycle length (600 ms), left atrial stimulation resulted in shorter A-H intervals than right atrial stimulation (73+/-3 ms versus 99+/-3 ms; P<0.05). In addition, atrial electrograms recorded close to the His bundle changed from near to far field potentials when stimulation was shifted to the left atrium. The A-H interval prolonged as the site of pacing was progressively moved from the distal to the proximal coronary sinus. During constant pacing from the distal coronary sinus, atrial activation close to the His bundle could be advanced by late extrastimuli delivered at the anterior and posterior approaches (up to 11+/-2 ms and 9+/-1 ms, respectively), without altering His bundle activation time. In contrast, late extrastimuli delivered at the inferoparaseptal mitral annulus advanced both the A and H electrograms in 19 of 20 patients, which is consistent with a left-sided input to the AV node. Right and left atrial stimulation resulted in similar AV nodal function. CONCLUSION: The mitral annulus provides a left atrial input to the human AV node.