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Previous studies have suggested that sinus node pacemaker function is distributed over a variable portion of the SVC/RA junction. Different areas may be responsible for different heart rates. We investigated the earliest site of endocardial activation during sinus rhythm and pharmacologically induced sinus tachycardia. Methods: 10 anaesthetised pigs (mean weight 83+/-12kg) were studied using non-contact mapping (NCM). Geometry reconstruction and labeling was aided by intracardiac ultrasound. The earliest sites of activation were identified with isopotential colour maps and earliest QS complexes in virtual unipolar electrograms. Sinus tachycardia was induced by isoprenolol infusion. 10 consecutive beats of equal cycle length from the same site of origin and identical P wave morphology were examined at 80, 100, 120, 150 and 180 beats per minute. Results: Earliest endocardial sinus node pacemaker activity occurred at a median of 2.5 (range 1-4) discrete sites along the crista terminalis (CT) Mid lateral CT High lateral CT SVC os High septal CT 552+/-202 513+/-178 491+/-129 524+/-158 msec msec msec msec Although the trend was for faster rates to originate from a more cranial position, within individual animals each site was able to generate tachycardias across a range of heart rates. Activation in the lateral CT occurred 32.2+/-14.4 msec before P wave onset vs 16.6+/-9.2 msec when arising from near the SVC os (p<0.001). NCM revealed that CT activation had to move up and down the CT before exiting into surrounding myocardium. The site of earliest sinus node activity determined subsequent RA activation. Conclusions: Sinus node pacemaker activity can arise from 1-4 discrete endocardial sites on the CT. Although faster heart rates tended to arise from more cranial sites, each site was capable of a range of sinus tachycardia cycle lengths. More cranial sites also result in more rapid global activation. This may influence ablation procedures in the high right atrium, including sinus node modification.


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