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1 University of Utah
2 Veterans Affairs Medical Center, Salt Lake City, UT
3 University of North Texas Health Science Center
* To whom correspondence should be addressed. E-mail: nathan.segerson{at}hsc.utah.edu.
Background: While modest elevations in pacing rate improve cardiac output and induce reflex sympathoinhibition, the threshold rate above which hemodynamic perturbations induce reflex sympathoexcitation remains unknown. Methods: Systolic, diastolic, and mean blood pressures (SBP, DBP, & MAP), and sympathetic nerve activity (SNA) were measured during normal sinus rhythm (NSR) and AV sequential pacing in 25 patients. Pacing was performed at 100, 120 and 140bpm with an AV interval of 100ms. Patients were divided into two groups based on normal or abnormal left ventricular ejection fraction (LVEF): Group 1 (n=11, mean LVEF=55%), Group 2 (n=14, mean LVEF=31%). Results: In Group 1, relative to NSR, SBP decreased an average of 2%, 3%, and 8% at 100, 120, and 140bpm (p<0.001). DBP and MAP increased 9%, 15%, 15% (p=0.001), and 3%, 6%, 5% (p=NS) respectively. In Group 2, SBP reductions were even greater, with an average decrease of 4%, 8%, and 16% (p<0.001). While DBP increased 9%, 9%, and 8% at 100, 120, and 140bpm, (p=NS), MAP increased 3% and 2% at 100 and 120bpm, but decreased 3% at 140bpm (p=0.001). SNA recordings were obtained in 11 patients (6 in Group 1, 5 in Group 2). In Group 1, SNA decreased during all rates, with a mean 21% reduction. In Group 2 however, SNA decreased at 100 and 120bpm (49% and 38%), but increased 24% at 140bpm. Conclusion: Patients with depressed LVEF exhibited altered hemodynamic and sympathetic responses to rapid sequential pacing. The implications of these findings in device programming await future studies.
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