Document Detail

The acute effect of atrioventricular pacing on sympathetic nerve activity in patients with normal and depressed left ventricular function.
MedLine Citation:
PMID:  18586896     Owner:  NLM     Status:  MEDLINE    
Although modest elevations in pacing rate improve cardiac output and induce reflex sympathoinhibition, the threshold rate above which hemodynamic perturbations induce reflex sympathoexcitation remains unknown. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressures (MAP) and sympathetic nerve activity (SNA) were measured during normal sinus rhythm (NSR) and atrioventricular (AV) sequential pacing in 25 patients. Pacing was performed at 100, 120, and 140 beats/min with an AV interval of 100 ms. Patients were divided into two groups based on normal or abnormal left ventricular ejection fraction (LVEF): group 1 (n = 11; mean LVEF, 55%) and group 2 (n = 14; mean LVEF, 31%). In group 1, relative to NSR, SBP decreased an average of 2%, 3%, and 8% at 100, 120, and 140 beats/min (P < 0.001), respectively. DBP and MAP increased 9%, 15%, and 15% (P = 0.001) and 3%, 6%, and 5% [P = not significant (NS)], respectively. In group 2, SBP reductions were even greater, with an average decrease of 4%, 8%, and 16% (P < 0.001). Whereas DBP increased 9%, 9%, and 8% at 100, 120, and 140 beats/min (P = NS), MAP increased 3% and 2% at 100 and 120 beats/min but decreased 3% at 140 beats/min (P = 0.001). SNA recordings were obtained in 11 patients (6 in group 1 and 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 120 beats/min (49% and 38%) but increased 24% at 140 beats/min. Patients with depressed LVEF exhibited altered hemodynamic and sympathetic responses to rapid sequential pacing. The implications of these findings in device programming and arrhythmia rate control await future studies.
Nathan M Segerson; Stephen L Wasmund; Marcos Daccarett; Manuel L Fabela; Christopher H Hammond; Gregory Stoddard; Michael L Smith; Mohamed H Hamdan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2008-06-27
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  295     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2008 Sep 
Date Detail:
Created Date:  2008-09-08     Completed Date:  2008-10-16     Revised Date:  2013-06-05    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1076-H1080     Citation Subset:  IM    
University of Utah, Salt Lake City, UT, USA.
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MeSH Terms
Arrhythmias, Cardiac / physiopathology
Blood Pressure / physiology
Cardiac Pacing, Artificial*
Central Venous Pressure / physiology
Heart Rate / physiology
Middle Aged
Peroneal Nerve / physiology
Stroke Volume / physiology
Sympathetic Nervous System / physiology*
Ventricular Dysfunction, Left / therapy*
Ventricular Function, Left / physiology*
Grant Support
5-T32-HL-007576/HL/NHLBI NIH HHS

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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