Effect of pacing site on systolic mechanical restitution curves in the in vivo canine model.
BACKGROUND
Pacing site is known to influence the contractile state of the ventricle. Non-physiologic pacing sites such as the right ventricular apex (RVA) or left ventricular freewall (LVFW) have been shown to decrease the contractile state of normal myocardium, due to abnormal electrical propagation. The impact of pacing at these sites may alter mechanical restitution (MR), a fundamental cardiac property involving the electro-mechanical regulation of contraction. This, in turn, may affect cardiac function. The present study was conducted to determine if pacing site alters the time constant of MR: tau.


RESULTS
Anesthetized canines (n = 6) were acutely paced at four sites: right atrium (RA), RVA, right ventricular septum (RVS), and LVFW. MR data was captured by the S1-S2 pacing protocol and used to create MR curves, generating a restitution time constant, tau, at each site. No significant difference in tau was found between pacing sites. A linear regression analysis of MR curves revealed that there was no significant difference in slope between pacing sites.


CONCLUSIONS
Although pacing site has been found to influence the contractile state of the ventricle, this is the first known study to demonstrate no change in tau in an in vivo preparation. This suggests that alteration of electro-mechanical coupling described by MR is not sufficiently robust to provide insight into pacing site and cardiac function in healthy hearts.
Ahlberg
Sarah E
SE
Department of Biomedical Engineering, University of Minnesota, Minneapolis, MN 55455, USA.
Grenz
Nathan A
NA
Ewert
Daniel L
DL
Iaizzo
Paul A
PA
Mulligan
Lawrence J
LJ
D000818:Animals; D016275:Atrial Function / Q000502:physiology*; D001696:Biomechanical Phenomena / Q000379:methods; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D003198:Computer Simulation; D004285:Dogs; D006329:Heart Conduction System / Q000502:physiology*; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology*; D013599:Systole / Q000502:physiology*; D016276:Ventricular Function / Q000502:physiology*