The effects of altering time delays of coupled pacing during acute atrial fibrillation.
BACKGROUND
Coupled pacing (CP), which consists of delivering a premature electrical stimulation to the heart after the effective refractory period of ventricular activation, is a novel method for controlling ventricular rate during atrial fibrillation (AF). It also has been established that CP improves pump function by enhancing external cardiac work and myocardial efficiency.


OBJECTIVE
The purpose of the present study was to determine if two time delays for CP (short and long) would result in similar improvements in ventricular function.


METHODS
In a canine model, we applied CP at two time delays (CP-S and CP-L) during two stages: sinus rhythm (SR) and acute AF. The cardiac responses to CP during SR served as the nontachycardic and nondepressed control. During both rhythms, we shortened the coupling interval until we obtained maximal contractility, designated CP-S. Next, we increased the delay until we started to see a measurable secondary contraction (left ventricular pressure development of approximately 20 mmHg). These longer delays were designated CP-L.


RESULTS
Our results showed that the ventricular rate of intrinsic activation (VRIA) remained decreased despite prolongation of the time delay of CP during both AF and SR. Also, both delays of CP increased left ventricular systolic pressure (LVSP) and dLVP/dt, which are indices of myocardial contractility. In contrast, CP increased external cardiac work only during AF. Prolonging this time delay did not markedly decrease the improvement in external cardiac work. Myocardial O(2) consumption (MVO(2)) did not significantly change as the result of CP during either SR or AF. Finally, myocardial efficiency improved during AF as the result of CP at both time delays.


CONCLUSIONS
In conclusion, shorter time delays for CP increased contractile strength during both SR and AF. However, extending the time delay of CP had minimal effects on diminishing the improved ventricular pump function and energetics that resulted from CP during AF. Thus, the maximal enhancement of myocardial contractility via CP-S was not needed to maintain the improved ventricular function during acute AF when CP is applied.
Yamada
Hirotsugu
H
Department of Cardiovascular Medicine, Cleveland Clinic Foundation, OH 44195, USA.
Popović
Zoran B
ZB
Martin
David O
DO
Civello
Kenneth C
KC
Wallick
Don W
DW
D000208:Acute Disease; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology / Q000628:therapy*; D002304:Cardiac Pacing, Artificial / Q000379:methods; D004195:Disease Models, Animal; D004285:Dogs; D004452:Echocardiography; D006439:Hemodynamics; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000503:physiopathology / Q000628:therapy; D010138:Pacemaker, Artificial; D013997:Time Factors; D016277:Ventricular Function, Left; D018879:Ventricular Premature Complexes / Q000503:physiopathology / Q000628:therapy