Effects of coupled pacing on cardiac performance during acute atrial tachycardia and fibrillation: an old therapy revisited for a new reason.
Atrial tachycardia (AT) and fibrillation (AF) result in rapid ventricular rates that are detrimental to optimal cardiac function. The purpose of this study was to determine whether the application of a coupled pacing (CP) regimen would improve ventricular function by decreasing the ventricular rate of mechanical contractions (VRMCs). We simulated AT by pacing either atrium at a rate that resulted in a rapid but regular ventricular rate in seven anesthetized dogs. AF was induced by increasing the atrial pacing rate until atrial activation did not follow the pacing. After the induction of either AT or AF, we applied CP after each intrinsic ventricular activation. We measured the VRMCs and left ventricular (LV) pressures and volumes via a pressure-conductance catheter. The marked reductions in VRMCs during CP resulted in increases in LV end-diastolic volume. The CP resulted in virtually no mechanical contractions, whereas the strength of contractions from the normal electrical activation increased. The increases in the positive LV rate of pressure development over time and LV ejection fraction during CP were the result of postextrasystolic potentiation. The average stroke work (area of the pressure-volume loops) increased as a result of CP during both AT and AF. Despite the large increases in stroke volume (approximately 2x) during CP, the changes in cardiac output were moderate because the VRMCs markedly decreased (approximately 1/2). We conclude that CP therapy may be a viable therapy for slowing the heart rate and improving cardiac performance in patients with AT and AF.
Yamada
Hirotsugu
H
Department of Cardiovascular Medicine, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195, USA.
Martin
David O
DO
Mowrey
Kent A
KA
Greenberg
Neil L
NL
Wallick
Don W
DW
D000208:Acute Disease; D000818:Animals; D001011:Aorta / Q000502:physiology; D001281:Atrial Fibrillation / Q000503:physiopathology* / Q000628:therapy*; D001794:Blood Pressure; D004285:Dogs; D004599:Electric Stimulation Therapy / Q000379:methods*; D009200:Myocardial Contraction / Q000502:physiology; D010138:Pacemaker, Artificial; D013318:Stroke Volume; D013612:Tachycardia, Ectopic Atrial / Q000503:physiopathology* / Q000628:therapy*; D014655:Vascular Resistance; D016277:Ventricular Function, Left