Moe G W, Stopps T P, Howard R J, Armstrong P W
Department of Medicine, St. Michael's Hospital, University of Toronto, Ontario, Canada.
J Lab Clin Med. 1988 Oct;112(4):426-32.
Chronic rapid ventricular pacing (250 beats/min) induces severe heart failure in a canine model. To assess the potential for recovery after cessation of pacing, simultaneous hemodynamic and two-dimensional echocardiographic studies were conducted in nine conscious dogs paced to severe heart failure (4.3 +/- 1.7 weeks). Heart failure was characterized by elevated left and right ventricular filling pressures from 9 +/- 3 and 7 +/- 2 mm Hg to 25 +/- 6 and 15 +/- 3 mm Hg (both p less than 0.01), respectively. Left ventricular cross-sectional area (an estimate of preload) and systolic wall stress (an estimate of afterload) increased from 12 +/- 2 cm2 and 119 +/- 23 10(3) dynes/cm2 to 17 +/- 3 cm2 and 210 +/- 46 10(3) dynes/cm2 (both p less than 0.01), respectively. Left ventricular ejection fraction decreased from 54% +/- 7% to 13% +/- 5% (p less than 0.01). When pacing was discontinued to allow resumption of sinus rhythm, left and right ventricular filling pressures declined rapidly at 48 hours after resumption of sinus rhythm, by 36% and 53%, respectively. Ejection fraction doubled, although left ventricular cross-sectional area and wall stress remained elevated at 48 hours. The recovery of systolic function in the absence of major changes in loading conditions suggests that pacing-induced heart failure is mediated by a decrease in left ventricular contractility. Moreover, the persistent dilation of the left ventricle after cessation of pacing suggests that structural remodeling of the left ventricle occurs during the development of pacing-induced heart failure.
