Rapid ventricular pacing in pigs: an experimental model of congestive heart failure

Abstract

To develop an improved animal model of congestive heart failure, 11 female farm pigs (wt, 42-46 kg) underwent rapid ventricular pacing at 230 beats/min for 7 days with a modified Medtronic unipolar pacemaker connected to an apical pacing lead. After 7 days the pacemaker was turned off, anesthesia induced, the chest opened, and cardiac hemodynamic and dimensional studies were performed. Results were subsequently compared with data from 12 control pigs that received no pacing. Two pigs died before measurements could be determined. Cardiac output in the paced animals (0.061 +/- 0.018 l.min-1.kg-1) was significantly less (P less than 0.05) than in control pigs (0.085 +/- 0.016 l.min-1.kg-1), when compared at the same resting heart rate. Left ventricular (LV) end-diastolic pressure (23.2 +/- 7.7 vs. 8.6 +/- 3.6 mmHg, P less than 0.01) and right ventricular (RV) end-diastolic pressure (9.0 +/- 3.1 vs. 4.4 +/- 1.7 mmHg, P less than 0.01) were significantly greater in the paced pigs. Significant increases in both septal-lateral LV end-diastolic dimension (60.3 +/- 3.9 vs. 52.1 +/- 7.2 mm, P less than 0.01) and RV end-diastolic dimension (47.2 +/- 5.7 vs. 40.8 +/- 4.7 mm, P less than 0.05) indicated biventricular dilation in the paced pigs. They also exhibited a significantly greater heart weight-to-total body weight ratio and clinical evidence of congestive heart failure, with hepatomegaly and ascites. These results demonstrate that 1 wk of rapid ventricular pacing at 230 beats/min produces a realistic model of congestive heart failure in the pig.

Alterations in left ventricular mechanics, energetics, and contractile reserve in experimental heart failure.

“…Because in many cases the ESPVR was obviously nonlinear, the end-systolic points were also fit to a parabolic relation Pes=a * (Ves-Vo)+b * (Ves-V0)2 (2) where a is the slope of the ESPVR at V., and b is the coefficient of nonlinearity. Stress-strain relations.…”

Alterations in left ventricular diastolic function in conscious dogs with pacing-induced heart failure.

“…In order to elucidate which of these mechanisms are important in mediating diastolic dysfunction during the development of heart failure and to determine whether alterations in diastolic function precede or follow alterations in systolic function, it is important to examine an experimental model in which the changes in systolic and diastolic function can be assessed longitudinally as the congestive heart failure state is induced, and potentially be studied early enough such that alterations in collagen content are not a confounding factor (6,7). The model ofpacing-induced cardiomyopathy and heart failure is ideal for this investigation because it has been well characterized in terms ofits alterations in LV systolic function (8)(9)(10)(11)(12), has been shown to be characterized by LV diastolic dysfunction as well (12), and can be studied as the lesion develops initially and progressively in the same animals, which serve as their own controls.…”

Tachycardia mediated cardiomyopathy: Pathophysiology, mechanisms, clinical features and management

“…This is characterized by increased ventricular filling pressures, decreased cardiac output and increased systemic vascular resistance, without a change in left ventricular (LV) mass (5,6,7). There is loss of intrinsic myocardial contractility with diminished contractile reserve.…”