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.
The volume and pressure of one ventricle have been demonstrated to modulate the volume and pressure in the contralateral chamber during systole and diastole. To quantitate the isolated systolic effects of left ventricular (LV) pressure on right ventricular (RV) mechanics, we rapidly withdrew blood from the LV immediately after diastole via an apex cannula during a single cardiac cycle in eight open-chest, open-pericardium anesthetized pigs (45 kg) and studied the effects on the RV. Reductions in LV pressure of up to 75 mm Hg were achieved in midsystolic without changing LV or RV diastolic volume or pressure. Resultant changes in RV flow and pressure development during these single unloaded beats may therefore be considered to result from pure systolic interaction. The instantaneous left-to-right systolic pressure gain [G(t)] was determined as the ratio of RV pressure change to LV pressure change as a function of time during systole, and the mean LV-to-RV systolic pressure gain was determined as the ratio of changes in mean systolic RV pressure to changes in mean systolic LV pressure. During LV unloading, there was an average reduction of 62.6 +/- 12.3% in the mean systolic LV pressure, which resulted in decreases of 13.6 +/- 6.4% in mean RV systolic pressure, 17.9 +/- 10.4% in RV stroke volume, and 27.0 +/- 11.3% in RV stroke work. G(t) was found to vary significantly within systole, reaching a minimum of 0.042 +/- 0.014 mm Hg/mm Hg at normalized time 0.70 of the systolic duration and a maximum of 0.079 +/- 0.029 at the end of RV ejection.(ABSTRACT TRUNCATED AT 250 WORDS)
These results suggest that dilated cardiomyopathy increases systolic but not diastolic interactions, that the pericardium increases diastolic but not systolic ventricular interactions, and that volume loading with and without the pericardium opened increases both systolic and diastolic interactions.
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