The effects of ventricular pacing on left ventricular (LV) dynamic geometry, function, and myocardial oxygen consumption (MVO2) were measured in 12 conscious dogs using sonomicrometry, micromanometry, ultrasonic flow probes, and oximetry catheters during right atrial (A-) and right ventricular (V-) pacing at 150 beats/min. Systolic function was quantified using slopes (MW) and volume-intercepts (VW) of linear relationships between end-diastolic volume (EDV) and stroke work (SW) for data obtained during vena caval occlusion. V-pacing shifted SW-EDV relationships downward (MW decreased from 97 +/- 21 to 81 +/- 21 Kerg/mL) and to the right (VW increased from 14 +/- 11 to 20 +/- 12 mL) in comparison with A-pacing (P < 0.02). These functional changes correlated with altered contractile geometry manifest as early shortening in the septal free wall relative to anterior-posterior dimension (increased minor axis mid-wall eccentricity at end-diastole and begin-ejection). Steady-state LV power output decreased from 802 +/- 213 mW during A-pacing to 514 +/- 170 mW during V-pacing (P < 0.05), while MVO2 remained relatively unchanged during V-pacing (10 +/- 3 mL O2/min vs 11 +/- 3 mL O2/min during A-pacing, P = NS). As a result, overall LV efficiency decreased from 0.24 +/- 0.08 during A-pacing to 0.16 +/- 0.06 during V-pacing (P < 0.05). These data illustrate the impact of V-pacing on dynamic LV geometry and function, including impaired LV work output at all physiological levels of preload. Most importantly, the relationship between LV work output and MVO2 is depressed during V-pacing, emphasizing the interaction between LV mechanics and pump efficiency in intact subjects. As a result, measures taken to restore normal contractile geometry might improve LV efficiency and performance when V-pacing is necessary.

Background: To date, no data exist on the linearity and, therefore, the usefulness of the preload recruitable stroke work (PRSW) and end-systolic pressure-volume (ESPVR) relationships during acute afterload changes in heart failure. Aims: Our aim was, therefore, to characterize both relationships in a model of ventricular pacing induced heart failure at baseline and during acute changes in afterload. Methods: Dynamic left ventricular volume and transmural pressure were measured in 10 conscious dogs using sonomicrometry and micromanometry under control conditions and during heart failure produced by 3 weeks of rapid right ventricular pacing. Afterload was varied from baseline with intravenous infusions of nitroprusside and phenylephrine. Left ventricular function was assessed using the PRSW and ESPVR relationships. Results: Cardiac output demonstrated a linear inverse relationship with afterload in both normal and failing hearts (r )0.5, P-0.001) with failure producing a parallel, downward 2 shift of the afterload (x) vs. cardiac output (y) relationship (P-0.01). Yet, afterload variation did not affect PRSW or ESPVR relationships in either normal or failing hearts (r -0.12, P)0.05). Conclusion: Thus, the PRSW and ESPVR relationships are 2 insensitive to acute afterload changes in both failing and normal hearts, and the failing left ventricle is no more afterload-sensitive than the normal heart.