Myocardial oxidative metabolism, blood flow and efficiency in rapid pacing induced heart failure in dogs.
Heart failure is the final common pathway for most forms of heart disease, and is characterized by a reduced energy status. Myocardial oxygen consumption (MV02) is closely related to the main determinants of systolic function (heart rate, pressure and contractility). The aim of the study was to compare myocardial blood flow, metabolism and mechanical efficiency in rapid pacing induced heart failure in dogs.5 dogs were paced for 3 weeks at 240 bpm, with regular follow up of hemodynamic characteristics. Coronary blood flow and oxidative metabolism were evaluated with [(15)O] water and [(11)C]acetate clearance respectively, in baseline conditions (B) and after 3 weeks of rapid pacing (3 wk RP) using positron emission tomography.Three weeks of rapid pacing in a dog model resulted in a severely depressed left ventricular function (LV dP/dtmax 3698 ± 314 mmHg (B) vs. 1365 ± 103 mmHg (3 wk RP)). On the contrary myocardial blood flow 1.29 ± 0.11 ml/min/g (B) vs. 1.05 ± 0.07 ml/min/g (3 wk RP) and oxidative metabolism 0.178 ± 0.1 min(-1) (B) vs. 0.161 ± 0.1 min(-1) (3 wk RP) remained essentially unchanged, indicating a reduced efficiency and a change in O2 utilization.Heart failure induced by rapid ventricular pacing in dogs provokes a clearly reduced mechanical efficiency, illustrating the occurrence of a metabolic remodeling in heart failure induced by rapid pacing.