BACKGROUND: Previous studies in patients and in dogs with experimentally induced heart failure (HF) showed that electrical signals applied to the failing myocardium during the absolute refractory period improved left ventricular (LV) function. We examined the effects these same cardiac contractility modulating (CCM) electrical signals on myocardial oxygen consumption (MVO(2)) in both patients and dogs with chronic HF. METHODS AND RESULTS: Six dogs with microembolizations-induced HF and 9 HF patients underwent CCM leads and generator (OPTIMIZER II) implantation. After baseline measurements, CCM signals were delivered continuously for 2 hours in dogs and for 30 minutes in patients. MVO(2) was measured before and after CCM therapy. In dogs, CCM therapy increased LV ejection fraction at 2 hours (26 +/- 1 versus 31 +/- 2 %, P = .001) without increasing MVO(2) (257 +/- 41 versus 180 +/- 34 micromol/min). In patients, CCM therapy increased LV peak +dP/dt by 10.1 +/- 1.5 %. As with dogs, the increase in LV function after 30 minutes of CCM therapy was not associated with increased MVO(2) (13.6 +/- 9.7 versus 12.5 +/- 7.2 mL O(2)/min). CONCLUSIONS: The study results suggest that unlike cAMP-dependent positive inotropic drugs, the increase in LV function during CCM therapy is elicited without increasing MVO(2).
BACKGROUND: Previous studies in patients and in dogs with experimentally induced heart failure (HF) showed that electrical signals applied to the failing myocardium during the absolute refractory period improved left ventricular (LV) function. We examined the effects these same cardiac contractility modulating (CCM) electrical signals on myocardial oxygen consumption (MVO(2)) in both patients and dogs with chronic HF. METHODS AND RESULTS: Six dogs with microembolizations-induced HF and 9 HF patients underwent CCM leads and generator (OPTIMIZER II) implantation. After baseline measurements, CCM signals were delivered continuously for 2 hours in dogs and for 30 minutes in patients. MVO(2) was measured before and after CCM therapy. In dogs, CCM therapy increased LV ejection fraction at 2 hours (26 +/- 1 versus 31 +/- 2 %, P = .001) without increasing MVO(2) (257 +/- 41 versus 180 +/- 34 micromol/min). In patients, CCM therapy increased LV peak +dP/dt by 10.1 +/- 1.5 %. As with dogs, the increase in LV function after 30 minutes of CCM therapy was not associated with increased MVO(2) (13.6 +/- 9.7 versus 12.5 +/- 7.2 mL O(2)/min). CONCLUSIONS: The study results suggest that unlike cAMP-dependent positive inotropic drugs, the increase in LV function during CCM therapy is elicited without increasing MVO(2).