BACKGROUND: Nonexcitatory electrical, signals termed cardiac contractility modulation (CCM) have been shown to improve contractile force of isolated papillary muscles. In this study, we examined the effects of CCM signal delivery on left ventricular function in dogs with chronic heart failure (HF). METHODS AND RESULTS: Chronic HF (ejection fraction </=35%) was produced in 7 dogs by intracoronary microembolizations. The CCM signal was delivered during the absolute refractory period using a lead implanted in the anterior coronary vein. A right ventricular and an atrial lead were implanted and used for timing of the CCM signal delivery. Hemodynamic measurements were made at baseline and at 1, 2, 3, 4, 5, and 6 hours after initiating CCM signal delivery. Ejection fraction increased from 31 +/- 1% at baseline to 41 +/- 1% at 1 hour (P <.05), 42 +/- 1% at 3 hours (P <.05), and 44 +/- 2% at 6 hours (P <.05). Similarly, stroke volume increased from 26 +/- 2 mL to 31 +/- 3 mL at 1 hour (P <.05), 33 +/- 3 mL at 3 hours (P <.05), and 34 +/- 3 mL at 6 hours (P <.05). There were no significant changes compared to baseline in ejection fraction or stroke volume in 5 HF control dogs studied for up to 4 hours. CONCLUSION: In dogs with HF, CCM signal delivery for 6 hours elicited marked improvement in LV function. This novel approach may represent a useful adjunctive therapy for the treatment of patients with HF.
BACKGROUND: Nonexcitatory electrical, signals termed cardiac contractility modulation (CCM) have been shown to improve contractile force of isolated papillary muscles. In this study, we examined the effects of CCM signal delivery on left ventricular function in dogs with chronic heart failure (HF). METHODS AND RESULTS:Chronic HF (ejection fraction </=35%) was produced in 7 dogs by intracoronary microembolizations. The CCM signal was delivered during the absolute refractory period using a lead implanted in the anterior coronary vein. A right ventricular and an atrial lead were implanted and used for timing of the CCM signal delivery. Hemodynamic measurements were made at baseline and at 1, 2, 3, 4, 5, and 6 hours after initiating CCM signal delivery. Ejection fraction increased from 31 +/- 1% at baseline to 41 +/- 1% at 1 hour (P <.05), 42 +/- 1% at 3 hours (P <.05), and 44 +/- 2% at 6 hours (P <.05). Similarly, stroke volume increased from 26 +/- 2 mL to 31 +/- 3 mL at 1 hour (P <.05), 33 +/- 3 mL at 3 hours (P <.05), and 34 +/- 3 mL at 6 hours (P <.05). There were no significant changes compared to baseline in ejection fraction or stroke volume in 5 HF control dogs studied for up to 4 hours. CONCLUSION: In dogs with HF, CCM signal delivery for 6 hours elicited marked improvement in LV function. This novel approach may represent a useful adjunctive therapy for the treatment of patients with HF.