Cardiac contractility modulation (CCM) is a device-based therapy that involves delivery of nonexcitatory electrical signals resulting in improved ventricular function and a reversal of maladaptive cardiac fetal gene programmes. Our aim was to evaluate whether acute application of CCM leads to an increase in myocardial oxygen consumption (MVO2) in patients with chronic heart failure using 11C-acetate positron emission tomography (PET).Methods
We prospectively enrolled 21 patients with severe heart failure. 11C-acetate PET was performed before and after activation of the CCM device. In 12 patients an additional stress study with dobutamine was performed.Results
Under resting conditions, the values of myocardial blood flow (MBF), MVO2 and work metabolic index (WMI, reflecting myocardial efficiency) with the CCM device activated did not differ significantly from the values with the device deactivated. MBF was 0.81 ± 0.18 ml min-1 g-1 with the device off and 0.80 ± 0.15 ml min-1 g-1 with the device on (p = 0.818), MVO2 was 6.81 ± 1.69 ml/min/100 g with the device off and 7.15 ± 1.62 ml/min/100 g with the device on (p = 0.241) and WMI was 4.94 ± 1.14 mmHg ml/m2 with the device off and 5.21 ± 1.36 mmHg ml/m2 with the device on (p = 0.344). Under dobutamine stress, the values of MBF, MVO2 and WMI with the CCM device activated did not differ from the values with the device deactivated, but were significantly increased compared with the values obtained under resting conditions.Conclusion
These results indicate that CCM does not induce increased MVO2, even under stress conditions.