Cardiac Contractility Modulation for Advanced Heart Failure

Abstract

Heart failure with reduced ejection fraction (HFrEF) is a major health burden affecting over 13 million people worldwide. Despite emergence of novel pharmacotherapies, it remains a condition with high mortality and morbidity. Currently, guidelines recommend cardiac resynchronization therapy (CRT) for the treatment of medically refractory HFrEF associated with widened QRS on ECG. However, clinical benefits of CRT do not extend to the majority of HFrEF patients who have no significant intraventricular conduction delay. In addition, even in those who fulfilled the stringent criteria for CRT implantation, two-thirds do not respond to therapy. Cardiac contractility modulation (CCM) is a device-based therapy that involves administration of non-excitatory electrical impulses to the right ventricular septum during the absolute refractory period. Studies have shown that these electrical impulses increase cytosolic calcium and regulates local gene expression, resulting in an improved functional capacity and reduces hospitalization in those with symptomatic HFrEF. In this presentation, we summarize the pathophysiological mechanisms, clinical data, potentials and limitations of CCM. Heart failure with reduced ejection fraction (HFrEF) is a major health burden affecting over 13 million people worldwide. Despite emergence of novel pharmacotherapies, it remains a condition with high mortality and morbidity. Currently, guidelines recommend cardiac resynchronization therapy (CRT) for the treatment of medically refractory HFrEF associated with widened QRS on ECG. However, clinical benefits of CRT do not extend to the majority of HFrEF patients who have no significant intraventricular conduction delay. In addition, even in those who fulfilled the stringent criteria for CRT implantation, two-thirds do not respond to therapy. Cardiac contractility modulation (CCM) is a device-based therapy that involves administration of non-excitatory electrical impulses to the right ventricular septum during the absolute refractory period. Studies have shown that these electrical impulses increase cytosolic calcium and regulates local gene expression, resulting in an improved functional capacity and reduces hospitalization in those with symptomatic HFrEF. In this presentation, we summarize the pathophysiological mechanisms, clinical data, potentials and limitations of CCM.