Heart failure (HF) is a debilitating disease that refers to a clinical syndrome in which an abnormality of cardiac function causes a below normal cardiac output that can fall below a level adequate to meet the metabolic demand of peripheral tissues. Heart failure can be due to a variety of etiologies with ischemic heart disease being the most common. Heart failure is usually treated with a drug regimen designed to augment cardiac function and/or relieve congestive symptoms.
Electrostimulation of the ventricles can also be useful in treating heart failure. It has been shown that some heart failure patients suffer from intraventricular and/or interventricular conduction defects (e.g., bundle branch blocks) such that their cardiac outputs can be increased by improving the synchronization of ventricular contractions with electrical stimulation. In order to treat these problems, implantable cardiac devices have been developed that provide appropriately timed electrical stimulation to one or more heart chambers in an attempt to improve the coordination of atrial and/or ventricular contractions, termed cardiac resynchronization therapy (CRT). Ventricular resynchronization is useful in treating heart failure because, although not directly inotropic, resynchronization can result in a more coordinated contraction of the ventricles with improved pumping efficiency and increased cardiac output. Currently, a most common form of CRT applies stimulation pulses to both ventricles, either simultaneously or separated by a specified biventricular offset interval, and after a specified atrio-ventricular delay interval with respect to the detection of an intrinsic atrial contraction or delivery of an atrial pace.
It has also been demonstrated that electrostimulatory pulses delivered to the heart during its refractory period can augment myocardial contractility. Applying contractility augmenting stimulation to the ventricles can thus aid in the treatment of heart failure. Such stimulation, sometimes referred to as cardiac contractility modulation (CCM), can be delivered during the refractory period after an intrinsic contraction and hence is non-excitatory. Presumably, such stimulation increases myocardial contractility by increasing intracellular calcium concentration and/or eliciting release of neurotransmitters.