Cardiac contractility modulation for heart failure, such as pacemaker therapy or implantable cardioverter defibrillators (ICD), Cardiac contractility modulation does not affect the cardiac rhythm directly. Rather, the aim is to enhance the heart’s natural contraction (the native cardiac contractility) sustainably over long periods of time. Furthermore, unlike most interventions that increase cardiac contractility, the Cardiac contractility modulation is not associated with an unfavorable increase in oxygen demand by the heart (measured in terms of Myocardial Oxygen Consumption or MVO). This may be explained by the beneficial effect the therapy has in improving cardiac efficiency. A meta-analysis in 2014 and an overview of device-based
Cardiac neural crest cells and GATA families of molecules. In addition to these signaling pathways, these processes are also mediated by environmental factors including blood flow, shear stress, and blood pressure. The CNCCs interact with the cardiogenic mesoderm cells of the primary and secondary heart fields, which are derived from the cardiac crescent and will give rise to the endocardium, myocardium, and epicardium. The CNCCs themselves are the precursors to vascular smooth muscle cells and cardiac neurons. For example, CNCCs are required for the formation of the aorticopulmonary septum (APS) that directs cardiac outflow into two tracts: the pulmonary trunk and the aorta of