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 excitation-contraction coupling into the cell. Secondly Ca indirectly activates proteins, called myofilaments, resulting in muscle contraction. The two main myofilaments in cardiac (and skeletal) muscle are actin and myosin. Ca binds to a protein called troponin, which is bound to the actin filament. This binding causes a shape change in the troponin which exposes areas on the actin, to which the head of the myosin filament binds. The binding of the myosin head to actin is known as a cross-bridge. A molecule, called adenosine triphosphate (ATP) which is produced by an intracellular structure called a mitochondrion, is then used, as a source