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 action potential membrane potential Ionic pumps as discussed above, like the sodium-calcium exchanger and the sodium-potassium pump restore ion concentrations back to balanced states pre-action potential. This means that the intracellular calcium is pumped out, which was responsible for cardiac myocyte contraction. Once this is lost the contraction stops and myocytic cells relax, which in turn relaxes the heart muscle. During this phase, the action potential fatefully commits to repolarisation. This begins with the closing of the L-type Cachannels, while the K channels (from phase 2) remain open. The main potassium channels involved in repolarization are the delayed rectifiers (I) and (I)