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 In the SAN cAMP binds to an ion channel involved in action potential initiation, speeding up the production of the action potential (see sinoatrial node for more detail). cAMP also, activates a protein called protein kinase A (PKA). PKA affects both the DHPR and RyR, increasing the rise in Ca within the contractile cells and therefore increasing rate of muscle contraction. PKA also affects the myofilaments as well as a protein called phospholamban (PLB; see sarcoplasmic reticulum for more details), speeding up the rate of Cadecline in the cell and so speeding up muscle relaxation. Parasympathetic nerves work by releasing