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
Heart rate levels have a great impact on heart rate and contractility: increased calcium levels cause an increase in both. High levels of calcium ions result in hypercalcemia and excessive levels can induce cardiac arrest. Drugs known as calcium channel blockers slow HR by binding to these channels and blocking or slowing the inward movement of calcium ions. Caffeine and nicotine are both stimulants of the nervous system and of the cardiac centres causing an increased heart rate. Caffeine works by increasing the rates of depolarization at the SA node, whereas nicotine stimulates the activity of the sympathetic neurons that deliver impulses