Pharmacological agents such as beta-blockers may reduce the risk of cardiovascular events but are associated with side-effects and may be contra-indicated in some patients. The mechanism of RIPC (remote ischemic preconditioning) may be humoral, neural, or a combination of both, and involves adenosine, opioids, bradykinins, protein kinase C, and K-ATP channels, although the precise end-effector remains unclear. Small studies provide some evidence that RIPC could reduce myocardial injury and other ischemic complications of surgery.Ischemic preconditioning renders the heart resistant to infarction from ischemia/reperfusion. While adenosine couples directly to PKC (protein kinase C) through the phospholipases, bradykinin and opioids do so through a complex pathway that includes in order: phosphatidylinositol 3-kinase (PI3-kinase), nitric oxide synthase, guanylyl cyclase, PKG, opening of mitochondrial KATP channels, and activation of PKC by redox signaling. These kinases are activated as a result of PKC somehow promoting signaling from adenosine A2 receptors early in reperfusion.If an acute myocardial infarction is preceded by preinfarction angina, it results in smaller infarction size, fewer cardiac arrhythmias, and better-left ventricular function. Preconditioning protects the myocardium during coronary artery bypass surgery, particularly in the off-pump procedure, yet the thoracic surgery community has not universally adopted this technique.Although not completely elucidated, the cellular and molecular mechanisms of APC appear to mimic those of ischemic preconditioning, the most powerful endogenous cardioprotective mechanism.