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Short periods of myocardial ischemia followed by reperfusion induce a cardioprotective mechanism when the myocardium is subsequently subjected to a prolonged period of ischemia, a phenomenon known as ischemic preconditioning. As well as its application in the myocardium, ischemic preconditioning can also be induced by brief interruptions of blood flow to other organs, particularly skeletal muscle. Transient ischemia induced noninvasively by inflating a cuff on a limb, followed by reperfusion, helps reduce the damage caused to the myocardium by interruption of the coronary circulation. Remote ischemic preconditioning involves activation of humoral and/or neural pathways that open mitochondrial ATP-sensitive potassium channels in the myocardium and close mitochondrial permeability transition pores, making cardiomyocytes less vulnerable to ischemia-induced cell death. This cardioprotective mechanism is now being translated into clinical practice, with positive results in several clinical trials in coronary artery bypass surgery, surgical repair of abdominal aortic aneurysms, valve replacement surgery and percutaneous coronary intervention. However, certain factors weaken the subcellular mechanisms of preconditioning - age, comorbidities, medication, anesthetic protocol - and appear to explain the heterogeneity of results in some studies. Detailed understanding of the pathways involved in cardioprotection induced by ischemic preconditioning is expected to lead to the development of new drugs to reduce the consequences of prolonged ischemia.

Pré-condicionamento isquémico remoto do miocárdio: dos mecanismos fisiopatológicos à aplicação na prática clínica