Myocardial injury in adult, pediatric, and newborn patients is a leading cause of mortality and morbidity. Although the underlying etiologies are different among patient populations, the sequence of initial ischemic-hypoxic injury followed by secondary
myocardial reperfusion injury is relatively consistent. Overall
infarct size is important because it is believed to be a key determinant of mortality. The detrimental effects of myocardial reperfusion have been proposed to be at least partially related to the formation of
mitochondrial permeability transition pore (MPTP). The
MPTP is a nonspecific pore, which forms during myocardial reperfusion and allows the release of apoptotic signaling molecules and may also lead to cellular
necrosis.
Cyclosporine A has been shown to be a potent inhibitor of the
MPTP, leading to its study as a potential treatment to limit
myocardial reperfusion injury. Multiple adult animal models have demonstrated the protective effects of
cyclosporine in
ischemia-reperfusion. A recent human pilot clinical trial also reported reduced myocardial injury and
infarct size in patients treated with
cyclosporine intravenously before
percutaneous coronary intervention for
ST-elevation myocardial infarction. Despite the paucity of evidence of
cyclosporine A demonstrating myocardial protection in pediatric and newborn patients, the existing animal experimental results are promising.