Administration of cyclosporine, an immunosuppressant, at the time of reperfusion is associated with a smaller infarct by some measures than that seen with placebo, according to a small, pilot trial published in the July 31 issue of the New England Journal of Medicine.
Christophe Piot, MD, from the Hospices Civils de Lyon, Université Claude Bernard in Lyon, France, and colleagues randomly assigned 58 patients who presented with acute STEMI to receive either an intravenous bolus of 2.5 mg of cyclosporine per kilogram of body weight (cyclosporine group) or normal saline (control group) immediately before undergoing PCI.
The investigators assessed infarct size in all patients by measuring the release of creatine kinase and troponin I and in a subgroup of 27 patients by performing MRI on day five after infarction.
Piot and colleagues found that cyclosporine and control groups were similar with respect to ischemia time, the size of the area at risk and the ejection fraction before PCI. The release of creatine kinase was significantly reduced in the cyclosporine group as compared with the control group, and the release of troponin I was not significantly reduced, according to the researchers.
On day five, the authors wrote that the absolute mass of the area of hyperenhancement (i.e., infarcted tissue) on MRI was significantly reduced in the cyclosporine group as compared with the control group, with a median of 37 g (interquartile range, 21 to 51) versus 46 g (interquartile range, 20 to 65).
The investigators noted that they did not detect any adverse effects of cyclosporine administration.
Piot and colleagues concluded that “these data are preliminary and require confirmation in a larger clinical trial.” Notably, they also wrote that the clinical significance of the reduction of creatine kinase and delayed hyperenhancement on MRI with cyclosporine needs to be defined by assessing meaningful differences in endpoints such as death, recurrent MI and heart failure on follow-up.