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GIPS-IV trial

Preservation of myocardial function after myocardial infarction

In the past decades, as a result of advances in pharmacological, reperfusion and preventive strategies, prognosis of patients with ST-elevated myocardial infarction has substantially improved and mortality has decreased. However, permanent myocardial injury related to the ischemia and subsequent reperfusion is still observed in the vast majority of patients and harbors a risk of heart failure development. Although many advances have been made, there is no specific treatment that targets myocardial reperfusion injury, which is considered to be a paradoxical form of myocardial damage that occurs as a result of the restoration of vessel patency. Reducing myocardial reperfusion injury is expected to further decrease infarct size, decreasing adverse cardiac remodeling and improving cardiac function as well as clinical outcome.

H2S has been shown to protect from (myocardial) ischemia reperfusion injury in various experimental models. It reduces infarct size and attenuates the loss of cardiac function. Inhibition of leukocyte endothelial cell interactions, neutralization of reactive oxygen species (ROS) and the reduction of apoptotic signaling were all suggested as mechanisms underlying the cardioprotective effect of H2S. The H2S donor sodium thiosulfate (STS) is already administered to humans for many years for calciphylaxis and cyanide poisoning. Recently, we demonstrated that STS is well tolerated in patients presenting with acute coronary syndrome.

The GIPS-IV study, designed by our group, will be the first study to determine the efficacy of a H2S-donor to reduce myocardial infarct size in patients with ST-elevated myocardial infarction. Currently, recruitment has completed. First results are expected fall 2021.

“We are good at restoring the coronary blood flow via percutaneous interventions. However, usually the oxygen shortage has already caused damage to the cardiac muscle. In our hospital we are testing new strategies to improve the response of the heart to oxygen shortages.”

People involved