Cardiac arrest (CA) with return of spontaneous circulation is associated with high mortality, exceeding 90% in out-of-hospital settings and approaching 50% in in-hospital settings. Despite management of the underlying cause of CA, patients often die from post-anoxic brain injury or from ischemia-reperfusion injury occurring after reperfusion and reoxygenation, which increases oxidative stress and leads to multi-organ failure. To date, no effective therapeutic strategy has been established in humans to limit these ischemia-reperfusion injuries. GC7 (N1-guanyl-1,7 diaminoheptane) has demonstrated a strong protective potential against ischemia reperfusion injury in rodent and porcine models, including myocardial infarction, stroke, and renal transplantation. These protective effects are attributed to the pleiotropic action of GC7 which renders cells and tissues energetically less dependent on oxygen, and reduces oxidative stress which play a major role in ischemia reperfusion injury. Degree of blood acidification and immune dysregulation may also represent parameters that GC7 could potentially influence. Although no adverse effects have been reported in these experimental models, GC7 has not yet been studied in human. Our study therefore aims to demonstrate the protective effect of GC7 on blood cells in patients after CA by evaluating oxidative stress levels, blood acidification and inflammatory profile.

Inclusion Criteria:

• Cardiac arrest as the primary reason for hospital admission
• Admission < 48 hours
• Age ≥ 18 years
• Affiliated with a social security system

Exclusion Criteria:

• Limitation or withdrawal of life-sustaining therapies prior to study screening
• Prior cardio-vascular ischemic event (> 24h) before cardiac arrest
• Patient deprived of liberty