Novel Therapeutic Targets to Improve Neurologic Outcome in Cardiac Arrest

Dear Colleagues,

Neurologic disability causes a high degree of morbidity in cardiac arrest survivors. Ischemic reperfusion is considered to trigger a complex cascade of pro-inflammatory and pro-thrombotic events, which impair microvascular perfusion and contribute to secondary neurologic damage. Lack of knowledge of the exact molecular mechanisms and pathways driving post-resuscitative neurologic damage, however, limit current post-resuscitation care to unselective targeted temperature management and no specific treatment strategies are available to diminish secondary organ damage. The potential of post-resuscitation care to improve neurologic outcome is yet to be realized. Timely targeted interventions could offer the opportunity to alleviate or even interrupt early organ damage cascades triggered by ischemia and/or reperfusion after or even during cardiac arrest. There is a pressing need to identify molecular structures, which have the potential to serve as future therapeutic targets in cardiac arrest survivors to prevent neurologic damage and improve outcome.

This Special Issue, “Novel therapeutic targets to improve neurologic outcome in cardiac arrest”, welcomes all basic and clinical research on molecular mechanisms and pathways involved in neurologic damage after cardiac arrest, which may serve as novel therapeutic targets in the future.

Dr. Michael Schwameis
Guest Editor

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