Small Molecules That Improve Post-cardiac Arrest Outcomes by Protecting Against Mitochondrial Damage



    • Post-CPR cardiogenic shock is associated with hemodynamic instability and poor neurological outcomes. The pathophysiology is unknown and current treatment approaches merely restore basal cardiac function and do not protect against longer term damage. 
    • The inventors demonstrated that the main mechanism leading to post-CPR cardiogenic shock is myocardial stunning, which is specifically caused by mitochondrial damage. This mitochondrial damage is perpetuated by decreased electron transport chain complex I function, and the associated formation of reactive oxygen species (ROS) by leaked electrons. 
    • The invention is a novel treatment method of improving post-CPR outcomes in cardiac arrest patients by administering an inhibitor of electron transport chain complex I superoxide (S1QEL). The treatment inhibits electron leaks, thereby blocking the production of ROS and associated myocardial stunning. 
    • In in vivo proof of concept experiments with a murine model of asystolic cardiac arrest, the inventors showed that post-CPR administration of 10uM of S1QEL was able to improve myocardial contractility, neurological function, and overall survival rate (74% for treated mice vs 30% for un-treated mice).



    Survival curve following cardiac arrest for mice treated with the S1QEL (CA+S, dotted line) and mice treated with the vehicle control (CA, solid line).





    • Addresses a novel mechanism of action for cardiogenic shock
    • Reduces neurological damage
    • Overall improvement of long-term outcomes following post-CPR



    • Cardiology
    • Critical care and emergency medicine










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