Ranolazine for cardiac arrest: moving from ex vivo studies to clinical relevant in vivo models
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Abstract
Despite successful cardiopulmonary resuscitation (CPR), the majority of patients succumb to post-resuscitation myocardial and cerebral dysfunction. Early post-resuscitation periods are marked by ventricular arrhythmias and severe myocardial dysfunction, often driven by cytosolic and mitochondrial calcium overload. The Ranolazine Implantable Cardioverter-Defibrillator (RAID) trial demonstrated that ranolazine reduces ventricular tachycardia (VT) burden by modulating intracellular calcium through sodium current inhibition. While these findings suggest a potential role for ranolazine in managing cardiac arrest (CA), our investigations in a rat model indicate that pretreatment with ranolazine improves CA outcomes, including defibrillation success and post-resuscitation myocardial function. However, administering ranolazine post-resuscitation unexpectedly increased mortality, likely due to severe hypotension. These results underscore the need for further studies to assess ranolazine’s therapeutic viability and safety in CA treatment.