Abstract
Epilepsy is a group of neurological disorders characterized by abnormal electrical activity in the central nervous system (CNS) and recurrent seizures representing the principal clinical manifestation. Sudden unexpected death in epilepsy (SUDEP) is the predominant cause of death in young epileptic patients. SUDEP patients displayed an increased cardiovascular (CV) risk, probably due to an impaired autonomic control of CV functions, but the underlying mechanisms need to be explored yet. Therefore, we aimed to examine the cardiac morphological alterations in a pentylenetetrazol (PTZ)-kindled rat model, a well-established tool for studying chronic epilepsy. To complete this, the distance between the atria, between the atrium and ventricle were measured, the heart was weighed, and the pathological morphology of dissected hearts was analyzed by histological assessment with hematoxylin and eosin staining. A significantly decreased distance between atria and a significant increase in heart weight were observed in PTZ-kindled rats which interestingly also displayed increased hemorrhagic content when compared with controls. Our findings provided evidence that changes in cardiac morphology may be related to autonomic CV dysfunctions occurring during SUDEP while also opening up more avenues to better develop novel drugs for the treatment of this disorder.
Highlights
Epilepsy is a group of chronic neurological disorders with a complex etiology and represents one of the most common serious brain conditions, affecting over 70 million people worldwide [1]
3rd and 4th injection, six deaths occurred in the PTZ-treated group
Our results provide evidence that changes in cardiac morphology may be related to autonomic CV dysfunctions in epilepsy
Summary
Epilepsy is a group of chronic neurological disorders with a complex etiology and represents one of the most common serious brain conditions, affecting over 70 million people worldwide [1]. It is clinically characterized by recurrent seizures caused by an imbalance between cerebral excitability and inhibition in the central nervous system (CNS) which may either affect specific brain systems or originate in a restricted area and spread to involve multiple cortical and subcortical circuits [2]. Epidemiological studies have largely reported that people with epilepsy show a higher prevalence of structural cardiac disorder than those without epilepsy [9]
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