| Description |
Status epilepticus (SE), which is characterized by any prolonged and sustained seizure without recovery of consciousness, increases mortality risk during SE and in the 30-day period following seizure cessation. Moreover, these seizures produce intense activation of the sympathetic nervous system (SymNS), diffuse myofilament damage, cardiac dysregulation, and autonomic nervous system (ANS) imbalance. It is proposed that these physiological effects of SE contribute to cardiac contractile dysfunctions, arrhythmias, and sudden death subsequent to seizure cessation. Indeed, clinical reports have indicated an increased occurrence of ventricular arrhythmias at the time of death in SE patients, although the mechanism has not been elucidated. Potentially, a sympathetically mediated mechanism may result in a reversible cardiac dysfunction called cardiac stunning, which persists after a cardiac insult, leaving only subtle myofilament damage with normal blood flow. Neurogenically mediated cardiac stunning results from prolonged sympathetic activation and hypersecretion of catecholamines, which over-stimulate adrenoceptors on cardiac myocytes and induces tachycardic ischemia. These changes cause diffuse myocyte damage, increased susceptibility to arrhythmias, and persistent risk of sudden cardiac death following the insult. We propose that a similar mechanism(s) may occur during SE, whereby prolonged seizure -induced sympathetic activation produces catecholamine mediated tachycardic ischemia, arrhythmias, myocardial stunning and ultimately an increased risk for mortality. Understanding how SE damages the heart and alters normal cardiac function may allow development of treatment paradigms and pharmacotherapeutic strategies to reduce cardiac morbidity and mortality following SE. |
