RESUMEN
OBJECTIVE: Sympathetic predominance and ventricular repolarization abnormalities represent epilepsy-associated cardiac alterations and may underlie seizure-induced ventricular arrhythmias. Myocardial ion channel and electrical remodeling have been described early in epilepsy development and may contribute to ventricular repolarization abnormalities and excitability. Using the pilocarpine-induced acquired epilepsy model we sought to examine whether altered myocardial ion channel levels and electrophysiological changes also occur in animals with long-standing epilepsy. METHODS: We examined myocardial adrenergic receptor and ion channel protein levels of epileptic and age-matched sham rats (9-20 months old) using western blotting. Cardiac electrical properties were examined using optical mapping ex vivo and electrophysiology in vivo. We investigated the propensity for ventricular tachycardia (VT) and the effects of ß-adrenergic blockade on ventricular electrical properties and excitability in vivo. RESULTS: In animals with long-standing epilepsy, we observed decreased myocardial voltage-gated K+ channels Kv4.2 and Kv4.3, which are known to underlie early ventricular repolarization in rodents. Decreased ß1 and increased α1A adrenergic receptor protein levels occurred in the myocardium of chronically epileptic animals consistent with elevated sympathetic tone. These animals exhibited many cardiac electrophysiological abnormalities, represented by longer QRS and corrected QT (QTc) intervals in vivo, slower conduction velocity ex vivo, and stimulation-induced VT. Administration of a ß-adrenergic antagonist late in epilepsy was beneficial, as the therapy shortened the QTc interval and decreased stimulation-induced VT. SIGNIFICANCE: Our findings demonstrate that myocardial ion channel remodeling and sympathetic predominance, risk factors for increased ventricular excitability and arrhythmias, persist in chronic epilepsy. The beneficial effects of ß-adrenergic antagonist treatment late in the course of epilepsy suggest that attenuating elevated sympathetic tone may represent a therapeutic target for ameliorating epilepsy-associated cardiac morbidity.
RESUMEN
OBJECTIVES/HYPOTHESIS: External auditory canal (EAC) trauma, although rare, can have significant long-term adverse outcomes. This study aims to investigate the frequency, treatment, and complications of external ear canal injury in association with mandibular and temporal bone trauma. STUDY DESIGN: Retrospective chart review. METHODS: Computed tomography images with mandibular or temporal bone trauma were reviewed for EAC fractures. Patient data were collected from initial presentation and subsequent follow-up clinic visits. RESULTS: Thirty-nine percent of temporal bone fractures and 3.3% of mandible trauma involved the EAC. In particular, 10% of condylar or subcondylar trauma included an EAC fracture (P = 0.0006). One patient sustained bilateral EAC fractures despite an isolated, unilateral condylar fracture. The most common presenting sign was blood in the external auditory canal. Two patients underwent exam under anesthesia and removal of debris and stenting as treatment, whereas 42% of the patients were placed on otic drops and 5% received packing or a stent. Follow-up data were only available for 16% of the patients. Hearing loss from otic capsule involvement or ossicular chain disruption were follow-up complaints, and one patient had persistent canal stenosis. CONCLUSIONS: External auditory canal trauma is present in a significant proportion of mandibular and temporal bone trauma, including both condylar and noncondylar fractures with a higher incidence of condylar fractures. One case was seen with bilateral EAC fractures despite a unilateral mandibular fracture. Complications of these fractures can include hearing loss and canal stenosis; however, additional outpatient follow-up is needed to further elucidate long-term complications and shape treatment recommendations.
