Left ventricular thrombus recurrence after anticoagulation discontinuation.

Background: Evidence regarding the duration of anticoagulation (AC) therapy for left ventricular thrombus (LVT) is lacking. This study aims to evaluate the rate and risk factors for LVT recurrence in patients with Anterior ST-Segment elevation Myocardial Infarction (STEMI) complicated by LVT. Methods: This was a retrospective analysis of patients with Anterior STEMI complicated by LVT and reduced ejection fraction (<35 %) from 2010 to 2020. Patients with atrial fibrillation and hypercoagulable state were excluded. Recurrence of LVT was defined as a new LVT on transthoracic echocardiography (TTE) after interval resolution and AC discontinuation. Demographics, comorbidities, guideline directed medical therapy, TTE, and angiographic characteristics were assessed and compared in patients with and without LVT recurrence. Results: 87 patients met the inclusion criteria. Nine (10.3 %) had LVT recurrence of which three (33.3 %) had cardioembolic events. More patients with recurrence had ventricular aneurysm/scarring (33 % vs 10.3 %) and multi-vessel disease (22.2 % vs 9 %). Conclusion: This study reveals that a portion of patients with Anterior STEMI complicated by LVT are at a higher risk of recurrence after initial resolution and AC discontinuation. Larger prospective trials are needed to re-address the appropriate duration of anticoagulation.

Neonatal exposure to monosodium glutamate results in impaired auditory brainstem structure and function.

Excitotoxic injury during the neonatal period has been shown to result in neurodegenerative changes in several different brain regions. Exposure to monosodium glutamate (MSG) during the first two postnatal weeks results in glutamate neurotoxicity in the cochlea and has been shown to result in damage to cochlear hair cells and fewer neurons in the spiral ganglion. Further, we have shown that such exposure results in fewer neurons in the cochlear nucleus and superior olivary complex and abnormal expression of the calcium binding proteins calbindin and calretinin. Based on these findings, we hypothesized that neonatal MSG exposure would result in loss of neurons at more rostral levels in the auditory brainstem, and this exposure would result in abnormal brainstem auditory evoked potentials. We identified a significantly lower density of neurons in the spiral ganglion, heterogenous loss of neurons in the globular bushy cell-trapezoid body circuit, and fewer neurons in the nuclei of the lateral lemniscus and central nucleus of the inferior colliculus. The most severe loss of neurons was found in the inferior colliculus. Click-evoked auditory brainstem responses revealed significantly higher thresholds and longer latency responses, but these did not deteriorate with age. These results, together with our previous findings, indicate that neonatal exposure to MSG results in fewer neurons throughout the entire auditory brainstem and results in abnormal auditory brainstem responses.

Auditory Midbrain Hypoplasia and Dysmorphology after Prenatal Valproic Acid Exposure.

Prenatal exposure to the antiepileptic valproic acid (VPA) is associated with an increased risk of autism spectrum disorder (ASD) in humans and is used as an animal model of ASD. The majority of individuals with ASD exhibit adverse reactions to sensory stimuli and auditory dysfunction. Previous studies of animals exposed to VPA reveal abnormal neuronal responses to sound and mapping of sound frequency in the cerebral cortex and hyperactivation, hypoplasia and abnormal neuronal morphology in the cochlear nuclei (CN) and superior olivary complex (SOC). Herein, we examine the neuronal populations in the lateral lemniscus and inferior colliculus in animals exposed in utero to VPA. We used a combination of morphometric techniques, histochemistry and immunofluorescence to examine the nuclei of the lateral lemniscus (NLL) and the central nucleus of the inferior colliculus (CNIC). We found that the VPA exposure resulted in larger neurons in the CNIC and the dorsal nucleus of the lateral lemniscus (DNLL). However, we found that there were significantly fewer neurons throughout all nuclei examined in the auditory brainstem of VPA-exposed animals. Additionally, we found significantly fewer calbindin-immunopositive neurons in the DNLL. VPA exposure had no impact on the proportions of perineuronal nets in the NLL or CNIC. Finally, consistent with our observations in the CN and SOC, VPA exposure resulted in fewer dopaminergic terminals in the CNIC. Together, these results indicate that in utero VPA exposure significantly impacts structure and function of nearly the entire central auditory pathway.