Background: Glycoprotein IIB/IIIA inhibitors are occasionally utilized during carotid artery stenting (CAS) in the presence or absence of a visualized intra-operative thrombus.Objective: We assess the hemorrhagic and clinical outcomes associated with the use of eptifibatide during CAS.Methods: A retrospective analysis of prospectively collected data on patients with the diagnosis of carotid artery stenosis underwent CAS in a single center. We identified those who received intravenous eptifibatide intra-operatively and compared to the rest of the cohort. Hemorrhagic outcomes included intracerebral hemorrhage (ICH) or groin hematoma that occurred during the hospital stay.Results: In this analysis, 81 patients had CAS during a 3-year span; 16 of those had received 15 mg of intravenous eptifibatide intra-operatively. The mean age of the treated and untreated patients was similar (65.6 ± 13.4 versus 65.4 ± 10.2; P = 0.13). One patient (1.2%) in this series had ICH in the perioperative period that occurred in the non-eptifibatide group. Five patients (6.2%) in this series had groin hematoma; only one in the non-eptifibatide group required surgical repair. No mortality was reported and clinical outcomes including discharge modified Rankin scale, NIH stroke scale, as well as discharge destination were similar in both groups. A stratified analysis among those who underwent an urgent CAS showed no significant differences in the risks of hemorrhages or any clinical outcome (P > 0.05).Conclusion: The use of eptifibatide during CAS is safe. The risk of any hemorrhagic complication is rare in this series; however, a prospective study to validate this observation will be helpful.
Central etiologies of bilateral vocal cord paralysis leading to respiratory stridor are uncommon, as they require bilateral disruption of the laryngeal motor fibers. Here we present a young woman with multiple vascular risk factors, including ischemic stroke in the right medulla occurring 3 months prior, who presented with acute inspiratory stridor. All respiratory parameters were normal including arterial blood gas, and neck and pulmonary imaging. Direct laryngoscopy showed bilaterally bowed vocal cords, with decreased mobility and paradoxical adduction with each inspiratory cycle. On the third hospital day, neurological signs including a right hemiparesis became evident. Brain magnetic resonance imaging showed a diffusion restriction in the left medial pons likely disrupting the laryngeal motor fibers to the ponto‐medullary neuronal network. In the absence of tracheobronchial obstruction, physicians should be alert to the central causes of stridor including ischemic stroke. Additionally, paradoxical movements of the vocal cords can be an ominous sign.
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