in five studies. Interestingly, none of the reviewed studies used computerized cognitive testing methods such as the Cambridge Neuropsychological Test Automated Battery (CANTAB). While these tools have been available for decades, their lack of adoption in cardiovascular studies is notable. Discussion: Despite the known association between CVD and cognitive decline, most observational studies did not include neuropsychological assessments. Those that did tended to focus on
a few cognitive domains, such as memory and processing speed, with a preference for traditional in-person testing. The absence of computerized testing methods, despite their potential advantages, raises questions about awareness and resource allocation in these studies. Future cardiovascular research should consider expanding the use of neuropsychological testing, including computerized tools, to better understand the cognitive impacts of CVD and related conditions.
OLANZAPINE-ASSOCIATED ANGIOEDEMA Elena Karras, Ruona Ebiai, David Yancey, Fareed Beaini, Abdul Khan; The University of Queensland – Ochsner Clinical School, New Orleans, LA.
Introduction: Angioedema often affects the face and oral cavity. When the larynx is involved, swelling may be fatal. Possible mechanisms include bradykinin- mediated, histamine-mediated, and idiopathic. Drugs such as ACE inhibitors, NSAIDs, and calcium- channel blockers are commonly implicated. Rare cases have associated angioedema with olanzapine. Case: An 85-year-old nonverbal woman with dementia, schizophrenia with tardive dyskinesia, and hypertension was brought in from a nursing home for severe tongue and lip swelling. The patient was intubated and sedated due to concerns for impending airway compromise. She had no history of angioedema or anaphylaxis, nor was she on an ACE inhibitor or taking NSAIDs. She had, however, been taking amlodipine for years. One to two months earlier, she had resumed olanzapine after discontinuing it for a year. The physical exam was notable for significant swelling of the tongue and lower lip. Cardiopulmonary auscultation was unremarkable, and there were no rashes nor urticaria. Laboratory results included a normal C4, not consistent with acquired C1 inhibitor deficiency. CT imaging showed no discrete soft tissue mass or fluid collection within the neck.
Olanzapine was held, and the patient was treated with steroids and antihistamines. Although the swelling of the lips and tongue improved over the next ten days, cuff leak tests were variable, despite imaging ruling out involvement of the neck and airway. Ultimately, the patient failed extubation three times. After an extensive hospital course and many goals of care discussions with the family, a tracheostomy and percutaneous endoscopic gastrostomy tube were placed, and the patient was discharged to a long-term acute care facility. Discussion: The pathophysiology of angioedema in this case remains unclear. However, the timing between olanzapine initiation and symptom onset suggests a potential association. Limitations include delayed symptom onset as well as previous olanzapine use. Further, the case is complicated by the patient’s long-term amlodipine use. Finally, the patient’s nonverbal status and dementia limited the ability to obtain a thorough history. Nonetheless, clinicians should remain aware of the potential adverse effects of olanzapine and consider a broad differential diagnosis when evaluating similar presentations.
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