Document Type

Conference Proceeding

Publication Date

5-2-2025

Abstract

Introduction: Stroke is the leading cause of long-term disability, with most cases being ischemic. In patients aged 18–60 years, patent foramen ovale (PFO) is implicated in 10% of strokes. Pathophysiologies include paradoxical thromboembolism and thrombus formation in the PFO, leading to cerebral or systemic embolism. Cancer is a comorbidity in 5–10% of patients with acute stroke, with mechanisms such as direct tumor effects, coagulopathy, and cancer therapy. Two common inherited thrombophilia predisposing to deep vein thrombosis (DVT) are Factor V Leiden (FVL) and G20210A Prothrombin gene mutation (PTM). FVL results in poor anticoagulant response to activated Protein C, while PTM increases prothrombin mRNA expression, causing hypercoagulation. Genetic testing via PCR is the gold standard for diagnosing these mutations. Case Report: A 51-year-old female with a history of DVT, diagnosed one week earlier at another hospital, presented with slurred speech. She was last known well the night before symptom onset and denied chest pain, shortness of breath, or palpitations. She was neither a smoker nor using oral contraceptives. At presentation, her NIHSS score was 2 out of 42. Head CT ruled out intracranial hemorrhage, but tissue plasminogen activator (tPA) was not administered due to a low NIHSS score and presentation beyond 4.5 hours therapeutic window. Given her recent DVT, embolic stroke was suspected, and IV heparin was initiated alongside hypercoagulable workup. Transthoracic echocardiogram revealed a PFO, with an ejection fraction of 60% and no left atrial or ventricular thrombus. Transesophageal echocardiogram confirmed the PFO, and brain MRI revealed acute infarction in bilateral superior frontal, parietal, and occipital lobes, consistent with an embolic source involving multiple vascular territories. The patient was transitioned to apixaban upon discharge after a 5-day IV heparin course. Loading dose of apixaban was given upon discharge and the patient was advised to transition to maintenance dose after 7 days. Genetic testing revealed heterozygous FVL and G20210A PTM mutations. Post-discharge, she experienced heavy vaginal bleeding requiring repeated hospital admissions for anemia and blood transfusions. Endometrial biopsy concerned hyperplasia. CT abdomen identified a right adnexal mass, with biopsy confirming high-grade serous carcinoma of the ovary. During this period, she underwent surgical PFO closure and began chemotherapy for ovarian cancer. Discussion: Persistent PFO is causally linked to 10% of ischemic strokes in patients aged 18–60 years. In this case, the hypercoagulable state from genetic mutations and malignancy led to an embolic stroke via the PFO. Closure of the PFO was performed to prevent recurrent embolic events. This case emphasizes the importance of evaluating for underlying malignancies in patients with unprovoked DVT and ischemic stroke. The co-occurrence of genetic thrombophilia further complicated the patient’s prothrombotic state. Conclusion: Approaching an acute ischemic stroke patient, persistent PFO and underlying malignancy must always be kept in the differential diagnosis, even if patients are presenting with genetic mutations that predispose them to hypercoagulable states. Understanding the underlying cause of an ischemic stroke can help providers address stroke prophylaxis, which may include surgical closure of PFO.

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American College of Physicians Michigan Chapter and Society of Hospital Medicine Michigan Chapter Resident and Medical Student Day, May 2, 2025, Troy, MI

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