Hadziahmetovic, U.

Introduction Hypoplastic left heart syndrome and Fontan procedure predispose to cardiac thrombus formation in the venous pathways due to the unique hemodynamic and hematologic disturbances inherent to the Fontan circulation. Systemic venous blood is routed passively to the pulmonary arteries without a subpulmonary pump, resulting in chronic low‐velocity flow, elevated central venous pressure, and venous stasis—all elements of Virchow's triad that favor clot formation 1 . Additionally, these patients exhibit reduced levels of protein C, coagulation factors II, V, VII, and X, plasminogen, and antithrombin III, along with increased levels of factor VIII 2,3 . Once a thrombotic event occurs, the rationale for lifelong anticoagulation is compelling. We report a case of an adult man that underwent Fontan palliation in infancy, with acute cerebral and renal infarcts, and discuss stroke and systemic embolism prevention. Case presentation A 22‐year‐old male with history of hypoplastic left heart syndrome status post Fontan procedure in infancy with congestive splenomegaly and liver disease presented with acute abdominal pain and was found to have bilateral renal infarcts. Anticoagulation was not initiated acutely and within 24 hours he developed left face and arm weakness, dysarthria and mild aphasia. Intravenous Tenecteplase was administered within 1 hour of symptom onset and was followed by symptoms’ complete resolution within 30 minutes of administration. Brain MRI confirmed scattered cerebral infarcts in the bilateral middle cerebral artery territories. Transthoracic echocardiogram showed atrial level shunting, expected due to fenestrated IVC to left atrium from prior Fontan procedure, and no evidence of atrial or ventricular thrombus. Due to the patient having evidence of multiple infarcts in multiple vascular beds within the brain and kidneys, an extensive hypercoagulable workup was undertaken which was unremarkable. The patient's stroke etiology was presumed to be cardioembolic from his altered cardiac anatomy with susceptibility to form venous thrombi and known surgically‐induced atrial level shunt. Low intensity heparin drip without bolus was started initially, and was transitioned to therapeutic apixaban upon discharge with proposed life long anticoagulation. Conclusions Subjects with hypoplastic heart syndrome display persistent unfavorable hemodynamics and procoagulant state after Fontan procedure. Either antiplatelet or anticoagulants are recommended after performing risk stratification. In high‐risk patients (recent thromboembolic event or stent, recurrent atrial arrhythmias, mechanical valve), therapeutic anticoagulation with either warfarin or direct oral anticoagulant is indicated, given increased vulnerability to recurrent events 1 . In intermediate‐risk subjects, antiplatelet or prophylactic doses of anticoagulation is indicated, whereas in low‐risk patients, antiplatelet agent is preferred.

Introduction/Purpose Vertebral artery dissection is a recognized cause of ischemic stroke in young and middle‐aged adults, often presenting with headache, neck pain, and focal neurologic deficits. Minor trauma, including neck manipulation, is a statistically significant risk factor for cervical artery dissection, with several case‐control and cohort studies demonstrating an association, particularly in younger patients. The vertebral arteries ascend through the transverse foramina of the cervical vertebrae, making them susceptible to mechanical stress from abnormal spinal curvature. Cervical scoliosis alters the bony alignment and curvature, causing the vertebral artery pathway to be elongated, kinked, or compressed, especially at the apex of the spinal curve. We suspect in patients with abnormal cervical biomechanisms the vertebral arteries are more vulnerable to injury during high velocity cervical manipulation. This case aims to highlight the risk of arterial dissection in a patient with scoliosis after undergoing neck manipulation. Materials/Methods A 37‐year‐old right‐handed male with a history of migraine headaches presented with acute onset diplopia and vertigo accompanied by nausea, vomiting, and right facial sensory loss on awakening. The patient reported recent chiropractic cervical manipulation days prior to symptom onset. Neurological examination revealed right‐sided facial sensory deficits, multidirectional nystagmus, and right homonymous hemianopia. CT angiography demonstrated right vertebral artery dissection in V2 and V3 and subtle luminal changes over the left V2 segment with scoliotic curve of the cervical spine and upper thoracic spine. MRI and MR angiography demonstrated multifocal acute infarcts in the posterior circulation and evidence of vertebral artery dissection. Additional workup included a lipid panel which showing an LDL of 137 mg/dL and a transthoracic echocardiogram revealing a bicuspid aortic valve. Results The patient was initiated on dual antiplatelet therapy with aspirin and clopidogrel for secondary prevention, consistent with American Heart Association guidance for extracranial cervical artery dissection, with plans to transition to single antiplatelet therapy after 3 months, assuming no recurrent events and stable follow up imaging. Ultimately, the patient had improvement in his visual symptoms including complete resolution of right homonymous hemianopia during his hospitalization. Given his elevated LDL, the patient was started on a high intensity statin therapy. Secondary prevention strategies included aggressive vascular risk factor modification, avoidance of further neck manipulation or trauma, and close outpatient follow‐up with repeat vascular imaging in 3 months. The patient was also referred to medical genetics to further evaluate possible underlying connective tissue disorders. He was counseled regarding the statistical association between cervical manipulative therapy and vertebral artery dissection, and the importance of prompt medical evaluation for any future neurological symptoms. Conclusions Cervical scoliosis is not a well‐established independent risk factor for vertebral artery dissection. However, when combined with cervical high velocity manipulations, the vertebral arteries are likely to be more vulnerable to injury and lead to dissections and strokes. Further research is warranted on this topic. Finally, early recognition and evidence‐based antithrombotic therapy are critical to optimizing outcomes in patients with arterial dissection.

Introduction/Purpose Diabetic striatopathy (DS) is a rare neurologic complication of poorly controlled diabetes mellitus characterized by hemichorea/hemiballism and distinctive basal ganglia imaging abnormalities, most commonly T1 hyperintensity in the putamen or caudate nucleus. Emerging evidence suggests that DS may coexist with acute ischemic stroke, particularly in the context of intracranial atherosclerotic disease (ICAS), complicating both diagnosis and management. The pathophysiological interplay between chronic hyperglycemia and impaired regional perfusion is postulated to increase basal ganglia vulnerability to metabolic and ischemic injury, leading to the characteristic clinical and radiological features of DS. This case report aims to highlight the clinical course, diagnostic evaluation, and management of a patient presenting with DS and stroke secondary to ICAS. Materials/Methods A 68‐year‐old female with hypertension, hyperlipidemia, and newly diagnosed diabetes presented with a one‐month history of left arm choreiform movements, episodic dizziness, and blurred vision. Movements correlated with hyperglycemia (home blood glucose in the 400s) and resolved with dietary modification and improved glycemic control. Initial MRI revealed right M1 segment MCA occlusion with multiple subacute‐chronic infarcts in the right MCA territory and T1 hyperintensity in the right putamen, suggestive of DS. CT angiography head and neck demonstrated distal right M1 severe stenosis vs occlusion with distal reconstitution, atherosclerotic calcification in the right carotid siphon, and severe stenosis in the right V4 segment and left AICA. Laboratory evaluation showed LDL 103 mg/dL and HbA1c 10.7%. Cardioembolic evaluation with echocardiography, transcranial doppler, and prolonged cardiac monitoring was unremarkable. The patient was managed with dual antiplatelet therapy (aspirin and clopidogrel for 90 days, then aspirin monotherapy), high‐intensity statin, and intensive glycemic control per current consensus guidelines for ICAS and DS. Results The patient's involuntary movements resolved with improved glycemic control, consistent with DS. Follow‐up imaging at three months demonstrated interval resolution of right lentiform nucleus edema and enhancement, with residual mild T1 hyperintensity and curvilinear susceptibility artifact. No new infarcts were identified; prior right MCA territory infarcts appeared subacute/chronic. Persistent right distal M1 MCA stenosis was noted. The cessation of choreiform movements with normalization of blood glucose and the radiological evolution of basal ganglia changes supported the diagnosis of DS in the context of ICAS. Aggressive medical management, including dual antiplatelet therapy and statin, was implemented per American Heart Association (SAMMPRIS) recommendations for symptomatic ICAS. The patient remained neurologically stable without recurrent stroke or movement disorder. Conclusion This case illustrates the complex interplay between chronic hyperglycemia and intracranial atherosclerotic disease in the pathogenesis of both stroke and diabetic striatopathy. The combination of metabolic and vascular insults likely increases basal ganglia susceptibility to injury, manifesting as DS and ischemic stroke. Recognition of this association is critical for accurate diagnosis and optimal management, as DS may herald imminent cerebrovascular events. Aggressive risk factor modification and guideline‐directed medical therapy are essential for secondary prevention in ICAS, while glycemic control remains the cornerstone of DS management. Further research is needed to elucidate the mechanistic links and refine therapeutic strategies for these overlapping entities.