Louisiana Research Day Program Book 2025

Case Studies: Section 2

Case Studies: Section 2

117 PARADOXICAL EMBOLISM TO THE CORONARY ARTERY: AN UNCOMMON CAUSE OF ACUTE MYOCARDIAL INFRACTION

118 OPIOID-INDUCED INTRAHEPATIC CHOLESTASIS IN HEMOGLOBIN SC DISEASE: A CHALLENGING ISSUE IN MANAGEMENT

Swesha Shrestha, MD 1 ; Shekhar Gurung, MD 2 ; Nisheem Pokharel, MD; Thomas R Smith, MD 4 1 St Francis Medical Center; 2 Department of Internal Medicine, Monroe, LA

Usman Haq, MD 1 ; Susmitha D Chalamalasetti, MD 2 ; Anam Shahid, MD 3 ; Navin Ramlal, MD 4 Department of Medicine, St Francis Medical Center, Monroe, LA.

Background: The most common cause of myocardial infarction (MI) is by atherosclerotic plaque disruption, which triggers thrombus formation and subsequent myocardial ischemia. Myocardial infarction with no coronary atherosclerosis (MINOCA), however, can occur in the absence of obstructive atherosclerosis. Coronary embolism, for example, accounts for approximately 3% of cases of MINOCA and is often linked to conditions like atrial fibrillation and infective endocarditis. (1-5) Even less commonly, MINOCA can occur via paradoxical embolism in the setting of a patent foramen ovale (PFO). (2) The coronary artery anatomy, with its right-angle departure from the aortic root and partial covering by aortic valve cusps, and its size disparity from the aorta with primarily diastolic filling, make this condition rare. Here, we present a rare case of a MI in a patient due to a paradoxical embolism via his PFO. A 48-year-old male with no significant history presented with a dull, aching central chest pain. This pain had been persistent for several hours prior to presentation and was unrelieved by rest or medications including use of both nitroglycerin and aspirin. He had a BMI of 24 and did not smoke or drink alcohol.

Initial workup revealed a significantly elevated troponin I level of 4.53 ng/mL, up trending to 13.56 ng/mL on repeat check (N <0.05). An EKG demonstrated sinus bradycardia without ST-segment changes. He was subsequently taken for emergent coronary angiography, which revealed no significant atherosclerotic disease however, there was a notable thrombus in the distal segment of a small-caliber diagonal branch with faint distal flow approximately 1 mm in diameter. This vessel was deemed too small and distal to be intervened on or evaluated with an intravascular ultrasound. Given the concern for a possible cardioembolic event, anticoagulation with heparin was initiated. Although further evaluation with a transthoracic echocardiogram demonstrated a structurally normal heart with a normal ejection fraction, a transesophageal echocardiogram with bubble study confirmed the presence of a PFO. Patient’s symptoms subsided in less than 24 hours and no arrhythmias were detected during his hospital stay. He was discharged in stable condition on apixaban and clopidogrel with plans for PFO closure and a loop recorder placement as outpatient. In the evaluation of non-atherosclerotic MI, important differential

diagnoses include coronary artery embolism, coronary vasospasm or spontaneous coronary artery dissection (SCAD). (3) While paradoxical coronary embolism via PFO remains a rare cause of MI, it must be considered in patients with no atherosclerotic disease or other traditional cardiovascular risk factors. Studies have shown significantly higher mortality rate among patients with MI secondary to coronary embolism verses those with atherosclerotic MI. (7) Hence, it is important to understand the etiology as workup and management of embolic MI requires additional considerations to prevent recurrence and improve patient outcomes. Transthoracic or transesophageal echocardiography should be performed, along with monitoring for occult arrhythmia. Depending on location and thrombus burden, treatment options include aspiration thrombectomy or thrombolysis with or without stenting/anticoagulation, followed by long-term antiplatelet therapy. (1) Consideration for PFO closure is also warranted and decisions are individualized based on the patient’s risk profile. (1,8)

Introduction Sickle cell disease (SCD) is an inherited autosomal recessive disorder resulting from a point mutation on chromosome 11. This mutation leads to the production of abnormal hemoglobin S (HbS), which, under deoxygenated conditions, causes red blood cells (RBCs) to adopt a rigid, crescent or sickle shape. Hemoglobin SC (HbSC) disease, a variant of Sickle cell disease, occurs when an individual inherits one HbS gene and one hemoglobin C (HbC) gene. Here we present a rare case of intrahepatic cholestasis in a patient with HbSC disease which was complicated by opioid use. Case: A 48-year-old male with a history of sickle cell HbSC disease, complicated by proliferative retinopathy and avascular necrosis (AVN) of both shoulders and hips presented to the emergency room with severe generalized pain. On arrival, the patient was afebrile, tachycardic, tachypneic and hypertensive. His Initial lab work was also significant for transaminitis and thrombocytopenia. Patient was admitted for sickle cell pain crisis and was conservatively managed with IV fluids and hydromorphone (Dilaudid) for pain management.

Despite receiving scheduled hydromorphone, the patient continued to report increasing intensity of generalized pain requiring additional doses of pain medications. His hospital course was subsequently complicated by worsening icterus and pruritus. Repeat labs now revealed hyperbilirubinemia with a peak total bilirubin of 19 mg/dl, of which his direct bilirubin level was 13.4 mg/dl. Patient’s hemoglobin remained stable and he did not require transfusion. His other lab work for acute liver injury was unremarkable as was right upper quadrant ultrasound and MRCP. With no identifiable cause for hyperbilirubinemia, a decision was made to discontinue hydromorphone because it was the only new medication he was started on. Once the hydromorphone was discontinued, the patient started showing significant improvement both symptomatically and in his lab results. His bilirubin levels began to trend down gradually and he had improvement in his pain, pruritus and scleral icterus. The patient was discharged in stable condition and scheduled for follow-up with his primary care provider (PCP) for further symptomatic management. Discussion: This case describes an instance of intrahepatic cholestasis in a patient with hemoglobin SC

disease, triggered by the use of hydromorphone (Dilaudid ), a commonly prescribed opioid for managing sickle cell pain crises. While HBSC disease is typically considered less severe than HBSS, this case highlights its potential to lead to serious complications. In our patient, opioid-induced cholestasis emerged as the most likely cause for conjugated hyperbilirubinemia after ruling out extrahepatic obstructive etiologies and active hemolysis. Since the patient had marked improvement after the discontinuation of dilaudid, this highlights the importance of considering cholestasis as a potential complication of high-dose opioid use in sickle cell patients. Hydromorphone, which is commonly used for pain management during sickle cell disease (SCD) crises, can lead to intrahepatic cholestasis by affecting bile flow at the bile canaliculi and inducing biliary spasms. Early recognition of this issue, along with the discontinuation of the opioid, may help differentiate from other serious complications such as Sickle cell hepatopathy.

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133 2025 Research Recognition Day