Patient: Female, 46-year-old Final Diagnosis: Coronary artery dissection and stent dislodgement Symptoms: Chest pain Medication: — Clinical Procedure: PCI Specialty: Cardiology Objective: Rare disease Background: Coronary stent dislodgement is rare but carries serious complications like thrombosis, myocardial infarction, disruption of the systemic circulation, and coronary dissection, which can lead to sudden death. Thus, rapid evaluation and intervention are needed to restore blood flow to vital organs. Case Report: A 46-year-old woman with no relevant past medical history except for smoking, presented to the Emergency Department (ED) with left-sided chest pain. The physical exam was unremarkable. EKG showed ST segment elevation, and troponin was 4.03. She underwent cardiac catheterization, which showed 100% occlusion of the left anterior descending coronary artery (LAD). A drug-eluting stent (DES) was placed. Later, she had chest pain similar to the initial episode. EKG showed 1-mm elevation at ST segment in leads V1 and V2 and T wave inversion in leads V2, V3, V4, and V5. She underwent a repeat heart catheterization, which revealed a dissection in the middle LAD distal to the initial stent placement. She was treated with another stent overlapping the proximal stent. While attempting to cross the proximal stent, the stent came off the balloon, slipped from the wire, and went down into the descending aorta. Conclusions: Coronary artery stent dislodgement is a rare event that can lead to significant complications during PCI. Patient restlessness and small-sized, severely angulated, and previously stented coronary arteries are associated risk factors. The main treatment option is stent retrieval, either surgically or using other available techniques. If retrieval of the stent is impossible, crushing it against the blood vessel wall could be considered.

Papillary fibroelastoma (PFE) and nonbacterial thrombotic endocarditis (NBTE) account for <1% of all cardioembolic strokes. When there is no evidence of infection, and an exophytic valve lesion is seen on echocardiography, PFE may be an initial imaging diagnosis. NBTE, or Libman-Sacks endocarditis, is a rare entity and can present with varied imaging findings. This report presents a case of embolic stroke and NBTE mimicking a PFE. We discuss a 49-year-old female with a past medical history of diabetes mellitus who presented with headache and right-hand numbness. The initial CT head was negative and the MRI brain showed multiple infarcts in the watershed areas where anterior and posterior brain circulation meet and overlap. A transesophageal echocardiogram (TEE) showed a left ventricle (LV) mass initially diagnosed as PFE. The patient was started on aspirin only with no anticoagulation since we thought the stroke was related to an embolus from a tumor, not a thrombus. The patient underwent surgery but the pathology report revealed a diagnosis of organizing thrombus with abundant neutrophilic infiltration and no neoplastic proliferation. This case report highlights the importance of a comprehensive evaluation of valvular masses and the diagnostic approaches currently available to help clinicians differentiate between various causes of embolic stroke like PFE, bacterial endocarditis, and NBTE. Early differentiation is critical because it can affect the treatment and outcome. This report shows that echocardiography of endocardial and valvular lesions may provide a differential diagnosis, but a definitive diagnosis requires microbiology and histopathology. Advanced imaging techniques such as cardiac CT or cardiac MRI may assist in identifying select cases that are at lower risk for subsequent embolic events, in which surgical intervention may safely be avoided.

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Background Serratia marcescens is a Gram-negative motile bacillus that is a facultative anaerobe and non-lactose fermenting. Serratia can be isolated from water, soil, plants, and the intestinal microbiome. Serratia produces a unique Identifying reddish pigment called prodigiosin. Serratia is responsible for only 0.14% of infective endocarditis cases, with a mortality rate of 85%. Methods A 37 YO female with a history of Intravenous heroin abuse was admitted with fevers and dyspnea. Vital signs were BP 76/50, HR 140, RR 26, temp 102 F, and SpO2 98% on room air. She was toxic-appearing. Labs: WBC 26000(4,000 – 11,000 /uL) with 14% bands, Hb 5.6 (12.6 – 17.0 g/dL), PLT 15*10^3(150-372*10^3/uL), creatinine 2.5 (0.50 - 1.60 mg/dL), lactic acid 15.8 (0.5-2.2 mmol/L). We started vancomycin, piperacillin-tazobactam, and norepinephrine for septic shock. A transthoracic echo showed a large mass on the tricuspid valve, and a transesophageal echo depicted it as vegetation. Blood cultures grew Serratia. She underwent excision of anterior and posterior tricuspid valve leaflets with reconstruction and ring annuloplasty. She reported washing her syringes with tab water and reusing them again. Serratia has a predilection for left-side heart valves even in the IVDU population but this patient presented with a tricuspid valve endocarditis. Results Serratia is a rare cause for IE in the ICE study; out of 2.761 definite IE cases identified over five years, only forty-nine instances were due to gram-negative bacilli. Of those, only four cases were due to Serratia. The clinical presentation of Serratia includes constitutional symptoms, new-onset murmur, and cutaneous and neurologic manifestations. Serratia produces multiple pathogenic factors allowing Serratia to result in valvular destruction and perivalvular complications, and distant septic emboli metastasis. Conclusion Serratia is sensitive to third and fourth-generation cephalosporins, monobactams, carbapenems, fluoroquinolones, and aminoglycosides. Treatment is complex due to the production of AmpC B-lactamase, which hydrolyzes third and fourth-generation cephalosporins. The 2005 IDSA suggested a combination of B-lactam and an aminoglycoside for Serratia endocarditis, and these are not guidelines but merely recommendations. Disclosures All Authors: No reported disclosures.