Nonbacterial Thrombotic Endocarditis of the Mitral Valve With Echocardiographic Appearances Mimicking a Papillary Fibroelastoma in a Middle-Aged Female Patient.

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.

A 77-Year-Old Man with Heparin-Induced Aldosterone Suppression Causing Hyperkalemia.

BACKGROUND Anticoagulation with heparin infrequently causes elevated serum potassium via a reduction in the number and affinity of adrenal angiotensin II receptors, causing reversible aldosterone suppression, thereby leading to enhanced sodium excretion and hyperkalemia. CASE REPORT A 77 year-old man presented with productive cough and shortness of breath and was subsequently found to have non-ST-elevation myocardial infarction and concomitant symptomatic COVID-19 infection, for which he was started on a high-dose unfractionated heparin infusion. A gradual increase in serum potassium followed, with a subsequent return to a normal potassium level after stopping treatment with heparin. An evaluation for hemolysis was unrevealing, and the patient was not on any other medications known to cause hyperkalemia. On day 6, heparin was restarted owing to a high suspicion of pulmonary embolism. There was a subsequent increase in serum potassium level, which was followed by a return to baseline after discontinuation of heparin, thereby confirming the suspected diagnosis. CONCLUSIONS Acute increases in serum potassium levels in hospitalized patients can result in weakness, paralysis, conduction abnormalities, and cardiac arrhythmias that, if left untreated, can result in serious morbidity and potentially death in a short period of time. As this clinical entity is infrequently encountered in clinical practice, it can easily be overlooked by clinicians. The prompt exclusion of alternative causes of acutely elevated serum potassium levels and the identification of heparin administration as an easily reversible trigger is imperative and can potentially be life-saving.

Coronary Artery Stent Dislodgement and Loss in the Bloodstream: A Case Report and Management Options.

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.