United States

Background: The incidence of gastro-intestinal stromal tumors is 1-2% of all gastrointestinal malignancies [1]. These rarely metastasize to the heart [2], causing atrial fibrillation. The drug of choice is imatinib. This is known to have GI side effects, and infrequently, direct cardiac toxicity. Here, we present a case of atrial fibrillation in a patient with GIST on imatinib therapy, and outline the workup of this rare presentation. 
Case: 84 year old male with spindle cell GIST (4.9 X 3.5 cm) in the gastric fundus, on imatinib 400mg OD for 3 weeks was hospitalized for new onset atrial fibrillation (Figure 1), fever and lymphadenopathy. No history of shortness of breath, chest pain, headaches or palpitations. There is history of severe diarrhea, vomiting and weakness in the last week.  On examination, vitals were normal. Bloodwork showed an eosinophil manual count of 73% (normal: &lt;7%) and atypical lymphocytosis. Workup for the cause of atrial fibrillation (echo, cardiac CT, chest X ray, electrolytes) was done and was normal. Patient was started on eliquis 2.5 mg BD and rate control for atrial fibrillation. Patient developed AKI and transaminitis during the course of hospitalization. Imatinib was held, and patient was started on steroids. On steroids, his eosinophil count normalized, rhythm returned to sinus, renal and liver function dropped back to baseline. The patient was referred to oncology to switch to a different tyrosine kinase inhibitor. Steroids were tapered and discontinued. Patient was asked to review in cardiology clinic for follow – up of atrial fibrillation. 
Discussion: Four potential causes of AF were considered in this patient: cardiac metastasis from the GIST, direct drug toxicity, dehydration induced, and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome due to imatinib [3,4]. Imaging revealed no evidence of cardiac metastasis. Electrolytes were normal, ruling out dehydration as a cause. AF is an uncommon side effect of imatinib (0.55% of patients) [5]. In this case, temporal correlation suggested a possible association. However, the markedly elevated eosinophil count raised suspicion for DRESS [6]. Scoring according to RegiSCAR system suggested probable DRESS. The patient markedly improved on steroids, further confirming our theory. Several studies have reported cases of imatinib-induced DRESS syndrome, and atrial fibrillation in DRESS (7.1%) [3] supporting our clinical findings.  In conclusion, this case is a good example of the importance of considering multiple etiologies for AF in cancer patients undergoing targeted therapy. Clinicians should remain vigilant, follow a comprehensive diagnostic approach and promptly intervene to mitigate adverse events. 

AMA Research Challenge 2024 

Atrial Fibrillation in a Patient with GIST on Imatinib – What are the causes?

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AMA Research Challenge 2022

Welcome to the largest national, multi-specialty research event featuring research from 750 medical students, residents and fellows, and international medical graduates.


Background: The incidence of gastro-intestinal stromal tumors is 1-2% of all gastrointestinal malignancies [1]. These rarely metastasize to the heart [2], causing atrial fibrillation. The drug of choice is imatinib. This is known to have GI side effects, and infrequently, direct cardiac toxicity. Here, we present a case of atrial fibrillation in a patient with GIST on imatinib therapy, and outline the workup of this rare presentation. 
Case: 84 year old male with spindle cell GIST (4.9 X 3.5 cm) in the gastric fundus, on imatinib 400mg OD for 3 weeks was hospitalized for new onset atrial fibrillation (Figure 1), fever and lymphadenopathy. No history of shortness of breath, chest pain, headaches or palpitations. There is history of severe diarrhea, vomiting and weakness in the last week.  On examination, vitals were normal. Bloodwork showed an eosinophil manual count of 73% (normal: <7%) and atypical lymphocytosis. Workup for the cause of atrial fibrillation (echo, cardiac CT, chest X ray, electrolytes) was done and was normal. Patient was started on eliquis 2.5 mg BD and rate control for atrial fibrillation. Patient developed AKI and transaminitis during the course of hospitalization. Imatinib was held, and patient was started on steroids. On steroids, his eosinophil count normalized, rhythm returned to sinus, renal and liver function dropped back to baseline. The patient was referred to oncology to switch to a different tyrosine kinase inhibitor. Steroids were tapered and discontinued. Patient was asked to review in cardiology clinic for follow – up of atrial fibrillation. 
Discussion: Four potential causes of AF were considered in this patient: cardiac metastasis from the GIST, direct drug toxicity, dehydration induced, and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome due to imatinib [3,4]. Imaging revealed no evidence of cardiac metastasis. Electrolytes were normal, ruling out dehydration as a cause. AF is an uncommon side effect of imatinib (0.55% of patients) [5]. In this case, temporal correlation suggested a possible association. However, the markedly elevated eosinophil count raised suspicion for DRESS [6]. Scoring according to RegiSCAR system suggested probable DRESS. The patient markedly improved on steroids, further confirming our theory. Several studies have reported cases of imatinib-induced DRESS syndrome, and atrial fibrillation in DRESS (7.1%) [3] supporting our clinical findings.  In conclusion, this case is a good example of the importance of considering multiple etiologies for AF in cancer patients undergoing targeted therapy. Clinicians should remain vigilant, follow a comprehensive diagnostic approach and promptly intervene to mitigate adverse events.

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AMA would like to thank Laurel Road for sponsoring a $10,000 grand prize for the winner of the AMA Research Challenge. Laurel Road is not involved in winner selection process. The winner will be announced on February 20, 2025 during the AMA Research Challenge finals. Payment of the grand prize will be directly from Laurel Road. See the AMA Research Challenge Official Rules for terms and conditions.

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Background: 
Pulmonary embolism (PE) is a life-threatening condition characterized by the blockage of a pulmonary artery or one of its branches. The intricate relationship between substance abuse and thromboembolic events has emerged as a significant concern in clinical medicine. Cocaine, a potent vasoconstrictor, has been associated with both arterial and venous thrombotic events due to its prothrombotic effects on the coagulation cascade and its impact on the vascular endothelium. We present a case of a 42-year-old male with a history of cocaine abuse who presented with a life-threatening PE. 
Case Presentation: 
A 42-year-old male with a past medical history of cocaine abuse presented after a syncopal episode. He described the episode as passing out from a standing position and regaining consciousness quickly on the ground. He endorsed a 3 day history of worsening dyspnea and lightheadedness. On examination, the patient was experiencing mild respiratory distress and was found to be tachycardic. ECG revealed sinus tachycardia with evidence concerning for right heart strain. Laboratory findings were significant for elevated troponin and pro-BNP. 
A ventilation/perfusion lung scan was ordered which showed a high probability of PE. A subsequent CT angiography of the chest was performed which confirmed acute bilateral pulmonary emboli with moderate-large clot burden and evidence of right heart strain with a right ventricle to left ventricle size ratio of 1.35. Lower extremity doppler ultrasound was positive for deep vein thrombosis in the right popliteal vein. 
The patient was evaluated by the interventional cardiology team and was taken for mechanical thrombectomy of the pulmonary emboli. Pre-intervention right heart catheterization was significant for a mean pulmonary artery pressure of 47 mmHg and a pulmonary capillary wedge pressure of 23 mmHg. The clot burden was reduced by greater than 90% and excellent filling with a good venous phase of all pulmonary arteries was noted. The patient improved symptomatically after the procedure. 
Discussion: 
Cocaine's prothrombotic properties are multifaceted, involving the activation of the coagulation process and the secretion of von Willebrand factor (VWF), among other factors, which collectively contribute to thrombus formation. The presence of adulterants in cocaine, such as levamisole, further complicates its pathophysiological impact, potentially exacerbating pulmonary damage and fibrosis, thus predisposing individuals to thromboembolic events. The reported case emphasizes the need for a high index of suspicion for cocaine-induced PE in patients with a history of substance abuse presenting with symptoms suggestive of thromboembolic events.

BEYOND TRADITIONAL RISK FACTORS: COCAINE ABUSE AND PULMONARY
EMBOLISM

Background:
Complete heart block (CHB) is a potentially life-threatening conduction disorder characterized by the complete absence of electrical impulse transmission from the atria to the ventricles. While commonly associated with advanced age and structural heart disease, CHB can also present atypically, particularly in elderly patients. Potential consequences of delayed diagnosis of CHB can consist of syncope, heart failure and even cardiac arrest. This case report describes a 79-year-old male with a history of hypertension and tobacco abuse who presented with atypical symptoms of CHB.
Case Presentation:
A 79-year-old male with a past medical history of hypertension and tobacco abuse presented with shortness of breath of several days duration. He noted body aches, upper respiratory symptoms, and malaise during the week prior. In the past month, he reports having intermittent episodes of lightheadedness. He was previously hospitalized a few months before for similar episodes of lightheadedness, but refused workup. At home in the morning before admission, a low oxygen saturation and heart rate were noted.
On examination the patient was alert, oriented, and answering questions appropriately. He was breathing comfortably on supplemental oxygen via nasal cannula. An ECG was then performed and the patient was found to have a complete heart block with a rate in the 30s. On continuous monitoring, his heart rate continued to drop into the 20s without worsening symptoms. He was then moved to the ICU for placement of transvenous pacemaker.
The patient was not taking any pharmacological agents that could have caused his condition. A transthoracic echocardiogram showed a preserved ejection fraction. Left heart catheterization revealed non-occlusive disease. He was taken for permanent pacemaker placement which led to resolution of all symptoms.
Discussion:
This case highlights the often atypical presentation of CHB in elderly patients. While the classic presentation involves syncope or near-syncope due to bradycardia, this patient primarily reported shortness of breath and malaise. Additionally, despite experiencing prior episodes suggestive of CHB, he initially declined a workup. This stresses the need for thorough clinical evaluation in elderly patients, even when symptoms appear mild or unrelated to cardiac dysfunction. The absence of structural heart disease on echocardiogram and non-occlusive coronary arteries on angiography suggest an idiopathic or functional etiology for the CHB in this case. The prompt diagnosis and placement of a permanent pacemaker resulted in complete symptom resolution. This emphasizes the critical role of early intervention in managing CHB and preventing potential complications such as heart failure or syncope-related injuries.

Complete Heart Block in an Elderly Male with Atypical Presentation


Abstract Title
Myocarditis post-COVID-19 Vaccination

Background: 
Reports to the Vaccine Adverse Event Reporting System (VAERS) have highlighted a possible association between mRNA COVID-19 vaccines and myocarditis, particularly in males between 12 and 39.1 This case report investigates a rare instance of myocarditis in an adult male following mRNA vaccination, emphasizing the need for heightened clinical awareness.

Case Presentation :
A 38-year-old male with no prior medical history presented with acute chest pain and shortness of breath one day after receiving his second Moderna COVID-19 vaccine dose. An EKG showed nonspecific ST elevations and elevated troponin levels, peaking at 16 ng/mL. Coronary angiography ruled out coronary artery disease, and cardiac MRI indicated myocarditis, characterized by delayed intramural enhancement.

Discussion :
This case exemplifies myocarditis as a potential adverse effect post-COVID-19 vaccination, a phenomenon that demands attention due to its potentially severe implications. Immunological reactions like those elicited by viral infections may play a role, potentially involving an exaggerated inflammatory response to the vaccine's spike protein, leading to myocardial injury.1 The rapid symptom onset post-vaccine and elevated cardiac biomarkers strongly suggest a causal relationship.
While vaccine-associated myocarditis generally follows a benign course, severe outcomes like arrhythmias and heart failure require vigilant monitoring and management. Treatment focuses on anti-inflammatory medications and, if necessary, immunosuppressive therapy, especially when cardiac function is compromised.1
Despite the low incidence of myocarditis relative to the millions of vaccine doses administered, these cases highlight the need for ongoing surveillance and research to refine our understanding and management strategies. Improved knowledge of vaccine-related myocarditis is essential for developing educational programs for healthcare providers and informing the public to ensure early detection and treatment.


Covid-19 Vaccine Induced Myocarditis

BACKGROUND
Immuno-oncology (IO) therapy is often associated with immune-related adverse effects (irAEs) varying in severity and involving different organs. There are many common irAEs; however, the rare irAEs include myocarditis, pericarditis, colitis, pneumonitis, dermatitis, and hepatotoxicity, which are associated with higher rates of morbidity and mortality. Approximately 0.06%–2.4% of SCLC patients develop IO-related myocarditis.
CASE PRESENTATION
A 74-year-old female with a past medical history of hypertension, O2-dependent COPD, pAF, SCLC, and a 40-pack-year history of tobacco abuse presented to the hospital with chest and back pain. Her pain radiated towards the epigastric region, and she was also experiencing nausea. She received two cycles of carboplatin/etoposide followed by two cycles of chemoradiation, during which substantial tolerance issues were noted, even with dose reductions and treatment delays due to AF, respiratory failure, and influenza. After deferring therapy, her condition relapsed within several months, and she was started on Nivolumab monotherapy four weeks prior to her admission.
Upon presentation, it was noted that the patient’s troponin T was elevated (177 ng/L). She also had an abnormal NT-proBNP (10,279 pg/ml), and the ECG suggested NSTEMI changes. The CT thoracic spine reports indicated a T9 compression fracture, which correlated with the site of back pain. For the concurrent chest pain, a TTE was performed, showing depressed RV systolic function, grade I diastolic dysfunction, and LVEF of 45-49% (previous LVEFs of 50–54%). Since multiple abnormalities were noted on TTE and ESR, CRP were elevated, and a cardiac MRI was performed. Due to a drop in EF, a diagnosis of immune-mediated myocarditis due to Nivolumab was suspected. The patient was started on Solumedrol-1 mg/kg, resulting in clinical improvement. A cardiac MRI was performed four days after initiation of treatment, demonstrating wall motion abnormalities in the mid/distal septal wall with patchy segments of non-CAD LGE in the mid-distal septum and apical septal wall. Findings were consistent with IO-associated myocarditis.
DISCUSSION
PD-1 inhibitors, such as Nivolumab, represent an effective treatment option for SCLC that induces irAEs. Myocarditis associated with ICIs necessitates immediate and continuous monitoring after starting immunotherapy. This case seeks to raise awareness for early detection and intervention, which are essential in managing ICI-induced myocarditis. Elevated cTnI levels and ECG changes are key biomarkers. Frequent ECG changes include T waves, ST segment abnormalities, and arrhythmias. As seen in this case, high doses of glucocorticoids are effective in alleviating symptoms, especially in cases of severe myocarditis.

Immunotherapy-Induced Myocarditis In The Setting Of Small Cell Lung Cancer

Aerococcus urinae is a gram-positive, catalase-negative bacterium first isolated in 1953 from samples of air and dust of occupied room of unknown clinical significance Later, the species was revealed as a causative organism with urinary tract infection in the 1990s. More recently, A. urinae has also been shown to cause invasive infections such as bacteremia and infective endocarditis (IE), more commonly in aortic valve, but mitral and tricuspid valve IEs have also been reported. We describe a case of a middle aged male who presented with A. urinae urosepsis complicated by aortic valve endocarditis, resulting in complete heart block and multi-territory strokes secondary to septic emboli.

Infective endocarditis with aortic root abscess secondary to Aerococcus Urinae sepsis

Background. Chronic kidney disease (CKD) affects more than 20 million people in the USA, who have 30 times greater risk of cardiovascular mortality compared to the general population. Sudden cardiac death (SCD) is a leading cause of death in patients with ESRD, accounting for 20% to 30% of all deaths [1]. Hyperkalemia is the main cause of fatal arrhythmias in this group of patients. We present a case of multiple cardiac arrests related to acute hyperkalemia secondary to consumption of potassium rich diet in the patient with ESRD.
Case Presentation. A 64-year-old male with past medical history of diabetes mellitus, ESRD on hemodialysis (HD), coronary artery disease, and hypertension presented to ED after two syncopal episodes that lasted for a few seconds. As per the patient's family, the patient was in his usual state of health, was compliant with his medications and HD, however, was non-compliant with a low potassium diet. The patient started a religious fasting and was abstaining from any food or liquids for several days. However, he has been consuming one box of dates containing 26 dates every evening. When presenting to ED, the patient was found to be hypertensive and bradycardic with HR of 17 beats/min. He lost consciousness twice, was pulseless, thus, CPR was initiated. In 2 minutes, the patient regained his pulse without any medications. His BGCAP showed hyperkalemia of 6.7 mmol/l. EKG demonstrated junctional rhythm with bradycardia of 10 BMP and subsequent 5-second pause. The patient had the third episode of loss of pulse, and regained consciousness after 4 minutes of CPR. Patient was given atropine, calcium gluconate, and epinephrine with improvement of heart rate to the 50s beats/min. The patient was taken to HD emergently which improved his hyperkalemia and symptoms. Patient had an ICD placed on the same admission to prevent SCD in the future.
Discussion. Besides traditional risk factors (LVH, dyslipidemia, DM, CAD), there are additional factors for SCD in ESRD patients. They include: uremic state, dialysis-induced oxidative stress and myocardial stunning, diffuse myocardial fibrosis and vascular calcification, anemia, fluid overload, fluid and electrolyte shifts, sympathetic overactivity and mineral bone disease. These factors contribute to arrhythmias and sudden cardiac death. Hyperkalemia with potassium levels of more than 6.7 mmol/l are strongly associated with mortality and can be avoided, when patients are educated and compliant with HD, low potassium diet and regular follow-up visits.

Multiple cardiac arrests due to consumption of potassium rich fruit in the patient with end-stage renal disease

Primary cardiac tumors are rare, with a prevalence of about 0.001-0.03% in autopsy series and myxomas constituting the most common subtype. Cardiac myxomas predominantly originate in the left atrium (75%) and, less frequently, the right atrium (15-20%). Although biologically benign, myxomas carry a risk of embolization associated with complications such as strokes, transient ischemic attacks (TIAs), and neurological deficits. Herein, a 46-year-old female presented with symptoms including dizziness, shortness of breath, and general fatigue. Initial electrocardiogram (ECG) evaluation revealed an inverted T wave in leads aVL and V1, poor R-wave progression (PRWP), nonspecific ST-T wave changes (NSSTTWC), and a right ventricular conduction delay (RVCD) with a primitive epsilon wave in lead V1. A 2D transthoracic echocardiography showed impaired diastolic filling, diminished relaxation, mild left atrium dilation, and a pedunculated mass suggestive of a right atrial myxoma. Cardiothoracic surgery successfully excised the mass weighing 35 grams and measuring 4.7 x 4.5 x 3.5 cm. Histopathological examination confirmed the cardiac myxoma diagnosis and revealed compelling additional findings of multiple dark red hemorrhagic foci and an inflammatory infiltrate, implying an atypical proinflammatory phenotype with potential postoperative complications. Despite successful resection of the myxoma, follow-up ECGs showed persistent inverted T wave morphology in leads aVL and V1, a primitive epsilon wave associated with RVCD, and a right axis deviation, though the NSSTTWC and PRWP patterns resolved. Subsequent echocardiograms noted no structural abnormalities, ruling out remnant intracavitary masses or atrial appendage thrombosis. These persistent electrophysiological abnormalities suggest underlying structural or conduction system abnormalities resembling a pseudo-arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) constellation. The mechanism(s) remains in question; however, genetic predisposition, mild congenital anomalies, and/or inflammation-induced fibrotic changes might have contributed to altered electrical conduction. In conclusion, our case highlights the complexity of cardiac myxoma presentations, offers insights into persistent conduction abnormalities, and suggests immunophenotyping to predict postoperative recovery while facilitating targeted therapies.

Persistent ARVD/C-like Electrophysiology Following Successful Excision of a Right Atrial Myxoma

Abstract Title
Reconnecting the dots in a patient with biventricular clots
Dany Toumajan MS-3, Priya Goyal MBBS, Jyotirmaya Jain MS-3, Karun Khanna MD

Background
This abstract delineates the complex interplay between pancreatitis and cardiac involvement, presenting a diagnostic conundrum in clinical practice.

Case Presentation
A 25-year-old male, with a background of alcoholism and cocaine use, presented with abdominal pain, fever, and vomiting. Clinical examination revealed epigastric tenderness, and ECG abnormalities indicative of cardiac dysfunction. Imaging studies unveiled necrotizing pancreatitis, accompanied by thrombotic complications, including portal vein and splenic vein thrombosis, alongside biventricular clots. Cardiac evaluations demonstrated global hypokinesia and progressive left ventricular systolic dysfunction, attributed to myocarditis, possibly exacerbated by substance abuse.

Discussion
The coexistence of acute pancreatitis and cardiac complications poses a diagnostic and therapeutic challenge. Proposed mechanisms include direct pancreatic enzyme injury, vasospasm, or thrombus formation, with underlying substance abuse potentially exacerbating myocardial damage. Despite ruling out coronary occlusion, the exact etiology remains elusive, necessitating further investigation. Management recommendations are scarce due to the rarity of this association, highlighting the need for tailored interventions and screening protocols in at-risk populations. Future research endeavors should focus on elucidating the pathophysiological mechanisms and optimizing therapeutic strategies to improve patient outcomes.

Reconnecting the dots in a patient with biventricular clots

Patients with bicuspid aortic valve (BAV) experience valvular complications at an accelerated rate. While BAV is generally regarded as a benign anatomical variant, recent histological and cardiac imaging studies suggest significant hemodynamic instability in even asymptomatic BAV patients.

A previously healthy 59-year-old man was referred for new-onset difficult-to-control hypertension. Echocardiography revealed a mildly calcified but well-functioning bicuspid aortic valve (BAV) and there were signs of chronically elevated left-sided heart pressures, though the patient denied any symptoms and exercise stress testing was normal. Over the next 2 years he failed multiple antihypertensive drug regimens despite proper compliance. He eventually presented to the hospital with profound hypotension and was found to have infective endocarditis complicated by a perivalvular abscess requiring mechanical aortic valve replacement (AVR). Prior to AVR, he struggled to maintain blood pressure on a 3-drug regimen and his response to atenolol reflected that of elderly patients with isolated systolic hypertension from age-related aortic stiffening. Following AVR, a dramatic improvement was observed in the patient’s blood pressure, now responsive to nebivolol monotherapy at half the previous dose, and he has remained stable at 1, 3, and 6-month follow up.

Hemodynamic instability and ascending aorta stiffness are obvserved in BAV patients independently of age, valvular function, aortic diameter, or atherosclerotic risk factors. While the exact etiology of aortic stiffening in BAV patients has not been confirmed, recent histological studies suggest a similar–but
accelerated–mechanical stress-induced phenotypic shift in vascular smooth muscle cells (VSMCs) which has previously been implicated in thoracic aortic disease and age-related aortic stiffening. Reactive deposition of extracellular matrix initially serves to dampen mechanical stress and maintain homeostasis; however this ultimately increases pulse wave velocity (PWV) and central systolic pressure, perpetuating a feedforward loop of maladaptive stiffening and increased myocardial demand. Supporting these findings are recent strain imaging studies revealing subclinical diastolic dysfunction associated with aortic stiffness in asymptomatic BAV patients. Consensus guidelines for BAV surveillance currently address aortic aneurysm detection but fail to address its likely precursor–loss of proximal aortic distensibility due to the intrinsic hemodynamic abnormalities of BAVs. Strain imaging offers immense value for this application but is not yet widely available in clinical practice. In the meantime, assessment of PWV on doppler echocardiography may be a valuable surrogate for aortic stiffness in BAV patients.


Resolution of Hypertension Following Replacement of a “Well-Functioning”
Bicuspid Aortic Valve: Re-examining Aortic Stiffness in Asymptomatic BAV Patients

BACKGROUND: Intracranial infected aneurysms (IIAs), also known as mycotic aneurysms, complicate infective endocarditis (IE) in around 2-4% of cases. IIAs can spontaneously rupture and present with intracerebral bleeding, which is usually straightforwardly recognized in brain imaging. This case documents a rare presentation of a ruptured IIA initially misdiagnosed as a brain neoplasm due to clearly suggestive radiologic features.

CASE PRESENTATION: A 43-year-old male with history of cocaine and tobacco consumption and treated tuberculosis was admitted for tonic-clonic seizures and right hemiparesis along with a 3-month history of persistent fever, malaise, and 15-kg weight loss. A head computed tomography (CT) showed a left frontal lesion having both solid and central hemorrhagic content along with surrounding vasogenic edema and intraventricular hemorrhage. In the magnetic resonance imaging, the brain lesion was expansive and showed contrast enhancement. The workup showed elevated inflammatory markers and glomerulonephritis but was otherwise unremarkable for infectious, autoimmune, or oncological etiologies. At present, the primary suspicion was a brain tumor based on the characteristic radiologic features, the otherwise unremarkable workup including negative pan-cultures and transthoracic echocardiogram (TTE), and the maintenance of afebrile status following oral prednisone for vasogenic edema. He was discharged for outpatient follow-up. Around 3 months later, he was readmitted for persistent fever; a new TTE showed mitral valve vegetations and blood cultures grew Streptococcus mutans, confirming IE. A brain CT angiography confirmed multiple IIAs. He received intravenous ceftriaxone and vancomycin. Besides, the hospital course was complicated by decompensated heart failure and myocardial infarction with an obstructive coronary artery that required mitral valve and coronary artery bypass graft surgery, respectively. He was discharged hemodynamically stable.

DISCUSSION: IIAs represent an embolic complication of IE caused by septic arterial emboli that travels to the vasa vasorum of cerebral arteries and triggers a local inflammation and dilation of the arterial wall. Ruptured IIAs present with intracranial hemorrhage in brain imaging studies. However, this case and other around two-to-four cases documented that ruptured IIAs can rarely mimic intra-axial masses, leading to misdiagnosis. For example, similarities between IIAs and glioblastoma multiforme were reported, as both conditions can enhance contrast in imaging. It is unclear if this presentation is extremely rare or is underreported. This case documents a ruptured IIA presenting radiologically as a brain cerebral neoplasm. As a final reminder, clinicians should be aware of this unique presentation to maintain a high index of suspicion for IIAs despite unremarkable blood cultures and echocardiography.

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