United States

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&#39;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.


AMA Research Challenge 2024 

Covid-19 Vaccine Induced Myocarditis

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.


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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.

Ruptured Intracranial Infectious Aneurysm (IAAs) Mimicking an Expansive Brain Tumor: Endocarditis Case

Background 
Cardiac myxomas are the most common primary cardiac tumors. They are benign, but considered “functionally malignant” due to high potential for embolization. Transthoracic and Transesophageal echocardiography (TTE/TEE) are the imaging modalities of choice when evaluating for myxoma. Cardiac MRI, CT and PET scan are also useful in establishing a diagnosis. There are few documented cases of cardiac myxomas associated with Atrial Septal Defect (ASD) occluder devices. At present, there is no established relationship between myxoma and ASD occluder devices. Interestingly, cardiac myxomas have been theorized to predispose patients to Takotsubo Cardiomyopathy through CNS and systemic mechanisms.

Case Presentation
A 75 year old female with a past medical history of hypertension, hyperlipidemia, atrial fibrillation, and an atrial septal defect with an ASD occluder device presented to an outside hospital with concerns for an acute cerebrovascular accident (CVA). Stroke workup revealed multiple embolic infarcts. Further evaluation with TTE revealed a normal ejection fraction and a semi-mobile mass in the left atrium, which appeared to be associated with the ASD closure device. During the hospitalization, the patient experienced another rapid decline, which was found to be a new embolic MCA infarct. Repeat TTE confirmed the pre-existing mobile mass and noted a hypokinetic apex with an ejection fraction of 20% concerning for Takotsubo cardiomyopathy. TEE visualized two left atrial mobile masses on the interatrial septum, and confirmed absence of a thrombus. Each mass appeared to be connected by a stalk, a finding highly suspicious of myxomas. MRI reported a well circumscribed, semi-mobile, spherical mass in the left atrium attached to the ASD occluder device and CT scan noted a large filling defect adjacent to the closure device. The patient was not a surgical candidate due to multiple comorbidities. She was kept comfortable and died shortly thereafter. 

Discussion
Thrombi are known to attach to ASD occluder devices. However, there are very few cases of cardiac myxomas doing so. A similar case report hypothesized that enhanced endothelialization after ASD occluder device placement may promote further cell transformation, leading to myxoma. Advanced imaging assists in further characterizing cardiac myxoma; However, there are still challenges in differentiating between myxoma and thrombus. In our case, TEE using real time 3D reconstruction provided the best visualization of the masses. Surgery is required to make a definitive diagnosis. Finally, myxomas may lower the threshold for development of Takotsubo cardiomyopathy, which can impact surgical planning.

Two Presumed Cardiac Myxomas Associated with ASD Occluder Device, and Subsequent Development of Takotsubo Cardiomyopathy: A Case Report

Cardiac tamponade, a critical medical emergency, mandates immediate intervention due to its life-threatening hemodynamic instability. While Coxsackie B virus infrequently leads to cardiac tamponade, documented cases are scarce. Moreover, the simultaneous occurrence
of bilateral pleural effusion adds an unusual dimension to its clinical presentation. Serositis, a hallmark of connective tissue disorders like systemic lupus erythematosus (SLE), is encountered often. Yet its co-presentation with hemorrhagic viral pleural
effusion and cardiac tamponade of this severity remains exceptionally rare. 

A 77-year-old male with a medical history notable for SLE, relapsing polychondritis, and paroxysmal atrial fibrillation, presented with palpitations and dyspnea. Electrocardiography revealed atrial fibrillation with rapid ventricular response, necessitating
immediate cardioversion in the emergency department due to hemodynamic instability. Subsequent chest computed tomography demonstrated moderate pericardial effusion alongside bilateral pleural effusions. Despite initial stabilization, recurrent episodes of
hemodynamic instability ensued. Prompt transthoracic echocardiography confirmed tamponade physiology, prompting urgent pericardiocentesis and thoracentesis with drainage of serosanguinous fluid. Fluid analysis confirmed an exudative nature. Exacerbation of
SLE was ruled out (by normal anti-dsDNA antibodies and complement levels (especially CH50, C3, C4)), while serological testing revealed elevated Coxsackie B1 virus titers (1:80). 

Coxsackie B virus exhibits diverse clinical manifestations, ranging from benign viral prodrome to severe cardiac involvement. Maintaining a high clinical suspicion is crucial to avoid anchoring bias and for timely diagnosis, especially in distinguishing viral-induced
pathology from more conventional causes like SLE. This case underscores the importance of recognizing rare viral etiologies in patients with similar presentations mimicking an exacerbation of underlying autoimmune disorders.

Unveiling Coxsackie B Virus-Induced Cardiac Tamponade with Bilateral Pleural Effusion in a Patient with Systemic Lupus Erythematosus: A Rare Case Report

Lipschütz ulcers (LU), also known as reactive non-sexually related acute genital ulcerations, are an uncommon condition that primarily affects sexually inactive girls under the age of 20 years. In this report, we describe a 13-year-old female with past medical history of periodic fever, aphthous stomatitis, pharyngitis, adenitis (PFAPA) in early childhood who presented to the emergency department (ED) for sudden onset of genital ulcerations and labial swelling. Based on her clinical presentation, negative primary infectious workup, unresponsiveness to broad-spectrum antimicrobials, and concurrent viral infection, she was diagnosed with LU. Her simultaneous presentation with aphthous stomatitis was unique and may indicate that PFAPA history potentially influences susceptibility to developing LU.

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

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