Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare but potentially progressive cause of pulmonary hypertension, often presenting with subtle exertional symptoms that delay diagnosis. We report the case of a 34-year-old man with no prior chronic medical conditions who presented with a three-month history of progressive exertional dyspnea and fatigue, accompanied by intermittent lower extremity edema and Raynaud-like color changes in the toes. Physical examination revealed mild ankle edema and subtle digital clubbing, with otherwise unremarkable cardiopulmonary and musculoskeletal findings. Laboratory evaluation showed elevated NT-proBNP, modestly raised D-dimer, and preserved renal and hepatic function. Transthoracic echocardiography revealed right ventricular dilation with preserved systolic function and an estimated pulmonary artery systolic pressure of 62 mmHg. Pulmonary function testing was largely normal, but computed tomography pulmonary angiography demonstrated organized thrombotic material in segmental and subsegmental pulmonary arteries bilaterally. Right heart catheterization confirmed pre-capillary pulmonary hypertension. Further evaluation revealed combined congenital deficiencies of protein S and protein C, explaining the thrombotic predisposition in the absence of prior venous thromboembolic events. The patient was managed with anticoagulation, cautious diuresis, supportive therapy, and initiation of pulmonary vasodilator therapy, with referral to a specialized center for consideration of surgical intervention. This case emphasizes the importance of thorough clinical evaluation, early imaging, and hemodynamic assessment in young adults presenting with unexplained exertional limitation. Recognition of underlying thrombophilic disorders is crucial to guide management, prevent recurrent thrombosis, and preserve right ventricular function, underscoring the value of a multidisciplinary approach in optimizing long-term outcomes in CTEPH.

Background. The problem of diagnosis and prevention of postoperative coagulopathies is quite relevant in modern orthopaedics, since an increasing number of patients with various pathologies of the hip joints undergo arthroplasty both in Ukraine and abroad. The purpose: based on the analysis of risk factors for the development of venous thromboembolic complications in patients with hip joint pathology after arthroplasty, to substantiate a set of measures for their prevention. Materials and methods. Patients who underwent hip arthroplasty were divided into the following groups: group I — low risk, 20–40 years old (n = 13); group II — moderate risk, 41–60 years old (n = 45); group III — high risk, 61–80 years old (n = 42). To assess the risk of thrombotic complications, a method similar to the J.A. Caprini score was used. Results. Analysis of thrombotic complications in the studied groups of patients after total hip replacement compared to the data of the scientific literature showed that complications in the form of pulmonary embolism were not observed in our patients. According to the literature, they are found in 1.08–30 % of cases. Deep vein thrombosis of the lower extremities was detected in 4.65 and 10–20 % of patients, respectively (an average decrease of 5.35 %), oedema of the lower extremities (chronic venous insufficiency) — in 15.5–20.9 and 17–25 % of cases (an average decrease of 3 %). Conclusions. Thromboprophylaxis of venous thromboembolic complications during total hip arthroplasty requires an individual approach to patients, taking into account risk factors both in the pre-operative and postoperative periods. The prevention program we proposed in the studied patients, compared to the literature data, allowed us to reduce the number of thrombotic complications: in group I of patients with a low risk, these complications were not observed, in groups II and III, deep vein thrombosis of the lower extremities decreased by 5.35 %, oedema of the lower extremities by 3 %, hematomas in the surgical area by 1.5 %. The data obtained indicate the effectiveness and feasibility of using a set of thromboprophylaxis measures proposed by us in patients after hip arthroplasty.

Objectives Etodolac (ETD), an insoluble anti-inflammatory drug, undergoes first-pass metabolism, which limits its oral bioavailability. The current study presents the trials for improvement of drug solubility on one hand and formulation of different emulgel systems loaded with modified drug on the other hand. Significance The Prolonged oral administration of ETD results in serious gastrointestinal problems. Therefore, the improvement of its solubility and modifying an alternative route of administration will increase its bioavailability and lessen its adverse effects, providing an alternative safe delivery system for inflammatory signs treatment. Methods The current study focused on the formulation of different emulgel systems since medicated emulgels were constructed by loading the emulgels with either pure ETD or modified ETD adsorbate (ETD/Avicel, 1:2 ratio). Finally, the in vivo studies were accomplished by studying the anti-inflammatory activity of ETD emulgels using albino rats. Results All the prepared emulgels showed acceptable physical properties since sodium alginate emulgel showed superior drug release compared with other gelling agents. The drug release profile was affected significantly by both emulsifying and gelling agents’ concentration. The release kinetics data showed that the main mechanism of drug release was the Higuchi diffusion model. concerning the in vivo results, the extreme edema inhibition was obtained upon using emulgel formulae containing modified ETD with penetration enhancer (5% PG + 5% oleic acid). The modified emulgels did not show any sign of irritation on rats’ dorsal skin. Conclusion The obtained results highlighted the promising application of topical ETD emulgels as an alternative anti-inflammatory drug delivery system.

Lupus podocytopathy (LP) is an increasingly recognised and histopathologically distinct entity within the spectrum of lupus nephritis (LN). It is defined by diffuse podocyte foot process effacement in the absence of subendothelial or subepithelial immune complex deposition and often mimics minimal change disease or focal segmental glomerulosclerosis. LP is typically observed at the onset of systemic lupus erythematosus (SLE) or in patients with known LN. We report a rare case of LP in a 28-year-old Japanese woman with a 12-year history of SLE and no prior renal involvement. She presented with fever, malar rash, arthralgia, and progressive bilateral lower extremity oedema. Laboratory studies revealed marked hypoalbuminemia (1.5g/dl), nephrotic-range proteinuria (15g/gCr), elevated anti-dsDNA antibody titers (>400IU/ml), and hypocomplementemia. Renal biopsy revealed ISN/RPS 2018 class II LN, with mild mesangial hypercellularity and mesangial deposition of IgG, C3, and C1q, without subendothelial or subepithelial immune complexes. Electron microscopy confirmed extensive foot process effacement, establishing the diagnosis of LP. The coexistence of class II LN and LP accounted for the acute onset of nephrotic syndrome in the absence of proliferative changes. The patient was treated with methylprednisolone pulse therapy, high-dose corticosteroids, and intravenous cyclophosphamide, followed by oral cyclosporine. This regimen resulted in prompt clinical and immunological improvement, including near-complete resolution of proteinuria. She remained in remission throughout a 6-month follow-up. This case emphasises the need to consider LP in SLE patients with nephrotic syndrome, even in the absence of prior renal complications during long-term follow-up.

Background: Chronic refractory edema in the lower extremities is a disabling condition characterized by persistent swelling and venous stasis skin changes, despite standard conservative therapies. Research Question: What are the underlying etiologies of chronic refractory lower extremity edema, and how effective is a structured, integrated diagnostic protocol in improving etiologic classification and guiding targeted management? Study Design and Methods: This was a single-center, retrospective analysis of 58 prospectively enrolled patients with chronic, refractory lower extremity edema persisting for ≥1 year, all of whom underwent a standardized diagnostic protocol. Superficial and deep venous insufficiency were assessed using duplex ultrasonography with reflux testing. Central venous anatomy was evaluated with iliocaval ultrasonography to detect potential obstructions in the inferior vena cava or iliac veins. Right heart catheterization was performed to assess for pulmonary hypertension, a possible contributor to chronic venous hypertension in the lower extremities. Iliocaval venography and intravascular ultrasound were employed to confirm or exclude obstructive pathology of the central veins. Right heart catheterization and invasive venous assessments were conducted concurrently. Etiologies were categorized as cardiopulmonary (pulmonary hypertension [PH]), central (non-thrombotic iliac vein lesion [NIVL]), peripheral (superficial venous insufficiency [SVI]), or multifactorial. Results: Of the 58 patients, 51.7% had a single identifiable etiology, while 41.4% had multifactorial causes. Non-thrombotic iliac vein lesion (NIVL) was the most common etiology, identified in 55.2% of cases, followed by pulmonary hypertension (PH) in 48.3%, and superficial venous insufficiency (SVI) in 43.1%. Among patients with multifactorial etiologies, NIVL frequently coexisted with either PH or SVI. Unknown etiology, not attributable to any of the specified categories (NIVL, PH, or SVI), was identified in 6.7% of patients. Endovascular intervention for iliocaval obstruction (n = 23) and venous ablation for isolated SVI (n = 10) led to sustained clinical improvement, with no recurrence or procedural complications observed during follow-up. Interpretation: This pathophysiology-based diagnostic algorithm enabled accurate etiologic classification and informed individualized treatment strategies for patients with chronic refractory edema and chronic venous skin changes of the lower extremities.

Description of Case: Giant coronary artery aneurysms (CAAs) are rare and pose diagnostic and therapeutic challenges, particularly when asymptomatic or incidentally discovered. Right atrial (RA) compression due to CAA is extremely uncommon and lacks standardized management guidelines. We report a 59-year-old man with prior inferior ST-elevation myocardial infarction (2009) and known right coronary artery (RCA) ectasia, presenting with dyspnea at rest and new-onset atrial fibrillation. Physical examination revealed hypoxemia, bilateral lower extremity edema, and bibasilar crackles. Transthoracic echocardiography showed mild biventricular dysfunction and biatrial enlargement. Pulmonary computed tomography angiography excluded thromboembolism but incidentally identified a 6.6 × 6.4 cm proximal RCA aneurysm. Coronary computed tomography confirmed RA compression without tamponade or restrictive physiology. Right heart catheterization showed normal pulmonary artery pressures, excluding pulmonary hypertension. The patient remained hemodynamically stable and was initially discharged on optimal medical therapy. Coronary angiography revealed RCA occlusion with retrograde perfusion via left anterior descending artery collaterals. After multidisciplinary Heart Team discussion, conservative management was initially considered. However, due to aneurysm size and risk of complications, an endovascular approach was pursued. Methods: The patient underwent percutaneous intervention under conscious sedation, utilizing dual arterial access (right femoral and left radial). The procedure included selective RCA catheterization, balloon occlusion testing proximal to the aneurysm, and deployment of a vascular plug at the RCA ostium. Discussion: Selective RCA catheterization was achieved, and a 0.014-inch guidewire was advanced into the aneurysmal sac. Balloon occlusion was performed proximal to the aneurysm to test for tolerance, followed by deployment of a vascular plug at the RCA ostium, achieving aneurysm exclusion. The patient remained stable throughout, with no clinical or electrical instability. Post-procedural imaging confirmed cessation of flow into the aneurysmal sac, without new compressive or ischemic complications. This case highlights the importance of individualized, multidisciplinary management in rare giant CAAs. In selected patients with preserved hemodynamics and suitable anatomy, endovascular exclusion with vascular plugs offers a safe and effective alternative to surgery.

Introduction: Constrictive pericarditis (CP) is a rare but reversible cause of diastolic heart failure caused by chronic pericardial inflammation, fibrosis, and calcification that impairs ventricular filling. Often misdiagnosed as HFpEF (heart failure with preserved ejection fraction), CP has an estimated U.S. prevalence of 9–10 cases per million. Early recognition is crucial, as surgical pericardiectomy can be curative. Case Presentation: A 60-year-old male with hypertension, type 2 diabetes, and obstructive sleep apnea presented with progressive exertional dyspnea, fatigue, bilateral lower extremity edema, intermittent exertional chest pain, orthostatic dizziness, and palpitations. Initial evaluation in 2022 showed preserved left ventricular ejection fraction and no pericardial abnormalities on transthoracic echocardiogram. Myocardial perfusion SPECT revealed a mild right coronary artery perfusion defect. EKG showed right bundle branch block with nonspecific ST-T changes. In February 2024, left heart catheterization revealed mild coronary artery disease and incidental pericardial calcifications. By June 2024, CT angiography confirmed diffuse pericardial thickening and dense calcifications around the left ventricular apex, consistent with prior pericarditis. Right heart catheterization in July 2024 demonstrated equalization of diastolic pressures (Right Atrium: 25 mmHg, Right Ventricular End Diastolic Pressure: 24 mmHg, Pulmonary Capillary Wedge Pressure: 24 mmHg, Left Ventricular End Diastolic Pressure: 24–25 mmHg), reduced cardiac output (1.6 L/min), low cardiac index (1.7 L/min/m 2 ), and mildly elevated Pulmonary Vascular Resistance (3.2 Wood units), confirming CP. The patient underwent pericardiectomy without cardiopulmonary bypass in August 2024. Pathology showed pericardial calcifications and chronic inflammation. Postoperatively, the patient reported improved exercise tolerance and resolution of symptoms. Discussion: This case highlights the diagnostic challenge of CP, especially in patients without classic risk factors such as prior surgery, radiation, or tuberculosis. The clinical picture mimicked HFpEF, but subtle clues—pericardial calcification and invasive hemodynamic findings—were critical for diagnosis. Timely pericardiectomy led to significant clinical improvement, emphasizing the importance of early recognition and intervention in CP.

Introduction: Primary cardiac synovial sarcoma (PCSS) is an extremely rare cardiac tumor, representing less than 1% of all primary cardiac tumors and approximately 5% of cardiac sarcomas. Case Report: 55-year-old male with a past medical history of hypertension, hyperlipidemia, autism spectrum disorder presented to the emergency department for evaluation of progressive dyspnea on exertion. It was not associated with chest pain, fevers, chills, cough, lower extremity edema, orthopnea, paroxysmal nocturnal dyspnea or night sweats. An electrocardiogram showed normal sinus rhythm with nonspecific T-wave changes. His blood pressure was normal. Initial blood work showed mild hyperbilirubinemia, thrombocytopenia, elevated BNP and D-dimer. A CT angiogram of pulmonary artery showed a 7.5 x 4.6 cm mass arising from the right ventricle (RV). A transthoracic echocardiogram (TTE) showed right atrial (RA) and RV dilation with a large mobile heterogeneous mass taking up most of the ventricular cavity and prolapsing into the right atrium during systole, obstructing flow through the tricuspid valve with 45% of Left ventricular ejection fraction (LVEF). A cardiac MRI confirmed heterogenous RV mass with late gadolinium enhancement, attached to inferior wall of the RV causing significant compromisation RV function. Patient underwent a TTE guided endomyocardial biopsy which confirmed diagnosis of biphasic synovial sarcoma with SS18 rearrangement. The patient was started on doxorubicin and ifosfamide. However, he had adverse reaction from ifosfamide. PET scan did not show any evidence of local or distant metabolically active metastasis. At this point patient’s liver function test has improved. After multidisciplinary discussion patient was planned to continue doxorubicin therapy as an outpatient pending final surgical decision after recovery from acute rehabilitation. RV mass reduced in size on subsequent TTE. Patient is currently under evaluation of surgical resection or advance therapy. Discussion: Due to the rarity of PCSS, there are currently no established guidelines for its standard management. This case highlights the safety and feasibility of performing a TTE guided endomyocardial biopsy of a RV mass. Additionally, it also highlights efficacy of combining neo-adjunctive therapy to reduce the tumor burden in hemodynamically stable patients. This strategy may improve the likelihood of successful surgical resection and help stabilize patients for subsequent advanced therapies.

Background: Amid the opioid pandemic, rising intravenous drug use (IVDU) has markedly increased the incidence of tricuspid valve endocarditis (TVE), a serious complication. While long-term IV antibiotics are the mainstay treatment, refractory cases may require surgery. Tricuspid valvectomy without prosthetic replacement is a rare option, chosen in select cases to reduce reinfection risk and support recovery from IVDU. However, this approach can cause chronic right heart volume overload, right atrial enlargement, and atrial fibrillation, leading to eventual valve replacement in a large number of cases. Case report: We report a rare case of a 61-year-old male with a longstanding history of IVDU who presented with progressive shortness of breath and peripheral edema, 32 years following isolated tricuspid valvectomy without valve replacement performed for refractory tricuspid valve endocarditis (TVE). His past medical history included COPD on home oxygen therapy, paroxysmal atrial flutter, and heavy tobacco use. Clinical examination revealed signs consistent with chronic venous congestion, including bilateral lower extremity edema and elevated jugular venous distention. Echocardiography assessment demonstrated preserved left ventricular ejection fraction (65%), markedly dilated right atrium and ventricle (ventricularization of the right atrium), absence of the tricuspid valve, and elevated central venous pressure. Due to underlying COPD, initial respiratory management led to clinical improvement, and the patient was discharged for outpatient cardiopulmonary follow-up. We decided against valve replacement during his clinic visit, given his medical history and ability to perform all daily activities independently without any symptoms. Discussion: This report underscores the remarkable feasibility of prolonged survival following tricuspid valvectomy without prosthetic replacement. Despite significant anatomical changes, including marked right-heart chamber dilation, severe right heart failure was notably absent even decades post-surgery. It challenges traditional surgical paradigms and suggests that conservative management may remain viable decades after valvectomy, calling for more nuanced decision-making frameworks. Our findings underscore the need for standardized guidelines and long-term echocardiographic surveillance in patients post-valvectomy to identify subtle signs of decompensation and optimize timing for potential intervention.

Background: Primary cardiac lymphoma (PCL) is an extremely rare malignancy, accounting for approximately 1–2% of primary cardiac tumors and about 0.5% of extranodal lymphomas. It primarily affects immunocompetent adults, with a median age of 55–65 years, and male predominance (65–85%). Case Presentation: A 44-year-old male with well-controlled HIV on Rilpivirine presented with a 2-week history of progressive shortness of breath, facial edema, and exertional peripheral cyanosis. His physical exam confirmed facial and upper extremities edema and jugular venous distension suggestive of superior vena cava syndrome. Contrast computed tomography (CT) of the chest identified a large 12 × 6.2 × 7.5 cm lytic rib lesion invading the pleura and chest wall, accompanied by left supraclavicular, axillary, mediastinal, and upper abdominal lymphadenopathy. CT also showed a large (8.3 × 5.8 × 6.0 cm) right atrial mass causing near-complete occlusion of the superior and inferior vena cava (Fig 1A). A transthoracic echocardiogram with contrast-enhanced imaging confirmed a large right atrial mass extending into the IVC (Fig 1B). Cardiac magnetic resonance imaging (MRI) further detailed an 8.3 × 6.5 × 6.4 cm mass nearly filling the right atrium, infiltrating the interatrial septum with mass effect on left atrium and encroaching on the right superior and inferior pulmonary veins (Fig 2A). Biopsy of the rib lesion confirmed high-grade B-cell lymphoma with 11q aberration. The patient was started on Rituximab combined with E-POCH chemotherapy on day 7 of admission. A follow-up PET-CT scan after the first cycle showed significant regression of the intracardiac mass (Fig 2B.) Discussion: PCL is an uncommon extranodal lymphoma, most often presenting as diffuse large B-cell lymphoma (DLBCL). High-grade B-cell lymphoma with 11q aberration (HGBCL-11q) is a distinct entity characterized by a unique 11q gain/loss cytogenetic pattern, typically lacking MYC rearrangement and frequently showing Burkitt-like morphology. Standard treatment for primary cardiac DLBCL involves immunochemotherapy, most commonly R-CHOP unless contraindicated. Curative regimens yield 5-year survival rates of 70–80% in selected cohorts; however, prognosis worsens with advanced or extracardiac disease.

Description of Case: A 53 year old female with past medical history of autoimmune thyroid disease post-thyroidectomy (not on levothyroxine for over one year), chronic lower extremity edema, generalized anxiety disorder, hysterectomy, and cholecystectomy, presented with 2 day history of progressive bilateral leg swelling and right lower extremity erythema. She reported worsening exertional dyspnea and orthopnea over several months. She denied chest pain, syncope, fever, chills, nausea, or diaphoresis. Initial labs were notable for anemia with a hemoglobin of 8.3, potassium 3.3, elevated TSH 38.21, with a low free T3 1.8 and low free T4 0.25, normal BNP 36 and elevated D-dimer 1.32. Chest X-ray showed cardiomegaly with mild perihilar pulmonary congestion. EKG showed normal sinus rhythm and nonspecific findings of an old anterior myocardial infarction. Transthoracic echocardiogram (TTE) revealed a large pericardial effusion with right atrial and right ventricular collapse, consistent with cardiac tamponade. Urgent pericardiocentesis was performed under echocardiographic and fluoroscopic guidance, and 500 mL of straw-colored pericardial fluid was aspirated. Post-procedural TTE confirmed complete resolution of the effusion and normalization of cardiac chamber function without evidence of residual tamponade physiology. The pericardial fluid was sent for diagnostic analysis which was exudate. A pericardial drain was left in place and removed after 24 hours. Plan is for repeat TTE in 2 weeks. Discussion: Hypothyroidism is a known but rare cause of large pericardial effusions and tamponade. This case underscores that while pericardial effusion is a relatively common finding in hypothyroidism, progression to tamponade is rare due to the typically slow accumulation of fluid. However, delayed recognition or additional stressors can tip a patient into hemodynamic compromise. Clinicians should maintain a high index of suspicion for pericardial effusion in patients with long-standing or untreated hypothyroidism presenting with dyspnea or hemodynamic instability. Prompt echocardiographic evaluation and thyroid hormone replacement are essential for optimal outcomes.

Left ventricular non-compaction cardiomyopathy (LVNC) is an infrequent cardiac disorder characterized by prominent trabeculations, deep intertrabecular recesses, and thinning of the compacted myocardial layer, predisposing to heart failure, arrhythmias, and thromboembolic complications. The relationship between myocardial inflammation and chordae tendineae rupture is clinically relevant, as prior inflammatory processes may compromise valvular structures, leading to acute mitral regurgitation and ventricular overload. We present the case of a 45-year-old male with a history of severe mitral regurgitation and heart failure with preserved ejection fraction, who presented with progressive dyspnea, oppressive chest pain, diaphoresis, and lower extremity edema. Clinical assessment revealed arterial hypertension, tachycardia, hypoxemia, a loud systolic mitral murmur, jugular venous distension, and peripheral edema. Complementary studies demonstrated LVNC, severe prolapse of the posterior mitral leaflet with chordae tendineae rupture, acute mitral regurgitation, and pulmonary hypertension. Thoracic computed tomography revealed chronic lesions compatible with a previous viral infection, although specific SARS-CoV-2 testing results were unavailable. The patient underwent mitral valve replacement with a mechanical prosthesis, with postoperative complications including acute pulmonary edema, pleural effusion, renal insufficiency, and left ventricular dysfunction, which resolved favorably during hospitalization. This case highlights the importance of early recognition of LVNC and its valvular complications, as well as a comprehensive approach and timely surgical intervention to optimize clinical outcomes in complex cardiovascular scenarios.

Subclavian venous valve stenosis is a rare but significant cause of upper extremity venous hypertension in hemodialysis patients. When standard endovascular treatments are not feasible, alternative techniques may be required. A man in his 60s with end-stage renal disease on maintenance hemodialysis for 19 years, with a right forearm prosthetic arteriovenous graft (AVG), presented with right upper extremity edema and dialysis dysfunction due to subclavian vein occlusion. Intravascular ultrasound (IVUS) revealed fibrotic valve leaflets at the occlusion site. An 8 mm balloon was pulled through the lesion under IVUS and fluoroscopic guidance, resulting in partial cusp rupture. A second 12 mm balloon and a kissing balloon technique with a cutting balloon achieved complete valve disruption. The pressure gradient dropped from 20 to 0 mmHg, and dialysis resumed without complications. This is the first reported case of IVUS-guided balloon-assisted cusp avulsion (BACA) technique for treating fibrotic venous valve stenosis. This approach may offer a viable stentless option when conventional stenting is not feasible due to anatomical or technical limitations.

Rapid post exercise venous refilling time is an independent contributor to chronic venous insufficiency.

Abstract Introduction/Objective Cardiac tumors are rare, with myxomas being the most common primary cardiac tumor. Low-grade neuroendocrine tumors (NETs) are neoplasms arising from neuroendocrine cells, and they are most frequently found in the gastrointestinal tract and lungs. Historically, they were referred to as “carcinoid” tumors. NETs are relatively rare, with an estimated incidence ranging from 2.5 to 5 cases per 100,000 population per year. Involvement of the heart by NETs is exceedingly rare and almost universally represents metastasis from a distant primary. Cardiac metastasis from carcinoid tumors occurs in approximately 4% of patients, many of which have advanced disease and carcinoid syndrome. Primary neuroendocrine tumors of the heart are even rarer, with limited cases described in the literature, and their occurrence within the interventricular septum is virtually unknown. This report highlights a unique case of a low-grade neuroendocrine tumor presenting as a cardiac mass, with a unique natural history. Methods/Case Report A 56-year-old woman with a history of mitral valve minimally invasive surgical repair in 2015 presented with new-onset dyspnea on exertion, dizziness, and a recent presyncopal episode, but no chest pain, orthopnea, flushing, diarrhea, or lower extremity edema. Transthoracic echocardiography revealed a 4 cm spherical mass (size 4 cm) attached to the apex of the interventricular septum, protruding into the right ventricle. Cardiac CT angiography confirmed a well circumscribed mass with no invasion. Whole-body PET-CT showed increased radiotracer uptake localized to the cardiac mass, with no evidence of abnormal uptake elsewhere in the body. The initial impression was a cardiac myxoma. Surgical resection was performed. Gross examination revealed a rounded firm, tan yellow mass measuring 4.0 cm. Histologically, the tumor consisted of a neuroendocrine tumor composed of uniform cells with low-grade features, with no mitotic activity or necrosis. Immunohistochemical stains were positive for Pancytokeratin (AE1/AE3), Chromogranin, and Synaptophysin, supporting the diagnosis of a neuroendocrine tumor. The Ki-67 proliferation index was approximately 1%, indicative of a low-grade tumor. Immunohistochemical stains for Cytokeratin 7, Cytokeratin 20, TTF-1, PAX8, and GATA3 were negative. Of note, immunohistochemical stain for CDX2 was diffusely positive, strongly suggesting origin from a primary tumor in the midgut. Results NA Conclusion Neuroendocrine tumors of the heart are exceedingly rare and often present with non-specific symptoms or no symptoms at all. Imaging findings may mimic more common cardiac tumors, such as myxomas. Histopathologic evaluation and immunohistochemical profiling are essential for definitive diagnosis. CDX2 positivity by immunohistochemistry within metastatic carcinoid tumors is strongly associated with a small intestinal primary, even in the absence of a detectable primary lesion. This case demonstrates the necessity of considering alternate diagnoses other than myxoma for tumors in the ventricle. It also highlights the unique natural history of some of these lesions that present as metastases before detection of a primary tumor, and without the clinical features of carcinoid syndrome.

Disclosure: S. Obialo: None. B. Moazzami: None. B. Hayes: None.Background: Myxedema coma is a rare, life-threatening complication of severe, untreated hypothyroidism characterized by altered mental status, hypothermia, and multi-organ dysfunction. While it’s known to lead to metabolic derangements, its association with acute compartment syndrome and rhabdomyolysis is exceedingly uncommon and rarely reported. We present a unique case of myxedema coma complicated by bilateral upper and lower extremity acute compartment syndrome and severe rhabdomyolysis. Clinical Case: A 46-year-old male presented with lethargy, bilateral upper and lower extremity swelling and slurred speech. Due to loss of insurance from lack of employment, he was unable to continue taking his medications for the past three to four months. On examination he was somnolent, mild slurring of speech, generalized edema in bilateral upper and lower extremities. Laboratory workup revealed profound hypothyroidism with a TSH of 342 uIU/ml (0.35 – 4.94 uIU/ml) and T4 of < 0.42 ng/dL (0.70 – 1.48 ng/dL). Creatine kinase (CK) was initially elevated at 25,095 IU/L (30 – 200 IU/L), then peaked at 74,000 IU/L (30 – 200 IU/L). Transaminitis was also present with initial AST 179 IU/L (5 – 34 IU/L) and ALT 53 IU/L (less than 55 IU/L) with a peak at AST 1201 IU/L (5 – 34 IU/L) and ALT 208 IU/L (less than 55 IU/L). The patient was started on liothyronine 5 mcg IV and a loading dose of levothyroxine 200 mcg IV followed by 50 mcg oral daily. Stress-dose hydrocortisone100 mg IV every 8 hours was initiated for suspicion of adrenal insufficiency and started on IV maintenance fluids for rhabdomyolysis. Due to increasing CK levels despite IV fluids, he was then upgraded to the ICU for continuous renal replacement therapy to enhance myoglobin clearance and to prevent rhabdomyolysis induced acute kidney injury. Within a few days into the admission, he underwent bilateral upper and lower extremity fasciotomies with later staged wound closure. His thyroid function improved with repeat TSH of 110 uIU/ml (0.35 – 4.94 uIU/ml). CK decreased to 2934 IU/L (30 – 200 IU/L). Glucocorticoids were tapered off near discharge. Conclusion: Early recognition of acute complications of myxedema coma, is paramount to getting the prompt treatment necessary. Clinicians should maintain a high index of suspicion for rhabdomyolysis and evolving compartment syndrome in patients with severe hypothyroidism presenting with extremity swelling and weakness, as early intervention is critical to prevent irreversible tissue damage and multiorgan failure.Presentation: Saturday, July 12, 2025

Disclosure: A. Dharia: None. M. Grimes: None.Introduction: POEMS syndrome is a rare paraneoplastic disorder linked to plasma cell dyscrasia, characterized by polyneuropathy, organomegaly, endocrinopathy, monoclonal plasma cell proliferation, and skin changes, often with additional clinical features. Clinical Case A 76 year old male presented with progressive lower extremity weakness over three months, eventually requiring a wheelchair. His symptoms developed gradually and included chest pain radiating to his back, vomiting, bilateral tingling and numbness in his hands and feet, visual changes, primarily decreased acuity, lower extremity edema, fatigue, and erectile dysfunction. Physical examination revealed hypertrichosis, white nails, hyperpigmentation, and a previously excised glomeruloid angioma. He was found to have an IgG lambda M protein, lambda serum free light chain of 177 mg/L (5.71 -26.3 mg/L) and VEGF 10,999 pg/mL (62-707 pg/mL). CT imaging revealed multiple sclerotic lesions in pelvis and T12 of the spine, and splenomegaly. EMG showed motor and sensory polyneuropathy with axonal and demyelinating features. Bone marrow biopsy confirmed a plasma cell clone and megakaryocytic hyperplasia. Endocrine was consulted for abnormal TFTs and a diagnosis of POEMS was considered. Labs revealed sodium 134 mmol/L (136-145 mmol/L), potassium 5.6 mmol/L (3.5-5.2 mmol/L) creatinine 2.28 mg/dL (0.7-1.2 mg/dL), platelet 561 k/mcL (145-445 k/mcL), TSH 12.3 mIU/L (0.4-4.5mIU/L), FT4 0.65ng/dl(0.7-1.9 ng/dl), ACTH 70 pg/ml (10-48 pg/ml), cosyntropin stimulation test showed a peak cortisol of 13 mcg/dL, total testosterone 40 ng/dL( 300-1,000 ng/dL), LH <1 mIU/mL(2-9 mIU/mL), FSH <1 mIU/mL( 1-12 mIU/mL), prolactin 35.9 ng/mL(4-15.2 ng/mL) and IGF-1 24 ng/mL (50-185 ng/mL). His prior brain MRI showed a normal sella/pituitary, and a dedicated pituitary MRI was deferred until renal function improved. His symptoms met major POEMS criteria (polyneuropathy, sclerotic bone lesions, M-protein spike) and minor criteria (splenomegaly, endocrinopathy, hyperpigmentation, hypertrichosis, glomeruloid angioma, and thrombocytosis). Treatment included initiation of physiologic hydrocortisone, weight-based levothyroxine and chemotherapy (daratumumab, dexamethasone, lenalidomide), which improved renal function and strength, with the patient transitioning to leg braces for ambulation. Despite clinical improvement, his hypogonadal symptoms, including erectile dysfunction persisted, so topical testosterone was initiated for secondary hypogonadism. Discussion POEMS syndrome demands high clinical suspicion due to its nonspecific presentation. Early diagnosis and a multidisciplinary approach are key to improving outcomes. Endocrinopathies like hypothyroidism, adrenal insufficiency, and hypogonadism complicate management, making prompt detection and hormone replacement crucial for optimal care.Presentation: Monday, July 14, 2025

Disclosure: M. Ayman: None. S. Manikonda: None.Introduction: Obesity is a major risk factor for cardiovascular and metabolic diseases, including pulmonary hypertension. Obesity-induced PH is associated with high body mass index (BMI), obstructive sleep apnea (OSA), and increased right ventricular strain. The pathophysiology involves increased cardiac output, hypoxia due to OSA, and the release of adipokines, contributing to pulmonary vascular remodeling. Case Presentation: A 45-year-old woman with a BMI of 42 kg/m² presented with dyspnea on exertion, fatigue, and lower extremity edema. She had a history of obstructive sleep apnea, hypertension, and type 2 diabetes. Despite management of these conditions, her symptoms worsened over the past year. Physical exam showed bilateral lower limb edema, jugular venous distension, and signs of right-sided heart failure (hepatomegaly, peripheral edema). Vital signs: heart rate 98 bpm, BP 130/85 mmHg, oxygen saturation 94% on room air. Lung auscultation revealed bilateral crackles. Investigations:Chest X-ray: Right heart enlargement and pulmonary congestion.Echocardiography: Right ventricular dilation with tricuspid regurgitation jet velocity of 3.8 m/s, RVSP of 55 mmHg, confirming PH.Pulmonary Function Tests (PFTs): Mild restrictive lung pattern, likely secondary to obesity.Sleep Study: Moderate OSA with oxygen desaturation.Right Heart Catheterization: Mean pulmonary artery pressure (mPAP) 45 mmHg and pulmonary vascular resistance (PVR) 5.2 Wood units, confirming obesity-induced PH.Discussion: Obesity-induced PH results from increased cardiac output, pulmonary vascular changes, and right-sided heart failure. OSA contributes to pulmonary vasoconstriction and right ventricular strain. Adipokines play a role in vascular remodeling. In this patient, obesity and OSA were key factors in PH development. Early diagnosis is crucial to prevent severe complications. PH progresses slowly and requires a comprehensive management approach addressing underlying factors.Management:Obesity Management: Referral to a weight management program, including diet, exercise, and bariatric surgery consideration.CPAP Therapy: Initiated to manage OSA and improve nocturnal oxygenation.Diuretics: Furosemide 40 mg daily to manage fluid overload and heart failure symptoms.Conclusion: Obesity-induced pulmonary hypertension is a serious condition requiring early recognition and multidisciplinary management. This case highlights the importance of addressing both obesity and OSA in PH treatment. Weight loss, CPAP therapy, and pulmonary vasodilators significantly improved the patient's symptoms and prognosis. Timely intervention can prevent further complications and improve outcomes.Presentation: Saturday, July 12, 2025

Abstract Disclosure: Z. Raad: None. L. Esper: None. N. Reyes: None. Background: Adrenal insufficiency due to metastatic disease most commonly is in the form of peripheral adrenal insufficiency (PAI), which is documented as an uncommon presentation of non-Hodgkin lymphoma (NHL).1 Here we discuss an even rarer case in which central adrenal insufficiency (CAI) resulted from suspected pituitary involvement of diffuse large B cell lymphoma (DLBCL).2Clinical case We consider the case of an 82 year old woman who was found to have DLBCL with central nervous system involvement due to presentation with adrenal insufficiency and central hypothyroidism. This patient presented with subacute progressive fatigue, exertional dyspnea, and deterioration of functional independence. She had tried and failed doxycycline for a presumed tick-borne illness as well as an additional antibiotic course for asymptomatic bacteriuria. Though she required a nasal cannula to maintain adequate oxygen saturation, apart from mild lower extremity edema her exam was benign. Initial workup was significant for severe hyponatremia (123 mmol/L, n 136-145 mmol/L) and marked central hypothyroidism with TSH 0.08 mIU/L (n 0.45-4.50 mIU/L), fT4 0.5 ng/dL (n 0.7-1.5 ng/dL), and fT3 1.4 pg/mL (n 1.6-3.9 pg/mL). Random cortisol obtained at 1 PM was 9.7 ug/dL, followed by an equivocal AM cortisol of 6.8 ug/dL. Due to concern for central hypothyroidism and CAI, brain MRI was obtained which showed asymmetric pituitary enlargement and other intracranial features concerning for neoplasm. Lumbar puncture showed mild leukocytic pleocytosis (9/uL, n 0-5/uL) without cerebrospinal fluid dyscrasia. Bone marrow biopsy revealed chronic lymphocytic leukemia (CLL), an unlikely culprit for her neuroradiology findings. Brain biopsy of the dura and frontal lobe revealed DLBCL likely resulting from CLL Richter transformation, elucidating the underlying cause of her CAI and central hypothyroidism. She was started on levothyroxine and hydrocortisone inpatient, which she was ultimately able to discontinue at outpatient follow up after starting dedicated treatment for DLBCL. Conclusion: This patient’s case represents an uncommon occurrence of NHL-induced CAI. Adrenal insufficiency without primary adrenal involvement in the setting of lymphoma warrants thorough investigation of central causes.

Abstract Disclosure: T. Jain: None. K. Zulqadar: None. S. Ifthikhar: None. R. Sharma: None. N. Jaafar: None. S. Israr: None. A. Khan: None. Background: Insulin therapy for diabetes management can occasionally trigger rare complications like insulin edema, leading to rapid fluid retention and volume overload. We present a case where insulin initiation unmasked heart failure with preserved ejection fraction (HFpEF), highlighting the need for vigilance in managing insulin in at-risk patients. Case Presentation: A 63-year-old male with a history of atrial fibrillation (AF), hypertension and type 1 diabetes mellitus presented to emergency department (ED) with progressive shortness of breath, orthopnea, leg swelling and 42 lb weight gain in 11 days. On exam, he had jugular venous distension and anasarca. The patient was diagnosed with uncontrolled diabetes, with an HbA1c of 17%, and was initiated on a basal-bolus insulin regimen 11 days prior to presentation. In the ED, labs revealed normal troponin levels, an elevated pro- brain natriuretic peptide at 1462 pg /mL and EKG revealed AF with rapid ventricular response, Q waves in II, III, AVF and poor R wave progression. He was admitted for acute decompensated HF. A transthoracic echocardiogram demonstrated mild concentric left ventricular hypertrophy with an ejection fraction of 55% with no wall motion abnormalities, and indetermined diastolic function. Thyroid, liver and renal function testing was normal with no proteinuria. The patient reported a notable decrease in urine output since starting insulin therapy. Previously, he experienced polyuria, voiding large volumes every 2-3 hours. His symptoms were attributed to new-onset HFpEF following insulin therapy, which led to reduced polyuria but exacerbated fluid retention, worsening his heart failure symptoms. He received intravenous diuretics, resulting in symptom resolution and was discharged with a titratable diuretic regimen. Conclusion: This case highlights a rare complication of insulin therapy—rapid fluid retention leading to HF symptoms, even in patients without a prior HF diagnosis. Insulin edema is rare complication of insulin use that can cause variety of manifestations ranging from lower extremity edema to anasarca and heart failure1. Clinicians should be vigilant about this potential complication when starting insulin in patients with predisposing conditions. 1.Chelliah A, Burge MR. Insulin Edema in the Twenty-first Century: Review of the Existing Literature. Journal of Investigative Medicine. 2004;52(2):104-108. doi:10.1177/108155890405200218 Presentation: Sunday, July 13, 2025