Double-chambered right ventricle (DCRV) is a rare congenital cardiac anomaly caused by hypertrophy of right ventricular muscular structures, most commonly the moderator band, resulting in intracavitary obstruction and division of the right ventricle into high- and low-pressure chambers. It accounts for approximately 0.5%-2% of congenital heart diseases and is usually diagnosed in childhood, though delayed presentation in adulthood may occur. DCRV is frequently associated with other congenital anomalies and is often discovered on cardiac imaging. A 55-year-old asymptomatic woman was referred for cardiology evaluation due to a family history of thoracic aortic aneurysms. Physical examination revealed pectus excavatum and a cardiac murmur. Electrocardiography showed left ventricular hypertrophy with repolarization abnormalities. Transthoracic echocardiography identified right ventricular apical obstruction, prompting cardiac MRI. This demonstrated marked right ventricular hypertrophy and a prominent moderator band dividing the ventricle into proximal and distal chambers, consistent with type 1 DCRV. Cine imaging revealed a focal high-velocity jet at the obstruction site. The patient was referred for cardiology follow-up to consider surgical management, though this was not found to be necessary due to her being asymptomatic. DCRV is diagnostically challenging due to nonspecific or absent symptoms in adults. While echocardiography may detect obstructive flow, cardiac MRI is essential for detailed anatomical assessment and identification of associated anomalies. Early diagnosis is important, as guidelines recommend surgical intervention to prevent right ventricular dysfunction. DCRV may present in asymptomatic adults. This case highlights the value of advanced cardiac imaging in diagnosing atypical right ventricular obstruction and guiding timely management to prevent disease progression.

Papillary fibroelastoma (PFE) is a benign primary cardiac tumor arising from the endocardial surface, most commonly affecting the valvular endocardium. Although often incidental, PFEs may lead to serious complications, including systemic embolization, valvular obstruction, or regurgitation. Aortic valve fibroelastoma resulting in severe aortic insufficiency (AI) may be rare. A 77-year-old woman with a history of hypertension and chronic kidney disease presented with progressive dyspnea, orthopnea, and bilateral lower extremity edema. Examination revealed a diastolic murmur at the left lower sternal border. Transthoracic echocardiography demonstrated a tri-leaflet aortic valve with preserved left ventricular systolic function and moderate eccentric aortic regurgitation due to incomplete cusp coaptation. A transesophageal echocardiogram was performed, which revealed a small, filamentous, and mobile mass that was visualized at the base of the noncoronary cusp (NCC), consistent with a PFE. There were no clinical or laboratory findings suggestive of infection, and the lesion's morphology was inconsistent with vegetation. Holodiastolic flow reversal in the descending aorta confirmed severe AI. The patient was diagnosed with acute decompensated heart failure secondary to severe aortic regurgitation. After medical optimization, she underwent surgical aortic valve replacement. Intraoperative histopathology confirmed the presence of a fibroelastoma originating from the NCC. Postoperative recovery was uneventful, and the patient demonstrated marked symptomatic improvement. This case illustrates a rare presentation of PFE causing severe aortic regurgitation through mechanical interference with cusp closure rather than leaflet destruction. PFEs are typically small, avascular, and pedunculated, and when located near the coaptation zone, they can prevent complete leaflet closure, resulting in significant hemodynamic compromise. Echocardiography remains the diagnostic modality of choice, and multimodal imaging may aid in differentiating PFEs from vegetations or thrombi. Surgical excision is recommended for symptomatic, mobile, or left-sided PFEs due to the risk of embolization and valvular dysfunction. Although rare, PFE of the aortic valve should be recognized as a potential cause of severe AI. Early diagnosis and timely surgical management are curative and prevent embolic complications.

A 17-year-old male presented with intermittent palpitations for 6 months, acutely worsening over 24 h. Physical examination revealed Marfanoid features (arachnodactyly, positive thumb/wrist signs, pectus carinatum) and cardiac abnormalities (irregular rhythm, 3/6 systolic murmur with mid-late click). Echocardiography demonstrated: (1) Aortic sinu (AS) dilation (41 mm); (2) Bileaflet mitral valve prolapse (Barlow's Disease) with myxomatous degeneration (anterior leaflet 3.8 mm, posterior 4.2 mm); (3) Mitral annular disjunction (MAD, 13 mm gap). Transesophageal echo revealed left atrial appendage sluggish flow ("smoke-like echo") without thrombus. CTA confirmed aortic root aneurysm (42 mm) and right hydronephrosis. Electrocardiogram demonstrated paroxysmal atrial flutter. Diagnoses included Marfan syndrome (Ghent criteria), Barlow's Disease with MAD, paroxysmal atrial flutter, and obstructive hydronephrosis. The multidisciplinary team recommended staged interventions. Following catheter ablation for atrial flutter, the patient declined further procedures. Subsequent follow-up showed clinical stability.

A six-year-old male, neutered Golden retriever was presented to the University of Minnesota Veterinary Medical Center Cardiology Service for exercise intolerance, two collapsing episodes, and a newly diagnosed heart murmur. Echocardiogram revealed an intracardiac mass within the left ventricle causing severe left ventricular outflow tract obstruction. The patient re-presented a few weeks later for respiratory distress and was euthanized. At necropsy, a large multilobular mass was noted, which coursed along the mitral valve base and was firmly adhered to the endocardium of the left ventricle. Histology and immunohistochemical staining were consistent with a poorly differentiated sarcoma.

Type A aortic dissection (TAAD) is a life-threatening condition that often presents diagnostic challenges, particularly when mimicking acute myocardial infarction (AMI). This case report describes a 31-year-old male with a history of fever and no cardiovascular history who presented with acute chest pain and rapidly developed hemodynamic instability. Initial assessments revealed mild aortic regurgitation (AR) and ascending aortic dilation but no aortic dissection was reported. ECG showed ST-segment changes, yet coronary angiography ruled out obstructive coronary disease. Serial daily echocardiograms demonstrated rapid progression of AR from mild to severe within 72 h, accompanied by worsening left ventricular dysfunction. Reassessment of aortic CT confirmed TAAD with left main coronary artery involvement. Different elements of his presentation suggested possible other diagnoses, including TAAD, AMI and myocarditis. We discuss how evaluating these other diagnostic possibilities led to the correct diagnosis. This case underscores the diagnostic pitfalls of TAAD masquerading as AMI, it demonstrates the need to consider aortic dissection in patients with AMI and/or emerging diastolic murmurs of AR.

A 73-year-old female presented with split second heart sound (S2) and ejection systolic murmur. The S2 split only during expiration (paradoxical splitting) with a softer second component (pulmonary component), which was in reverse order compared to typical paradoxical splitting (termed reversed paradoxical splitting). Furthermore, the murmur increased during expiration and decreased during inspiration (reversed Rivero-Carvallo's sign). Transthoracic echocardiography revealed a mass adherent to the free wall of the right ventricular outflow tract. Open-heart surgery was performed, and the tumor was surgically resected. Histopathological examination confirmed the diagnosis of a capillary hemangioma. The patient's recovery was smooth and uneventful.

Patent ductus arteriosus (PDA) is a common congenital cardiac condition in neonates. Its frequency is substantially higher in preterm infants, and it is frequently associated with other congenital heart defects. Its persistence into adulthood has become increasingly uncommon due to advances in neonatal screening, echocardiographic diagnosis, and timely therapeutic intervention. The hemodynamic burden imposed by PDA depends on the magnitude of the left-to-right shunt and may result in both short- and long-term complications. While small shunts may remain asymptomatic throughout life, moderate and large shunts can cause pulmonary congestion, cardiac volume overload, organ hypoperfusion, and even death, early in life. When left untreated, particularly in small-to-moderate defects that may not initially meet the criteria for intervention, chronic shunting may progressively result in pulmonary hypertension and heart failure. In adults, heart failure related to PDA is usually associated with preserved or moderately reduced left ventricular ejection fraction (LVEF), whereas severe systolic dysfunction and acquired dilated cardiomyopathy are exceptionally rare. Here, we present the case of a 70-year-old male who was admitted with progressive dyspnea, orthopnea, dry cough, and bilateral lower extremity edema over one month. His medical history included PDA diagnosed in childhood, without intervention or regular follow-up. On admission, physical examination revealed signs of acute heart failure, including tachypnea, jugular venous distension, pulmonary congestion, and marked peripheral edema. Cardiac auscultation demonstrated a prominent second heart sound and systolic murmurs consistent with mitral and tricuspid regurgitation, and a characteristic continuous, "machinery" murmur suggestive of PDA. Electrocardiography showed sinus rhythm with frequent atrial and ventricular premature beats, poor R-wave progression in the precordial leads, and nonspecific ST-T abnormalities in the limb leads. Chest radiography demonstrated cardiomegaly, pulmonary vascular congestion, alveolar edema, and bilateral pleural effusions. Laboratory evaluation revealed elevated natriuretic peptide levels and mildly increased high-sensitivity cardiac troponin I, consistent with the setting of acute heart failure. Transthoracic echocardiography revealed dilation of all four chambers and severe biventricular systolic dysfunction, with an LVEF of 25%, mild mitral and tricuspid insufficiency, and increased systolic pressure in the pulmonary artery. A moderate left-to-right shunt was found. Evaluation by coronary angiography ruled out obstructive coronary artery disease. Further assessment with cardiac magnetic resonance imaging demonstrated a persistent communication between the aortic isthmus and the main pulmonary artery, confirming PDA. A diagnosis of acquired dilated cardiomyopathy secondary to long-standing left-to-right shunt, likely precipitated by frequent atrial and ventricular arrhythmias, was established. Although the patient was a candidate for transcatheter percutaneous ductal closure, he declined any intervention, and optimized guideline-directed medical therapy was initiated. This case represents an exceptionally rare presentation of PDA in adulthood and highlights the importance of lifelong medical surveillance in patients with congenital heart defects.

Transcatheter aortic valve replacement has become an established therapy for severe aortic stenosis, demonstrating prosthesis durability for at least five years (and up to eight years) in recent studies. Structural valve deterioration within 5 years is rare, particularly with self-expanding Evolut prostheses. We present an 88-year-old man with prior coronary artery bypass grafting and severe aortic stenosis who underwent transfemoral transcatheter aortic valve replacement with a 34 mm Evolut valve in 2019. Five years later, he developed progressive dyspnea and chest pain. Examination revealed a grade IV/VI decrescendo diastolic murmur and a markedly wide pulse pressure, raising concern for severe aortic regurgitation. Transesophageal echocardiography demonstrated moderate to severe aortic insufficiency. Coronary angiography revealed patent grafts, without new obstructive native coronary disease. He underwent surgical aortic valve replacement with an Inspiris Resilia bioprosthesis. This case underscores the possibility of rapid prosthetic valve failure and highlights the ongoing importance of physical examination in detecting severe regurgitation. It also contributes to the growing literature on early valve degeneration.

A 57-year-old female patient presented to our outpatient clinic with complaints of anginal chest pain. She had a history of mitral commissurotomy and later mechanical mitral valve replacement via a robotic surgical approach due to rheumatic heart disease. On physical examination, a pansystolic murmur at the apex and an arrhythmic mechanical heart sound were noted. Transesophageal echocardiography (TEE) revealed severe tricuspid valve insufficiency, pulmonary hypertension, moderate to severe aortic stenosis, acquired discrete subaortic membrane (DSM), a paravalvular leak with mild insufficiency in the mechanical prosthetic mitral valve, and non-obstructive pannus on the left ventricular side. The patient underwent reoperation, including DSM resection, aortic and tricuspid valve replacement, and paravalvular leak repair. Postoperative recovery was uneventful. Acquired DSM following mitral valve replacement (MVR) is a rare but increasingly recognized entity. The underlying mechanism may involve postoperative hemodynamic alterations, excessive leaflet preservation, or residual fibrosis. Extended myectomy techniques may offer a more durable solution in selected cases, reducing the risk of recurrence and reoperation.

Subaortic membrane (SAM) is a subtype of left ventricular outflow obstruction, rarely seen in adults. In some cases, SAM may be associated with other congenital defects. The association of patent ductus arteriosus (PDA) and SAM is the rarest, especially in adult patients. The management of these patients is delicate in terms of diagnosis, timing, and the appropriate surgical technique. A 34-year-old patient with a known aortic heart murmur presented with exertional syncope. She was referred to our hospital for aortic valve replacement due to symptomatic aortic stenosis. Transthoracic and transesophageal echocardiography demonstrated a SAM with significant stenosis (mean gradient 48 mmHg) associated with a PDA, mild to moderate aortic regurgitation (AR), and an ascending aortic aneurysm. The heart team decided to proceed with membrane resection, aortic valve replacement, and ascending aortic graft. This case highlights the challenge of managing adult congenital heart disease, particularly regarding diagnosis and optimal timing for surgical intervention. The subaortic membrane is a structural anomaly that can be either congenital or acquired. The primary indication for surgery is the symptomatic form or its association with severe AR. We believe that prophylactic surgery should be considered in isolated cases of mixed anomalies.

A 30-year-old South Asian male with no specific medical history presented with shortness of breath of insidious onset for two months, with facial puffiness and progressive dysphagia. Physical examination revealed dilated veins over the upper chest, upper arms, and back, with an ejection systolic murmur. Thoracic imaging revealed a large mass occupying the anterior mediastinum, encasing the aorta with mass effect on the esophagus, and causing superior vena cava obstruction. Histopathological and immunohistochemical examination of the mass revealed a seminomatous germ cell tumor. Ultrasonography of the testes was normal except for microlithiasis. The patient was initiated on cisplatin-based chemotherapy and showed symptomatic improvement after two cycles. This case describes an uncommon presentation of primary extragonadal germ cell malignancy with testicular microlithiasis, a premalignant condition linked to gonadal germ cell malignancy. Further studies are needed to determine a correlation, if any, between testicular microlithiasis and extragonadal germ cell malignancy.