Left ventricular noncompaction (LVNC) is a rare cardiomyopathy marked by excessive myocardial trabeculations and profound intertrabecular recesses, frequently identified incidentally, yet occasionally linked to significant cardiac dysfunction and adverse outcomes. It is uncommon for LVNC to coexist with other congenital cardiac anomalies, and the concurrent occurrence of LVNC, patent ductus arteriosus (PDA), and bicuspid aortic valve has not been previously reported. We report a 7-month-old female infant who exhibited exertional cyanosis and an episode of syncope in early infancy. Transthoracic echocardiography revealed that the left ventricle was not functioning correctly and that the aorta was too narrow. Therefore, a cardiac computed tomography angiography (CTA) was performed to gather further information. The CTA showed a significant PDA with flow in both directions, predominantly right-to-left shunting. This was caused by pulmonary arterial hypertension, which caused the pulmonary arteries (PAs) and descending thoracic aorta to have different levels of contrast opacification. There was significant dilation in all the heart's chambers and PAs. In addition, classic imaging features of LVNC were identified, including prominent trabeculations and deep intertrabecular recesses, with a noncompacted to compacted myocardial ratio > 3. The aortic valve had two cusps and thickened leaflets and raphes, which caused severe valvular stenosis. These three congenital defects probably worked together to cause early heart failure, pulmonary hypertension, and a high risk of death. This case exemplifies an extraordinarily rare congenital cardiac triad that manifests in infancy, emphasizing the critical importance of CTA in thorough anatomical and functional evaluation. Early identification of intricate associations is essential for risk stratification, multidisciplinary management, and prognostication in affected infants.

Partial anomalous pulmonary venous return (PAPVR) is a congenital cardiovascular malformation in which one or more pulmonary veins drain abnormally into the right atrium or systemic venous circulation, producing a pretricuspid left-to-right shunt. In anatomic terms, this condition is more precisely described as a partial anomalous pulmonary venous connection, whereas PAPVR refers to the physiological consequence of anomalous venous drainage. Historically, these anomalies were most often diagnosed during childhood; however, with increasing use of cross-sectional imaging modalities such as cardiac computed tomography and cardiovascular magnetic resonance, the condition is increasingly identified in adults. Adult presentations are heterogeneous, ranging from incidental imaging findings to clinically significant disease characterized by right ventricular volume overload, atrial arrhythmias, and pulmonary arterial hypertension. Recognition of PAPVR/partial anomalous pulmonary venous connection in adults remains clinically important, as delayed diagnosis may allow progressive right-sided cardiac remodeling and pulmonary vascular changes. This narrative review aims to move beyond classic anatomical descriptions and provide a clinically oriented overview of PAPVR in adults. We summarize the embryologic basis, anatomic variants, epidemiology, clinical manifestations, and hemodynamic consequences of this condition. Particular emphasis is placed on multimodality imaging-including transthoracic echocardiography, cardiac computed tomography, and cardiovascular magnetic resonance-for accurate diagnosis and procedural planning. The review also discusses hemodynamic evaluation with right-heart catheterization, risk assessment for pulmonary hypertension, and indications for intervention. Management strategies are reviewed in detail, including surgical techniques such as intracardiac baffling, single-patch and 2-patch repairs, and the Warden procedure, as well as the evolving role of transcatheter and hybrid approaches in carefully selected adult patients. Special clinical scenarios-including late presentation, pregnancy, and coexisting pulmonary hypertension-are also addressed. By integrating diagnostic, therapeutic, and longitudinal follow-up perspectives, this review provides a practical framework for the evaluation and management of adults with PAPVR in modern cardiology practice.

The Gerbode defect is a rare left ventricle-to-right atrium shunt caused by an anatomic deficiency of the membranous septum. Infective endocarditis is one of the main etiologies for Gerbode defect. This manuscript presents a rare case of Gerbode defect secondary to Streptococcus agalactiae endocarditis. Transthoracic echocardiography visualized the Gerbode defect. Cardiac computed tomography and 3D reconstruction delineated the anatomy. This multimodality imaging approach was pivotal in early diagnosis and guiding successful surgical planning. Trial Registration: This article is a case report and does not describe a clinical trial; therefore, trial registration was not required.

Atrial septal defects (ASDs) are among the most common congenital heart defects diagnosed in adulthood, with percutaneous device closure being the standard treatment for suitable secundum ASDs. However, the presence of anomalous coronary artery anatomy, particularly a high-risk interarterial course, may complicate procedural planning due to potential myocardial ischemia and sudden cardiac death. Single-ostium coronary artery anomalies are exceptionally rare, and their coexistence with a secundum ASD is even more uncommon, providing distinct diagnostic and treatment issues. We report the case of a 42-year-old woman with a secundum ASD. Her background included obesity, hypertension, and anxiety. Investigations revealed a significant left-to-right shunt (Qp/Qs 1.72:1), raised pulmonary artery pressures, and right-heart dilation. As part of pre-procedural assessment, CT coronary angiography unexpectedly identified a single coronary artery arising from the right coronary sinus. This single ostium gave rise to three branches: a right coronary artery (RCA) with a normal course, a retroaortic left circumflex (LCx), and a left anterior descending (LAD) artery with an interarterial course between the aorta and pulmonary artery. Despite the anatomical anomaly, high-intensity treadmill testing showed no chest pain, electrocardiogram (ECG) changes, or wall-motion abnormalities. Multidisciplinary evaluation confirmed that no coronary intervention was required due to the absence of ischemia. Therefore, percutaneous transcatheter closure was indicated, given the adequate septal rims. The procedure was successfully performed using a 22 mm Amplatzer septal occluder without complications, and complete elimination of the shunt was achieved. Follow-up imaging confirmed normal device position and stability, reduced pulmonary pressures, and preserved coronary artery patency. This case highlights the critical role of multimodality imaging, in particular CT angiography and functional testing, in the pre-procedural evaluation of coronary anatomy prior to device closure in ASD patients. It emphasizes that in the absence of functional ischemia, even a potentially high-risk single-ostium coronary anomaly may not be a contraindication to safe transcatheter ASD closure. It also underlines the value of a multidisciplinary approach in complex congenital presentations where routine pathways may need to be adapted.

Giant coronary artery aneurysms with fistulas are extremely rare and high-risk. This manuscript presents a rare case of a giant left circumflex (LCX) branch aneurysm rupturing into the superior vena cava-right atrial (SVC-RA) junction, accompanied by severe valvular regurgitation. Transesophageal echocardiography visualized the aneurysm and turbulent shunt flow, cardiac computed tomography angiography (CCTA) precisely delineated the anatomical details, and 3D CT reconstruction clarified spatial relationships. This multimodality imaging approach was pivotal in guiding successful single-stage surgical intervention. Trial Registration: This article is a case report and does not describe a clinical trial; therefore, trial registration was not required.

Ectopic embolism is an infrequent but potentially life-threatening complication following esophageal variceal embolization. Although it has been hypothesized to result from right-to-left shunting via pulmonary arteriovenous malformations or patent foramen ovale, definitive anatomical routes often remain undetected. The present case study reports a 57-year-old male patient with decompensated cirrhosis who developed acute bilateral visual loss and lower limb weakness within 24 h after undergoing transjugular intrahepatic portosystemic shunt placement combined with endovascular embolization of esophageal varices. Brain imaging confirmed multiple acute cerebral infarctions; notably, angiographic review revealed an abnormal direct venous connection between the esophageal variceal plexus and the left heart/ascending aorta, bypassing the pulmonary circuit. No cardiac or pulmonary shunts were identified. This direct communication likely permitted embolic material to enter the systemic circulation, causing cerebral artery occlusion. In conclusion, to the best of our knowledge, the present case provides the first angiographic evidence of a direct vascular route from esophageal varices to the systemic arterial system. The present finding underscores the importance of comprehensive imaging before embolization and suggests that solid embolic agents such as coils may be preferable in select patients to prevent ectopic embolism.