Tuberculous pericarditis (TBP) is a potentially severe manifestation of extrapulmonary tuberculosis that may lead to pericardial effusion and constrictive physiology and, in some patients, progress to fixed constrictive pericarditis. Diagnosis can be particularly challenging in young immunocompetent patients without overt pulmonary involvement. We report the case of a 20-year-old immunocompetent man presenting with a one-month history of weight loss, profuse night sweats, nocturnal fever, and typical pericarditic chest pain. Clinical examination revealed fever and signs of systemic venous congestion. Transthoracic echocardiography demonstrated marked pericardial thickening, moderate circumferential effusion, septal bounce, approximately 25% respiratory variation in transmitral flow, annulus reversus, and annulus paradoxus, supporting the presence of pericardial effusion with constrictive physiology. Contrast-enhanced computed tomography confirmed diffuse pericardial thickening and effusion without calcification or pulmonary parenchymal involvement. At the same time, cardiac magnetic resonance demonstrated intense late gadolinium enhancement of the thickened pericardium, supporting active pericardial inflammation. Xpert Mycobacterium tuberculosis/Rifampicin assay (Xpert MTB/RIF; Cepheid, Sunnyvale, CA, USA) testing of the pericardial fluid detected Mycobacterium tuberculosis, subsequently confirmed by positive mycobacterial culture. Following multidisciplinary discussion, a six-month antituberculous regimen combined with adjunctive corticosteroid therapy was initiated, with close clinical and multimodality imaging follow-up and reassessment for pericardiectomy according to clinical evolution. This case highlights the complementary value of echocardiography, computed tomography, and cardiac magnetic resonance in characterizing tuberculous pericardial disease associated with constrictive physiology and defining its inflammatory substrate. Identification of active pericardial inflammation in the presence of constrictive physiology may indicate a potentially reversible component; however, actual reversibility requires confirmation during longer-term follow-up.

A quadricuspid mitral valve is an uncommon congenital anomaly whose imaging features are inconsistently reported. Prior case reports frequently describe this finding in patients with hypertrophic cardiomyopathy (HCM), complicating characterization of this anomaly as an isolated finding. We report a 64-year-old male with severe mitral regurgitation of incompletely defined origin and atrial fibrillation presenting for robotic thoracoscopic mitral valve repair and a Cox-Maze III procedure. Intraoperative transesophageal echocardiography demonstrated a thickened, myxomatous mitral valve with deep fissures in both the anterior and posterior leaflets extending to the mitral annulus, with the anterior defect being the predominant origin of regurgitation. The opposing mitral valve defects created four apparent leaflet segments, which were suspicious for a quadricuspid mitral valve but ultimately described as a quadricuspid-appearing mitral valve created by opposing true clefts in the anterior and posterior leaflets. No HCM or other structural cardiac anomalies were identified. Surgical repair included direct closure of the anterior leaflet defect, release of two anterior chordae, and placement of a 38-mm annuloplasty band. Post-bypass imaging showed only trivial residual mitral regurgitation. This case highlights the value of three-dimensional transesophageal echocardiography for defining complex mitral leaflet morphology and its importance in surgical planning.

We study the formation of ring-like structures in interacting active particle systems in two dimensions. The emergent structure shows signatures of both spatial and orientational organization. The spatial organization is characterized by the radial distance of a tagged particle from the centroid of the assembly, while orientational organization is characterized by the radial alignment of its self-propulsion direction. We derive exact analytical expressions for the radial and polarization distributions for systems of active Brownian particles and run-and-tumble particles. While both models exhibit annular steady states, we show that their spatial and orientational organization differ qualitatively in the strongly active regime. A direct comparison of the two models reveals how the nature of the propulsion mechanism leads to the distinction in both the structure of the annulus and the statistics of particle orientations. Our results provide a unified analytical framework for characterizing emergent annular states in active matter and identify robust signatures that distinguish persistent active dynamics with continuous and discrete reorientation.

Management of aortic valve and aortic root disease has evolved alongside an expanding therapeutic landscape that includes valve repair, valve-sparing root replacement, composite graft reconstruction, transcatheter therapies, and autograft-based approaches. Because these strategies differ in durability, hemodynamic performance, and implications for future reintervention, procedural selection must be individualized. Multimodality imaging is central to this process, integrating valve phenotype, annulus-root geometry, ventricular remodeling, and clinical context to refine procedural planning. As surgical and transcatheter options continue to expand, imaging remains fundamental to durable, patient-centered management of aortic valve and root disease.

Intimal sarcoma is a malignant mesenchymal tumour arising in large blood vessels of systemic and pulmonary circulation, depicted as undifferentiated and aggressive. Clinical presentation of these cardiac masses is often subtle, making misdiagnosis possible. We discuss the case of a 27-year-old woman with a recent history of delivery, admitted for dyspnoea and signs of right-heart failure. A diagnosis of pulmonary embolism was made on a computed tomography angiogram and transoesophageal echocardiography basis. Emergency surgery was performed due to haemodynamic instability. Pulmonary arteriotomy revealed a large solid polylobate mass instead of a thrombus. Surgical debulking, with reconstruction of the right ventricle outflow tract, and pulmonary valve replacement were therefore necessary. Partial pulmonary annulus reconstruction was furthermore performed with a strip of heterologous pericardium with a 'sandwich technique'. Prompt diagnosis of intimal sarcoma was made, permitting initiation of timely treatment with anthracycline. Surgical resection of malignancies involving either the heart or great vessels is uncommonly performed because of the potential morbidity and mortality and the unknown probability of significant cure. Preoperative imaging is then of paramount importance in determining the diagnosis and planning for surgery. In this specific case, the haemodynamic instability, the high suspicion of a thrombotic nature of the mass, and young age precluded the performing of any second-level examination, leading surgeons to an unexpected reconstruction.

Sutureless aortic valve replacement (AVR) is generally avoided in type A aortic dissection (TAAD) because fragile, dissected tissue may provide inadequate stent fixation. We describe 2 patients with TAAD in whom a Perceval Plus sutureless bioprosthesis was successfully deployed as a bailout after failed aortic valve repair. In both cases, prior ascending aortic replacement created a stable prosthetic landing zone that allowed reliable radial fixation. Conversion to sutureless AVR increased aortic cross-clamp time by only 20-23 minutes, approximately half the time required for conventional sutured implantation. Postoperative imaging showed appropriate valve positioning without paravalvular leakage, and hemodynamic function remained stable at 7 and 8 months. Sutureless AVR may therefore offer a viable, time-saving bailout strategy for selected patients with TAAD, an intact aortic annulus, and a stabilized proximal aorta.

Chronic low back pain (CLBP) is a leading cause of disability, yet radiographic degeneration correlates poorly with symptoms. This mini-review examines how immune-neural crosstalk may link intervertebral disc degeneration to pain initiation and persistence. Degenerated nucleus pulposus and annulus fibrosus cells develop inflammatory and catabolic phenotypes and release mediators that may promote neural and vascular ingrowth, sensitize nociceptors, and increase dorsal root ganglion neuron excitability. Sustained peripheral input may engage spinal glial pathways and contribute to central sensitization. Pain may persist through expectation, learning, affective processes, and altered central prediction even when peripheral inflammatory input is limited. These interactions are bidirectional: immune signaling may affect mood, cognition, sleep, and threat processing, whereas stress, pain-related beliefs, and social context may modify immune and neural responses through autonomic and neuroendocrine pathways. Vertebral endplate inflammation, sometimes reflected by Modic type I changes, may mark an immune-associated phenotype. Although mechanistic and preclinical evidence supports targets such as NGF and pro-inflammatory cytokines, clinical benefit has been inconsistent, potentially because of safety concerns, patient heterogeneity, insufficient target engagement, and trial-design limitations. We propose a systems framework integrating inflammatory biomarkers, endplate imaging, quantitative sensory testing, neuroimmune imaging, and contextual measures. This framework may help distinguish inflammation-dominant, peripherally sensitized, central-sensitization-associated, nociplastic (pain arising from altered nociception), and mixed profiles. Validation requires prospective longitudinal studies, biomarker-stratified cohorts, and adequately powered randomized controlled trials.

Annulus fibrosus (AF) rupture is a key structural event in intervertebral disc degeneration, but effective repair is hindered by the acidic, hypoxic and oxidative microenvironment of the avascular disc. Single-cell transcriptomic reanalysis and clinical AF specimens identified ferroptosis-associated redox imbalance as a prominent feature of advanced degeneration. Here, we developed an acid-responsive nanobot-integrated core-shell microneedle system for staged annulus fibrosus repair. The shell layer released TA@MgO2 metal-phenolic nanobots that consumed pathological H[+], generated O2, and provided NIR-amplified redox buffering, thereby normalizing the early degenerative microenvironment. The core layer enabled sustained quercetin release to reinforce anti-ferroptotic and matrix-preserving effects. Mechanistically, TMH/QG+NIR suppressed ferroptosis in AF cells by epigenetically silencing ATF3 through DNMT3A-dependent promoter methylation, thereby relieving ATF3-mediated repression of SLC7A11 and restoring GPX4-dependent antioxidant defense. In a puncture-induced degeneration model, this system alleviated ferroptotic injury, improved AF integrity, preserved disc height and enhanced biomechanical resilience. These findings identify the DNMT3A-ATF3-SLC7A11 axis as a therapeutically tractable ferroptosis-regulatory pathway and establish a staged microenvironment-reprogramming strategy for AF repair.