Background/Objectives: Cardiac hemangiomas are rare benign vascular tumors, accounting for less than 2% of primary cardiac tumors. Despite their rarity, they can cause significant clinical effects depending on their size and location. This systematic review aims to provide an updated analysis of recent cases, focusing on epidemiology, histopathological subtypes, clinical presentation, diagnostic approaches, and treatment outcomes. Methods: A systematic search of the PubMed database identified case reports and series published between 2019 and 2025. After applying inclusion and exclusion criteria, 55 eligible cases were selected for analysis. Data were extracted on patient demographics, tumor characteristics, imaging methods, treatment strategies, and follow-up outcomes. Results: Cavernous hemangiomas were the most commonly reported subtype. Patient ages ranged from infancy to over 85 years, with a slight predominance in females. Presentations varied from asymptomatic incidental findings to symptoms such as dyspnea and chest pain. Echocardiography was the primary diagnostic tool in over 80% of cases. Surgical resection was performed in 87.3% of patients, yielding favorable outcomes and low recurrence. However, follow-up duration was inconsistent, and long-term outcomes were underreported, underscoring the lack of standardized surveillance protocols. This variability limits clinicians’ ability to assess recurrence risk and long-term prognosis, highlighting the need for evidence-based guidelines to inform structured follow-up and improve patient care. Conclusions: The increasing number of published cases likely reflects improved diagnostic imaging and greater clinical awareness. While surgery remains the preferred treatment, the variability in follow-up and diagnostic reporting highlights the need for standardized protocols. Further studies are warranted to clarify the natural history, refine classification systems, and establish evidence-based guidelines for the management of this rare cardiac tumor.

Atrial fibrillation (AF) is the most prevalent sustained arrhythmia worldwide and is now increasingly regarded as a disease of chronic inflammation and progressive atrial fibrosis. Understanding of molecular mechanisms that mediate the linkage between systemic metabolic dysregulation, inflammation, and structural atrial changes is crucial for informing risk stratification and targeting of prevention strategies. This review provides evidence from 105 studies focusing on the contributions of transforming growth factor-β1 (TGF-β1), tumor necrosis factor-a (TNF-α), interleukin-6 (IL-6), galectin-3, and galectin-1 to cardiac fibrogenesis, atrial fibrosis, and AF pathogenesis. We also link metabolic syndrome to these biomarkers and to atrial remodeling, as well as echocardiographic correlates of fibrosis. TGF-β1 is established as the central profibrotic cytokine and promotes Smad-based fibroblast activation, collagen accumulation, and structural atrial remodeling. Its role is highly potentiated by thrombospondin-1 by turning latent TGF-β1 into its potent form. TNF-α and IL-6 also play an integral role in the inflammatory fibrotic continuum by activating NF-κB and STAT3 signaling, promoting fibroblast proliferation, electrical uncoupling, and extracellular matrix accumulation. Galectin-3 is a potent profibrotic mediator that promotes TGF-β signaling and is a risk factor for negative outcomes, whereas Gal-1 seems to regulate inflammation resolution and may exert context-dependent protective or maladaptive roles. Metabolic syndrome is strongly associated with excessive levels of these biomarkers, chronic low-grade inflammation, oxidative stress, and ventricular and atrial fibrosis. Chronic clinical findings show that metabolic syndrome (MetS) increases AF risk, exacerbates atrial dilatation, and is associated with worse postoperative outcomes. Echocardiographic data are connected to circulating biomarkers and are non-invasive for evaluating atrial remodeling. The evidence to date supports that atrial fibrosis should be considered an end point of systemic inflammation, metabolic dysfunction, and activation of profibrotic molecular pathways. Metabolic syndrome, due to its chronic low-grade inflammatory environment and prolonged levels of metabolic stress, manifests as an important upstream factor of fibrotic remodeling, which continuously promotes the release of cytokines, oxidative stress, and fibroblast activation. Circulating fibrotic biomarkers, in comparison with metabolic syndrome, serve separate yet interdependent pathways that help orchestrate atrial structural remodeling through the simultaneous process but can also provide a long-term indirect measure of ongoing profibrotic activity. The integration of these biomarkers with superior atrial imaging enables a broader understanding of the fibrotic substrate of atrial fibrillation. This combined molecular imaging approach can facilitate risk stratification, refine therapeutic decisions, and facilitate early identification of higher-risk metabolic phenotypes, thus potentially facilitating directed antifibrotic and anti-inflammatory therapy in atrial fibrillation.

Background: Obstructive sleep apnea (OSA) is a prevalent but frequently underdiagnosed comorbidity in patients undergoing cardiac surgery, including coronary artery bypass grafting (CABG), aortic valve replacement (AVR), and mitral valve repair or replacement (MVR). This systematic review and meta-analytic synthesis investigates the relationship between OSA and postoperative morbidity and mortality, with particular attention to the predictive utility of established screening instruments. Methods: A systematic search of the PubMed database was conducted (April 2025), identifying 724 articles published in the last ten years. Seventeen primary studies met the inclusion criteria for qualitative synthesis, and four additional studies were included in the meta-analyses. Outcomes assessed included atrial fibrillation, major adverse cardiac and cerebrovascular events (MACCE), acute kidney injury (AKI), respiratory complications, pneumonia, hospital length of stay (LOS), and mortality. Risk of bias was assessed qualitatively based on study design and reporting limitations. This review was registered in the PROSPERO database under registration number CRD420251049574. Results: Meta-analyses demonstrated significantly elevated odds of atrial fibrillation (OR = 2.44, 95% CI: 1.46–4.07), major adverse cardiac and cerebrovascular events (OR = 2.06, 95% CI: 1.61–2.63), acute kidney injury (OR = 2.24, 95% CI: 1.67–3.01), and respiratory complications (OR = 1.15, 95% CI: 1.05–1.25) among patients with OSA. Additionally, OSA was associated with a significantly prolonged hospital length of stay (standardized mean difference [SMD] = 0.62, 95% CI: 0.46–0.78) and a marginal increase in pneumonia risk (OR = 1.07, 95% CI: 1.00–1.15). Evidence regarding stroke, intensive care unit (ICU) stay, and mortality was inconsistent or underpowered. Conclusions: Across core outcomes, findings were consistent across multiple studies involving a large patient population. Obstructive sleep apnea is a clinically consequential risk factor in cardiac surgery, associated with increased perioperative complications and prolonged hospitalization. These findings support the integration of routine OSA screening into preoperative risk assessment protocols. Further prospective, multicenter trials are warranted to assess the efficacy of perioperative management strategies, including continuous positive airway pressure (CPAP) therapy, in improving surgical outcomes.

Background: Primary cardiac tumors are exceedingly rare, accounting for less than 0.2% of cases in autopsy series. Myxomas represent the majority, while hemangiomas are exceptionally uncommon, accounting for less than 2% of benign cardiac tumors. Their rarity, nonspecific clinical presentation, and overlapping imaging features make preoperative diagnosis particularly challenging. Case presentation: We report the case of a 47-year-old woman with exertional dyspnoea and a large right atrial mass initially suggestive of myxoma on transthoracic echocardiography. Coronary angiography revealed a small fistulous connection, raising suspicion of a vascular lesion. Surgical resection was performed, and histopathological examination confirmed a cavernous hemangioma. The postoperative course was favorable, with no residual mass on follow-up imaging. Discussion: Cardiac hemangiomas are often misdiagnosed as myxomas due to similar clinical and echocardiographic appearances. This case illustrates the diagnostic challenges posed by cardiac hemangiomas and the importance of correlating multiple imaging modalities when assessing atypical atrial masses. Our case highlights the potential role of multimodal imaging, including contrast echocardiography, cardiac MRI, and coronary angiography, in differentiating vascular from non-vascular cardiac tumors. Based on recurrent patterns in the literature, we outline a conceptual diagnostic framework that may assist preoperative evaluation. Conclusions: Although rare, cardiac hemangiomas should be considered in the differential diagnosis of atrial masses. Multimodal imaging may improve diagnostic accuracy, but additional data from multicenter registries are required to establish validated diagnostic pathways.

Mechanical complications after acute myocardial infarction (MI)—ventricular septal rupture (VSR), free-wall rupture (FWR), and papillary muscle rupture (PMR)—have become uncommon in the primary percutaneous coronary intervention (PCI) era, yet remain among the most lethal cardiovascular emergencies, with contemporary mortality largely driven by cardiogenic shock and delays to definitive treatment. Although major society documents agree on urgent imaging, early mechanical circulatory support when shock is present, and multidisciplinary decision-making, important transatlantic differences persist, particularly regarding timing of intervention in ventricular septal rupture. This review synthesises current surgical and transcatheter evidence and proposes a unified, physiology-centred framework integrating shock staging, anatomical feasibility, and response to mechanical support. We also introduce STABLE, a structured bedside checklist designed to support consistent daily triage across all three lesions and to align timing decisions with haemodynamic stabilisation rather than centre-specific habit.

Background/Objectives: Giant atrial chambers are rare but clinically important conditions, most often linked to rheumatic mitral valve disease, though they may also occur in congenital or other acquired disorders. Despite their low prevalence, they entail major hemodynamic, arrhythmogenic, and extracardiac risks. This study aimed to review recent evidence on giant atrial pathology—including giant left atrium (GLA), giant right atrium (GRA), and atrial appendage aneurysms—and to illustrate its relevance through cases of symptomatic extracardiac compression. Methods: A PubMed search on 15 September 2025 using “giant atrium” and limited to human, free full-text studies from the last 10 years yielded 93 results. After screening, 21 reports describing 24 cases were analyzed and compared with institutional experience. Results: GLA is most often defined by an anteroposterior diameter ≥6.5 cm or ≥8 cm, while criteria for GRA and appendage aneurysms remain inconsistent. Reported complications include atrial fibrillation, thromboembolism, and compression of mediastinal structures, with presentations such as dysphagia or airway obstruction. While valve surgery alone may suffice, many authors recommend concomitant atrial reduction or aneurysm resection in symptomatic patients. Conclusions: Giant atrial pathology, though uncommon, carries significant cardiac and extracardiac implications. Management should be individualized, and awareness of atypical manifestations is critical for timely diagnosis and treatment.