Search Results (109)

Background/Objectives: Left atrial thrombus (LAT) is a clinically important finding in nonvalvular atrial fibrillation (AF). The Fibrosis-4 (FIB-4) index reflects systemic fibrotic burden. We investigated the association between FIB-4 and LAT. Methods: This retrospective study included 859 patients with nonvalvular paroxysmal AF undergoing transesophageal echocardiography (TEE). ROC analysis and multivariable logistic regression were performed. Results: Left atrial thrombus (LAT) was detected in 10.2% of patients. Patients with thrombus exhibited significantly higher admission FIB-4 scores compared to those without (1.5 vs. 1.1, p < 0.001). ROC analysis yielded an optimal FIB-4 cut-off of 1.47 (AUC: 0.65, 95% CI: 0.57–0.70, p < 0.001), providing 71.6% sensitivity and 72.0% specificity. After adjusting for CHA₂DS₂-VASc score, renal function, and left atrial diameter, a FIB-4 > 1.47 remained a strong independent predictor of LAT (OR: 5.200; 95% CI: 3.105–8.708, p < 0.001). However, the addition of FIB-4 to the CHA₂DS₂-VASc score did not significantly improve discriminatory performance (p = 0.314, DeLong’s test). Spearman’s correlation showed a modest relationship between FIB-4 and CHA₂DS₂-VASc (r = 0.321). Conclusions: Elevated FIB-4 index values are independently associated with LAT in patients with paroxysmal AF. This simple, noninvasive marker may reflect a systemic fibro-inflammatory milieu that promotes an atrial thrombogenic substrate beyond traditional clinical risk scores. Full article

Background: Atrial fibrillation (AF) remains the most common cardiac arrhythmia, with pulmonary vein isolation (PVI) established as the cornerstone of interventional treatment. However, in patients with persistent AF (PersAF), the success rates of PVI alone tend to be limited. A promising additional target is the left atrial appendage (LAA). In recent years, cryoballoon (CB) technology has become a tool for achieving durable PVI. Its application for LAAI has been investigated as a potentially advantageous alternative to radiofrequency ablation, and a positive effect on long-term outcome has been reported. However, the available data is limited. This study sought to investigate the clinical impact of CB-based LAAI in addition to PVI. Methods: This is a prospective, interventional, single-centre study. Consecutive patients with symptomatic PersAF were prospectively enrolled. In total 23 patients with PersAF underwent PVI plus LAAI using the CB system. Percutaneous LAA closure was performed within 2–3 months in all patients by implanting an endocardial LAA-closure device. Prior to LAA closure, LAAI durability was systematically assessed by invasive remapping studies. Results: A total of 100% of PVs were successfully isolated using the CB only (n = 91/91). Concerning LAAIs, a total of 21/23 (91%) remained isolated at the end of the procedure. After the ablation procedure including LAAI, all patients were scheduled for TEE assessment and LAA closure. TEE was performed after a mean of 54 ± 19 days. In 6/23 (26%) patients, LAA thrombus formation was detected after LAAI. A total of 23/23 patients (100%) received LAAC after a mean of 72 ± 45 days. Durability of LAAI was assessed utilizing a spiral mapping catheter in 23/23 patients (100%). In a total of 17/23 (74%) patients, durable LAA isolation was detected. Durable PVI of all PVs was detected in 16/23 (70%) patients. During a mean follow-up of 13 ± 3.4 months, stable sinus rhythm was maintained in 15 (65%) patients. The LAA showed reconnection in 3/23 (13%) patients, with arrhythmia recurrence. During follow-up, one stroke (318 days after LAAC) and one device thrombus (56 days after LAAC) occurred. Conclusions: While CB-based LAAI may offer benefits in managing persistent AF, it presents a significant risk of thrombus formation in the LAA, even with appropriate OAC. Early closure of the LAA following LAAI appears promising in mitigating these risks, but further evidence is needed to establish clear best practices. Full article

Background: Endovascular aneurysm repair (EVAR) requires lifelong imaging surveillance because endoleaks, aneurysm sac expansion, and severe adverse events occur in up to one-third of the patients. Conventional follow-up based on sac diameter and visual assessment may fail to detect early microstructural changes that precede clinical deterioration. Methods: This narrative review summarizes the current evidence on texture-based radiomics and artificial intelligence (AI) applied to computed tomography (CT) and CT angiography (CTA) for post-EVAR outcome prediction and surveillance. Original studies evaluating radiomic features and AI-based models for endoleak detection, aneurysm sac behavior, and EVAR-related adverse events were included and qualitatively synthesized. Results: Ten studies were included. Radiomic features describing texture heterogeneity, gray-level nonuniformity, entropy, and spatial complexity were extracted from the aneurysm sac, intraluminal thrombus, and perivascular adipose tissue. Machine learning and deep learning models achieved good to excellent performance, with reported AUC values ranging from 0.78 to 0.95 for predicting endoleaks, sac expansion, and severe adverse events. Texture-based radiomics consistently outperformed morphology-only assessments and showed complementary value to deep learning, including applications on non-contrast CT. Conclusions: CT texture radiomics combined with AI represents an emerging research approach with potential relevance for post-EVAR surveillance, although current evidence remains limited. By capturing tissue heterogeneity beyond conventional morphology, radiomics may enable the earlier detection of complications and support risk-adapted follow-up. However, the heterogeneity of methods limited external validation, and reproducibility issues remain major barriers to clinical translation. Full article

Aortic diseases, including abdominal aortic aneurysm (AAA), thoracic aortic aneurysm (TAA), aortic dissection (AD), and Takayasu arteritis (TAK), are characterized by vascular remodeling and chronic immune–inflammatory activation, with AD often representing an acute complication of long-standing aortic wall vulnerability. Increasing evidence suggests that gut dysbiosis, impaired intestinal barrier integrity, and microbiota-derived metabolites may contribute to aortic wall injury. We synthesized current evidence linking the gut microbiome to aortic diseases and explored potential translational implications. PubMed, Scopus, and Web of Science were searched for microbiome-related studies on AAA, TAA, AD, and TAK published up to December 2025. Human observational and interventional studies were integrated with relevant experimental research. The strongest evidence was identified for AAA, where multiple cohorts report gut dysbiosis and reduced microbial diversity. Translational studies have detected bacterial DNA and microbial products in blood, aneurysm wall, or intraluminal thrombus, consistent with barrier-related microbial signaling and vascular inflammation, although these low-biomass findings do not establish microbial viability or causality. Microbiota-derived mediators—including trimethylamine-N-oxide, lipopolysaccharides, short-chain fatty acids, and bile acid derivatives—interact with pathways involved in cytokine signaling, oxidative stress, innate immune activation, and extracellular matrix degradation. Evidence for TAA and AD remains limited and suggests mainly modifier effects, whereas early studies in TAK indicate disease-associated microbiome and metabolite alterations. Mendelian randomization analyses have explored genetically proxied microbiome–AAA associations; however, results are heterogeneous, and causal inference remains provisional. Overall, the gut microbiome emerges as a plausible modifier of aortic disease, with the greatest translational relevance in AAA, highlighting the need for longitudinal multi-compartment studies and targeted interventions with aortic endpoints. Full article

Left ventricular (LV) apical obliteration represents a convergent imaging phenotype arising from diverse cardiac conditions, including thrombotic, hypertrophic, infiltrative, congenital, and neoplastic diseases. These conditions, despite sharing overlapping morphological features, require profoundly different management strategies. In this context, an accurate characterization of the LV apex is a cornerstone point, and can be performed through various techniques. Advances in multimodality imaging have substantially improved diagnostic precision, allowing clinicians to differentiate true obliteration from mimicking conditions such as hypertrabeculation, apical hypertrophy, or subendocardial fibrosis. This review provides a comprehensive overview of the anatomical variability of the LV apex and its implications for imaging interpretation. We appraise the role of echocardiography, including contrast-enhanced and speckle-tracking studies—alongside cardiac magnetic resonance (CMR), computed tomography (CT), and selective nuclear imaging in the evaluation of apical pathology. For each principal cause of apical obliteration—LV thrombus, apical hypertrophic cardiomyopathy, left ventricular non-compaction, endomyocardial fibrosis, cardiac amyloidosis, and intracardiac tumors—we outline key diagnostic clues, imaging red flags, and distinguishing tissue characteristics. Special emphasis is given to the incremental value of CMR for tissue characterization, thrombus detection, and fibrosis mapping, as well as to the interpretative challenges posed by apical foreshortening, near-field artefacts, and suboptimal acoustic windows. A practical, stepwise imaging framework is proposed to guide clinicians through the differential diagnosis of apical obliteration using an integrated multimodality approach. Future directions include the incorporation of 4D flow, advanced mapping techniques, and artificial intelligence-powered analysis to refine apical phenotyping and identify early disease signatures. Recognizing the full spectrum of apical pathology and its imaging manifestations is essential to prevent misdiagnosis, enable timely therapeutic decisions, and improve risk stratification. Full article

Background and Clinical Significance: The crista terminalis (CT) is a fibromuscular ridge located on the posterolateral wall of the right atrium, formed by the junction of the sinus venosus and the primitive right atrium. A hypertrophic or prominent CT (HCT) refers to a thickened or conspicuous configuration of this normal anatomical structure. In prenatal ultrasound (US) and/or echocardiographic assessments, HCT can mimic a right atrial mass, such as a tumor or a thrombus. Case Presentation: Herein, we describe a case of a fetal right atrial echogenic mass detected at 32 weeks, which remained stable through gestation and was confirmed postnatally as a likely HCT. No hemodynamic compromise, growth, or pathological sequelae were observed. Conclusions: Our case reinforces the importance of including atrial structural variants in the differential diagnosis of intracardiac masses, particularly when features favor stability and low risk. Serial imaging, avoidance of premature invasive measures, and careful counseling are key to appropriate management. Full article

Methamphetamine (MA) abuse has emerged as a multisystem insult driving cardiovascular and neurovascular consequences. Methamphetamine-associated cardiomyopathy (MACM) remains an underrecognized cause of cardioembolic stroke through left ventricular thrombus (LVT) formation. MA-induced gut dysbiosis and enteric neural disruption exacerbate systemic inflammation and autonomic imbalance, resulting in broader dysregulation of the brain–heart–gut axis. This study aimed to synthesize contemporary evidence on chronic MA exposure and its role in LVT formation, stroke pathogenesis, diagnostic approaches, and anticoagulation management. We conducted a focused narrative review of PubMed- and Scopus-indexed literature (1990–2025) addressing cardiovascular, neurovascular, and gut-mediated consequences of chronic MA exposure. Observational cohorts and case reports were integrated to characterize pathophysiology, imaging approaches, and therapeutic considerations, supplemented by a representative clinical case. Chronic MA exposure mediates persistent catecholamine excess, myocardial fibrosis, ventricular dysfunction, and a prothrombotic milieu. Gut dysbiosis-related inflammation and autonomic dysregulation further promote intracardiac stasis. Affected individuals are typically young men with severe systolic dysfunction (left ventricular ejection fraction 20–30%), with a substantial proportion demonstrating apical or mural LVT on systematic imaging. Case-level evidence highlights a broader systemic embolic burden, involving the limbs, kidneys, and aorta. Echocardiography remains the first-line screening method, while cardiac CT and MRI offer greater sensitivity for thrombus detection. Anticoagulation is challenged by bleeding risk, inconsistent adherence, and the absence of standardized protocols. MACM represents a critical and underrecognized etiology of cardioembolic stroke in young adults. Early recognition of brain–heart–gut axis disruption, systematic cardiac imaging, and individualized anticoagulation are crucial for preventing emboli. Prospective registries and standardized imaging-guided treatment strategies are needed to improve outcomes in this high-risk population. Full article

Background: Central retinal artery occlusion (CRAO) is an ophthalmic emergency attributed to a vessel occlusion with an embolus or a thrombus and may occur during the hypercoagulable state, inflammation, or vasculitis. CRAO may occur in children; however its incidence is very rare. Most pediatric cases have detectable etiologies. Case Presentation: We describe the case of an otherwise-healthy six-year-old female, who presented with the sudden and complete vision loss of the left eye lasting over twelve hours after a six-day chickenpox exanthema, followed by a high fever. All the ophthalmological, laboratory, and instrumental investigations led to the diagnosis of a left CRAO. Laboratory testing was unremarkable except for the transient elevation of D dimers (1363 µg/L), IgM anticardiolipin antibodies (238.5 CU), and IgG anti-beta-2 glycoprotein-1 antibodies (76.1 CU) on admission. Thrombolytic treatment was not exerted because of late presentation to the hospital. Treatment with steroids, antiviral medications, antibiotics, and anticoagulants was obtained, but the visual outcome was poor during the hospitalization and at the last follow-up. We could not ascribe features of this case to any etiological condition apart from the documented ongoing chickenpox infection. Conclusions: This is the first case report of CRAO in a child with transient aPL elevation and acute chickenpox infection. Full article

Fragmented thrombolytic actuators address the limited time window of thrombolysis agents and the risk of intimal injury from mechanical thrombectomy, emerging as a crucial method for rapid vascular recanalization. However, occluded vessels are often tortuous and narrow, imposing strict size constraints on the actuator. Moreover, the inability to assess thrombolysis efficacy in real-time during procedures impedes timely adjustments to control strategies for the actuator. To address these challenges, this study designs a conical piezoelectric actuator that employs high-frequency vibration in conjunction with a small dose of thrombolytics to fragment and accelerate thrombus dissolution. Firstly, structural parameters of the actuator are optimized using grey relational analysis combined with an improved entropy-weighting method, and the optimal design is prototyped and tested. Next, a real-time thrombolytic solution concentration detection algorithm based on an Improved Grey Wolf Optimizer–Support Vector Regression (IGWO-SVR) model is proposed. Finally, an experimental platform is constructed for validation and analysis. The results show that compared to the initial design, the optimized actuator has significantly improved kinematic and force performance, with the tip amplitude increasing by 42% and the output energy density reaching 3.3726 × 10⁻² W/mm³. The IGWO-SVR model yields highly accurate, stable concentration estimates, with a coefficient of determination (R²) of 0.9987 and a root-mean-square error (RMSE) of 0.8118. This work provides a pathway toward actuator miniaturization and real-time thrombolysis monitoring, with positive implications for future clinical applications. Full article

Conventional whole-blood flow assays for quantifying thrombus formation are typically performed at room temperature and are technically demanding, which limits their translational applicability. We engineered a novel, disposable, mountable, and single-channel microfluidic chip (MC-2S), which is based on the Maastricht chamber (MC) and designed for automated evaluation of platelet function, coagulation and fibrinolysis under physiological conditions. The MC-2S chip allows customizable choices of thrombogenic surfaces, such as collagen and tissue factor. The chip was used in combination with an adapted, 1.3 kg brightfield/fluorescence microscope, operating at physiological temperature (37 °C), and with scripts for automated multicolor analysis of image features. The integrated system enables a robust, rapid, and high-content quantification of the kinetics of thrombus formation and dissolution. In platelet-sensitive mode, MC-2S demonstrated high sensitivity to antiplatelet therapy with aspirin or cangrelor. In coagulation-sensitive mode, it detected the anticoagulant effect of rivaroxaban plus its reversal by andexanet-α. In fibrinolysis-sensitive mode, it monitored tissue-type plasminogen activator-induced thrombus dissolution, inhibited by tranexamic acid. Collectively, the MC-2S platform was found to provide a versatile, physiologically relevant tool for functional hemostasis testing, with high potential for the acute and subacute evaluation of patient blood samples in the context of bleeding disorders, thrombosis risk, and drug monitoring. Full article

Both primary and secondary hemostasis consist of finely regulated pathways, forming a blood clot to stop bleeding. These orchestrated mechanisms involve multiple plasma- and platelet/endothelial-derived receptors, factors, enzymes, and proteins, such as the von Willebrand factor (vWF), fibrinogen, and thrombin. Over-activation or improper resolution of the coagulation cascade leads to severe pathological disorders, arterial and venous. Despite the fact that the genetic etiology of thrombophilia has gained the main research interest, there is growing evidence that the disturbed redox network of key hemostatic pathways signals thrombus formation. Oxidized LDL in dyslipidemias and many endogenous and exogenous compounds act as pro-oxidant stimuli that lead to post-translational modifications of proteins, such as sulfenylation, nitrosation, disulfide formation, glutathionylation, etc. Oxidation of cysteine and methionine residues of vWF, fibrinogen, and thrombomodulin has been detected at thrombotic episodes. Increased homocysteine levels due to, but not restricted to, methylenetetrahydrofolate reductase gene (MTHFR) mutations have been incriminated as a causative factor for oxidative stress, leading to a pro-thrombotic phenotype. Alterations in the vascular architecture, impaired vascular relaxation through decreased bioavailability of NO, accumulation of Nε-homocysteinylated proteins, ER stress, and endothelial cells’ apoptosis are among the pro-oxidant mechanisms of homocysteine. This review article focuses on describing key concepts on the oxidant-based molecular pathways that contribute to thrombotic episodes, with emphasis on the endogenous compound, homocysteine, aiming to promote further molecular, clinical, and pharmacological research in this field. Full article

Background: A persistent connection between the atria, known as a patent foramen ovale (PFO), is present in approximately 25% of the general population. PFO closure is indicated in patients under 60 years of age who have experienced an embolic stroke of undetermined source (ESUS) or transient ischemic attack (TIA) confirmed by neurological imaging, and in selected cases of peripheral embolism. Follow-up after the procedure is indicated to confirm the position of the occluder, assess the effectiveness of the closure, and evaluate any potential thrombus formation on the device. Methods: We analyzed data from 75 consecutive patients who underwent percutaneous PFO closure procedures and were followed up for at least one year. The procedure was performed under fluoroscopy and transesophageal echocardiography (TEE) guidance, and occluder size selection was made using TEE multiplanar imaging (MPR). All patients had standard transthoracic echocardiography (TTE) at 1 and 6–12 months after the procedure. To assess the long-term efficacy, contrast-enhanced transcranial Doppler (ce-TCD) was performed at 12 months to record high-intensity transient signals (HITSs). Cases with positive ce-TCD had TEE performed. Results: During follow-up evaluations after 1 and 6–12 months (TTE), we did not observe any device dislodgements, thrombi, or residual leaks visible in TTE. ce-TCD detected HITSs in eight patients, prompting additional TEE examinations performed in seven cases. In five out of seven patients, a leak around the occluder was identified, including two patients with grade 2 HITSs. Conclusions: Assessing the effectiveness of PFO occluder placement is crucial for the residual embolic risk and thus the necessity of antithrombotic therapy. Even low grades of HITSs observed in ce-TCD help to identify patients with residual leaks confirmed in TEE. Full article

Acute pulmonary embolism (APE) represents a significant cause of morbidity and mortality worldwide, requiring rapid and precise diagnosis and effective therapy strategies. Computed Tomography Pulmonary Angiography (CTPA) is currently the gold standard technique for diagnosing PE; however, it presents some disadvantages, including limited sensitivity in detecting sub-segmental emboli and contrast-related risks. Recent advancements in imaging technologies, including Dual-Energy Computed Tomography (DECT) and Photon Counting (PC), offer improved sensitivity and specificity for APE and perfusion abnormalities detection. Digital Dynamic Radiography (DDR) perfusion imaging represents a novel imaging that allows pulmonary perfusion assessment without contrast medium administration, able to detect anomalies at the patient’s bedside, representing a promising advancement, particularly for critically ill or contrast-allergic patients. In parallel, interventional radiology has become integral to APE management, particularly for high-risk and intermediate–high-risk patients, with evolving intravascular treatment techniques such as catheter-directed thrombolysis, mechanical thrombectomy, and thrombus aspiration. This narrative review provides an overview of the latest developments in APE diagnostic imaging and interventional radiology, contextualizing them within current guideline recommendations for endovascular treatment. Full article

Knowing the precise etiology in ischemic stroke is necessary to ensure accurate diagnosis and decide on appropriate preventive treatments, especially in those of undetermined cause. Analysis of the thrombus protein composition could be useful to identify diagnostic biomarkers to help determine the stroke origin. Thrombi from 54 ischemic stroke patients with large vessel occlusion (LVO), of cardioembolic and atherothrombotic etiology, were analyzed using a proteomics approach. The proteome profile was compared between them to detect differential proteins of each etiology. Peptides of those differential proteins were quantified and related to the neurological function and clinical status of the patients. Of the 516 proteins identified, three showed significant differences between atherothrombotic and cardioembolic thrombi. These were fibronectin (FINC), 2,3-bisphosphoglycerate mutase (PMGE), and tropomyosin-1 (TPM1). Combining these proteins in a biomarker panel provided good sensitivity and high specificity for differentiating cardioembolic and atherothrombotic strokes. In addition, several of the quantified peptide levels correlated with clinical parameters related to stroke severity and prognosis. Three proteins differentially detected in ischemic stroke thrombi could be useful tools for accurately diagnosing ischemic stroke etiology, particularly in cases of undetermined cause. These biomarkers should be further analyzed in prospective multicenter studies to demonstrate their usefulness. Full article

Background/Objectives: This study investigated whether serum salusin-α and salusin-β levels could support the diagnosis and prognosis of confirmed acute pulmonary embolism (APE) cases. Methods: A prospective observational study was conducted including 57 patients diagnosed with APE using computed tomography pulmonary angiography (CTPA) and 30 control participants without any acute or chronic disease. APE patients were categorized based on the Pulmonary Artery Obstruction Index (PAOI) into low (≤20) and high (>20) thrombus burden groups. Serum salusin-α and salusin-β levels were measured at diagnosis using an enzyme-linked immunosorbent assay. Associations with PAOI and Pulmonary Embolism Severity Index (PESI) scores were analyzed. Results: Salusin-α and salusin-β levels were markedly reduced in APE patients versus controls (p < 0.001). In multivariate analysis, salusin-α remained independently associated with APE (p = 0.042), whereas salusin-β was not significant. A receiver operating characteristic analysis showed good diagnostic performance for salusin-α (AUC = 0.799; sensitivity = 89.5%; specificity = 46.7%). Neither peptide correlated with PAOI or PESI. At a 305.85 pg/mL cut-off, salusin-α yielded a positive predictive value of 76.1% and a negative predictive value of 70% in this cohort. Conclusions: The findings suggest that salusin-α has high sensitivity in detecting acute pulmonary embolism and may serve as a supportive diagnostic marker in emergency settings. Although its specificity is limited, it could contribute to guiding additional testing. While salusin-β showed no significant diagnostic value, the potential role of salusin peptides in prognostic evaluation requires further exploration. Full article