Search Results (701)

Obstructive sleep apnea syndrome (OSAS) is heavily implicated in subclinical cardiovascular disease; however, traditional polysomnographic metrics fail to capture the localized mechanical trauma exerted on the carotid artery. To address this methodological gap, this study evaluated exploratory associations between frequency-domain snoring characteristics and right carotid artery alterations in 50 patients with OSAS. Snoring was quantified using a dual-modality bioelectronic approach: an ambient microphone captured airborne snoring sound energy (SSE), while a portable neck-surface piezoelectric sensor recorded tissue-conducted snoring vibratory energy (SVE). Subclinical vascular changes, including carotid intima-media thickness (CIMT) and atherosclerosis, were assessed via ultrasonography. Hierarchical multivariable regression demonstrated that acoustic SSE%-404–500 Hz and mechanical SVE%-112–144 Hz independently correlated with preliminary CIMT increases (adjusted β = 0.033 and 0.021, respectively; both p < 0.05), alongside neck circumference. Conversely, SSE%-404–500 Hz emerged as an exploratory marker for focal carotid atherosclerosis (adjusted odds ratio = 1.828; p = 0.009). Integrating this metric with baseline parameters yielded exploratory diagnostic capacity (area under the curve = 0.833; p < 0.001), achieving 89% sensitivity and 69% specificity. These findings suggest that dual-modality spectral analysis provides a non-invasive exploratory framework for cardiovascular risk stratification, isolating localized mechanotransduction phenotypes independently of systemic hypoxia. Full article

Background/Objectives: Carotid–femoral pulse-wave velocity (cfPWV) is the reference-standard non-invasive measure of central arterial stiffness and a validated marker of cardiovascular risk in hypertension. While lipoprotein(a) [Lp(a)] and homocysteine have each been implicated in vascular injury, their independent and combined associations with arterial stiffness in treated hypertension remain uncertain. In this study, we examined the associations of Lp(a), homocysteine, and peripheral artery disease (PAD) with cfPWV and assessed whether concomitant elevation of Lp(a) and homocysteine was associated with excess arterial stiffness. Methods: We conducted a single-centre, cross-sectional study of 366 consecutive adults with treated hypertension attending a tertiary hypertension centre and associated vascular service between February 2016 and October 2019. cfPWV was measured non-invasively through applanation tonometry using the SphygmoCor XCEL system. Multivariable robust linear regression was used to assess associations with cfPWV after adjustment for age, sex, body mass index, mean 24 h systolic blood pressure (BP), diabetes mellitus, chronic kidney disease, smoking status, low-density lipoprotein cholesterol, and PAD. Joint associations and interactions on multiplicative and additive scales were also evaluated. Results: Of 366 participants, 99 (27.0%) had high arterial stiffness, defined as cfPWV ≥ 10 m/s. After full adjustment, cfPWV increased by 0.13 m/s per 0.1 g/L increase in Lp(a) (95% CI, 0.08 to 0.18; p < 0.001) and by 0.26 m/s per 5 μmol/L increase in homocysteine (95% CI, 0.02 to 0.49; p = 0.03). Participants with concomitantly elevated Lp(a) and homocysteine had the highest adjusted cfPWV, with a mean difference of 1.56 m/s versus the low-Lp(a)/low-homocysteine group (95% CI, 1.00 to 2.13; p < 0.001). No meaningful multiplicative or additive interaction was observed. Conclusions: In adults with treated hypertension, higher Lp(a), higher homocysteine, and PAD were independently associated with greater central arterial stiffness. Concomitant elevation of Lp(a) and homocysteine identified participants with the highest cfPWV without evidence of synergistic interaction, supporting a complementary vascular-risk model. Full article

Cardiovascular disease (CVD) remains the leading global cause of morbidity and mortality. While low-dose aspirin is well established for secondary prevention, its role in primary prevention is controversial because modest benefits in cardiovascular benefits must be balanced against increased bleeding risk, as highlighted by recent large trials. Current guidelines recommend restricting aspirin use to individuals at higher cardiovascular risk without elevated bleeding risk, yet significant heterogeneity persists in defining these thresholds. Evidence from randomized trials, guidelines, cohort and modeling analyses, and post hoc or observational subgroup studies suggests that selected patients with advanced subclinical atherosclerosis or specific high-risk markers may have a more favorable risk–benefit profile, although the certainty and directness of evidence vary across subgroups. This narrative review and pragmatic clinical guide presents an illustrative tiered framework based on clinical, imaging, and biomarker markers—such as coronary artery calcium score, carotid plaque score, and lipoprotein(a)—to support individualized discussion of preventive aspirin therapy. The framework is not a validated risk calculator or standalone treatment algorithm, and decisions should balance absolute cardiovascular risk, major bleeding risk, evidence certainty, and patient preferences. Full article

Background/Objectives: Patients undergoing carotid revascularization may show distinct patterns of bilateral carotid vulnerability and clinical risk. This study used latent class analysis (LCA) to identify high-resolution magnetic resonance imaging (HR-MRI)-based clinical–radiological phenotypes and evaluate their association with long-term major adverse cardiovascular events (MACE). Methods: This retrospective cohort included 289 patients who underwent carotid endarterectomy (CEA) or carotid artery stenting (CAS) between April 2017 and April 2024 and had preoperative carotid HR-MRI within 90 days. Ipsilateral and contralateral plaque features were assessed on multi-contrast vessel-wall HR-MRI. LCA included five indicators: ipsilateral intraplaque hemorrhage, ipsilateral lipid-rich necrotic core, contralateral intraplaque hemorrhage, cardiovascular disease history, and symptomatic status. MACE comprised cardiovascular death, nonfatal myocardial infarction, coronary revascularization, or stroke. Outcomes were assessed using Kaplan–Meier analysis and multivariable Cox regression. Results: Among 289 patients undergoing carotid revascularization, the mean age was 65.12 ± 9.46 years, and 237 (82.0%) patients were men. LCA identified three phenotypes: Systemic High-Risk (n = 128), Silent High-Risk (n = 37), and Stable/Moderate (n = 124). The Systemic High-Risk phenotype showed high probabilities of symptomatic presentation, cardiovascular disease history, and bilateral carotid vulnerability, whereas the Silent High-Risk phenotype showed marked ipsilateral plaque vulnerability despite lower clinical risk. During a median follow-up of 4.4 years, MACE-free survival differed significantly across phenotypes (log-rank p = 0.043). Compared with the Stable/Moderate phenotype, the Systemic High-Risk and Silent High-Risk phenotypes were both associated with increased MACE risk (HR 1.65, 95% CI 1.15–2.37, p = 0.039; HR 1.43, 95% CI 1.12–2.15, p = 0.034). Conclusions: HR-MRI-based LCA identified clinically meaningful carotid vulnerability phenotypes associated with long-term MACE after carotid revascularization. These findings support integrated assessment of bilateral plaque vulnerability and clinical risk for postoperative cardiovascular risk stratification. Full article

Cardiovascular disease (CVD) is closely linked to metabolic disorders such as obesity, dyslipidemia, and hepatic steatosis. This study investigated the anti-thrombotic and metabolic effects of KoreaGinseng F Max (KGF), a standardized extract rich in ginsenosides, in high-fat diet (HFD)-induced obese rats, and complementary in silico analyses were used to explore putative molecular targets and pathways. The extract was standardized to contain 36.97 mg/g of ginsenosides Rg1, Rb1, and Rf. Male rats were administered KGF (50, 100, or 200 mg/kg) orally for six weeks. KGF significantly improved lipid profiles by reducing serum triglycerides, total cholesterol, and low-density lipoprotein (LDL) levels. Histological analysis revealed a dose-dependent reduction in hepatic steatosis and adipocyte size. Potential anti-thrombotic activity was evaluated using a FeCl₃-induced carotid artery thrombosis model, with aspirin (30 mg/kg) included as a positive control. KGF200 delayed thrombus formation and produced a carotid blood flow pattern comparable to that observed in the aspirin-treated group, without significant alterations in serum ALT, AST, BUN, or creatinine levels. To further generate mechanistic hypotheses, complementary in silico analyses, including target prediction, GO/KEGG enrichment, network analysis, and molecular docking, were performed using the marker compounds. Eight overlapping genes, including STAT3, PTAFR, VEGFA, FGF2, HPSE, IL2, HSP90AA1, and LGALS3, associated with thrombotic regulation were identified. Pathway analysis suggested that PI3K–Akt signaling, calcium signaling, Th17 cell differentiation, and proteoglycan/ECM-related signaling may represent putative pathway-level mechanisms underlying the observed protective effects. Molecular docking suggested possible interactions between the marker ginsenosides and several predicted hub targets. Collectively, these findings suggest that KGF may have potential for further investigation as a natural product-derived material for improving HFD-associated metabolic and thrombotic dysfunction, while the predicted multi-target and multi-pathway effects require further experimental validation. Full article

Background and Objectives: Despite the presence of atherosclerosis risk factors and symptoms associated with occlusive atherosclerotic cardiovascular disease (ASCVD), up to 30% of individuals do not present significant atherosclerotic lesions at the point of diagnostic evaluation. Those in whom ASCVD was ruled out once might be believed to be at low risk of future major cerebral and cardiac events (MACCEs). Despite this, they might still have some residual risk for MACCEs. Therefore, in the present study we aimed to evaluate risk factors for atherosclerosis progression to the stage of occlusive arterial disease in patients with cardiovascular risk factors but initially free from significant ASCVD. Materials and Methods: Between March 2012 and February 2014, a total of 686 consecutive patients presenting with clinical suspicion of significant coronary artery disease were evaluated. The actual status of atherosclerosis burden was verified in four major arterial territories (coronary, carotid, renal, lower limb arteries) with the use of angiography, computed tomography and ultrasonography. For the present study purpose, 188 (27.4%) patients were enrolled, in whom significant ASCVD (in any of the examined territories) was ruled out. In all patients, the incidence and severity of atherosclerotic risk factors, carotid intima–media complex thickness (CIMT) and carotid plaque presence were evaluated during first hospital admission. A ten-year follow-up period for a composite endpoint of MACCEs was included. Univariate and multivariate Cox proportional hazard analyses with the Simon–Makuch method for new-onset type 2 diabetes mellitus (T2DM) were performed for MACCEs. Results: MACCEs occurred in 30 (16%) of 188 patients, including 5 cardiovascular deaths, 19 non-fatal myocardial infarctions, and 6 non-fatal ischemic strokes, in a median of 48 (Q1; Q3: 25; 86) months. Univariate Cox proportional hazard analysis revealed that individuals who presented with baseline LDL cholesterol > 3.2 mmol/L, CIMT > 1 mm, carotid plaque, or experienced new-onset T2DM were predisposed to MACCE with hazard ratios (HRs) of 3.21 (p = 0.003), 3.82 (p = 0.001), 5.41 (p < 0.001), and 36.89 (p < 0.001), respectively. In multivariate Cox analysis, its associations with MACCEs were retained (HRs between 2.19 and 21.47), respectively. Conclusions: Our findings support the need for continued risk factor optimization despite the initial exclusion of obstructive ASCVD. In this study, we identified new-onset T2DM, initial LDL cholesterol, and the presence of subclinical atherosclerosis as risk factors for MACCEs. Full article

Carotid atherosclerosis is a major contributor to ischemic stroke, driven by complex interactions between inflammation, lipid metabolism, and vascular dysfunction. MicroRNAs (miRNAs) have emerged as key regulators of the molecular mechanisms underlying plaque formation, progression, and instability. This review summarizes current evidence on the role of miRNAs in endothelial dysfunction, vascular smooth muscle cell proliferation, macrophage activation, and plaque vulnerability. Specific miRNAs, including miR-21, miR-145, and miR-200c, demonstrate context-dependent effects on atherogenic and protective pathways. Circulating miRNA profiles show strong potential as noninvasive biomarkers for assessing plaque instability and predicting cardiovascular ischemic events, and as promising therapeutic targets. Despite these advances, challenges remain in standardization and clinical implementation. Integration of multi-miRNA panels with imaging modalities, conventional biomarkers, and emerging artificial intelligence approaches may improve risk stratification and support personalized management of carotid artery disease. Full article

Background: Cardiovascular disease (CVD) remains the leading cause of mortality across the European Union (EU), with a fourfold to fivefold east–west gradient in standardized circulatory-disease mortality. Romania ranks second highest in the EU (787 per 100,000 inhabitants in 2023). Primary-prevention practice is organized around two quantitative frameworks—the 2021 European Society of Cardiology (ESC) SCORE2/SCORE2-OP system and the 2018/2019 American College of Cardiology/American Heart Association (ACC/AHA) Pooled Cohort Equations (PCE)—which converge on therapy but diverge on patient selection. Methods: We conducted a structured narrative review (SANRA-compliant) of contemporary primary-prevention guidelines, validation studies, key trials of risk-modifier interventions, and Romanian epidemiological data through April 2026. On this basis, we developed ROMA-CV (Risk Of Multifactorial Atherosclerosis—CardioVascular) as a conceptual, country-specific risk-stratification framework anchored to existing Class I/IIa recommendations or Level A/B evidence, rather than as a fully developed, ready-to-use clinical tool Results: Four structural limitations of SCORE2 are clinically consequential in Romania: (i) an age floor of 40 years that excludes the population in which premature myocardial infarction is most preventable; (ii) a country-level calibration coefficient applied to individuals; (iii) permissive treatment of lipoprotein(a) [Lp(a)]; and (iv) an under-emphasis of subclinical-atherosclerosis imaging. We propose ROMA-CV (Risk Of Multifactorial Atherosclerosis—Cardiovascular), a four-step algorithm retaining SCORE2 as the quantitative spine while embedding once-in-a-lifetime Lp(a) measurement, a mandatory amplifier checklist, and selective coronary artery calcium (CAC) or carotid/femoral ultrasound imaging. Conclusions: ROMA-CV is a hypothesis-generating proposal that operationalizes existing evidence-based recommendations into a deterministic Romanian pathway aligned with the 2025–2030 Romanian National Plan for Non-Communicable Diseases and the EU Cardiovascular Health Plan. The algorithm is not a validated clinical decision tool and requires prospective external validation in Romanian cohorts—alongside feasibility, cost-effectiveness, and implementation studies—before any consideration of routine clinical adoption. Full article

Per- and polyfluoroalkyl substances (PFAS) are persistent environmental contaminants increasingly associated with cardiovascular disease. Identifying early manifestations of vascular aging before the onset of overt disease is essential for improving cardiovascular risk stratification and prevention. Emerging evidence suggests that PFAS exposure contributes to early vascular and atherosclerotic alterations detectable by imaging techniques, including increased carotid intima–media thickness (CIMT), arterial stiffness, and endothelial dysfunction. In contrast, evidence for associations with coronary artery calcium progression and coronary stenosis remains scarce. Mechanistically, PFAS exposure promotes endothelial dysfunction, oxidative stress, chronic inflammation, lipid dysregulation, and genetic and epigenetic modifications, all of which contribute to premature vascular aging and metabolic disturbances. The integration of imaging and molecular biomarkers may provide complementary insights into the structural, functional, and biological processes underlying PFAS-related vascular damage; however, to date, this field remains largely unexplored. This narrative review summarizes current evidence on imaging and molecular biomarkers of PFAS-induced vascular aging and discusses their potential role in cardiovascular risk assessment. It also highlights key knowledge gaps and the need for robust epidemiological and multi-omics studies to validate these biomarkers, clarify causal mechanisms, and support their application in cardiovascular and environmental health surveillance. Full article

Objective: To determine the prevalence and independent predictors of postoperative blood transfusion following carotid endarterectomy (CEA) and to quantify its association with in-hospital morbidity and 30-day mortality. Methods: A retrospective, single-centre cohort study was conducted. All consecutive patients undergoing CEA for carotid artery stenosis for two years were included without exclusion criteria. Preoperative and serial postoperative haemoglobin (Hb) and platelet values were collected at 6, 12, 24, and 48 h after surgery, together with demographic variables, cardiovascular risk factors, neurological presentation, anaesthetic risk (ASA classification), operative details, transfusion characteristics, postoperative complications, length of stay, and 30-day mortality. Red cell concentrate was indicated when postoperative Hb was ≤9 g/dL and platelet concentrate when postoperative platelets fell below 100 × 10³/mm³. The primary outcome was 30-day mortality. Univariate and multivariate linear regression analyses were used to identify independent predictors of mortality and transfusion need. Statistical significance was set at p < 0.05; analyses were performed with SPSS v30.0. Results: A total of 182 patients underwent CEA; 87.4% were male with a mean age of 71.84 years. The 30-day mortality rate was 3.8% (n = 7). Blood transfusion was required in 8.2% of patients (n = 15). On multivariate analysis, postoperative transfusion (p = 0.001) and postoperative complications (p = 0.001) were the only independent predictors of mortality, with transfusion conferring an approximately five-fold increase in mortality risk (relative risk [RR] 4.99; 95% confidence interval [CI] 0.88–28.24). Transfused patients had significantly higher complication rates (60.0% vs. 13.8%; p < 0.001) and longer total hospital stays (11.2 ± 14.9 vs. 4.9 ± 2.3 days; p = 0.001). On multivariate analysis, independent predictors of transfusion were low preoperative Hb (p < 0.001), peripheral arterial disease (PAD; RR 5.09, 95% CI 1.70–15.21; p = 0.002), postoperative complications (p = 0.004), and prolonged hospital stay (p < 0.001). Conclusions: Postoperative blood transfusion is an independent risk factor for mortality after CEA, multiplying mortality risk approximately five-fold. Low preoperative Hb and peripheral arterial disease are the principal preoperative predictors of transfusion requirement. These findings underscore the importance of systematic preoperative anaemia optimisation and the application of evidence-based restrictive transfusion thresholds in patients undergoing carotid surgery. Full article

Background: Recent research has drawn attention to potential systemic inflammation in patients with inherited epidermal differentiation disorders (EDD)—rare genetic skin conditions that may contribute to vascular dysfunction. Objective: This study assessed selected vascular, inflammatory, and biochemical parameters in 20 patients with selected EDD and 20 matched healthy controls. Methods: Assessments included Doppler ultrasound, ankle-brachial index, intima-media thickness (IMT), and laboratory profiling focused on lipid metabolism and systemic inflammation. Results: EDD patients showed significantly lower LDL cholesterol and higher interleukin-17A (IL-17A) than controls. IMT values were similar across groups and disease types, but correlated positively with age, body weight, waist circumference, triglycerides, and glucose, and negatively with reactive lymphocytes. No link was found between IMT and self-reported cardiovascular symptoms. Conclusions: In patients with selected EDD, we observed a distinct biochemical profile characterized by lower LDL cholesterol and higher IL-17A concentrations, without accompanying structural arterial changes—carotid IMT and ABI did not differ from controls and remained stable at short-term follow-up. These alterations may reflect disease-specific disturbances of lipid and inflammatory homeostasis rather than classical atherosclerosis. Although they could be of theoretical relevance to long-term vascular health, no structural arterial abnormality was demonstrated. Longitudinal studies incorporating endothelial function testing are needed to clarify their significance. Full article

Carotid artery stenting (CAS) is an established revascularization option for patients with carotid disease at high surgical risk. Periprocedural cerebral embolization remains a clinical concern, and plaque prolapse, the extrusion of atherosclerotic material through the stent struts into the lumen, has emerged as an actionable mechanism directly linked to embolic events and adverse neurological outcomes. This narrative review provides a structured, practice-oriented framework addressing one specific question: how can plaque prolapse be prevented during CAS? Drawing on prospective registries, comparative cohort studies and intravascular imaging analyses based on optical coherence tomography (OCT) and intravascular ultrasound (IVUS), we discuss the main determinants of prolapse risk, plaque morphology, procedural variables and device selection, converging on dual-layer micromesh stent (DLMS) technology as the most advanced device-based solution available. Pooled clinical data indicate a 30-day stroke rate of approximately 1.4% when DLMSs are used in combination with embolic protection, and OCT studies confirm reduced prolapse compared with single-layer stents. Prevention requires an integrated strategy combining lesion-specific characterisation, optimised technique and tailored device selection, while standardised imaging definitions and adequately powered randomised trials with hard clinical endpoints remain research priorities. Full article

Background: Hyperhomocysteinemia (homocysteine [Hcy] ≥15 μmol/L) is frequently observed in patients with impaired kidney function and has been associated with vascular remodeling and increased cardiovascular risk. We aimed to evaluate the relationship between Hcy, arterial stiffness, coronary artery disease (CAD), peripheral arterial disease, and biomarkers of kidney injury in patients undergoing elective coronary angiography. Methods: In this prospective observational study, 133 patients undergoing elective coronary angiography were stratified according to serum Hcy levels (Hcy <15 vs. Hcy ≥15 μmol/L). CAD severity was assessed angiographically. Arterial stiffness was evaluated using carotid–femoral pulse wave velocity (cfPWV), while peripheral arterial disease was assessed using ankle–brachial index (ABI). Kidney function was evaluated using serum creatinine, estimated glomerular filtration rate (eGFR), cystatin C, and urinary albumin-to-creatinine ratio (UACR). Correlation, multivariable regression, logistic regression, and receiver operating characteristic (ROC) analyses were performed. Results: Patients with hyperhomocysteinemia demonstrated significantly worse kidney function, including higher serum creatinine, cystatin C, and UACR levels, and lower eGFR (all p < 0.01). Patients with elevated Hcy levels also exhibited significantly higher cfPWV values (11.4 ± 3.3 vs. 9.7 ± 2.1 m/s, p < 0.001). Hcy correlated positively with cystatin C, creatinine, UACR, and cfPWV, and inversely with eGFR. In multivariable linear regression analysis, Hcy remained independently associated with increased cfPWV after adjustment for age, sex, and eGFR (β = 0.137, 95% CI 0.047–0.226, and p = 0.003). This association remained significant in sensitivity analyses incorporating hypertension, diabetes mellitus, LDL cholesterol, and statin therapy (β = 0.124, 95% CI 0.032–0.216, and p = 0.008). No independent associations were observed between Hcy and angiographic CAD severity or ABI values. ROC analysis demonstrated modest discrimination for elevated arterial stiffness (AUC = 0.66, 95% CI 0.56–0.76) and good discrimination for impaired kidney function (AUC = 0.82, 95% CI 0.69–0.92). Conclusions: Elevated Hcy levels were independently associated with impaired kidney function and increased central arterial stiffness, but not with angiographic CAD severity or peripheral arterial disease. These findings suggest that hyperhomocysteinemia may reflect cardiorenal vascular dysfunction and diffuse vascular remodeling rather than focal obstructive atherosclerotic disease. Further studies are needed to determine its clinical utility and prognostic value. Full article

Background: Panoramic radiography is one of the most widely used imaging examinations in dental practice, providing a broad view of the jaws and adjacent head and neck structures. Although primarily prescribed for odontogenic assessment, its field of view may reveal non-odontogenic findings with potential clinical significance. Methods: A structured narrative review was conducted according to SANRA criteria. A literature search was performed in PubMed/MEDLINE, Embase, Scopus, and Web of Science for English-language publications from January 2010 to May 2026. Backward and forward citation tracking of relevant articles, key reviews, and reference textbooks was also performed. Eligible studies and authoritative sources addressing non-odontogenic findings detectable on panoramic radiographs were qualitatively synthesized. Results: The review focuses on carotid artery calcifications, maxillary sinus abnormalities, mandibular radiomorphometric signs related to low skeletal bone mineral density, elongation or calcification of the stylohyoid complex, sialoliths, tonsilloliths, calcified lymph nodes, phleboliths, and laryngeal cartilage calcifications. These findings range from benign anatomical variants to radiographic indicators that may require medical or specialist evaluation. Conclusions: Panoramic radiography should be regarded as a tool for recognition and clinical suspicion rather than definitive diagnosis of extraoral or systemic disease. Dentists play a central role in systematically assessing the entire image, documenting relevant abnormalities, correlating them with patient history and risk factors, and initiating appropriate referral when indicated. Full article

Background: Cardiovascular (CV) risk is increased in psoriatic arthritis (PsA), yet vascular assessment has largely focused on carotid arteries, potentially underestimating systemic atherosclerosis. Objective: The objective of this study was to characterize the distribution and concordance of atherosclerotic plaques across carotid, femoral, and aortic territories in PsA and evaluate their incremental value over SCORE2. Methods: In this cross-sectional study, 250 unselected patients with PsA underwent carotid and femoral ultrasound and abdominal X-ray. Plaque prevalence and multiterritorial involvement (≥2 vascular beds) were assessed. Agreement between territories was evaluated using Cohen’s κ. In patients aged 50–69 years, the incremental value of vascular territories over SCORE2 was evaluated using ROC curves, bootstrap-corrected decision curve analysis (DCA), and reclassification metrics (IDI and continuous NRI). Results: Plaques were detected in carotid (36.0%), femoral (62.8%), and aortic (31.6%) territories, with multiterritorial involvement in 43.2%. Agreement between vascular beds was moderate (κ ≈ 0.35). Notably, 48.1% of patients without carotid plaques had femoral involvement. SCORE2 categories showed a strong gradient with plaque prevalence (p < 0.0001). In patients aged 50–69 years, adding vascular imaging improved discrimination for multiterritorial disease (AUC 0.73 vs. 0.86–0.90). Reclassification analyses demonstrated that carotid plaque substantially improved the identification of multiterritorial atherosclerosis (IDI 0.32, 95% CI 0.18–0.50; continuous NRI 1.33, 95% CI 1.08–1.60), with similar results observed for aortic plaque (IDI 0.33, 95% CI 0.20–0.50; continuous NRI 1.24, 95% CI 0.99–1.48). Femoral plaque provided a more modest improvement (IDI 0.26, 95% CI 0.16–0.37; continuous NRI 1.11, 95% CI 0.80–1.33). Conversely, when the outcome was defined as the presence of any plaque, femoral plaque provided the greatest incremental value over SCORE2 (AUC 0.96, 95% CI 0.93–0.99). Bootstrap-corrected DCA confirmed improved net benefit. Conclusions: The incremental value of vascular imaging over SCORE2 appears to be phenotype-dependent. Femoral plaque provided the greatest improvement for detecting the presence of subclinical atherosclerosis, whereas carotid and aortic plaques offered greater incremental value for identifying multiterritorial vascular involvement. These findings support a tailored, multiterritorial approach to cardiovascular risk assessment in patients with PsA. Full article