Search Results (244)

Background/Objectives: Gut microbiota has been implicated in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) and cardiovascular disease (CVD). This study aimed to identify associations between gut dysbiosis and MASLD, regarding body mass index (BMI) and subclinical coronary atherosclerosis (SCA). Methods: We conducted a cross-sectional study of 202 patients with MASLD who had no previous history of CVD. The severity of MASLD was evaluated using a magnetic resonance imaging-based method, and SCA was measured by assessing coronary artery calcification (CAC). Gut microbiota was assessed in fecal specimens using sequencing targeting the V4 region of the 16S rRNA gene. Results: Our results demonstrated that gut microbial profiles between low- and high-BMI groups (<30 vs. ≥30 kg/m²) differed significantly in beta-diversity, but not in alpha-diversity indices. At the genus level, we identified Megamonas, Sutterella, Catenibacterium, and Odoribacter, enriched in the high BMI group. Compared to the low CAC group (<100 AU), MASLD patients with high CAC scores (≥100 AU) exhibited enrichment in Ruminococcus gnavus, Bacteroides, and Lachnoclostridium, along with depletion of several short-chain fatty acid (SCFA)-producing bacteria, such as Faecalibacterium. Multivariate analysis demonstrated that older age, the presence of diabetes, high BMI, fibrosis stage F3-F4, and high plasma trimethylamine oxide (TMAO) levels were independently associated with a high CAC score in patients with MASLD. Conclusions: These data indicated that gut dysbiosis and related metabolites, in association with advanced liver disease, were potential contributors to the progression of SCA in obese patients with MASLD. Full article

Atherosclerosis (AS) is directly linked to the aging and damage of endothelial cells (ECs). As ECs and vascular smooth muscle cells (VSMCs) age, more autocrine and paracrine signals are released, extending a vicious cycle of tissue aging and physiological dysfunction. The recruitment of immune cells to inflamed arteries, including coronary arteries, and an increase in the uptake of oxidised low-density lipoprotein (ox-LDL) by macrophages (foam cells) onto the tunica intima (intima) of coronary arteries restrict blood flow. The inability of aging and damaged ECs to accommodate vast changes in signalling molecules, many produced by gut microbiota, leads to a range of anatomical and physiological arterial anomalies. These include degradation of cardiovascular membranes, fibrosis, calcification, plaque formation, and an increasingly dysfunctional immune system. Changes in the gut microbiome of the elderly have a direct effect on the immune response, as the signalling molecules produced by gut microbiota target specific receptors on inflamed arteries. This review summarizes the anatomical and physiological changes associated with the aging of coronary arteries and emphasizes the conditions leading to AS. The importance of butyrate-producing gut microbiota in preventing AS, especially in the elderly, is discussed. Full article

Background: Coronary artery calcium (CAC) scores are a widely used surrogate marker for atherosclerotic burden, but they do not fully reflect plaque vulnerability or coronary inflammation. This study aimed to evaluate the relationship between CACs, coronary plaque characteristics, and perivascular inflammatory activity using advanced CCTA and CaRi-Heart^® analysis. Methods: A total of 250 patients with no prior cardiovascular disease were retrospectively evaluated and stratified by CACs into three groups: 0 (n = 28), 1–100 (n = 121), and >100 (n = 101). Coronary plaque morphology, high-risk plaque (HRP) features, CAD-RADS scores, and AI-derived fat attenuation index (FAI) centiles were assessed. Results: Significant differences across CAC categories were observed for several key parameters. The number of diseased coronary segments increased markedly (from 1.39 ± 1.10 vs. 2.97 ± 1.57 vs. 3.94 ± 2.10; p < 0.0001, one-way ANOVA). A similar upward trend was seen for segment involvement scores, HRP prevalence, and the proportions of mixed and calcified plaque components. Regression analysis demonstrated that CACs correlated significantly with segment burden (r² = 0.2520), CAD-RADS (r² = 0.1352), and the FAI score centile (r² = 0.0568). Conclusions: This study highlights the limitations of CACs as a standalone risk stratification tool. Vulnerable and inflamed plaques may already be present in patients with low or zero CACs. Integrating CCTA with perivascular FAI mapping enables earlier detection of biologically active atherosclerosis and supports more precise clinical decision-making. Full article

Early stages of chronic kidney disease (CKD) are closely associated with vascular remodeling and coronary artery calcification. The aim of this study is to determine whether adropin is associated with asymptomatic coronary calcification in patients in the early stages of CKD. This study enrolled 337 individuals fulfilling the inclusion criteria of the early stages of CKD (G1–2, A1–3) and divided them into two subgroups with (n = 196) and without (n = 141) asymptomatic coronary artery calcification. Native coronary multi-detector computed tomography angiography was conducted to determine coronary artery calcification, which was stratified into four grades according to the Agatston method. Serum levels of adropin were measured by ELISA. The patients with known asymptomatic coronary artery calcification had significantly lower levels of adropin than those without this condition. The levels of adropin in individuals with mild (130–199 HU), moderate (200–299 HU), severe (300–399 HU) and very severe (≥400 HU) calcification were 3.13 (95% CI = 1.92–4.21) ng/mL, 2.3 (95% CI = 1.45–3.6) ng/mL, 2.1 (95% CI = 1.22–3.25) ng/mL and 1.26 (95% CI = 1.13–1.98) ng/mL, respectively. In multivariate logistic regression low adropin (<2.95 ng/mL), a presence of hypertension, type 2 diabetes mellitus (T2DM) exerted their independent potencies to predict asymptomatic coronary calcification. Moreover, adropin demonstrated better discriminative potency than concomitant hypertension and T2DM. Conclusions: Low levels of circulating adropin significantly predicted a risk of coronary artery calcification in patients in the early stages of CKD. Full article

Radiographic axial spondyloarthritis (r-axSpA) is associated with increased cardiovascular disease (CVD) risk. The coronary artery calcification (CAC) score, an atherosclerosis burden indicator that predicts CVD risk, is not well studied in r-axSpA. This study investigates CAC scores in patients with r-axSpA compared to controls without rheumatic disease and factors associated with CAC scores in r-axSpA patients. Fifty-eight r-axSpA patients from southwestern Sweden were assessed cross-sectionally using clinical disease measures, physical function, spinal mobility, lipid profiles, inflammation markers, and long-term time-averaged C-reactive protein (CRP). Four controls per patient were selected from the Swedish CArdioPulmonary bioImage Study (SCAPIS). CAC was scored on cardiac computed tomography (CT) using the Agatston method. The presence of CAC in the right coronary artery (RCA) was higher in patients compared to controls. However, no significant difference in total CAC scores was observed between r-axSpA patients and controls, despite numerically higher total CAC scores in patients. In r-axSpA patients, CAC scores correlated positively with time-averaged CRP, reduced physical function, and impaired spinal mobility. These findings suggest that chronic inflammation may contribute to coronary calcification and CVD risk in r-axSpA, highlighting the need for effective anti-inflammatory treatments. Further research is warranted to explore the association between coronary calcification, spinal immobility, and limitations in physical function. Full article

Background/Objectives: Nowadays, intravascular lithotripsy (IVL) has emerged as a novel technique for treatment of vascular calcifications, first in coronary and then in peripheral arteries. In the current literature there is little evidence that describes IVL as an effective and safe solution in treating severe aortic and aorto-iliac calcifications. The aim of this study is to report current available data about the use of IVL in treating aortic and aorto-iliac calcified lesions and its application in facilitating other endovascular procedures. Methods: the present review was conducted and reported in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) Guidelines. Preliminary searches were conducted on MEDLINE and Pubmed from January 2015 to February 2025. Studies were divided into 3 main categories depending on the location of calcifications and the type of treatment: IVL in visceral and infrarenal obstructive disease (group 1), IVL in aorto-iliac obstructive disease (group 2), IVL used to facilitate other endovascular procedures. Main primary outcomes in the perioperative period were technical and clinical successes and perioperative complications. Primary outcomes at 30 days and mid-term (2 years) were overall survival, limb salvage rate, primary patency, primary assisted patency, secondary patency, and residual stenosis. Results: Sixteen studies were identified for a total of 1674 patients. Technical and clinical successes were 100%, with low rates of perioperative complications. Dissection rate reaches up to 16.1% in some studies, without any differences compared to plain old balloon angioplasty (POBA) alone (22.8%; p = 0.47). At 30 days, limb salvage and survival rates were 100%. At 2 years, primary patency, assisted primary patency, and secondary patency were 95%, 98%, and 100%, respectively, with no difference compared to IVL + stenting. Conclusions: IVL has emerged as a novel approach to treat severe calcified lesions in visceral and aorto-iliac atherosclerotic disease and to facilitate other endovascular procedures. This technique seems to offer satisfactory early and mid-term outcomes in terms of primary, primary assisted patency, and secondary patency with low complication rates. Full article

Background: Delirium is a common, underdiagnosed neuropsychiatric syndrome in older adults, associated with high mortality and functional decline. Given its multifactorial nature and overlap with frailty, radiological markers may improve risk stratification in the emergency department (ED). Methods: We conducted a retrospective study on a small sample of 30 patients diagnosed with delirium in the emergency department who had recently undergone brain, thoracic, or abdominal CT scans for unrelated clinical indications. Using post-processing software, we analyzed radiological markers, including coronary artery calcifications (to estimate vascular age), cerebral atrophy (via the Global Cortical Atrophy scale), and cachexia (based on abdominal fat and psoas muscle volumetry). Results: Five domains were identified as significant predictors of 12-month mortality in univariate Cox regression: vascular age, delirium etiology, cerebral atrophy, delirium subtype (hyperactive vs. hypoactive), and cachexia. Based on these domains, we developed an exploratory 10-point delirium score. This score demonstrated acceptable diagnostic accuracy for mortality prediction (sensitivity 0.93, specificity 0.73, positive predictive value 0.77, negative predictive value 0.91) in this limited cohort. Conclusions: While preliminary and based on a small, retrospective sample of 30 patients, this multidimensional approach integrating clinical and radiological data may help improve risk stratification in elderly patients with delirium. Radiological phenotyping, particularly in terms of vascular aging and sarcopenia/cachexia, offers objective insights into patient frailty and could inform more personalized treatment pathways from the ED to safe discharge home, pending further validation. Full article

Background and Objectives: Galectin-3 (Gal-3), a pro-inflammatory cytokine, has been implicated in atherosclerosis and adverse cardiovascular outcomes. While its role in coronary artery disease (CAD) is increasingly recognized, its association with systemic atherosclerosis remains underexplored. Objective: To investigate serum Gal-3 levels in patients with CAD and evaluate correlations between CAD severity and extra-coronary atherosclerotic involvement (carotid, femoral, and radial territories). Materials and Methods: We prospectively enrolled 56 patients with CAD undergoing coronary angiography (42.8% with acute-ACS; 57.2% with chronic coronary syndromes-CCS). Gal-3 levels were measured within 24 h of admission. Atherosclerosis severity was assessed angiographically and through vascular ultrasound of the carotid, femoral, and radial arteries. Patients were stratified by median Gal-3 levels, and clinical follow-up was performed at 1 and 3 months. Results: Gal-3 levels were significantly higher in CAD vs. controls (20.7 vs. 10.1 ng/mL; p < 0.00001) and in ACS vs. CCS (22.18. vs. 17.93 ng/mL; p = 0.019). Gal-3 correlated positively with culprit lesion diameter stenosis (DS) (R = 0.30; p = 0.023) and maximum severity of additional treated lesions (R = 0.62; p = 0.006). Gal-3 also correlated positively with carotid plaque thickness (R = 0.32; p = 0.016), while patients with Gal-3 levels above the median showed increased median values for femoral plaque thickness (32.4 vs. 26.45 mm, p = 0.046). No correlation was found with radial artery calcification. Gal-3 showed moderate discrimination for ACS (AUC = 0.685; cut-off 20.18 ng/mL). On multivariate analysis age, DS, and ACS presentation were independent predictors of Gal-3 above 19.07 ng/mL. Conclusions: Gal-3 levels are elevated in ACS and correlate with atherosclerotic burden, particularly in coronary, carotid, and femoral territories. These findings support Gal-3 as a potential marker of lesion severity and systemic vascular involvement, highlighting its possible role in risk stratification and the monitoring of atherosclerotic disease progression. This study provides integrated insights into the impact of Gal-3 across multiple vascular beds by assessing them concurrently within the same patient cohort. Full article

Background/Objectives: Bisphosphonates may influence vascular calcification and atheroma formation via farnesyl pyrophosphate synthase inhibition in the mevalonate pathway regulating bone and lipid metabolism. However, the clinical impact of NCB use on cardiovascular outcomes remains uncertain, largely due to methodological heterogeneity in prior studies. We aimed to evaluate the association between nitrogen-containing bisphosphonate (NCB) therapy and coronary artery calcium (CAC) progression, as well as the incidence of cardiovascular disease (CVD) and coronary heart disease (CHD) events. Methods: From 6814 participants in MESA Exam 1, we excluded males (insufficient male NCB users in the MESA cohort), pre-menopausal women, baseline NCB users, and users of hormone replacement therapy, raloxifene, or calcitonin. Among 166 NCB initiators and 1571 non-users with available CAC measurements, propensity score matching was performed using the available components of FRAX, namely age, race, BMI, LDL cholesterol, alcohol, smoking, and steroid use, and baseline CAC yielded 165 NCB initiators matched to 473 non-users (1:3 ratio). Linear mixed-effects models evaluated CAC progression, and Cox models analyzed incident CVD and CHD events. Results: In the overall cohort, NCB use was not significantly associated with CAC progression (annual change: −0.01 log Agatston units; 95% CI: −0.05 to 0.01). However, among participants with a baseline estimated glomerular filtration rate (eGFR) < 65 mL/min/1.73 m², NCB use was associated with attenuated CAC progression compared with non-users (−0.06 log Agatston units/year; 95% CI: −0.12 to −0.007). No significant association was observed between NCB use and incident CVD events in the overall cohort (HR: 0.90; 95% CI: 0.60−1.36) or within kidney function subgroups. Conclusions: Incident NCB use among postmenopausal women with mild or no CAC at baseline was associated with reduced CAC progression only in women with impaired kidney function. However, this association did not correspond to a decreased risk of subsequent cardiovascular events, suggesting that the observed imaging benefit may not translate into meaningful clinical association. Full article

Background/Objectives: Patients with chronic kidney disease (CKD) are associated with a significantly elevated cardiovascular risk. The incidence and prevalence of mediated cardiac disorders and major adverse cardiac events (MACEs), such as heart failure, arrhythmias, acute coronary syndrome (ACS) based on coronary artery disease (CAD), stroke, venous thromboembolism, and peripheral artery disease, are significantly higher in CKD patients as compared with the general population. Methods: This narrative review summarizes the current clinical understanding, the pathophysiological mechanisms, and the clinical consequences in the context of cardiovascular risk and disease in CKD. Results: The impact of CKD on mediated cardiovascular disorders and elevated MACE prevalence is complex and multifactorial. The underlying mechanisms involve various traditional cardiovascular risk factors, such as arterial hypertension, smoking, dyslipidemia, and diabetes. Furthermore, CKD-specific molecular and pathophysiological factors, such as chronic inflammation and associated oxidative stress and endothelial cell dysfunction, pro-coagulatory status, uremic toxins and uremic lipids, progressive vascular calcification, and alterations in the regulation of the renin–angiotensin–aldosterone system (RAAS) and sympathetic activation cause an increased cardiovascular risk. Conclusions: Understanding the complex disease mechanisms between CKD and elevated cardiovascular risk might contribute to optimizing individual patients’ risk stratification and result in individualized diagnostic and treatment strategies via appropriate clinical biomarker application and individualized anti-inflammatory approaches. Full article

Mitral annular calcification (MAC) is usually considered an incidental, benign, age-related finding without serious complications in patients evaluated for cardiovascular or pulmonary disease with imaging studies that may result in mitral regurgitation or stenosis when severe. Therefore, it is usually not considered a significant alteration. However, there is accumulating evidence that it is associated with a higher risk of cardiovascular events, such as atherosclerotic coronary artery disease, aortic artery disease, carotid artery disease, peripheral artery disease, stroke, atrial fibrillation, atrioventricular and/or intraventricular conduction disturbance, systemic embolization, infective endocarditis, heart failure and mortality. The presence of MAC also significantly influences the outcome of mitral valve transcatheter and surgical interventions. Several conditions may predispose to MAC. MAC is strongly related to cardiovascular risk factors, such as hypertension, diabetes, smoking and cardiovascular atherosclerosis, and inflammation may also play a role in the pathogenesis of MAC. Also, conditions that increase mitral valve stress, such as hypertension, aortic stenosis and hypertrophic cardiomyopathy, predispose to accelerated degenerative calcification of the mitral annulus area. Congenital disorders, e.g., Marfan syndrome and Hurler syndrome, are also associated with MAC, due to an intrinsic abnormality of the connective tissue composing the annulus. Full article

Calcium (Ca²⁺) signaling is a fundamental regulatory mechanism controlling essential processes in the endothelium, vascular smooth muscle cells (VSMCs), and the extracellular matrix (ECM), including maintaining the endothelial barrier, modulation of vascular tone, and vascular remodeling. Cytosolic free Ca²⁺ concentration is tightly regulated by a balance between Ca²⁺ mobilization mechanisms, including Ca²⁺ release from the intracellular stores in the sarcoplasmic/endoplasmic reticulum and Ca²⁺ entry via voltage-dependent, transient-receptor potential, and store-operated Ca²⁺ channels, and Ca²⁺ elimination pathways including Ca²⁺ extrusion by the plasma membrane Ca²⁺-ATPase and Na⁺/Ca²⁺ exchanger and Ca²⁺ re-uptake by the sarco(endo)plasmic reticulum Ca²⁺-ATPase and the mitochondria. Some cell membranes/organelles are multifunctional and have both Ca²⁺ mobilization and Ca²⁺ removal pathways. Also, the individual Ca²⁺ handling pathways could be integrated to function in a regenerative, capacitative, cooperative, bidirectional, or reciprocal feed-forward or feed-back manner. Disruption of these pathways causes dysregulation of the Ca²⁺ signaling dynamics and leads to pathological cardiovascular conditions such as hypertension, coronary artery disease, atherosclerosis, and vascular calcification. In the endothelium, dysregulated Ca²⁺ signaling impairs nitric oxide production, reduces vasodilatory capacity, and increases vascular permeability. In VSMCs, Ca²⁺-dependent phosphorylation of the myosin light chain and Ca²⁺ sensitization by protein kinase-C (PKC) and Rho-kinase (ROCK) increase vascular tone and could lead to increased blood pressure and hypertension. Ca²⁺ activation of matrix metalloproteinases causes collagen/elastin imbalance and promotes vascular remodeling. Ca²⁺-dependent immune cell activation, leukocyte infiltration, and cholesterol accumulation by macrophages promote foam cell formation and atherosclerotic plaque progression. Chronic increases in VSMCs Ca²⁺ promote phenotypic switching to mesenchymal cells and osteogenic transformation and thereby accelerate vascular calcification and plaque instability. Emerging therapeutic strategies targeting these Ca²⁺-dependent mechanisms, including Ca²⁺ channel blockers and PKC and ROCK inhibitors, hold promise for restoring Ca²⁺ homeostasis and mitigating vascular disease progression. Full article

Background/Objectives: In 2024, Lithuania developed a national lung cancer screening program (the Program), targeting individuals aged 50 to 70 years, regardless of their smoking history, with screenings conducted once every three years. The Program aims not only to actively detect lung nodules (lung cancer) but also to identify clinically significant concomitant findings. The pilot study aimed to evaluate the screening process’s feasibility and organizational efficiency of the screening process, as well as its potential clinical effectiveness. Methods: Three family medicine centers were selected for participation. The Coordinating Center contacted individuals aged 50 to 70 sequentially and invited them to participate, regardless of smoking status. In total, 1014 individuals were prospectively enrolled and underwent low-dose chest computed tomography (LDCT) screening between 26 September 2024 and 14 February 2025. Results: Of the individuals invited, 76.1% agreed to participate. Lung-RADS v2022 category 4 nodules were identified in 1.4% of participants (n = 14), including six smokers and eight non-smokers. Additionally, one participant with a Lung-RADS category 2 nodule was diagnosed with squamous cell carcinoma originating from peripheral lung changes. Newly identified significant incidental findings were detected in 25.9% of participants: 5.1% had pulmonary or mediastinal findings (most commonly emphysema, interstitial lung changes, and bronchiectasis), 18.7% had cardiovascular findings (usually coronary artery calcification, aortic valve calcification, and aorta dilation), and 2.1% had other clinically relevant conditions (e.g., thyroid nodules, diaphragmatic changes). Following assessment by family physicians, 17.6% of all participants were referred to medical specialists, including pulmonologists, cardiologists, and others. Conclusions: This pilot study demonstrated that the Lithuanian lung cancer screening model is feasible, well-organized, and clinically valuable. The findings support the Program’s readiness for broader implementation at the national level. Full article

Background/Objectives: Given the conflicting results and limited published data on the correlation of vitamin A, E, and D, parathyroid hormone (PTH), and thyroid-stimulating hormone (TSH) levels, the triglyceride to high-density lipoprotein (TG/HDL) ratio, and glucose levels with the coronary artery calcium score (CAC score) in individuals at risk of coronary artery disease (CAD), this relationship requires extensive investigation. Therefore, our study aimed to investigate the correlations between the aforementioned metrics and the CAC score in individuals at risk of CAD in Saudi Arabia. Methods: This analytical cross-sectional study was conducted at the Department of Physiology, College of Medicine at King Saud University Medical City (KSUMC), King Saud University, Riyadh, Saudi Arabia, between November 2024 and April 2025, targeting patients at risk of CAD. After recruiting patients from cardiology and primary care clinics, data regarding blood vitamin A, E, and D and PTH and TSH levels and CAC scores were collected from each patient’s electronic medical records. A score of 10 points was used as a cutoff between low and high CAC scores. Results: Our sample size was 172 patients. The majority of the patients were male (62.2%), and 37.8% were female. The mean age of the sample was 59.98 ± 9.26 years, with an age range spanning 40 years. Serum vitamin A levels had a significant negative correlation with CAC scores, (odds ratio (OR) = 0.147, p-value = 0.002), whereas vitamin D and E, PTH, and TSH levels did not correlate with this score. The TG/HDL ratio was positively and significantly correlated with CAC scores (OR = 1.654, p-value = 0.030). The analysis model showed that a patient’s mean serum glycated hemoglobin (HbA1c) level positively and significantly influenced their odds of having a high CAC score (OR = 1.364, p-value = 0.018). Patient ethnicity was not significantly associated with the CAC score (CAC ≥ 10 points) (p = 0.749). Similarly, BMI did not correlate with the CAC score (p = 0.722). However, male patients were 3.42 times more likely than females to have a high CAC score (CAC ≥ 10 points), a statistically significant difference (p = 0.005). No significant differences were observed between males and females in terms of their mean vitamin A (1.74 ± 0.58 vs. 1.80 ± 0.52, p = 0.633), vitamin E (41.41 ± 15.99 vs. 37.61 ± 11.78, p = 0.189), or vitamin D levels (80.35 ± 31.07 vs. 77.16 ± 26.15, p = 0.479). Additionally, the patient’s age was significantly positively associated with the likelihood of having a high CAC score, with OR = 1.102 times (p < 0.001). Conclusions: The findings of our study indicate the strong impact of vitamin A, the TG/HDL ratio, and HbA1c on CAC scores, among other factors affecting CAC scores, and they need more concern and attention. Understanding the cellular mechanism of vitamin A correlation with calcification is of great clinical value. The TG/HDL ratio is emerging as a novel index for CVD when compared to other lipid profile parameters. Intensive large-scale studies are needed to explore the interpretations as well as cutoff values of this valuable index. Males are more prone to CVD due to their high correlation with CAC scores. Therefore, vitamin A administration and strict HbA1c and TG/HDL ratio monitoring could help as prophylactic measures to prevent cardiovascular disease in these patients. These findings could influence specific preventive measures or screening strategies for cardiovascular disease in high-risk populations. A lifestyle medicine approach that involves caregivers as well as patients should be implemented to minimize the incidence and complications of detrimental diseases. Full article

Background and Objectives: To examine individual-level sex differences in traditional and non-traditional risk factors and their potential effects on the severity of coronary artery disease (CAD). Materials and Methods: A cross-sectional analysis was performed on 208 patients with a low-to-intermediate pretest probability of CAD, referred to a Coronary CT angiography (CCTA) at the Department of Radiology, Maribor University Medical Centre, from January 2022 to January 2024. CCTA-derived EAT (epicardial adipose tissue) attenuation and CAC (coronary artery calcification) values were measured. The association between CAD, EAT, and risk factors was analyzed by sex, using correlation analysis and multivariate regression. Results: In the results obtained using the univariate logistic regression model, age (OR 1.122, p < 0.001) and hypertension (OR 4.087, p = 0.048) were significantly associated with the presence of obstructive CAD in women, while in men, age (OR 1.052, p = 0.008), hypercholesterolemia (OR 3.765, p = 0.042), and EAT attenuation (OR 1.053, p = 0.011) were significant factors. In results obtained using the multivariable logistic regression analysis model, EAT attenuation was found to be significantly associated with the presence of obstructive CAD in men (OR 1.087, p = 0.012), and age was a significant factor in women (OR =1.108, p = 0.033), while hypertension, body mass index (BMI), diabetes, hypercholesterolemia, angina pectoris, and smoking were not. Conclusions: In the sex-specific multivariable logistic regression analysis model, EAT attenuation was significantly associated with obstructive CAD in men, while in women, it was associated with age. EAT may function as a beneficial alternative indicator in identifying patients with CAD. Full article