Coronary artery calcium (CAC) score is a predictor of ischemic heart disease and closely linked to metabolic syndrome (MS). This study investigates the relationship between CAC and benign hepato-pancreaticobiliary disorders. A retrospective, cross-sectional, observational study was conducted on individuals who underwent cardiac computed tomography scans between 2015 and 2022 at a tertiary medical center. Multivariate logistic regression explored the association between CAC and potential confounders. Additionally, a logistic regression model was applied to determine whether CAC independently predicts benign hepato-pancreaticobiliary disorders [steatotic liver disease (SLD), fatty pancreas, gallstones, choledocholithiasis, pancreatic calcifications, and pancreatic duct stones]. Among 2422 individuals, 725 met inclusion. Univariate regression analysis indicated CAC was significantly linked to SLD, older age, male sex, and MS. Both SLD and fatty pancreas showed an association with CAC in individuals with and without MS (P < 0.001). Multivariate analysis demonstrated that CAC was independently associated with increasing age [OR: 1.18 (95% CI: 1.15-1.62), P < 0.001], male sex [OR: 3.12 (95% CI: 2.52-4.26), P < 0.001], MS [OR: 1.29 (95% CI: 1.25-2.45), P < 0.001], SLD [OR: 1.26 (95% CI: 1.12-2.42), P < 0.001], fatty pancreas [OR: 1.79 (95% CI: 1.19-1.98), P < 0.001], gallstones [OR: 1.82 (95% CI: 1.64-2.05), P < 0.001], choledocholithiasis [OR: 1.21 (95% CI: 1.19-2.62), P < 0.001], and pancreatic calcifications [OR: 1.74 (95% CI: 1.12-2.32), P < 0.001], regardless of MS. The CAC score is correlated with an increased prevalence of SLD, fatty pancreas, and other benign pancreaticobiliary conditions, independent of MS.

Coronary artery calcium (CAC) scoring is a well-established marker of atherosclerotic burden in the general population. Limited research has examined CAC progression and clinical implications in heart transplant (HT) recipients. We evaluated CAC progression in HT patients during long-term follow-up. We included adult HT recipients (≥ 5 years post-HT) from a retrospective single-center cohort undergoing annual cardiac CT with ≥ 4 years of follow-up. CAC scores were assessed using non-contrast CT. Patients were classified into two groups: no CAC progression (CAC = 0 across all CT scans) or any increase in CAC during follow-up. Generalized linear mixed models evaluated temporal changes in CAC; logistic regression identified variables associated with CAC progression. Among 116 patients (median age at baseline CT: 52 [38-63] years, 62% male), 65 showed CAC progression. From baseline to final CT, the proportion of patients with cardiac allograft vasculopathy (CAV) score 0 declined (90-83%), while CAV 1 and 3 increased (3-6%; 8-11%). CAC scores showed an annual increase in Ln(CAC + 1) of 0.4 (95% CI: 0.4-0.5; p < 0.001), corresponding to a 55% relative yearly increase. Significant interactions were found with recipient age at baseline CT (p = 0.008), donor heart age (p < 0.001), sex (p = 0.024), and recipient ischemic cardiomyopathy (p < 0.001). Only donor heart age was independently associated with CAC progression (p < 0.001). CAC progression is common post-HT, with donor heart age showing the strongest association. Younger recipient and donor heart age, male sex, and ischemic cardiomyopathy were associated with faster CAC progression, suggesting the need for closer surveillance and more aggressive cardiovascular management. Question Longitudinal changes in CAC score were assessed in HT recipients to provide insights into cardiovascular risk and disease progression. Findings Over half of HT recipients showed CAC progression, which was significantly associated with donor age. Recipient age, sex, and primary diagnosis influenced progression rate. Clinical relevance Routine CAC monitoring may help identify patients at higher risk of cardiovascular events after heart transplantation, allowing for closer surveillance and more aggressive cardiovascular management, which in turn might improve long-term outcomes.

Cardiac graft rejection and allograft vasculopathy (CAV) are major causes of morbidity and mortality in heart transplant (HT) patients. While endomyocardial biopsy and invasive coronary angiography remain diagnostic gold standards, their invasiveness highlights the need for safer, noninvasive alternatives. Cardiac computed tomography (CT) has emerged as a promising modality for evaluating both coronary and myocardial status. The primary aim of this study is to evaluate CT-measured extracellular volume (ECVCT) in HT patients compared to a control group and identify its clinical determinants. The secondary objective is to explore the association between ECVCT and CAV severity. In a reference HT center, we conducted a retrospective cohort study of 163 patients comprising 80 HT patients and 83 age- and sex-matched controls without structural heart disease studied with a standardized CT protocol. Twenty-two control patients had concomitant cardiac CT and magnetic resonance (CMR) to validate ECVCT measurements. Determinants of ECVCT including rejection history, CAD-RADS, CAV and cardiovascular risk factors were studied. Median ECVCT was significantly higher in HT patients (34%, IQR 30-38) compared to controls (29%, IQR 27-31; p<0.001). ECVCT was highly correlated with MR-ECV (r=0.88, p<0.001). In HT recipients, elevated ECVCT was independently associated to hypertension , smoking, presence of CAV, elevated CAD-RADS scores and a history of graft rejection, whereas in controls only higher coronary artery calcium scores correlated with increased ECVCT. CONCLUSION: ECVCT is increased in HT patients compared to controls and associated with rejection history and CAV. ECVCT emerges as a promising noninvasive tool for the simultaneous assessment of myocardial alterations and CAV in HT patients showing strong concordance with CMR and high reproducibility. Further multicenter studies are warranted to confirm its role in transplant surveillance protocols.

Background: Genetic determinants may offer incremental value over routine clinical risk factors for the prediction of coronary atherosclerosis, possibly with different outcomes across populations. Methods: In Asian subjects without known cardiovascular disease and/or diabetes, coronary atherosclerosis was quantified by coronary artery calcium (CAC), with a score of ≥100 indicating moderate-severe calcification. Relevant single nucleotide polymorphisms (SNPs) were identified through published studies with genotypes extracted through whole genome sequencing. Multivariate logistic regression modelling was performed to derive a clinical, genetic and combined model. Models’ performance was assessed using the area under the curve (AUC), Akaike’s information criterion (AIC), and Brier score. Results: Of 845 participants, 74 individuals (8.8%) had a CAC score of at least 100. Independent clinical predictors of a CAC score ≥100 were higher age, male sex, higher systolic blood pressure, higher glucose, longer time asleep, larger number of daily steps and family history of ischemic heart disease. This clinical model had an AUC of 0.89, AIC of 323, and Brier score of 0.0570. The genetic model, with independent SNPs rs515135, rs2047009 and rs10757272, had an AUC of 0.64 (p&lt;0.001 versus clinical model), AIC of 444, and Brier score of 0.0831. The combined model had an AUC of 0.91 (p=0.0026 versus clinical model), AIC of 280, and Brier score of 0.0570. Conclusion: In this healthy Asian cohort, a purely genetic prediction model for moderate-severe subclinical coronary atherosclerosis did not perform as well as its clinical counterpart. Incorporating both clinical and genetic variables allowed for only minor incremental predictive capabilities.

Recent studies have demonstrated a greater prevalence of coronary atherosclerosis in male masters endurance athletes, but the underlying contributors remain unclear. We explored the relationship between occult resting and exercise-induced hypertension with coronary atherosclerosis characteristics. 198 male masters endurance athletes with a low Framingham risk score (<10%) and no clinical diagnosis of hypertension underwent 24-hour ambulatory blood pressure (ABP) monitoring and exercise BP assessment. Coronary CT angiography assessed coronary artery calcification (CAC) score, luminal stenosis and high-risk plaque features. Seventy-eight (39%) athletes were hypertensive on ABP monitoring and 93 (47%) demonstrated a hypertensive response to exercise. A CAC score of 1-99 Agatston units (AU), 100-399 AU and ≥400 AU was present in 94 (47%), 32 (16%) and 15 (8%) athletes, respectively. Twenty-four (12%) athletes had coronary stenoses >50%. Sixty-two athletes (31%) had calcified plaque, 32 (16%) had mixed plaque, 2 (1%) had non-calcified plaque and 26 (13%) had markers of high-risk plaque. Hypertension on ABP monitoring was significantly associated with a CAC score ≥100 AU (OR: 2.56; 1.08 to 6.04) and coronary stenosis >50% (OR: 2.92; 1.17 to 7.33). A hypertensive response to exercise was significantly associated with coronary stenosis >50% (OR: 4.72; 1.65 to 13.5) and the presence of high-risk plaque (OR: 3.27; 1.27 to 8.43). Masters male endurance athletes have a high prevalence of occult hypertension, which is associated with high-risk features of coronary atherosclerosis. Both ambulatory and exercise-induced hypertension are associated with a higher prevalence of atherosclerotic coronary artery disease in male endurance athletes. Early identification and timely clinical management of this classic cardiovascular disease risk factor may reduce the burden of coronary atherosclerosis in athletes.

Association between deep learning-based coronary artery calcium score on non-gated chest CT and progression of chronic kidney disease: a retrospective observational cohort study.

ABSTRACT Subclinical hypothyroidism (SCH), characterized by elevated thyroid-stimulating hormone levels (typically &gt;4.5–5.0 mIU/L) with normal free thyroxine concentrations, affects 3%–16.9% of the general Indian population, with prevalence increasing substantially with age, particularly among women. This comprehensive review examines current evidence linking SCH to coronary artery calcium (CAC) scores in elderly individuals, exploring underlying pathophysiological mechanisms, diagnostic considerations, and clinical implications. Multiple studies demonstrate that SCH patients have significantly higher CAC scores compared to euthyroid controls, with increased prevalence of moderate to severe coronary calcification (CAC &gt;100–400). The relationship is mediated through multiple mechanisms, including lipid metabolism alterations (elevated low-density lipoprotein cholesterol [LDL-C] and oxidized LDL), endothelial dysfunction with impaired nitric oxide production, chronic low-grade inflammation (elevated C-reactive protein, interleukin-6), and direct vascular effects promoting calcium deposition. CAC scoring provides an objective assessment of atherosclerotic burden and may enhance cardiovascular risk stratification in elderly SCH patients, particularly identifying high-risk individuals misclassified by traditional risk scores like Framingham. Treatment decisions remain individualized based on age, thyroid-stimulating hormone levels, symptoms, and cardiovascular risk factors, with CAC scoring potentially guiding personalized therapeutic strategies in this vulnerable population.

Vascular calcification, a common complication of metabolic diseases such as diabetes and obesity, is closely associated with chronic inflammation and contributes to cardiovascular morbidity. The adipokine visfatin, which is secreted by visceral fat, is a proinflammatory mediator linked to metabolic dysfunction. In this study, we investigated its role in vascular calcification. A murine model was established by vitamin D injection. Serum visfatin levels were significantly elevated in patients with higher coronary artery calcification scores and in calcified mice, accompanied by increased visfatin expression in visceral fat. Adipose tissue-specific overexpression of visfatin further exacerbated vitamin D-induced vascular calcification. In cultured vascular smooth muscle cells (VSMCs), visfatin increased osteogenic differentiation under calcification conditions. Mechanistically, visfatin directly bound to TLR4 to promote osteogenic transformation of VSMCs, whereas TLR4 knockout markedly attenuated visfatin- and calcification medium-induced aortic calcification both in vivo and in vitro. Furthermore, the sodium-glucose cotransporter 2 inhibitor (SGLT2i) empagliflozin alleviated vascular calcification and reduced serum visfatin levels in mice. Mechanistically, empagliflozin suppressed p38/NF-κB activation, inhibited NF-κB nuclear translocation, and reduced NF-κB binding to the visfatin promoter, thereby decreasing visfatin expression in adipocytes. Collectively, these findings identify visfatin as a proinflammatory adipose-derived regulator of vascular calcification via TLR4 and a potential therapeutic target for vascular calcification and related cardiovascular disorders.

This study aimed to evaluate the prognostic value of segment involvement score (SIS) from coronary computed tomography angiography (CCTA) and compare it with coronary artery calcium score (CACS) in clinical practice. Patients undergoing CCTA for suspected coronary artery disease between 2006 and 2022 at 27 centers were included. SIS was defined by the number of segments with plaque. CACS was calculated using the Agatston method. Patients were followed for all-cause death and/or myocardial infarction (MI).A total of 23,034 patients were followed for a median of 2.5 years. SIS=0 was found in 61.4% of patients, SIS=1 in 12.6%, SIS=2 in 8.2%, SIS=3 in 5.7%, and SIS≥4 in 12.2%. Compared with SIS=0, SIS≥4 was associated with higher adjusted risk of death (HR [95% CI]: 1.39 [1.17-1.66]), MI (3.53 [2.72-4.59]), and death or MI (1.88 [1.62-2.18]). Obstructive stenosis (≥50%) was also independently associated with all outcomes but showed lower discrimination than SIS in receiver operating characteristic curve analyses. SIS and CACS had similar ability to predict death or MI (Area under the curve: 0.70 [0.67-0.74] vs. 0.68 [0.65-0.72], p=0.08) and MI alone (0.72 [0.67-0.77] vs. 0.72 [0.67-0.78], p=0.69). CACS performed better than SIS in predicting death (0.70 [0.66-0.74] vs. 0.67 [0.63-0.70], p=0.008). Both the extent of coronary atherosclerosis, measured by SIS, and the presence of obstructive disease are important predictors of outcomes. However, they do not provide additional prognostic value over CACS when used in routine clinical practice.

Coronary artery calcium (CAC) scoring on non-contrast ECG-gated CT remains a robust, reproducible marker of total coronary atherosclerotic burden with clear prognostic value and consistent risk reclassification beyond contemporary clinical calculators. Recent studies (2018–2026) reinforce the ‘power of zero’ for near-term risk de-escalation, identify very high CAC (≥1,000) as a distinct, very-high-risk phenotype, and, importantly, provide randomized evidence that CAC-guided treatment reduces plaque progression. Advances in artificial intelligence (AI), spectral CT, and standardized reporting (SCCT/STR; CAC-DRS) expand opportunities for automated and incidental CAC detection. This mini-review summarizes updated strengths, limitations, and practice guidance; synthesizes new evidence (2024–2026); and includes a practical clinical decision flowchart for the selective use of CAC in prevention pathways.

The AI-CVD initiative aims to extract actionable insights from coronary artery calcium (CAC) scans beyond the traditional CAC score. Although AI-derived cardiac chamber volumes predict atrial fibrillation (AF) and stroke, the long-term prognostic value of chamber ratios is less established. We evaluated the predictive value of AI-derived left atrial volume index and related chamber ratios (left atrial [LA]/right atrial [RA], LA/left ventricular) from routine CAC scans for incident AF and stroke, and their incremental value beyond established risk scores. Pooled participant-level data from 2 prospective cohorts, the MESA (Multi-Ethnic Study of Atherosclerosis, 2000-2002, n=5670) and the FHS (Framingham Heart Study Offspring cohort, 1998-2001, n=1142), were analyzed. Primary outcomes were incident AF and incident stroke. AI-enabled volumetry (AutoChamber, AI-CVD platform) quantified cardiac chamber metrics from noncontrast CAC scans. Cox proportional hazards models, net reclassification improvement, time-dependent area under the curve, calibration metrics, and least absolute shrinkage and selection operator regression were applied to evaluate predictive performance. Over a median 17-year follow-up, 1302 participants developed AF, and 365 experienced stroke events. Individuals in the ≥95th percentile of chamber metrics had a significantly increased risk. Adjusted hazard ratios for AF were 2.66 (95% CI, 2.23-3.17) for left atrial volume index, 2.04 (95% CI, 1.71-2.45) for LA/left ventricular (LV) ratio, and 1.87 (95% CI, 1.55-2.26) for LA/RA ratio. For stroke, corresponding hazard ratios were 1.96 (95% CI, 1.38-2.77), 1.64 (95% CI, 1.15-2.33), and 1.83 (95% CI, 1.29-2.59), respectively. AI-derived metrics improved reclassification beyond Cohorts for Heart and Aging Research in Genomic Epidemiology Atrial Fibrillation risk score and Framingham Stroke Risk Profile, with greatest improvements for AF from left atrial volume index (net reclassification improvement, 0.48) and stroke from LA/RA ratio (net reclassification improvement, 0.39), driven mainly by nonevent classification. Although discrimination improvements (area under the curve ) were modest, chamber measurements substantially improved Framingham Stroke Risk Profile calibration (slope, 0.448 to 0.834-0.902). Among all chamber metrics (including volumes and ratios), the least absolute shrinkage and selection operator identified left atrial volume index as the strongest predictor for AF, and LA/RA ratio as the strongest for stroke. AI-enabled left atrial volumetric and ratio-based metrics derived opportunistically from CAC scans provide incremental predictive value for AF and stroke prediction.

Traditional lipid biomarkers, such as cholesterol, HDL, LDL, and triglycerides, are frequently used to assess cardiometabolic health in clinical practice. However, these measures provide a limited view of the human lipidome, leaving clinically relevant information untapped. Lipidomic profiling using LC-MS/MS enables the measurement of hundreds of individual lipid species, yet low throughput and complex data processing have limited clinical integration. To overcome these limitations, we developed a Clinical Lipidomics Platform (CLP), a high-throughput (6 min runtime) LC-MS/MS assay measuring 270 lipid species (248 analytes + 22 internal standards) from 37 lipid subclasses in human plasma. The CLP incorporates automated data processing and normalization to an external reference material (NIST SRM 1950) to ensure reproducible and accurate data. We validated the CLP using the BioHEART-CT Discovery Cohort (n = 994) and compared lipidomic data to those from our Research Lipidomics Platform (RLP), which used a 16 min LC gradient and manual data processing to measure >800 lipids. CLP and RLP lipid measurements were highly correlated. A Lipidomic Risk Score (LRS), previously developed to model 10-year cardiovascular event risk using lipidomic, clinical, and demographic data, was calculated for each individual. CLP-derived LRS showed a strong correlation with RLP-derived LRS (R2 = 0.97). The LRS outperformed traditional risk scores, such as the Framingham Risk Score (FRS), in predicting the coronary artery calcium score (CACS), particularly in intermediate-risk individuals. These findings demonstrate the clinical utility of the CLP for cardiovascular risk assessment and its potential for broader clinical application.

To investigate the association between serum fibroblast growth factor 21 (FGF21) levels and the severity of coronary artery calcification (CAC) in patients with chronic total occlusion (CTO), as well as the complexity and outcomes of percutaneous coronary intervention (PCI). We enrolled 128 CTO patients who underwent PCI and preprocedural coronary computed tomography angiography, dividing them into severe CAC (n = 48) and nonsevere CAC (n = 80) groups according to an Agatston score of greater than or equal to 400. Serum FGF21 levels were significantly lower in patients with severe CAC, negatively correlated with CAC scores, and independently associated with severe CAC after multivariable adjustment [odds ratio (OR) per 1-SD increase: 0.481, 95% confidence interval (CI): 0.244-0.947; P < 0.05]. Patients with low FGF21 levels had significantly higher complexity scores, increased use of guidewires, longer procedural times, and lower procedural success rates (all P < 0.05). Receiver operating characteristic analysis identified 226.13 pg/ml as the optimal cut-off value of serum FGF21 for predicting procedural success. The area under the curve was 0.664 (95% CI: 0.527-0.802; P = 0.029). Serum FGF21 levels were negatively correlated with CAC severity and independently predicted severe CAC in patients with CTO. Serum FGF21 was associated with procedural difficulty and had a diagnostic value for procedural success.

Joint use of multiple molecular layers can be useful to prioritize targets for mechanistic studies. Application of coronary disease in large populations is an emerging field. We used reported circulating proteomic data (Somascan aptamer-based) from ≈3000 individuals in the CARDIA study (Coronary Artery Risk Development in Young Adults), measuring association with prevalent and 10-year incident coronary artery calcium (CAC) score. We used a multiparametric approach to prioritize circulating protein-CAC associations via genomics of circulating protein levels and coronary artery transcription. Proteins linked to prevalent/incident CAC in CARDIA implicated pathogenic mechanisms of vascular disease, including fibrosis and inflammation (GDF-15 [growth/differentiation factor 15], CDCP1 [CUB domain-containing protein 1], GSN [gelsolin], THBS2 [thrombospondin-2], chemokines, RNAS6), oxidative lipid metabolism (CILP2), extracellular matrix remodeling and signaling (MMPs [matrix metalloproteinases], TIMP-1, integrins), calcification (Notch 1, ARHGAP36 [Rho GTPase-activating protein 36]), and metabolism (GIP [gastric inhibitory polypeptide]), as well as new proteins not previously reported. Using protein-wide association study genetic approaches, several targets with nominal evidence in CAC proteomics were associated with atherosclerosis or myocardial infarction in over 300K individuals, including PCSK9 (proprotein convertase subtilisin/kexin type 9) and APO C1. Finally, the coronary artery-specific transcriptome-wide association study of CAC yielded genes with previously implicated mechanistic roles in vascular homeostasis, inflammation, and metabolism, as well as genes without previously described function in CAC. Overlap across CAC proteomics and transcriptome-wide association study highlighted genes involved in vascular inflammation (S100A9), cardiac development (HES1), vessel wall structure (SPARCL1), and vascular dysfunction or plaque (NOTCH3, TNFSF12, S100A12). These results report population-level multiomics in human coronary calcification, presenting a method to identify disease-relevant targets through integration of human genetic approaches with multiomics.

Primary Hyperparathyroidism Associated With Elevated Coronary Artery Calcium Scores and Increased Cardiovascular Risk.

The relationship between serum calcium levels at the initiation of hemodialysis and coronary artery calcium score (CACS) remains unclear. This study examined whether albumin-corrected calcium (correctedCa; Payne's formula) and ionized calcium (ionizedCa) measured at dialysis initiation are associated with CACS assessed by screening coronary computed tomography. This single-center cross-sectional study included 176 adults who initiated hemodialysis between 2015 and 2023 and underwent coronary computed tomography with CACS measurement within ±30 days. Restricted cubic spline (RCS) logistic regression was used to evaluate the associations of correctedCa and ionizedCa with CACS ≥ 400, adjusting for clinical covariates. Subgroup analyses were performed according to the median serum albumin level. For models in which nonlinearity was not significant, logistic models treating the variable as a linear term were fitted to calculate odds ratios (OR) per 1-standard deviation (SD) increase. The mean age was 70.9 years, 32.9% were women, 54.3% had diabetes, and the mean eGFR was 5.45 mL/min/1.73 m2. Higher calcium levels were associated with higher CACS. ionizedCa showed a linear association with CACS ≥ 400 (OR per 1-SD, 1.51; 95% CI, 1.08-2.11). correctedCa also showed a statistically linear association (OR per 1-SD, 1.53; 95% CI, 1.09-2.13), although the RCS curve visually plateaued at higher correctedCa levels. Subgroup analyses revealed that this convex pattern was driven by the low-albumin group. Higher calcium at hemodialysis initiation was associated with increased coronary calcification. ionizedCa tended to show a more stable linear relationship with CACS than correctedCa, as correctedCa may overestimate ionizedCa in patients with low albumin. Measurement of ionizedCa at dialysis initiation may help refine vascular calcification risk stratification as patients enter the dialysis period.

Purpose To evaluate the coronary artery disease (CAD) profile and valvular and structural alterations seen at coronary CT angiography (CTA) after radiation therapy (RT) for breast cancer in a case-control study. Materials and Methods Patients who underwent clinically indicated coronary CTA were included in this retrospective study. The following parameters were evaluated: coronary artery calcium (CAC) score, Coronary Artery Disease Reporting and Data System (CAD-RADS) score, high-risk plaque (HRP) phenotypes, and extracoronary findings (valvular fibrosis, fibrous adherence). Patients with breast cancer who underwent RT were propensity score-matched with controls (level: P = .05) for age, body mass index, and major cardiovascular risk factors to reduce selection bias and confounding. Results Among 154 female patients (mean age, 65.23 years ± 10.4 [SD]; 77 patients in RT group, 77 patients in control group), there was no evidence of a difference in CAC score between the RT and control groups (201.1 vs 75.4 Agatston units [AU], P = .64). No difference was seen in coronary stenosis severity (CAD-RADS score) (P = .40) or obstructive disease (>50% stenosis) rate (29% [22 of 77] vs 23% [18 of 77], P = .46; odds ratio [OR], 1.31 [95% CI: 0.63, 2.73]). No between-group difference was observed in high-risk plaque phenotype rate (9% [seven of 77] vs 17% [13 of 77], P = .23) or CAC or CAD-RADS scores. There was no evidence of a difference between left versus right RT for CAC (309 vs 120 AU, P = .23), coronary stenosis severity (CAD-RADS score, P = .43), or HRP phenotype rate (left, 11% [four of 36]; right, 6% [two of 34]). The prevalences of valvular fibrosis and calcifications were low (5% [four of 77] vs 3% [two of 77] [P = .68] and 16% [12 of 77] vs 9% [seven of 77] [P = .37], respectively; OR, 1.84 [95% CI: 0.68, 5.25]). The prevalence of fibrous adherence of the left anterior descending coronary artery or right coronary artery to the chambers was 1.4-fold higher in the RT group (29% [22 of 77] vs 13% [17 of 77] [P = .46]; OR, 1.41 [95% CI: 0.68, 2.97]). Conclusion RT for breast cancer was not associated with more severe coronary stenosis, HRP phenotypes, or valvular fibrosis in this case-control population cohort. Keywords: Coronary Arteries, Radiation Effects, CT-Coronary Angiography, Cardiac, Breast, Breast Cancer, Radiation Therapy, Cardiovascular Risk, Computed Tomography, Coronary Artery Disease Supplemental material is available for this article. © RSNA, 2026.

Association of cardiovascular risk scores with coronary plaque and its progression among individuals with family history of coronary artery disease.

Deep LearningReconstruction Combined with Contrast-Enhancement Boost Technique in "Quadruple-low" CCTA Protocol: Evaluation of Image Quality and Diagnostic Accuracy.

Impact of using the 2024 ESC guideline-recommended method to estimate the likelihood of obstructive coronary disease - a cardiac CT study.