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Background: The aim of our current systematic dynamic phantom study was first, to optimize reconstruction parameters of coronary CTA (CCTA) acquired on photon counting CT (PCCT) for coronary artery calcium (CAC) scoring, and second, to assess the feasibility of calculating CAC scores from CCTA, in comparison to reference calcium scoring CT (CSCT) scans. Methods: In this phantom study, an artificial coronary artery was translated at velocities corresponding to 0, < 60, and 60–75 beats per minute (bpm) within an anthropomorphic phantom. The density of calcifications was 100 (very low), 200 (low), 400 (medium), and 800 (high) mgHA/cm3, respectively. CCTA was reconstructed with the following parameters: virtual non-iodine (VNI), with and without iterative reconstruction (QIR level 2, QIR off, respectively); kernels Qr36 and Qr44f; slice thickness/increment 3.0/1.5 mm and 0.4/0.2 mm. The agreement in risk group classification between CACCCTA and CACCSCT scoring was measured using Cohen weighted linear κ with 95% CI. Results: For CCTA reconstructed with 0.4 mm slice thickness, calcium detectability was perfect (100%). At < 60 bpm, CACCCTA of low, and medium density calcification was underestimated by 53%, and 15%, respectively. However, CACCCTA was not significantly different from CACCSCT of very low, and high-density calcifications. The best risk agreement was achieved when CCTA was reconstructed with QIR off, Qr44f, and 0.4 mm slice thickness (κ = 0.762, 95% CI 0.671–0.853). Conclusion: In this dynamic phantom study, the detection of calcifications with different densities was excellent with CCTA on PCCT using thin-slice VNI reconstruction. Agatston scores were underestimated compared to CSCT but agreement in risk classification was substantial. Clinical relevance statement: Photon counting CT may enable the implementation of coronary artery calcium scoring from coronary CTA in daily clinical practice. Key Points: Photon-counting CTA allows for excellent detectability of low-density calcifications at all heart rates. Coronary artery calcium scoring from coronary CTA acquired on photon counting CT is feasible, although improvement is needed. Adoption of the standard acquisition and reconstruction protocol for calcium scoring is needed for improved quantification of coronary artery calcium to fully employ the potential of photon counting CT. [ABSTRACT FROM AUTHOR]

Background: The survival of pediatric chronic kidney disease (CKD) patients has improved in recent decades due to advances in dialysis and transplantation. However, cardiovascular disease (CVD) emerges as the main cause of mortality in patients with CKD. Objectives: To estimate cardiovascular risk in children with CKD at least 1 year after kidney transplantation. In addition, the possible association of cardiovascular risk with classic biochemical markers and potential new markers of this outcome was investigated. Methods: An observational ambidirectional (retrospective capture of risk factors and prospective study of outcomes) research including 75 patients who underwent renal transplant between 2003 and 2013 with postoperative follow‐up of at least 1 year was conducted. The outcome variables adopted were the LV mass Z‐score and the presence of coronary calcification on computed tomography using calcium Agatston score. Result: Only one patient had an elevated calcium score, and three children (4%) had an LV mass Z‐score ≥ 2.0. After multivariable analysis, only gender, serum triglyceride, and serum renalase concentration remained significantly associated with LV mass. Conclusion: The low incidence of cardiovascular changes in the population studied confirms the benefit of transplantation for the cardiovascular health of children. Nevertheless, long‐term follow‐up of these patients is recommended, given the limited duration of kidney function provided by transplantation and the high likelihood of further dialysis and kidney transplants being required in these children. [ABSTRACT FROM AUTHOR]

Cardiac hybrid positron emission tomography/computed tomography (PET/CT) has become a valid screening modality for cardiac allograft vasculopathy (CAV) following heart transplantation (HT). Visually estimated coronary artery calcium (VECAC) can be quantified from CT images obtained as part of PET/CT and has been shown to be associated with adverse cardiovascular outcomes in coronary artery disease. We investigated the prognostic value of VECAC following HT. A retrospective analysis of 430 consecutive adult HT patients who underwent 13N-ammonia cardiac PET/CT from 2016 to 2019 with follow-up through October 15, 2022, was performed. VECAC categories included: VECAC 0, VECAC 1–9, VECAC 10–99, and VECAC 100+. The association between VECAC categories and outcomes was assessed using univariable and multivariable proportional hazards regression. The primary outcome was death/retransplantation. The cohort was 73% male, 33% had diabetes, 67% had estimated glomerular filtration rate <60 ml/min, median age was 61 years, and median time since HT was 7.5 years. VECAC alone was insufficiently sensitive to screen for CAV. During a median follow-up of 4.2 years ninety patients experienced death or retransplantation. Compared with those with VECAC 0, patients VECAC 10–99 (HR 2.25, 95% CI 1.23–4.14, p = 0.009) and VECAC 100+ (HR 3.42, 95% CI 1.96–5.99, p < 0.001) experienced an increased risk of death/retransplantation. The association was similar for cardiovascular death and cardiovascular hospitalization. After adjusting for other predictors of death/retransplantation, VECAC 10–99 (VECAC 10–99: aHR 1.95, 95% CI 1.03–3.71 p = 0.04) and VECAC 100+ (VECAC 100+: aHR 2.33, 95% CI 1.17–4.63, p = 0.02) remained independently associated with death/retransplantation. VECAC is an independent prognostic marker of death/retransplantation following HT and merits inclusion as a part of post-HT surveillance PET/CT. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the relationship between the stress‐hyperglycaemia ratio (SHR) and the clinical prognosis of patients with moderate‐to‐severe coronary artery calcification (MSCAC). Methods: We consecutively enrolled 3841 patients with angiography‐detected MSCAC. The individuals were categorized into three groups based on SHR tertiles: T1 (SHR ≤ 0.77), T2 (0.77 < SHR ≤ 0.89) and T3 (SHR > 0.89). The SHR value was calculated using the formula SHR = [admission glucose (mmol/L)]/[1.59 × HbA1c (%) − 2.59]. The primary outcomes were major adverse cardiovascular and cerebrovascular events (MACCEs), including all‐cause death, non‐fatal myocardial infarction and non‐fatal stroke. Results: During a median follow‐up of 3.11 years, 241 MACCEs were recorded. Kaplan–Meier survival analysis showed that the SHR T3 group had the highest incidence of MACCEs (P <.001). Moreover, findings from the restricted cubic spline analysis showed a significant and positive association between the SHR and MACCEs. This correlation remained consistent even after considering other variables that could potentially impact the results (Pnon‐linear =.794). When comparing SHR T1 with SHR T3, it was found that SHR T3 was significantly associated with an increased risk of the primary outcome (adjusted hazard ratio = 1.50; 95% confidence interval: 1.10‐2.03). Conclusions: Patients with MSCAC showed a positive correlation between the SHR and MACCE rate over a 3‐year follow‐up period. The study showed that an SHR value of 0.83 is the key threshold, indicating a poor prognosis. Future large‐scale multicentre investigations should be conducted to determine the predictive value of the SHR in patients with MSCAC. [ABSTRACT FROM AUTHOR]

Several risk prediction models exist to predict atherosclerotic cardiovascular disease in asymptomatic individuals, but systematic reviews have generally found these models to be of limited utility. The coronary artery calcium score (CACS) offers an improvement in risk prediction, yet its role remains contentious. Notably, its negative predictive value has a high ability to rule out clinically relevant atherosclerotic cardiovascular disease. Nonetheless, CACS 0 does not permanently reclassify to a lower cardiovascular risk and periodic reassessment every 5 to 10 years remains necessary. Conversely, elevated CACS (> 100 or > 75th percentile adjusted for age, sex and ethnicity) can reclassify intermediate-risk individuals to a high risk, benefiting from preventive medication. The forthcoming update to the Dutch cardiovascular risk management guideline intends to re-position CACS for cardiovascular risk assessment as such in asymptomatic individuals. Beyond CACS as a single number, several guidelines recommend coronary CT angiography (CCTA), which provides additional information about luminal stenosis and (high-risk) plaque composition, as the first choice of test in symptomatic patients and high-risk patients. Ongoing randomised studies will have to determine the value of atherosclerosis evaluation with CCTA for primary prevention in asymptomatic individuals. [ABSTRACT FROM AUTHOR]

Background: Coronary artery calcification (CAC) is a common risk factor of cardiovascular disease. Although triglyceride glucose (TYG) index and high-density lipoprotein cholesterol (HDL-c) are both associated with CAC, no study has evaluated the correlation between the TYG/HDL-c ratio and CAC. In the present study, we investigated the relationships between CAC and the TYG index and the TYG/HDL-c ratio. Methods: A total of 9585 participants who underwent computed tomography (CT) screening for lung cancer from 2018 to 2020 were included in this cross-sectional study. Demographic data, laboratory test data and medical history data were collected from medical records. TYG = Ln[fasting glucose (mg/dL)×fasting TG (mg/dL/2]. The triglyceride glucose-HDL-c ratio was calculated as TYG/HDL-c. CAC was evaluated on chest CT images. Multivariate logistic regression analysis and restricted cubic splines were used to determine the relationships among the TYG index, TYG/HDL-c ratio and risk of CAC. The receiver operating characteristic (ROC) curve was used to evaluate the performance of the TYG index and TYG/HDL-c ratio in identifying CACs in individuals aged 60 years and above. Results: CAC was detected in 2515 of 9585 participants (mean age 51.8 ± 15.5 years, 61.2% men). The prevalence of CAC was significantly greater in participants with a high TYG/HDL-c ratio (32.6% in the fourth quartile vs. 19.1% in the first quartile, p < 0.001). Multivariate logistic regression revealed that both the TYG index (odds ratio (OR) = 1.06, 95% confidence interval (CI): 1.02–1.10) and the TYG/HDL-c ratio were associated with coronary artery calcification (OR = 1.32, 95% CI: 1.14–1.51). No such association was observed between the TYG index and CAC when further adjusted for the serum lipid level (OR = 1.23, 95% CI: 0.99–1.54). The TYG/HDL-c ratio was still associated with CAC after further adjustment for low-density lipoprotein cholesterol and total cholesterol (OR = 1.21, 95% CI: 1.09–1.35). TYG/HDL-c ratio was associated both with single vessel and multivessel calcification (OR = 1.14, 95%CI:1.05–1.23; OR = 1.15, 95%CI: 1.05–1.21). Similar trends were observed when we categorized individuals by TYG index and TYG/HDL-c quartiles and in subjects older than 60 years. Restricted cubic splines revealed that the TYG/HDL ratio had a better dose‒responsive relationship than did the TYG index. Subgroup analysis revealed that the association between the TYG/HDL-c ratio and coronary artery calcification was mainly observed in nondiabetic or nonhypertensive participants, regardless of low-density lipoprotein cholesterol levels. The ROC curve also revealed that the TYG/HDL-c ratio was better able to identify CAC than the TYG index was (area under the curve = 0.54 vs. 0.52, p < 0.01) in subjects older than 60 years. Conclusion: An increase in the TYG/HDL-c ratio is significantly positively associated with the risk of CAC, and the TYG/HDL-c ratio has a more stable association with CAC than TYG. [ABSTRACT FROM AUTHOR]

Background: Dietary patterns and lifestyle factors can influence the intensity of systemic inflammation and, consequently, the development and progression of coronary artery calcification (CAC). This study aimed to explore the relationship between the inflammatory potentials of diet and lifestyle, as captured by novel dietary and lifestyle inflammation scores (DIS and LIS), with CAC incidence and progression. Methods: We analyzed data on 5949 Black and White men and women ≥ 45 years old participating in the Multi-Ethnic Study of Atherosclerosis (MESA) cohort. Baseline data on diet and lifestyle factors were collected from 2000 to 2002 and used to construct the DIS and LIS, which reflect the overall inflammatory potential of diet and lifestyle. Cox proportional hazard regression was used to calculate the hazard ratios (HR) and 95% confidence intervals (95% CI) for CAC incidence and progression across quartiles of DIS and LIS, adjusting for potential confounders. Results: Over a median follow-up of 8.0 years, among 2638 participants with zero CAC score at baseline, 977 individuals developed positive scores, and 1681 out of 2561 participants showed CAC progression. For individuals in the highest (more pro-inflammatory) compared to the lowest (more anti-inflammatory) quartiles of the LIS, the multivariable-adjusted HR for CAC incidence was 1.35 (95% CI, 1.10–1.65; P trend < 0.002). This association was stronger among younger adults aged < 60 years compared to those aged ≥ 60 years, with respective values of 1.76 (1.34–2.30) and 1.02 (0.78–1.35) (P interaction < 0.001). However, the LIS was not significantly associated with the progression of existing CAC. Among the components of the LIS, a body mas index (BMI) ≥ 25 kg/m2 and current smoking were significant predictors for the incidence and progression of CAC, respectively. No significant association was found between DIS and CAC incidence and progression. Conclusions: Lifestyle factors, through their impact on systemic inflammation, may be associated with a higher risk of CAC incidence in middle and late adulthood. [ABSTRACT FROM AUTHOR]

Introduction: Arterial calcification, an independent predictor of cardiovascular events, increases morbidity and mortality in patients with diabetes mellitus (DM), but its mechanisms remain unclear. Extracellular vesicles (EVs) play an important role in intercellular communication. The study investigates the role and potential mechanisms of EVs derived from endothelial cells (ECs) in regulating vascular smooth muscle cell (VSMC) calcification under high glucose (HG) condition, with a goal of developing effective prevention and treatment strategies for diabetic arterial calcification. Results: The results showed that EVs derived from HG induced ECs (ECHG-EVs) exhibited a bilayer structure morphology with a mean diameter of 74.08 ± 31.78 nm, expressing EVs markers including CD9, CD63 and TSG101, but not express calnexin. ECHG-EVs was internalized by VSMCs and induced VSMC calcification by increasing Runx2 expression and mineralized nodule formation. The circ_0008362 was enriched in ECHG-EVs, and it can be transmitted to VSMCs to promote VSMC calcification both in vitro and in vivo. Mechanistically, miR-1251-5p might be one of the targets of circ_0008362 and they were co-localization in the cytoplasm of VSMCs. Runx2 was identified as the downstream target of miR-1251-5p, and circ_0008362 acted as a sponge, enhancing Runx2 expression and then promoted VSMC calcification. Besides, circ_0008362 could directly interact with Runx2 to aggravate VSMC calcification. Notably, DiR-labelled ECHG-EVs was detected in the vessels of mice. Meanwhile, the level of circ_0008362 and Runx2 were increased significantly, while the expression of miR-1251-5p was decreased significantly in calcified artery tissues of mice. However, inhibiting the release of EVs by GW4869 attenuated arterial calcification in diabetic mice. Finally, the level of circulation of plasma EVs circ_0008362 was significantly higher in patients with DM compared with normal controls. Elevated levels of plasma EVs circ_0008362 were associated with more severe coronary and aorta artery calcification in patients with DM. Conclusions: Our findings suggested that circ_0008362 was enriched in EVs derived from ECs and promoted VSMC calcification under HG conditions, both by sponging miR-1251-5p to upregulate Runx2 expression and through direct interaction with Runx2. Furthermore, elevated levels of plasma EVs circ_0008362 were associated with more severe coronary and aorta artery calcification in patients with DM. These results may serve as a potential prevention and therapeutic target for diabetic arterial calcification. [ABSTRACT FROM AUTHOR]

Background/Objectives: The role of body composition parameters in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) with presence and severity of coronary artery calcification (CAC) is still not fully elucidated. We aimed to evaluate the impact of computed tomography (CT)-based body composition parameters in patients with MASLD with CAC severity. Methods: In this multicenter study, 1870 individuals underwent cardiac CT for the detection of CAC as well as ultrasonography for the diagnosis of hepatic steatosis. The presence of CAC was defined by a CAC score threshold of >0, while severe CAC was defined by a threshold of >300. Using the abdominal cross-sectional CT images at the L3 vertebra level, we analyzed the skeletal muscle index, visceral to subcutaneous adipose tissue ratio, and muscle density using the Hounsfield unit. Results: Of 648 patients with MASLD, the proportions of presence of CAC and severe CAC were 45.2% and 9.9%, respectively. Visceral obesity was not associated with the presence of CAC after adjustment for age, sex, smoking, statin therapy, type 2 diabetes, and advanced fibrosis (adjusted odds ratio (aOR), 1.38; 95% confidence interval (CI), 0.86–2.23; p = 0.180). However, visceral obesity was independently associated with severe CAC after adjustment for several metabolic risk factors (aOR, 3.54; 95% CI, 1.25–14.90; p = 0.039), and adjustment for atherosclerotic cardiovascular disease risk scores (aOR, 3.74; 95% CI, 1.31–15.79; p = 0.032). Conclusions: Visceral obesity may serve as a novel prognostic CT-based radiological biomarker for patients with MASLD with severe CAC. [ABSTRACT FROM AUTHOR]

Exposure to metals, a newly recognized risk factor for cardiovascular disease (CVD), could be related to atherosclerosis progression. The authors hypothesized that higher urinary levels of nonessential (cadmium, tungsten, uranium) and essential (cobalt, copper, zinc) metals previously associated with CVD would be associated with baseline and rate of change of coronary artery calcium (CAC) progression, a subclinical marker of CVD in MESA (Multi-Ethnic Study of Atherosclerosis). We analyzed data from 6,418 MESA participants with spot urinary metal levels at baseline (2000-2002) and 1 to 4 repeated, continuous measures of CAC over a 10-year period. We used linear mixed-effect models to assess the association of baseline urinary metal levels with baseline CAC and cumulative change in CAC over a 10-year period. Urinary metals (μg/g creatinine) and CAC were log transformed. Models were adjusted for baseline sociodemographic factors, estimated glomerular filtration rate, lifestyle factors, and clinical factors. At baseline, the median CAC was 6.3 (Q1-Q3: 0.7-58.2). Comparing the highest to lowest quartile of urinary cadmium, CAC levels were 51% (95% CI: 32%, 74%) higher at baseline and 75% (95% CI: 47%, 107%) higher over the 10-year period. For urinary tungsten, uranium, and cobalt, the corresponding CAC levels over the 10-year period were 45% (95% CI: 23%, 71%), 39% (95% CI: 17%, 64%), and 47% (95% CI: 25%, 74%) higher, respectively, with no difference for models with and without adjustment for clinical factors. For copper and zinc, the corresponding estimates dropped from 55% to 33% and from 85% to 57%, respectively, after adjustment for clinical factors. The associations of metals with CAC were comparable in magnitude to those for classical CVD risk factors. Exposure to metals was generally associated with extent of coronary calcification at baseline and follow-up. These findings support that metals are associated with the progression of atherosclerosis, potentially providing a novel strategy for the prevention and treatment of atherosclerosis progression. [ABSTRACT FROM AUTHOR]

Vascular calcification (VC) arises from the accumulation of calcium salts in the intimal or tunica media layer of the aorta, contributing to higher risk of cardiovascular events and mortality. Despite this, the mechanisms driving VC remain incompletely understood. We previously described that nesfatin-1 functioned as a switch for vascular smooth muscle cells (VSMCs) plasticity in hypertension and neointimal hyperplasia. In this study, we sought to investigate the role and mechanism of nesfatin-1 in VC. The expression of nesfatin-1 was measured in calcified VSMCs and aortas, as well as in patients. Loss- and gain-of-function experiments were evaluated the roles of nesfatin-1 in VC pathogenesis. The transcription activation of nesfatin-1 was detected using a mass spectrometry. We found higher levels of nesfatin-1 in both calcified VSMCs and aortas, as well as in patients with coronary calcification. Loss-of-function and gain-of-function experiments revealed that nesfatin-1 was a key regulator of VC by facilitating the osteogenic transformation of VSMCs. Mechanistically, nesfatin-1 promoted the de-ubiquitination and stability of BMP-2 via inhibiting the E3 ligase SYTL4, and the interaction of nesfatin-1 with BMP-2 potentiated BMP-2 signaling and induced phosphorylation of Smad, followed by HDAC4 phosphorylation and nuclear exclusion. The dissociation of HDAC4 from RUNX2 elicited RUNX2 acetylation and subsequent nuclear translocation, leading to the transcription upregulation of OPN, a critical player in VC. From a small library of natural compounds, we identified that Curculigoside and Chebulagic acid reduced VC development via binding to and inhibiting nesfatin-1. Eventually, we designed a mass spectrometry-based DNA-protein interaction screening to identify that STAT3 mediated the transcription activation of nesfatin-1 in the context of VC. Overall, our study demonstrates that nesfatin-1 enhances BMP-2 signaling by inhibiting the E3 ligase SYTL4, thereby stabilizing BMP-2 and facilitating the downstream phosphorylation of SMAD1/5/9 and HDAC4. This signaling cascade leads to RUNX2 activation and the transcriptional upregulation of MSX2, driving VC. These insights position nesfatin-1 as a potential therapeutic target for preventing or treating VC, advancing our understanding of the molecular mechanisms underlying this critical cardiovascular condition. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a dynamic process. There is little evidence regarding whether quantification of atherosclerosis extent and progression, particularly in the carotid artery, in asymptomatic individuals predicts all-cause mortality. This study sought to evaluate the independent predictive value (beyond cardiovascular risk factors) of subclinical atherosclerosis burden and progression and all-cause mortality. A population of 5,716 asymptomatic U.S. adults (mean age 68.9 years, 56.7% female) enrolled between 2008 and 2009 in the BioImage (A Clinical Study of Burden of Atherosclerotic Disease in an At Risk Population) study underwent examination by vascular ultrasound to quantify carotid plaque burden (cPB) (the sum of right and left carotid plaque areas) and by computed tomography for coronary artery calcium (CAC). Follow-up carotid vascular ultrasound was performed on 732 participants a median of 8.9 years after the baseline exam. All participants were followed up for all-cause mortality, the primary outcome. Trend HRs are the per-tertile increase in each variable. Over a median 12.4 years' follow-up, 901 (16%) participants died. After adjustment for cardiovascular risk factors and background medication, baseline cPB and CAC score were both significantly associated with all-cause mortality (fully adjusted trend HR: 1.23; 95% CI: 1.16-1.32; and HR: 1.15; 95% CI: 1.08-1.23), respectively (both P < 0.001), thus providing additional prognostic value. cPB performed better than CAC score. In participants with a second vascular ultrasound evaluation, median cPB progressed from 29.2 to 91.3 mm3. cPB progression was significantly associated with all-cause mortality after adjusting for cardiovascular risk factors and baseline cPB (HR: 1.03; 95% CI: 1.01-1.04 per absolute 10-mm3 change; P = 0.01). Subclinical atherosclerosis burden (cPB and CAC) in asymptomatic individuals was independently associated with all-cause mortality. Moreover, atherosclerosis progression was independently associated with all-cause mortality. [ABSTRACT FROM AUTHOR]

Coronary artery calcification (CAC) is an early marker for atherosclerosis and is mainly induced by the osteoblast-like phenotype conversion of vascular smooth muscle cells (VSMCs). Recent reports indicate that NOD-like receptor protein 3 (NLRP3)-mediated pyroptosis plays a significant role in the calcification of vascular smooth muscle cells (VSMCs), making it a promising target for treating calcific aortic valve disease (CAC). Ligustrazine, or tetramethylpyrazine (TMP), has been found effective in various cardiovascular and cerebrovascular diseases and is suggested to inhibit NLRP3-mediated pyroptosis. However, the function of TMP in CAC is unknown. Herein, influences of TMP on ß-glycerophosphate (ß-GP)-stimulated VSMCs and OPG-/-mice were explored. Mouse Aortic Vascular Smooth Muscle (MOVAS-1) cells were stimulated by ß-GP with si- caspase-3, si- Gasdermin E (GSDME) or TMP. Increased calcification, reactive oxygen species (ROS) level, Interleukin-1beta (IL-1ß) and Interleukin-18 (IL-18) levels, lactate dehydrogenase (LDH) release, enhanced apoptosis, and activated cysteine-aspartic acid protease-3 (caspase-3)/GSDME signaling were observed in ß-GP-stimulated MOVAS-1 cells, which was sharply alleviated by si-caspase-3, si-GSDME or TMP. Furthermore, the impact of TMP on the ß-GP-induced calcification and injury in MOVAS-1 cells was abolished by raptinal, an activator of caspase-3. Subsequently, OPG-/- mice were dosed with TMP or TMP combined with raptinal. Calcium deposition, increased nodules, elevated IL-1ß and IL- 18 levels, upregulated CASP3 and actin alpha 2, smooth muscle (ACTA2), and activated caspase-3/GSDME signaling in OPG-/- mice were markedly alleviated by TMP, which were notably reversed by the co-administration of raptinal. Collectively, TMP mitigated CAC by inhibiting caspase-3/GSDME mediated pyroptosis. [ABSTRACT FROM AUTHOR]

Background: Coronary artery calcium score (CACS) and carotid intima-media thickness (CIMT) are important markers for early detection of coronary atherosclerosis. The study aimed to investigate the relationship between the CIMT and the CACS as markers for atherosclerotic coronary artery disease (CAD). Methods: This single-center prospective study enrolled 41 cases with suspected CAD. The cases underwent carotid artery US and CA noncontrast CT (NCCT). A radiologist with eight years of experience in vascular US imaging performed the carotid artery US, while two radiologists with ten years of experience in cardiac imaging analyzed the coronary artery CT images and assigned a CAC-DRS category for each case. We used the Pearson correlation test to calculate the correlation between CIMT and CACS. The receiver operating characteristics (ROC) curve was used to estimate the best cutoff value of CIMT in predicting CA heavy calcification. Results: The study included 41 cases of suspected CAD, of which 12-showed heavy, and 29 showed non-heavy CA calcification. The mean CACS was 163, and the highest CIMT was 0.785 mm among the included patients. There was a significant positive correlation between the CACS and the highest CIMT (r 0.606 and P <0.001). A CIMT > 0.8 mm was the best cutoff for predicting heavy calcification, with a sensitivity of 91.7%, a specificity of 65.5%, and an accuracy of 73.2% based on ROC curve analysis. Conclusions: CIMT and CACS can be considered non-invasive predictive measures for CA atherosclerosis and subsequent CAD. Moreover, these markers might help cardiologists in clinical management. [ABSTRACT FROM AUTHOR]

We aimed to compare the associations of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated fatty liver disease (MAFLD) with coronary artery calcification (CAC). Patients who simultaneously underwent ultrasonography to diagnose hepatic steatosis and cardiac computed tomography to detect CAC were included. The presence and severity of CAC were defined with CAC-score thresholds of > 0 and > 300, respectively, and patients were divided into the following groups: no MASLD or MAFLD (reference), MASLD-only, MAFLD-only, and overlapping groups. Overall, 1,060/2,773 (38.2%) patients had CAC, of which 196 (18.5%) had severe CAC. The MASLD and MAFLD prevalence rates were 32.6% and 45.2%, respectively, with an overlap of 30.7%. In an ASCVD risk score-adjusted model, both MASLD (adjusted odd ratios [aOR], 1.21; 95% confidence interval [CI], 1.02–1.44; p = 0.033) and MAFLD (aOR 1.20; 95% CI 1.01–1.42, p = 0.034) were associated with CAC, whereas only MASLD (aOR 1.38; 95% CI 1.01–1.89, p = 0.041) was associated with severe CAC. Compared to the reference group, the overlapping group showed an association with CAC (aOR 1.22; 95% CI 1.01–1.47; p = 0.038); however, the MASLD and MAFLD subgroups did not differ in their association with CAC. MASLD may predict a higher risk of ASCVD more effectively than MAFLD. [ABSTRACT FROM AUTHOR]

Objectives: We aim to explore the prevalence of coronary artery calcification (CAC) and ascending/descending thoracic aorta (AA/DA) dilation in idiopathic inflammatory myopathies (IIM) and systemic lupus erythematosus (SLE) patients, and to assess associations between cardiovascular disease (CVD) risk factors and these imaging signatures. Methods: This study recruited 151 IIM patients, 140 SLE patients, and 195 controls. The CAC and AA/DA diameters were quantified using non-gated chest CT images. The independent samples t-test or Mann–Whitney test was chosen for comparisons of continuous variables between patients and healthy controls. For categorical data, comparisons were made using the chi-square test or Fisher's exact test. Multivariate regression or Spearman's correlation analysis was employed to probe the associations between CVD risk factors and Framingham risk score (FRS) with imaging signatures. Results: The IIM and SLE patients showed significantly higher prevalence of CAC and AA/DA dilatation (P < 0.01). Age was a risk factor for both CAC and AA/DA dilatation in all cohorts (P < 0.01). In IIM patients, the AA/DA dilatation was associated with BMI (P = 0.05). In SLE patients, CAC was associated with the elevated CRP level (P = 0.05). Without CAC, both IIM and SLE patients showed significant correlations between AA/DA diameters and FRS (P < 0.01, P < 0.01). Only in SLE patients, the interleukin-6 (IL-6) level correlated with AA/DA diameters. Conclusion: The IIM and SLE patients more commonly exhibit CAC and AA/DA dilation. These subclinical atherosclerosis signs are associated with traditional CVD risk factors. For AID patients without CAC, AA/DA diameters could serve as a potential biomarker for early CVD risk. Key Points • The study characterized the manifestation of subclinical atherosclerosis imaging biomarkers (CAC, AA/DA dilation) in IIM and SLE patients. • AA/DA diameters could serve as an early imaging biomarker in clinical management for IIM and SLE patients with early-onset and no CAC present. [ABSTRACT FROM AUTHOR]

Advanced signal processing of photoplethysmographic data enables novel analyses which may improve the understanding of the pathogenesis of dysglycemia associated with sleep disorders. We aimed to identify sleep-related pulse wave characteristics in diabetic patients compared to normoglycemic individuals, independent of cardiovascular-related comorbidities. This cross-sectional evaluation of the population-based Swedish CArdioPulmonary bioImage Study (SCAPIS) included overnight oximetry-derived pulse wave data from 3997 subjects (45 % males, age 50–64 years). Metabolic status was classified as normoglycemic (n = 3220), pre-diabetic (n = 544), or diabetic (n = 233). Nine validated pulse wave features proposed to influence cardiovascular risk were derived and compared between metabolic status groups. Logistic prediction models and genetic matching were applied to capture diabetes-related pulse wave characteristics during sleep. The model was controlled for anthropometrics, lifestyle, sleep apnea, and in the final adjustment even for cardiometabolic factors like dyslipidaemia, hypertension, and coronary artery calcification. Pulse wave-derived parameters differed between normoglycemic and diabetic individuals in eight dimensions in unadjusted as well as in the partially adjusted model (anthropometric factors and sleep apnea, p ≤ 0.001). All covariates confirmed significant differences between normoglycemic and diabetic subjects (all p ≤ 0.001). Reduced cardio-respiratory coupling (respiratory-related pulse oscillations) (β = −0.010, p = 0.012), as well as increased vascular stiffness (shortened pulse propagation time (β = −0.015, p = 0.001), were independently associated with diabetes even when controlled for cardiometabolic factors. These results were confirmed through a matched cohort comparative analysis. Photoplethysmographic pulse wave analysis during sleep can be utilized to capture multiple features of modified autonomic regulation and cardiovascular consequences in diabetic subjects. Dampened heart rate variability and increased vascular stiffness during sleep showed the strongest associations with diabetes. • Several characteristics of the nocturnal pulse wave signal (PPG) are associated with diabetes. • Elevated vascular stiffness and reduced heart rate modulation identified in diabetic subjects. • Overnight PPG may detect diabetes-related consequences of metabolic dysfunction during sleep. [ABSTRACT FROM AUTHOR]

Coronary artery calcification is an integral part of atherosclerosis. It has been suggested that early coronary artery calcification is associated with active inflammation, and advanced calcification forms as inflammation subsides. Inflammation is also an important factor in plaque vulnerability. However, the relationship between coronary artery calcium burden, vascular inflammation, and plaque vulnerability has not been fully investigated. This study aimed to correlate calcified plaque burden (CPB) at the culprit lesion with vascular inflammation and plaque vulnerability. Patients with coronary artery disease who had both computed tomography angiography and optical coherence tomography were included. The authors divided the patients into 4 groups: 1 group without calcification at the culprit lesion; and 3 groups based on the CPB tertiles. CPB was calculated as calcified plaque volume divided by vessel volume in the culprit lesion. The authors compared pericoronary adipose tissue (PCAT) attenuation for vascular inflammation and optical coherence tomography–derived vulnerable features among the 4 groups. Among 578 patients, the highest CPB tertile showed significantly lower PCAT attenuation of culprit vessel compared with the other groups. The prevalence of features of plaque vulnerability (including lipid-rich plaque, macrophage, and microvessel) was also lowest in the highest CPB tertile. In the patients with calcification, higher age, statin use, and lower PCAT attenuation were independently associated with CPB. Greater calcium burden is associated with a lower level of vascular inflammation and plaque vulnerability. A greater calcium burden may represent advanced stable plaque without significant inflammatory activity. (Massachusetts General Hospital and Tsuchiura Kyodo General Hospital Coronary Imaging Collaboration; NCT04523194) [Display omitted] [ABSTRACT FROM AUTHOR]

Background: Despite the majority of studies have identified smoking as a risk factor for coronary artery calcification (CAC), some studies have not identified this relationship. Differences on results reached by studies on the association of alcohol consumption with CAC exist. Moreover, studies have almost exclusively investigated the association between smoking and alcohol consumption independently. Whether an interaction effect of alcohol on the association of smoking and CAC exists has hardly been investigated. Methods: The data of 2431 adult patients who visited Fuwai Hospital, Chinese Academy of Medical Sciences from September, 2001 to December, 2023 and had Agaston coronary artery calcification score (CACS) reported were utilized. Patients who (1) underwent percutaneous coronary intervention, coronary bypass graft and heart transplantation, or (2) were complicated by acute medical conditions, chronic kidney disease or malignant neoplasms were excluded. Data from 1528 patients were eventually analyzed. Logistic regression was employed to investigate the association of smoking and alcohol consumption with presence of CAC and severe CAC. Interaction effects of alcohol consumption history on the association of current smoking and both presence of and severe CAC were examined. Results: Smoking history was significantly associated with presence of CAC and severe CAC. Current alcohol consumption was also significantly associated with presence of CAC and severe CAC. After adjusting for confounders, alcohol consumption history demonstrated an interaction effect on the association of current smoking with both presence of and severe CAC. Using non-alcohol consumers not smoking at the time of the study as reference, current smokers with an alcohol consumption history suffered from an increased risk of presence of CAC and severe CAC. Conclusions: Both smoking history and current alcohol consumption were associated with presence of and severe CAC. Alcohol consumption history demonstrated an interaction effect on the association of current smoking with both presence of and severe CAC. [ABSTRACT FROM AUTHOR]

Polycystic Ovarian Syndrome (PCOS) is a prevalent endocrine disorder affecting women of reproductive age, with significant variations in presentation characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. Beyond reproductive health, it may also pose crucial long-term cardiometabolic risks, especially for women with specific types of PCOS, contributing to early subclinical cardiovascular atherosclerotic alterations such as endothelial dysfunction, increased arterial stiffness, and coronary artery calcium levels, respectively. Moreover, the precise relationship between clinical cardiovascular disease (CVD) and PCOS remains debated, with studies demonstrating an elevated risk while others report no significant association. This review investigates the pathophysiology of PCOS, focusing on insulin resistance and its link to subclinical and clinical cardiovascular disease. Diagnostic challenges and novel management strategies, including lifestyle interventions, medications like metformin and glucagon-like peptide-1 receptor agonists (GLP-1RAs), hormonal contraceptives, and bariatric surgery, are further discussed. Recognizing the cardiometabolic risks associated with PCOS, a comprehensive approach and early intervention should address both the reproductive and cardiometabolic dimensions of the syndrome. [ABSTRACT FROM AUTHOR]

Objective. To evaluate the progression of coronary artery calcification (CAC) and associated risk factors in a systemic lupus erythematosus (SLE) cohort. Methods. We reassessed the presence of CAC in patients with SLE who were screened 9 years before, using multidetector computed tomography. Clinical variables (cumulated disease activity and damage accrual), antiphospholipid syndrome and SLE serology, and cardiovascular (CV) risk factors (hypertension, BMI [kg/m²], modified Framingham risk score, lipid profile, menopausal status) were assessed longitudinally. Results. We included 104 patients from the parent study. Most of them were women (94.2%), with a mean age of 41.0 (SD 8.3) years and mean disease duration of 14.8 (SD 2.9) years. We documented CAC in 17 patients (16.3%). Seven cases were from the parent study and 10 were incident cases. The cumulative incidence of CAC was 9% and the incidence density was 1 per 100 person-years. CAC occurred more frequently in the age groups 30-39 years and 40-44 years. All patients with previous CAC had worsening of their calcium indexes, and none developed clinical CV events. When comparing prevalent CAC cases (n = 17) vs patients without calcification (n = 87), both groups were similar in traditional CV risk factors, disease duration, Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) area under the curve (AUC), and Systemic Lupus International Collaborating Clinics (SLICC) score, but were more likely to be postmenopausal and have higher apolipoprotein B (apoB) levels. Patients with previous CAC had higher apoB levels, SLEDAI-2K AUC scores, and anticardiolipin IgG antibodies than incident cases. Conclusion. CAC in patients with SLE progressed over time but was not associated with adverse CV events during the first 9 years of follow-up. ApoB levels and postmenopausal status might be associated with this progression. [ABSTRACT FROM AUTHOR]

Despite the well-established significance of the CAC score as a cardiovascular risk marker, the timing of using CAC score in routine clinical practice remains unclear. We aim to develop a prediction model for patients visiting outpatient cardiology units, which can recommend whether CAC score screening is necessary. A prediction model using retrospective cross-sectional design was conducted. Patients who underwent CAC score screening were included. Eight candidate predictors were preselected, including age, gender, DM or primary hypertension, angina chest pain, LDL-C (≥130 mg/dl), presence of low HDL-C, triglyceride (≥150 mg/dl), and eGFR. The outcome of interest was the level of CAC score (CAC score 0, CAC score 1–99, CAC score ≥100). The model was developed using ordinal logistic regression, and model performance was evaluated in terms of discriminative ability and calibration. A total of 360 patients were recruited for analysis, comprising 136 with CAC score 0, 133 with CAC score 1–99, and 111 with CAC score ≥100. The final predictors identified were age, male gender, presence of hypertension or DM, and low HDL-C. The model demonstrated excellent discriminative ability (Ordinal C-statistics of 0.81) with visually good agreement on calibration plots. The implementation of this model (CAC-prob) has the potential to enhance precision in recommending CAC screening. However, external validation is necessary to assess its robustness in new patient cohorts. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of a drug‐coated balloon (DCB) on inflammatory cytokines in patients with coronary artery calcification (CAC) after interventional therapy. Methods: This study included 58 patients with coronary heart disease who underwent coronary angiography (CAG) from October 2020 to September 2021. Patients were divided into CAC and non‐CAC groups, and a DCB was used to intervene in the target lesions. Ten‐milliliter preoperative and postoperative blood samples were drawn from the coronary lesions in both groups to detect the expression of serum interleukin‐6 (IL‐6), tumor necrosis factor‐alpha (TNF‐α), and intercellular adhesion molecule‐1 (ICAM‐1). All patients were subjected to a 6‐month follow‐up to observe the incidence of major adverse cardiac events (MACEs). Results: No significant differences in baseline clinical data were found between the groups. Serum IL‐6, TNF‐α, and ICAM‐1 expressions in coronary blood samples immediately before DCB were not significantly different from those after DCB in all patients. After DCB, serum TNF‐α expression in the CAC group was significantly lower than that in the non‐CAC group (p < 0.05). In contrast, no significant difference in serum IL‐6 and ICAM‐1 expression was found between the groups. During the 6‐month follow‐up, no significant difference in the incidence of MACE was found between both groups. Conclusions: DCB reduced the expression of inflammatory cytokine TNF‐α in CAC, which may be one of the key mechanisms underlying the treatment of CAC by DCB. [ABSTRACT FROM AUTHOR]

Background and Objectives Methods Results Conclusion Coronary artery calcification (CAC) is a frequent additional finding on lung cancer screening (LCS) low‐dose computed tomography (LDCT). Cardiovascular disease (CVD) is a major cause of death in LCS participants. We aimed to describe prevalence of incidental CAC detected on LDCT in LCS participants without prior history of coronary artery disease (CAD), evaluate their CVD risk and describe subsequent investigation and management.Prospective observational nested cohort study including all participants enrolled at a single Australian site of the International Lung Screen Trial. Baseline LDCTs were reviewed for CAC, and subsequent information collected regarding cardiovascular health. 5‐year CVD risk was calculated using the AusCVD risk calculator.55% (226/408) of participants had CAC on LDCT and no prior history of CAD, including 23% with moderate–severe CAC. Mean age of participants with CAC was 65 years, 68% were male. 53% were currently smoking. Majority were high risk (51%) or intermediate risk (32%) of a cardiovascular event in 5 years. 21% of participants were re‐stratified to a higher CVD risk group when CAC detected on LCS was incorporated. Only 10% of participants with CAC received lifestyle advice (only 3% currently smoking received smoking cessation advice). 80% of participants at high‐risk did not meet guideline recommendations, with 47% of this group remaining without cholesterol lowering therapy.LCS with LDCT offers the potential to identify and communicate CVD risk in this population. This may improve health outcomes for high‐risk LCS participants and further personalize management once screening results are known. [ABSTRACT FROM AUTHOR]

Background: The coronary artery calcium score and left atrial volume have been shown to predict the incidence of acute myocardial infarction and death from cardiovascular disease in patients undergoing peritoneal dialysis. However, the association between these factors has not been well-established. Methods: This cross-sectional, prospective, single-center study was conducted on patients undergoing outpatient peritoneal dialysis, who were followed up at a university hospital between March 2018 and August 2019. The coronary artery calcium score was calculated based on cardiovascular computed tomography findings. The score was "positive" when it was ≥100 Agatston and "negative" when it was <100 Agatston. The left atrial volume was obtained using the biplane disc method at the end of the left ventricular systole, and then it was indexed to the body surface. Results: Forty-four patients were evaluated. They had an age [mean (range)] of 56 (43–65) years and had been on dialysis therapy for 11.7 (6.8–25.4) months. Univariate analysis revealed a relationship between the coronary artery calcium score and left atrial volume index and the following variables: age, diabetes, overhydration, pulse wave velocity, E/A ratio, and left ventricular mass index. In multivariate logistic regression analysis, only the left atrial volume index was independently associated with a positive coronary artery calcium score. Conclusions: The left atrial volume index was associated with a positive coronary artery calcium score in patients on peritoneal dialysis, regardless of other factors. It may be a useful risk marker for coronary artery disease in this population. [ABSTRACT FROM AUTHOR]

Coronary CT angiography (CCTA) is now endorsed by all major cardiology guidelines for the investigation of chest pain and assessment for coronary artery disease (CAD) in appropriately selected patients. CAD is a leading cause of morbidity and mortality. There is extensive literature to support CCTA diagnostic and prognostic value both for stable and acute symptoms. It enables rapid and cost-effective rule-out of CAD, and permits quantification and characterization of coronary plaque and associated significance. In this comprehensive review, we detail the road traveled as CCTA evolved to include quantitative assessment of plaque stenosis and extent, characterization of plaque characteristics including high-risk features, functional assessment including fractional flow reserve-CT (FFR-CT), and CT perfusion techniques. The state of current guideline recommendations and clinical applications are reviewed, as well as future directions in the rapidly advancing field of CT technology, including photon counting and applications of artificial intelligence (AI). [ABSTRACT FROM AUTHOR]

Background: Coronary artery disease (CAD) imposes a significant global health burden, necessitating a deeper comprehension of its genetic foundations to uncover innovative therapeutic targets. Employing a comprehensive Mendelian randomization (MR) approach, we aimed to explore the genetic associations between lipid profiles, immune cell phenotypes, and CAD risk. Methods: Utilizing data from recent large-scale genome-wide association studies (GWAS), we scrutinized 179 lipid and 731 immune cell phenotypes to delineate their genetic contributions to CAD pathogenesis, including coronary artery calcification (CAC). Moreover, specific immune cell phenotypes were examined as potential mediators of the lipid-CAD/CAC causal pathway. Results: Among the 162 lipid species with qualified instrumental variables (IVs) included in the analysis, we identified 36 lipids that exhibit a genetic causal relationship with CAD, with 29 being risk factors and 7 serving as protective factors. Phosphatidylethanolamine (18:0_20:4) with 8 IVs (OR, 95% CI, P-value: 1.04, 1.02-1.06, 1.50E-04) met the Bonferroni-corrected significance threshold (0.05/162 = 3.09E-04). Notably, all 18 shared lipids were determined to be risk factors for both CAD and CAC, including 16 triacylglycerol traits (15 of which had ≥ 3 IVs), with (50:1) exhibiting the highest risk [OR (95% CI) in CAC: 1.428 (1.129-1.807); OR (95% CI) in CAD: 1.119 (1.046-1.198)], and 2 diacylglycerol traits. Furthermore, we identified HLA DR+ natural killer cells (IVs = 3) as nominally significant with lipids and as potential mediators in the causal pathway between diacylglycerol (16:1_18:1) or various triacylglycerols and CAD (mediated effect: 0.007 to 0.013). Conclusions: This study provides preliminary insights into the genetic correlations between lipid metabolism, immune cell dynamics, and CAD susceptibility, highlighting the potential involvement of natural killer cells in the lipid-CAD/CAC causal pathway and suggesting new targets for therapy. Further evidence is necessary to substantiate our findings. [ABSTRACT FROM AUTHOR]

Objectives: This study attempts to compare the predictive effects of several prediction models on obstructive coronary artery disease (OCAD) in young patients (30–50 years old), with a view to providing a new evaluation tool for the prediction of premature coronary artery disease (PCAD). Methods: A total of 532 hospitalized patients aged 30–50 were included in the study.All of them underwent coronary computed tomography angiography (CCTA) for suspected symptoms of coronary heart disease.Coronary artery calcium score (CACS) combined with traditional risk factors and pre-test probability models are the prediction models to be compared in this study.The PTP model was selected from the upgraded Diamond-Forrester model (UDFM) and the Duke clinical score (DCS). Results: All patients included in the study were aged 30–50 years. Among them, women accounted for 24.4%, and 355 patients (66.7%) had a CACS of 0. OCAD was diagnosed in 43 patients (8.1%). The CACS combined with traditional risk factors to predict the OCAD area under the curve of receiver operating characteristic (ROC) (AUC = 0.794,p < 0.001) was greater than the PTP models (AUCUDFM=0.6977,p < 0.001;AUCDCS=0.6214,p < 0.001). By calculating the net reclassification index (NRI) and the integrated discrimination index (IDI), the ability to predict the risk of OCAD using the CACS combined with traditional risk factors was improved compared with the PTP models (NRI&IDI > 0,p < 0.05). Conclusion: The predictive value of CACS combined with traditional risk factors for OCAD in young patients is better than the PTP models. [ABSTRACT FROM AUTHOR]

AbstractAsthma continues to cause morbidity and mortality despite advances in treatment that include biologics targeting Type 2 inflammation. The International Collaborative Asthma Network (ICAN) forum was developed with the primary goal of promoting innovative, collaborative research that focuses on mechanisms and treatment for asthma that does not respond or that responds poorly to currently available treatments. The mission of ICAN is innovation, collaboration, translation, and increasing high quality research. At the second ICAN meeting, presenters covered a broad scope and depth of asthma-related topics in the categories of complex data, novel therapeutics and diagnostics, breath analysis and microbiome, disease mechanisms, systemic effects, and circadian rhythm. Key actionable needs and research topics were identified during the group discussions. The presentations and discussions that occurred at the second ICAN had an immediate impact on asthma research in the form of new collaborations and implementation of new research ideas and techniques. The forum also served to connect early-stage investigators with investigators who are well established, thereby fostering innovation, translation, and collaboration well into the future. A third ICAN meeting is planned for 2025 to further the innovations and collaborations that will translate into novel therapies and diagnostics to improve the lives of patients with asthma. [ABSTRACT FROM AUTHOR]

Background: The aim of this study (EPIDIAB) was to assess the relationship between epicardial adipose tissue (EAT) and the micro and macrovascular complications (MVC) of type 2 diabetes (T2D). Methods: EPIDIAB is a post hoc analysis from the AngioSafe T2D study, which is a multicentric study aimed at determining the safety of antihyperglycemic drugs on retina and including patients with T2D screened for diabetic retinopathy (DR) (n = 7200) and deeply phenotyped for MVC. Patients included who had undergone cardiac CT for CAC (Coronary Artery Calcium) scoring after inclusion (n = 1253) were tested with a validated deep learning segmentation pipeline for EAT volume quantification. Results: Median age of the study population was 61 [54;67], with a majority of men (57%) a median duration of the disease 11 years [5;18] and a mean HbA1c of7.8 ± 1.4%. EAT was significantly associated with all traditional CV risk factors. EAT volume significantly increased with chronic kidney disease (CKD vs no CKD: 87.8 [63.5;118.6] vs 82.7 mL [58.8;110.8], p = 0.008), coronary artery disease (CAD vs no CAD: 112.2 [82.7;133.3] vs 83.8 mL [59.4;112.1], p = 0.0004, peripheral arterial disease (PAD vs no PAD: 107 [76.2;141] vs 84.6 mL[59.2; 114], p = 0.0005 and elevated CAC score (> 100 vs < 100 AU: 96.8 mL [69.1;130] vs 77.9 mL [53.8;107.7], p < 0.0001). By contrast, EAT volume was neither associated with DR, nor with peripheral neuropathy. We further evidenced a subgroup of patients with high EAT volume and a null CAC score. Interestingly, this group were more likely to be composed of young women with a high BMI, a lower duration of T2D, a lower prevalence of microvascular complications, and a higher inflammatory profile. Conclusions: Fully-automated EAT volume quantification could provide useful information about the risk of both renal and macrovascular complications in T2D patients. Article Highlights: Why did we undertake this study? What is the specific question(s) we wanted to answer? This study addresses the unmet need to assess epicardial fat volume quantification in high-risk people living with type 2 diabetes using a fully-automated deep learning AI tool. What did we find? Fully automated epicardial fat volume quantification with cardiac CT performed for CAC scoring is possible and reliable in T2D. Epicardial fat volume was associated with all cardiovascular risk factors, CKD and macrovascular complications but not with diabetic retinopathy or peripheral neuropathy. We identified a subgroup of T2D patients with a null CAC score and high EAT volume which was characterized by a higher systemic proinflammatory profile. What are the implications of our findings? This study provides new insights for non-invasive deep phenotyping of patients living with type 2 diabetes with epicardial fat volume quantification using cardiac CT performed for CAC scoring, that could be used in clinical practice. These findings set the stage for personalized medicine and prospective randomized trials testing new antihyperglycemic drugs that target inflammation. [ABSTRACT FROM AUTHOR]

Complex coronary atherosclerosis may exhibit different phenotypes of coronary plaques, from non-calcified highly vulnerable atheroma to heavily calcified ones. Computed coronary tomography angiography (CCTA) may identify these different phenotypes and the recently introduced CCTA-based techniques for mapping coronary inflammation along the coronary arteries may provide useful additional information on cardiovascular risk. Here we present the case of a 68-year-old male patient with acute coronary syndrome in whom invasive coronary angiography and CCTA revealed a severe three-vessel disease with a heavily calcified lesion. Mapping of the CT fat attenuation index along the coronary arteries identified a high level of coronary inflammation, especially associated with the non-calcified lesions. All lesions were successfully revascularized by implantation of drug-eluting stents. A cutting balloon was used for the lesion identified by CCTA as heavily calcified, followed by stent implantation, with good results. In conclusion, CCTA, in association with novel techniques for mapping coronary inflammation, may represent an extremely useful tool for preparing complex interventions in multivessel diseases, helping preprocedural planning in high-risk patients. [ABSTRACT FROM AUTHOR]

This document discusses the use of computed tomography coronary angiography (CTCA) as an imaging technique for evaluating coronary artery abnormalities (CAAs) in children with Kawasaki disease (KD). It compares CTCA to other imaging modalities such as 2D-echocardiography (2DE) and magnetic resonance coronary angiography (MRCA), highlighting the advantages of CTCA in terms of radiation exposure, detection of distal CAAs, and evaluation of temporal changes in CAAs. The document also mentions the use of calcium scoring in identifying undiagnosed CAAs. It concludes that with advancements in technology, CTCA is likely to become the preferred imaging modality for evaluating coronary arteries in children with KD. [Extracted from the article]

Objectives: CT-derived fractional flow reserve (CT-FFR) can improve the specificity of coronary CT-angiography (cCTA) for ruling out relevant coronary artery disease (CAD) prior to transcatheter aortic valve replacement (TAVR). However, little is known about the reproducibility of CT-FFR and the influence of diffuse coronary artery calcifications or segment location. The objective was to assess the reliability of machine-learning (ML)-based CT-FFR prior to TAVR in patients without obstructive CAD and to assess the influence of image quality, coronary artery calcium score (CAC), and the location of measurement within the coronary tree. Methods: Patients assessed for TAVR, without obstructive CAD on cCTA were evaluated with ML-based CT-FFR by two observers with differing experience. Differences in absolute values and categorization into hemodynamically relevant CAD (CT-FFR ≤ 0.80) were compared. Results in regard to CAD were also compared against invasive coronary angiography. The influence of segment location, image quality, and CAC was evaluated. Results: Of the screened patients, 109/388 patients did not have obstructive CAD on cCTA and were included. The median (interquartile range) difference of CT-FFR values was −0.005 (−0.09 to 0.04) (p = 0.47). Differences were smaller with high values. Recategorizations were more frequent in distal segments. Diagnostic accuracy of CT-FFR between both observers was comparable (proximal: Δ0.2%; distal: Δ0.5%) but was lower in distal segments (proximal: 98.9%/99.1%; distal: 81.1%/81.6%). Image quality and CAC had no clinically relevant influence on CT-FFR. Conclusions: ML-based CT-FFR evaluation of proximal segments was more reliable. Distal segments with CT-FFR values close to the given threshold were prone to recategorization, even if absolute differences between observers were minimal and independent of image quality or CAC. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) is the leading global cause of mortality, accounting for approximately 30% of all deaths. It is primarily characterized by the accumulation of atherosclerotic plaques within the coronary arteries, leading to reduced blood flow to the heart muscle. Early detection of atherosclerotic plaques is crucial to prevent major adverse cardiac events. Notably, recent studies have shown that 15% of myocardial infarctions occur in patients with non-obstructive CAD, underscoring the importance of comprehensive plaque assessment beyond merely identifying obstructive lesions. Cardiac Computed Tomography Angiography (CCTA) has emerged as a cost-effective and efficient technique for excluding obstructive CAD, particularly in patients with a low-to-intermediate clinical likelihood of the disease. Recent advancements in CCTA technology, such as improved resolution and reduced scan times, have mitigated many technical challenges, allowing for precise quantification and characterization of both calcified and non-calcified atherosclerotic plaques. This review focuses on two critical physiological aspects of atherosclerotic plaques: the burden of calcifications, assessed via the coronary artery calcium score (CACs), and perivascular fat attenuation index (pFAI), an emerging marker of vascular inflammation. The CACs, obtained through non-contrast CT scans, quantifies calcified plaque burden and is widely used to stratify cardiovascular risk, particularly in asymptomatic patients. Despite its prognostic value, the CACs does not provide information on non-calcified plaques or inflammatory status. In contrast, the pFAI, derived from CCTA, serves as an indirect marker of coronary inflammation and has shown potential in predicting adverse cardiac events. Combining both CACs and pFAI assessment could offer a comprehensive risk stratification approach, integrating the established calcification burden with novel inflammatory markers to enhance CAD prevention and management strategies. [ABSTRACT FROM AUTHOR]

Physical activity is recommended for the prevention of primary and secondary cardiovascular (CV) disease as it is linked to a number of health benefits, especially CV. However, recent research suggests that high-volume, long-term endurance exercise may hasten rather than slow the coronary atherosclerosis progression. This contentious theory has generated a great discussion and is still a major source of doubt when it comes to the clinical treatment of coronary artery disease (CAD) in athletes. CAD is the primary cause of sudden cardiac death in athletes over 35 years. Thus, recent studies evaluated the prevalence of CAD in athletes and its clinical and prognostic implications. Indeed, many studies have shown a relationship between endurance sports and higher volumes of coronary calcified plaque as determined by computed tomography. However, the precise pathogenetic substrate for the existence of an increased coronary calcification burden among endurance athletes remains unclear. Moreover, the idea that coronary plaques in elite athletes present a benign morphology has been cast into doubt by some recent studies showing potential association with adverse cardiovascular events. This review aims to analyze the association between physical activity and CAD, explaining possible underlying mechanisms of atherosclerotic progression and non-ischemic coronary lesions, focusing primarily on clinical and prognostic implications, multimodal evaluation, and management of CAD in endurance athletes. [ABSTRACT FROM AUTHOR]

Aging affects the cardiovascular system, and this process may be accelerated in individuals with cardiovascular risk factors. The main vascular changes include arterial wall thickening, calcification, and stiffening, together with aortic dilatation and elongation. With aging, we can observe left ventricular hypertrophy with myocardial fibrosis and left atrial dilatation. These changes may lead to heart failure and atrial fibrillation. Using multimodality imaging, including ultrasound, computed tomography (CT), and magnetic resonance imaging, it is possible to detect these changes. Additionally, multimodality imaging, mainly via CT measurements of coronary artery calcium or ultrasound carotid intima-media thickness, enables advanced cardiovascular risk stratification and helps in decision-making about preventive strategies. The focus of this manuscript is to briefly review cardiovascular changes that occur with aging, as well as to describe how multimodality imaging may be used for the assessment of these changes and risk stratification of asymptomatic individuals. [ABSTRACT FROM AUTHOR]

The aim of this paper is to demonstrate the difference in usefulness of the coronary artery calcium score (CACS) and the full assessment of the severity of coronary artery disease in coronary computed tomography angiography (CCTA) studies. The difference between the population risk of coronary artery disease (CAD) assessed by the CACS and the severity of CAD was demonstrated in images from two CCTA studies. The first image is from a patient with a CACS of 0 and significant coronary artery stenosis. In the native phase of CCTA examination, no calcified changes were detected in the topography of the coronary arteries. In the middle section of the left descending artery (LAD), at the level of the second diagonal branch (Dg2), a large non-calcified atherosclerotic plaque was visible. Mid-LAD stenosis was estimated to be approximately 70%. The second image features a patient with a high CACS but no significant coronary artery stenosis. The calcium score of individual coronary arteries calculated using the Agatston method was as follows: left main (LM) 0, LAD 403, left circumflex (LCx) 207.7, right coronary artery (RCA) 12. CACS was 622.7, representing a significant population risk of significant CAD. In the proximal and middle sections of the LAD, numerous calcified and mixed atherosclerotic plaques with positive remodeling were visible, causing stenosis of 25–50%. Similarly, in the proximal and middle sections of the LCx, numerous calcified and mixed atherosclerotic plaques with positive remodeling were visualized, causing stenoses of 25–50%. Calcified atherosclerotic plaques were found in the RCA, causing stenosis <25%. The entire CCTA image met CAD-RADS 2 (coronary artery disease reporting and data system) criteria. In summary, CACS may be applicable in population-based studies to assess the risk of significant CAD. In the evaluation of individual patients, a comprehensive assessment of CAD severity based on the angiographic phase of the CCTA examination should be used. [ABSTRACT FROM AUTHOR]

Purpose: The value of preoperative multidisciplinary approach remains inadequately delineated in forecasting postoperative outcomes of patients undergoing coronary artery bypass grafting (CABG). Herein, we aimed to ascertain the efficacy of multi-modality cardiac imaging in predicting post-CABG cardiovascular outcomes. Methods: Patients with triple coronary artery disease underwent cardiac sodium [18F]fluoride ([18F]NaF) positron emission tomography/computed tomography (PET/CT), coronary angiography, and CT-based coronary artery calcium scoring before CABG. The maximum coronary [18F]NaF activity (target-to-blood ratio [TBR]max) and the global coronary [18F]NaF activity (TBRglobal) was determined. The primary endpoint was perioperative myocardial infarction (PMI) within 7-day post-CABG. Secondary endpoint included major adverse cardiac and cerebrovascular events (MACCEs) and recurrent angina. Results: This prospective observational study examined 101 patients for a median of 40 months (interquartile range: 19–47 months). Both TBRmax (odds ratio [OR] = 1.445; p = 0.011) and TBRglobal (OR = 1.797; P = 0.018) were significant predictors of PMI. TBRmax>3.0 (area under the curve [AUC], 0.65; sensitivity, 75.0%; specificity, 56.8%; p = 0.036) increased PMI risk by 3.661-fold, independent of external confounders. Kaplan–Meier test revealed a decrease in MACCE survival rate concomitant with an escalating TBRmax. TBRmax>3.6 (AUC, 0.70; sensitivity, 76.9%; specificity, 73.9%; p = 0.017) increased MACCEs risk by 5.520-fold. Both TBRmax (hazard ratio [HR], 1.298; p = 0.004) and TBRglobal (HR = 1.335; p = 0.011) were significantly correlated with recurrent angina. No significant associations were found between CAC and SYNTAX scores and between PMI occurrence and long-term MACCEs. Conclusion: Quantification of coronary microcalcification activity via [18F]NaF PET displayed a strong ability to predict early and long-term post-CABG cardiovascular outcomes, thereby outperforming conventional metrics of coronary macrocalcification burden and stenosis severity. Trial registration: : The trial was registered with the Chinese Clinical Trial Committee (number: ChiCTR1900022527; URL: www.chictr.org.cn/showproj.html?proj=37933). [ABSTRACT FROM AUTHOR]

Background: Metabolic dysfunction associated steatotic liver disease (MASLD) is associated with an increased risk of coronary artery disease. Computed Tomography Coronary Angiography (CTCA) can assess both the extent and the features of coronary plaques. We aimed to gather evidence about the prevalence and features of coronary plaques among MASLD patients. Methods: PubMed, Scopus, and Google Scholar databases were searched for randomized controlled trials and adjusted observational studies assessing the prevalence and features of coronary plaques by means of CTCA in MASLD patients as compared with a control group. The prevalence of coronary stenosis (defined as >30% and >50% diameter of stenosis), of increasing coronary artery calcium (CAC) score and of high‐risk features (namely low‐attenuation plaques, napkin ring sign, spotty calcification and positive remodelling) in MASLD patients were the endpoints of interest. Results: Twenty‐four observational studies were included. MASLD was associated with an increased prevalence of critical coronary stenosis compared with controls (odds ratio [OR] 1.54, 95%CI 1.23–1.93). Increased values of CAC score were observed in MASLD patients (OR 1.35, 95%CI 1.02–1.78 and OR 2.26, 95%CI 1.57–3.23 for CAC score 0–100 and >100, respectively). An increased risk of 'high‐risk' coronary plaques was observed in MASLD patients (OR 2.13, 95%CI 1.42–3.19). As high‐risk features plaques, a higher prevalence of positive remodelling and spotty calcification characterize MASLD patients (OR 2.92, 95%CI 1.79–4.77 and OR 2.96, 95%CI 1.22–7.20). Conclusions: Patients with MASLD are at increased risk of developing critical coronary stenosis and coronary plaques characterized by high‐risk features as detected by CTCA. [ABSTRACT FROM AUTHOR]

Aim: The association of overweight/obesity and metabolic dysfunction‐associated steatotic liver disease (MASLD) in young adulthood with subclinical atherosclerosis [coronary artery calcification (CAC) and abdominal aortic calcification (AAC)] by middle age is unknown. Method: In total, 2274 participants aged 28‐39 years from the coronary artery risk development in young adults study at year 10 (1995‐1996) who were re‐examined 15 years later were included. CAC and AAC were measured at year 25 using computed tomography. We examined the utility of three young adult phenotypes (lean group; overweight/obese group; overweight/obese MASLD group) at year 10 in predicting CAC or AAC by middle age. Modified Poisson regression was used to estimate the association between groups and CAC, and AAC. Independent determinates of CAC and AAC were determined with linear regression models. Results: Compared with individuals categorized as lean in young adulthood, the relative risk for CAC by middle age was 1.09 (95% confidence interval: 0.93‐1.28) for those with overweight/obesity and 1.32 (95% confidence interval: 1.08‐1.61) for those with overweight/obesity‐related MASLD. For AAC, no difference was observed between these three groups. Group, systolic blood pressure and group × systolic blood pressure interaction were all the independent determinates for CAC. Conclusion: In this study, young adults with overweight/obesity‐related MASLD have a higher risk of developing CAC by middle age. These abnormalities are only partially explained by traditional cardiovascular risk factors, and overweight/obesity‐related MASLD has an independent impact on CAC. Our study provides evidence for identifying young adults at higher risk of developing subclinical atherosclerosis. [ABSTRACT FROM AUTHOR]

High-risk coronary plaques (HRP) are characterized in clinical radiological imaging by the presence of low plaque attenuation, a napkin-ring sign (NRS), spotty calcifications (SC) and a positive remodeling index (RI). To evaluate if these signs are detectable in postmortem imaging by a multi-phase postmortem CT angiography (MPMCTA), a retrospective study of a series of autopsy well-documented coronary plaques related to sudden cardiac death (SCD) was performed. Then correlations between histological and radiological findings were described. Fourty SCD cases due to acute coronary syndrome based on clinical history and confirmed at autopsy were selected (28 men and 12 women, age 53.3 ± 10.9). The culprit lesion was mainly situated in the proximal segments of coronary arteries, in the right coronary artery in 23 cases (57.5%), the left anterior descending artery in 13 cases (32.5%), the circumflex artery in 3 cases (7.5%) and in one case in the left main stem. MPMCTA showed a positive RI (≥ 1.1) in 75% of cases with a mean RI 1.39 ± 0.71. RI values were lower in cases with fibrotic plaques. NRS was observed in 40% of cases, low attenuation plaque in 46.3%, and SC in 48.7% of cases. There were significant correlations of the radiological presence of NRS for fibrolipid composition of the plaque (p-value 0.007), severe intraplaque inflammation (p-value 0.017), severe adventitial inflammation (p-value 0.021) and an increased vasa vasorum (p-value 0.012). A significant correlation (p-value 0.002) was observed between the presence of SC at radiological examination and the presence of punctuate/fragmented calcification at histology. In addition, in 58.3% of cases, plaque enhancement was observed, which correlated with plaque inflammation and the fibrolipid composition of the plaque. The coronary artery calcium score was 314 (± 455). There was a poor agreement between stenosis of the lumen at histology versus radiology. Our study shows that the various radiological signs of HRP can be detected in all plaques by MPMCTA, but individually only to a variable extent; plaque enhancement appeared as a new sign of vulnerability. In the postmortem approach, these radiological markers of HRP, should always be applied in combination, which can be useful for developing a predictive model for diagnosing coronary SCD. [ABSTRACT FROM AUTHOR]

Objectives: Utilising readily available clinical variables, we aimed to develop and validate a novel machine learning (ML) model to predict severe coronary calcification, and further assessed its prognostic significance. Methods: This retrospective study enrolled patients who underwent coronary CT angiography and subsequent invasive coronary angiography. Multiple ML algorithms were used to train the models for predicting severe coronary calcification (cardiac CT-measured coronary artery calcium [CT-CAC] score ≥ 400). The ML-based CAC (ML-CAC) score derived from the ML predictive probability was stratified into quartiles for prognostic analysis. The primary endpoint was a composite of all-cause death, nonfatal myocardial infarction, or nonfatal stroke. Results: Overall, 5785 patients were divided into training (80%) and test sets (20%). For clinical practicability, we selected the nine-feature support vector machine model with good and satisfactory performance regarding both discrimination and calibration based on five repetitions of the 10-fold cross-validation in the training set (mean AUC = 0.715, Brier score = 0.202), and based on the test in the test set (AUC = 0.753, Brier score = 0.191). In the test set cohort (n = 1137), the primary endpoint was observed in 50 (4.4%) patients during a median 2.8 years' follow-up. The ML-CAC system was significantly associated with an increased risk of the primary endpoint (adjusted hazard ratio for trend 2.26, 95% CI 1.35–3.79, p = 0.002). There was no significant difference in the prognostic value between the ML-CAC and CT-CAC systems (C-index, 0.67 vs. 0.69; p = 0.618). Conclusion: ML-CAC score predicted from clinical variables can serve as a novel prognostic indicator in patients referred for invasive coronary angiography. Clinical relevance statement: In patients referred for invasive coronary angiography who have not undergone preoperative CT-measured coronary artery calcium scoring, machine learning–based coronary artery calcium score assessment can serve as an alternative for predicting the prognosis. Key Points: • The coronary artery calcium (CAC) score, a solid prognostic indicator, can be predicted using non-CT methods. • We developed a machine learning (ML)-CAC model utilising nine clinical variables to predict severe coronary calcification. • The ML-CAC system offers significant prognostic value in patients referred for invasive coronary angiography. [ABSTRACT FROM AUTHOR]

Objectives: The impact of coronary calcification on the diagnostic accuracy of computed tomography-derived fractional flow reserve (CT-FFR) and coronary computed tomography angiography (CCTA) remains a crucial consideration. This meta-analysis aims to compare the diagnostic performance of CT-FFR and CCTA at different levels of coronary artery calcium score (CACS). Methods and results: We searched PubMed, Embase, and the Cochrane Library for relevant articles on CCTA, CT-FFR, and invasive fractional flow reserve (FFR). Ten studies were included to evaluate the diagnostic performance of CT-FFR and CCTA at the per-patient and per-vessel levels in four CACS groups. Invasive FFR was used as the reference standard. Except for the CACS ≥ 400 group, the AUC of CT-FFR was higher than those of CCTA in other subgroups of CACS (in CACS < 100 (per-patient, 0.9 (95% CI 0.87–0.92) vs. 0.32 (95% CI 0.28–0.36); per-vessel, 0.92 (95% CI 0.89–0.94) vs. 0.66 (95% CI 0.62–0.7); both p < 0.001), CACS ≥ 100 (per-patient, 0.86 (95% CI 0.82–0.88) vs. 0.44 (95% CI 0.4–0.48); per-vessel, 0.88 (95% CI 0.85–0.9) vs. 0.51 (95% CI 0.46–0.55); both p < 0.001), and CACS < 400 (per-patient, 0.9 (95% CI 0.87–0.93) vs. 0.74 (95% CI 0.7–0.78), p < 0.001; per-vessel, 0.8 (95% CI 0.76–0.83) vs. 0.74 (95% CI 0.7–0.78); p = 0.02)). Conclusions: CT-FFR demonstrates superior diagnostic performance in low CACS groups (CACS < 400) than CCTA in detecting hemodynamic stenoses in patients with coronary artery disease (CAD). Clinical relevance statement: Computed tomography-derived fractional flow reserve might be utilized to determine the necessity of invasive coronary angiography in coronary artery disease patients with coronary artery calcium score < 400. Key Points: • There is a lack of meta-analysis comparing the diagnostic performance of computed tomography-derived fractional flow reserve and coronary computed tomography angiography at different levels of calcification. • Computed tomography-derived fractional flow reserve only has a better diagnostic performance than coronary computed tomography angiography with low amounts of coronary calcium. • For the low coronary artery calcium score group, computed tomography-derived fractional flow reserve might be a good non-invasive method to detect hemodynamic stenoses in coronary artery disease patients. [ABSTRACT FROM AUTHOR]

The present study evaluated 10-year atherosclerotic cardiovascular disease (ASCVD) risk using ASCVD and Systematic Coronary Risk Evaluation (SCORE2) risk models in combination with aortic arch calcification (AAC) to identify those at high risk for significant coronary artery disease (CAD) in patients undergoing coronary angiography. Of the 402 patients enrolled, 48 had normal coronary angiograms and served as group 1. The 131 patients with CAD with stenosis of <70% as group 2 and 223 patients with CAD with stenosis of ≥70% as group 3. ASCVD and SCORE2 risk scores, and the presence of AAC differed significantly among these groups. For prediction of significant CAD, the area under the curve (AUC) of ASCVD and SCORE2 risk scores in receiver operating characteristic (ROC) curve analysis were statistically similar ([AUC:.647, P <.001] and [AUC:.654, P <.001], respectively). When AAC was added to ASCVD risk and SCORE2, it increased their predictive value for significant CAD in the ROC curve analysis (P =.003, and P =.019, respectively). In addition, significant net reclassification improvement (NRI) values were obtained by adding AAC to ASCVD and SCORE2 risk models ([NRI =.10, P =.04], and [NRI =.19, P =.04], respectively). These results suggest that the predictive value of ASCVD and SCORE2 increases when AAC is combined. [ABSTRACT FROM AUTHOR]

Background: The role of treadmill stress echocardiography (TSE) in symptomatic patients may be limited. We evaluated whether carotid intima-media thickness (cIMT) and coronary artery calcium (CAC) scores can predict cardiovascular (CV) outcomes in patients with negative TSE. Methods: Patients who had negative TSE and measured cIMT or CAC scoring were enrolled and followed up. The primary CV outcome was defined as a composite of acute coronary syndrome, coronary revascularization, heart failure, stroke, and CV death. Results: Overall, 1095 patients participated. The median follow-up duration was 5.8 years. Patients with increased cIMT and CAC scores experienced a high incidence of primary CV outcomes (normal vs. increased group on cIMT and CAC scoring: 4.4% vs. 20.0% and 0.4% vs. 25.0%, respectively, p < 0.001). In the Cox proportional hazard model, increased cIMT and CAC scores were associated with increased primary CV outcomes (adjusted hazard ratio [95% confidence interval], p-value for increased cIMT and increased CAC scores = 2.939 [1.241–6.960], p = 0.014 and 45.192 [5.497–371.505], p < 0.001, respectively). Conclusions: Patients with increased cIMT and CAC scores have poor CV outcomes even though they have negative TSE results, and therefore, they should be carefully monitored. [ABSTRACT FROM AUTHOR]

Abstract Background Coronary artery calcification (CAC) is a common risk factor of cardiovascular disease. Although triglyceride glucose (TYG) index and high-density lipoprotein cholesterol (HDL-c) are both associated with CAC, no study has evaluated the correlation between the TYG/HDL-c ratio and CAC. In the present study, we investigated the relationships between CAC and the TYG index and the TYG/HDL-c ratio. Methods A total of 9585 participants who underwent computed tomography (CT) screening for lung cancer from 2018 to 2020 were included in this cross-sectional study. Demographic data, laboratory test data and medical history data were collected from medical records. TYG = Ln[fasting glucose (mg/dL)×fasting TG (mg/dL/2]. The triglyceride glucose-HDL-c ratio was calculated as TYG/HDL-c. CAC was evaluated on chest CT images. Multivariate logistic regression analysis and restricted cubic splines were used to determine the relationships among the TYG index, TYG/HDL-c ratio and risk of CAC. The receiver operating characteristic (ROC) curve was used to evaluate the performance of the TYG index and TYG/HDL-c ratio in identifying CACs in individuals aged 60 years and above. Results CAC was detected in 2515 of 9585 participants (mean age 51.8 ± 15.5 years, 61.2% men). The prevalence of CAC was significantly greater in participants with a high TYG/HDL-c ratio (32.6% in the fourth quartile vs. 19.1% in the first quartile, p