Median Coronary Artery Calcium Research Articles

Coronary artery dominance influences the distribution of calcified plaques in the coronary tree.

Coronary artery dominance is determined by the coronary artery emitting the posterior descending artery. In the left dominant system, a greater proportion of coronary flow enters the left coronary artery, potentially influencing calcified plaque development in the left anterior descending artery (LAD). This retrospective single-center cohort study analyzed patients who underwent computed tomography angiography from September 2006 to December 2022 at Harbor-UCLA in Los Angeles, California. Coronary artery calcium (CAC) was quantified for the three coronary vessels. The LAD calcium score was divided by the total calcium score to calculate the LAD calcium percentage, which was compared between left and right dominant coronary systems. Multivariable linear regression assessed the association between LAD calcium percentage and coronary dominance, adjusting for age, gender, BMI, hyperlipidemia, hypertension, family history of cardiovascular disease, and past smoking. Among 9560 subjects, 6766 with CAC greater than zero were enrolled. The average age was 64.8 ± 10.7 years: 68% were male, and 9% had left dominant coronary systems. The median CAC was 51 [0-352] in the right dominant and 49 [0-358] in the left dominant system (P = 0.73). Adjusted analysis revealed that individuals with left dominant coronary systems had a 10.1% higher (CI 7.5-12.8%, P < 0.001) LAD calcium percentage than those with right dominant systems. Although coronary dominance does not influence overall plaque burden of atherosclerosis, it affects calcified plaque distribution. The left dominant system is associated with a higher proportion of calcified plaque in the LAD, potentially heightening the risk of adverse cardiovascular events.

Leptin levels are associated with coronary artery calcification in patients with advanced prostate cancer.

Convergent data suggest that advanced prostate cancer and coronary heart disease (CHD) share biological vulnerabilities that may be linked to adiposity. Here we explore whether leptin, as a marker and mediator of adiposity, could link prostate cancer to CHD. Patients with metastatic castration-resistant prostate cancer (mCRPC) enrolled in a phase II trial (NCT02703623) studying androgen deprivation therapy, abiraterone, prednisone, and apalutamide were eligible if they had plasma and a chest CT scan available. Coronary artery calcium (CAC) scores and adipokine levels were measured upon enrollment. Of 164 patients, 87% were white. The mean age was 65.6 ± 7.5 years, 88% were either overweight or obese, 59% had hypertension, 48% had hyperlipidemia (HLD), 20% had type 2 diabetes mellitus, and 41% were former or current smokers. Coronary calcifications were found in 115 patients (70%). Among 47 patients with non-contrast chest CT scans, the median total CAC score was 133 AU (IQR 22.6-704.6). Four patients (9%) had a score of 0 AU (low risk) and 24 (51%) scores ≥100 AU, associated with high risk for major adverse cardiovascular events. Leptin levels correlated positively with the right coronary artery (RCA) CAC score [Pearson correlation coefficient (ρ) = 0.3715 (P = .0142)]. In a multivariate logistic regression analysis, older age, HLD, and higher leptin levels were independently associated with RCA calcification and a higher number of calcified coronary arteries. Among men with mCRPC, there was a high burden of CHD, and higher leptin levels were associated with coronary atherosclerosis independently of traditional cardiac risk factors.

Polygenic Risk Scores and Extreme Coronary Artery Calcium Phenotypes (CAC=0 and CAC≥1000) in Adults ≥75 Years Old: The ARIC Study.

Coronary artery calcium (CAC) is heterogeneous in older age and is incompletely explained by traditional atherosclerotic cardiovascular disease risk factors. The extremes of subclinical atherosclerosis burden are strongly associated with either a low or high 10-year risk of incident atherosclerotic cardiovascular disease, respectively. However, the genetic underpinnings of differences in arterial aging remain unclear. We sought to determine the independent association of 2 polygenic scores for coronary heart disease (CHD) with CAC in adults ≥75 years of age. There were 1865 ARIC (Atherosclerosis Risk in Communities) participants who underwent genetic testing at visit 1 (1987-1989) and CAC scans at visit 7 (2018-2019). In the primary analysis, an externally derived multi-ancestry polygenic CHD risk score was calculated for both White and Black participants. Results were confirmed using a separate ARIC-derived polygenic CHD risk score, including ≥6 million variants computed for White participants. We used multivariable logistic regression models to assess the association of polygenic CHD risk with CAC, after adjusting for baseline, time-averaged lifestyle, traditional risk factors, and local ancestry principal components. In the primary analysis, the average age was 80.6 years old, 61.6% were women, and the median CAC score was 246 (189 participants with CAC=0, 364 participants with CAC≥1000). Compared with persons below the 20th percentile of polygenic CHD risk, persons with polygenic-CHD risk above the 80th percentile had 82% lower odds of having CAC=0 (odds ratio, 0.18 [95% CI, 0.09-0.37]) and had >4-fold higher odds of CAC≥1000 (odds ratio, 4.77 [95% CI, 2.88-7.88]). On a continuous scale, each SD increment increase in the polygenic risk score was associated with a 78% higher CAC score. Results were nearly identical using a second confirmatory polygenic CHD risk score in White participants. Polygenic CHD risk is robustly associated with a lower prevalence of CAC=0 and a higher prevalence of CAC≥1000 in adults ≥75 years of age, beyond lifestyle and traditional risk factors. These results suggest a heritable contribution to distinct healthy and unhealthy arterial aging phenotypes that persist throughout the life course.

Urinary Metal Levels and Coronary Artery Calcification: Longitudinal Evidence in the Multi-Ethnic Study of Atherosclerosis

BackgroundExposure to metals, a newly recognized risk factor for cardiovascular disease (CVD), could be related to atherosclerosis progression. ObjectivesThe 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). MethodsWe 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. ResultsAt 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. ConclusionsExposure 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.

Impact of successful secondary hyperparathyroidism treatment on cardiovascular morbidity in patients with chronic kidney disease KDIGO stages G3b-5.

Chronic kidney disease is common, with a projected increase to 5.4 million people in need of kidney replacement therapy by 2030. As many as 61.7% of patients on hemodialysis have secondary hyperparathyroidism (SHPT). This has been associated with high cardiovascular morbidity. The present study investigates the effect of SHPT treatment success on cardiovascular morbidity in patients with CKD KDIGO stages G3b, 4, and 5. A retrospective single center analysis of 211 chronic kidney disease stages G3b-5 patients undergoing computed tomography for coronary artery calcium (CAC) scoring at the University Hospital of Zurich between 2015 and 2019was performed. The presence of and control of SHPT was assessed at the timepoint of CAC scoring and 6-12 months prior. Information on left ventricular ejection fraction (LVEF), left ventricular hypertrophy (LVH), and left ventricular myocardial mass index (LVMMI) were calculated from echocardiography values obtained at the timepoint of CAC scoring. Occurrence of major acute cardiovascular events, including acute coronary syndrome (ACS), within 1 year of CAC scoring was drawn from the charts. Independent predictive factors for ACS and LVH were assessed by multivariable analysis. Thirty-four percent (n=72) of the patients had uncontrolled SHPT, whereas 66% (n=139) had either no (n=18%, n=39) or a controlled SHPT (n=48%, n=100). The CKD stage G3b-5 patients with uncontrolled SHPT had a significantly lower LVEF (p=0.028) and significantly more pronounced LVH (p=0.003) and a higher LVMMI (p=0.002) than the group with either no SHPT or well-controlled SHPT. Uncontrolled SHPT in the observed CKD cohort had a significantly higher risk for developing ACS (p=0.011, HR 2.76, 95%CI 1.26-6.05) compared to no or controlled SHPT patients (41.7% vs 31.7%). While patients with uncontrolled SHPT showed a median CAC score of 290 (IQR 18-866), those with no or controlled SHPT had a lower median CAC score of 194 (IQR 14-869), although not significant (p=0.490). Patients with CAC scores >400 displayed a significantly higher incidence of ACS (56.8% vs 33.1%, p=0.010). SHPT is common (82%) in advanced CKD (≥G3b) patients and insufficiently controlled in one-third of patients. Insufficient control of SHPT is associated with higher cardiovascular morbidity, lower LVEF, increased LVH, and a higher incidence of ACS. Thus, increased focus on SHPT control in CKD patients may have a beneficial impact on cardiovascular outcomes.

Coronary Artery Calcium for Risk Stratification Among Persons With Very High HDL Cholesterol

BackgroundCompared to normal high-density lipoprotein (HDL) cholesterol values, very high HDL cholesterol is associated with a higher incidence of mortality and atherosclerotic cardiovascular disease (ASCVD). As such, clinical risk stratification among persons with very high HDL cholesterol is challenging. ObjectivesAmong persons with very high HDL cholesterol, the purpose was to determine the prevalence of coronary artery calcium (CAC) and compare the association between traditional risk factors vs CAC for all-cause mortality and ASCVD. MethodsThe primary analysis was completed among 446 participants from the Cedars-Sinai Medical Center of the CAC Consortium with very high HDL cholesterol (≥77 mg/dL in men, ≥97 mg/dL in women). Cox proportional hazards regression assessed the association of CAC and traditional risk factors with all-cause mortality during a median follow-up of 10.7 years. Replication and validation analyses were performed for all-cause mortality among 119 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) with very high HDL cholesterol, who also had information on incident ASCVD. ResultsThe mean age was 57.9 years old, 49% were women, and the median HDL cholesterol was 98 mg/dL. One-half of participants (50%) had prevalent CAC, in whom the median CAC score was 118. Prevalent CAC conferred a 3.6-fold higher risk of all-cause mortality (HR: 3.64; 95% CI: 1.21-11.01), which appeared to be a more robust predictor than individual traditional risk factors beyond age. In the validation sample, prevalent CAC but not individual traditional risk factors were associated with all-cause mortality (HR: 2.39; 95% CI: 1.07-5.34) and a 4.0-fold higher risk of ASCVD (HR: 4.06; 95% CI: 1.11-14.84). ConclusionsMeasurement of CAC may facilitate clinical risk assessment among individuals with very high HDL cholesterol.

Abstract P513: Coronary Artery Calcium Burden in Rural Alabama: Initial Findings From the Risk Underlying Rural Areas Longitudinal Cohort Study

Introduction: Individuals living in rural areas have a disproportionately high rate of cardiovascular disease (CVD) mortality. Coronary artery calcium (CAC) scanning may inform CVD risk stratification. However, the prevalence of CAC in rural areas is unknown. Research Question: What is the prevalence of CAC according to age, sex, and self-reported race (Black, White) in two rural counties in Alabama? Aims: To determine the prevalence of a CAC score &gt;0, a CAC score ≥100, and premature CAC among rural persons without clinical CVD and the extent to which they differ by demographic group. Methods: We studied 789 participants between the age of 25 and 64 years in the Risk Underlying Rural Areas Longitudinal (RURAL) Cohort Study sample in Alabama who underwent CAC scoring on non-contrast cardiac computed tomography. Premature CAC was defined as CAC &gt;0 for men &lt;45 years old, and women &lt;55 years old. Multivariable logistic regression (including age, sex, race) estimated adjusted odds ratios (aOR) for CAC &gt;0 and CAC ≥100. Results: The median age was 51 years, 70% were women, and 80% were Black. Among the were 37% with CAC &gt;0 the median CAC score was 64, while 14% had CAC ≥100 and 12% had premature CAC. Significant differences in all three CAC categories were consistently observed across age and sex, but not race ( Figure ). After adjusting for age and race, women had an approximate 70% lower odds of CAC &gt;0 (aOR=0.29, 95% CI: 0.19-0.44) and CAC ≥100 (aOR=0.28, 95% CI: 0.18-0.43) compared to men. There were no significant differences in CAC &gt;0 (aOR=0.70, 95% CI: 0.43-1.12) or CAC ≥100 (aOR=0.76, 95% CI: 0.46-1.25) for Black versus White persons independent of age and sex. Conclusion(s): In a Southern rural cohort of young and middle-aged persons, approximately one in three had prevalent CAC and one in eight had premature CAC. In contrast to previously published urban cohorts, rural Black adults had a similar CAC burden to their White counterparts. There is a need to explore the factors implicated in the high CAC burden within Southern rural communities.

Left Main Coronary Artery Calcium and Diabetes Confer Very-High-Risk Equivalence in Coronary Artery Calcium >1,000

BackgroundAlthough a coronary artery calcium (CAC) of ≥1,000 is a subclinical atherosclerosis threshold to consider combination lipid-lowering therapy, differentiating very high from high atherosclerotic cardiovascular disease (ASCVD) risk in this patient population is not well-defined. ObjectivesAmong persons with a CAC of ≥1,000, the authors sought to identify risk factors equating with very high-risk ASCVD mortality rates. MethodsThe authors studied 2,246 asymptomatic patients with a CAC of ≥1,000 from the CAC Consortium without a prior ASCVD event. Cox proportional hazards regression modelling was performed for ASCVD mortality during a median follow-up of 11.3 years. Crude ASCVD mortality rates were compared with those reported for secondary prevention trial patients classified as very high risk, defined by ≥2 major ASCVD events or 1 major event and ≥2 high-risk conditions (1.4 per 100 person-years). ResultsThe mean age was 66.6 years, 14% were female, and 10% were non-White. The median CAC score was 1,592 and 6% had severe left main (LM) CAC (vessel-specific CAC ≥300). Diabetes (HR: 2.04 [95% CI: 1.47-2.83]) and severe LM CAC (HR: 2.32 [95% CI: 1.51-3.55]) were associated with ASCVD mortality. The ASCVD mortality per 100 person-years for all patients was 0.8 (95% CI: 0.7-0.9), although higher rates were observed for diabetes (1.4 [95% CI: 0.8-1.9]), severe LM CAC (1.3 [95% CI: 0.6-2.0]), and both diabetes and severe LM CAC (7.1 [95% CI: 3.4-10.8]). ConclusionsAmong asymptomatic patients with a CAC of ≥1,000 without a prior index event, diabetes, and severe LM CAC define very high risk ASCVD, identifying individuals who may benefit from more intensive prevention therapies across several domains, including low-density lipoprotein-cholesterol lowering.

Artificial intelligence coronary computed tomography, coronary computed tomography angiography using fractional flow reserve, and physician visual interpretation in the per-vessel prediction of abnormal invasive adenosine fractional flow reserve.

A comparison of diagnostic performance comparing AI-QCTISCHEMIA, coronary computed tomography angiography using fractional flow reserve (CT-FFR), and physician visual interpretation on the prediction of invasive adenosine FFR have not been evaluated. Furthermore, the coronary plaque characteristics impacting these tests have not been assessed. In a single centre, 43-month retrospective review of 442 patients referred for coronary computed tomography angiography and CT-FFR, 44 patients with CT-FFR had 54 vessels assessed using intracoronary adenosine FFR within 60 days. A comparison of the diagnostic performance among these three techniques for the prediction of FFR ≤ 0.80 was reported. The mean age of the study population was 65 years, 76.9% were male, and the median coronary artery calcium was 654. When analysing the per-vessel ischaemia prediction, AI-QCTISCHEMIA had greater specificity, positive predictive value (PPV), diagnostic accuracy, and area under the curve (AUC) vs. CT-FFR and physician visual interpretation CAD-RADS. The AUC for AI-QCTISCHEMIA was 0.91 vs. 0.76 for CT-FFR and 0.62 for CAD-RADS ≥ 3. Plaque characteristics that were different in false positive vs. true positive cases for AI-QCTISCHEMIA were max stenosis diameter % (54% vs. 67%, P < 0.01); for CT-FFR were maximum stenosis diameter % (40% vs. 65%, P < 0.001), total non-calcified plaque (9% vs. 13%, P < 0.01); and for physician visual interpretation CAD-RADS ≥ 3 were total non-calcified plaque (8% vs. 12%, P < 0.01), lumen volume (681 vs. 510 mm3, P = 0.02), maximum stenosis diameter % (40% vs. 62%, P < 0.001), total plaque (19% vs. 33%, P = 0.002), and total calcified plaque (11% vs. 22%, P = 0.003). Regarding per-vessel prediction of FFR ≤ 0.8, AI-QCTISCHEMIA revealed greater specificity, PPV, accuracy, and AUC vs. CT-FFR and physician visual interpretation CAD-RADS ≥ 3.

Associations of galectin-3 levels with measures of vascular disease in patients with rheumatoid arthritis

ObjectivesGalectin-3 is a beta-galactoside-binding lectin and is a marker of cardiovascular disease (CVD) in the general population. It may also play a role in joint inflammation. We asked whether serum galectin-3 is a useful marker of subclinical vascular disease in patients with rheumatoid arthritis (RA). MethodsRA patients without clinical CVD underwent assessment of coronary artery calcium (CAC) score, aortic inflammation (using 18Fluorodeoxyglucose positron emission-computed tomography [FDG PET/CT]), and myocardial flow reserve (MFR). Aorta FDG uptake was measured as standardized uptake values (SUV). Generalized linear models were constructed to explore the associations of galectin-3 levels with CAC score, aortic SUV, and MFR. ResultsA total of 124 RA patients (mean age 57; 82 % women, 45 % Hispanic; median RA duration 6.8 years; 75 % seropositive; median CDAI 16; 33 % on prednisone; 89 % on DMARDs; median CAC score 0; median aorta SUV 2.59; mean MFR 2.86; median galectin-3 level 8.54 ng/mL) were analyzed. In univariable analysis, higher galectin-3 levels were associated with higher aortic SUV (p = 0.007) but CAC score and MFR were not. In multivariable analysis, higher galectin-3 level remained significantly associated with higher aortic SUV (ß Coefficient=0.1786, p value=0.002). ConclusionIn our cohort of RA patients without clinical CVD, higher serum galectin-3 levels were independently associated with higher levels of aortic inflammation, but not CAC score or MFR. This suggests that galectin-3 may be a biomarker for an inflammatory and potentially reversible stage, but not a later (calcified) stage, of atherosclerosis in patients with RA.

Integrated omics analysis of coronary artery calcifications and myocardial infarction: the Framingham Heart Study

Gene function can be described using various measures. We integrated association studies of three types of omics data to provide insights into the pathophysiology of subclinical coronary disease and myocardial infarction (MI). Using multivariable regression models, we associated: (1) single nucleotide polymorphism, (2) DNA methylation, and (3) gene expression with coronary artery calcification (CAC) scores and MI. Among 3106 participants of the Framingham Heart Study, 65 (2.1%) had prevalent MI and 60 (1.9%) had incident MI, median CAC value was 67.8 [IQR 10.8, 274.9], and 1403 (45.2%) had CAC scores > 0 (prevalent CAC). Prevalent CAC was associated with AHRR (linked to smoking) and EXOC3 (affecting platelet function and promoting hemostasis). CAC score was associated with VWA1 (extracellular matrix protein associated with cartilage structure in endomysium). For prevalent MI we identified FYTTD1 (down-regulated in familial hypercholesterolemia) and PINK1 (linked to cardiac tissue homeostasis and ischemia–reperfusion injury). Incident MI was associated with IRX3 (enhancing browning of white adipose tissue) and STXBP3 (controlling trafficking of glucose transporter type 4 to plasma). Using an integrative trans-omics approach, we identified both putatively novel and known candidate genes associated with CAC and MI. Replication of findings is warranted.

Association of coronary artery calcification with mortality and myocardial injury after noncardiac surgery

Abstract Objectives This study aimed to evaluate the prognostic value of preoperative coronary artery calcium (CAC) scores for predicting in-hospital death and myocardial injury after noncardiac surgery (MINS). Backgrounds The CAC score is a surrogate marker for atherosclerosis and coronary artery disease. However, the association between preoperative CAC score and development of MINS has not been studied. Methods From 2010 to 2019, patients with CAC scores measured within three years prior to noncardiac surgery were enrolled from a tertiary hospital. Patients with a history of coronary revascularization were excluded from this study. The Agatston method was used to calculate CAC scores. The primary outcome was in-hospital death or MINS, defined as a peak high-sensitivity troponin I level higher than 0.040 ng/ml within 30 days after noncardiac surgery. The secondary outcome was 1-year mortality. Results A total of 740 patients were included in the analysis. The mean age was 67.0 years, and 68.9% were male. In-hospital death or MINS occurred in 129 (17.4 %) patients. The median CAC score was 164.0 and 70.5 in patients with and without in-hospital death or MINS, respectively (p=0.001). The preoperative CAC score was significantly associated with the development of in-hospital death or MINS (per 100 increases, odds ratio [OR] 1.05; 95% confidence interval [CI] 1.02–1.07). The best CAC score cutoff value for predicting in-hospital death or MINS was 619 (&amp;lt;619 vs. ≥619, OR 2.47; 95% CI 1.60–3.81; p&amp;lt;0.001), which was significant after adjustment for clinical risk factors. The 1-year mortality rate was significantly different according to CAC score strata. Conclusions A high preoperative CAC score was associated with a significant increase in in-hospital death or MINS independent of clinical risk factors.1-year mortality rate : CAC score1yr mortality rate by CAC score cut-off

Coronary calcium scoring on virtual non-contrast and virtual non-iodine reconstructions compared to true non-contrast images using photon-counting computed tomography

ObjectivesTo compare coronary artery calcification (CAC) scores measured on virtual non-contrast (VNC) and virtual non-iodine (VNI) reconstructions computed from coronary computed tomography angiography (CCTA) using photon-counting computed tomography (PCCT) to true non-contrast (TNC) images.MethodsWe included 88 patients (mean age = 59 years ± 13.5, 69% male) who underwent a TNC coronary calcium scan followed by CCTA on PCCT. VNC images were reconstructed in 87 patients and VNI in 88 patients by virtually removing iodine from the CCTA images. For all reconstructions, CAC scores were determined, and patients were classified into risk categories. The overall agreement of the reconstructions was analyzed by Bland–Altman plots and the level of matching classifications.ResultsThe median CAC score on TNC was 27.8 [0–360.4] compared to 8.5 [0.2–101.6] (p < 0.001) on VNC and 72.2 [1.3–398.8] (p < 0.001) on VNI. Bland–Altman plots depicted a bias of 148.8 (ICC = 0.82, p < 0.001) and − 57.7 (ICC = 0.95, p < 0.001) for VNC and VNI, respectively. Of all patients with CACTNC = 0, VNC reconstructions scored 63% of the patients correctly, while VNI scored 54% correctly. Of the patients with CACTNC > 0, VNC and VNI reconstructions detected the presence of coronary calcium in 90% and 92% of the patients. CACVNC tended to underestimate CAC score, whereas CACVNI overestimated, especially in the lower risk categories. According to the risk categories, VNC misclassified 55% of the patients, while VNI misclassified only 32%.ConclusionCompared to TNC images, VNC underestimated and VNI overestimated the actual CAC scores. VNI reconstructions quantify and classify coronary calcification scores more accurately than VNC reconstructions.Clinical relevance statementPhoton-counting CT enables spectral imaging, which might obviate the need for non-contrast enhanced coronary calcium scoring, but optimization is necessary for the clinical implementation of the algorithms.Key Points• Photon-counting computed tomography uses spectral information to virtually remove the signal of contrast agents from contrast-enhanced scans.• Virtual non-contrast reconstructions tend to underestimate coronary artery calcium scores compared to true non-contrast images, while virtual non-iodine reconstructions tend to overestimate the calcium scores.• Virtual non-iodine reconstructions might obviate the need for non-contrast enhanced calcium scoring, but optimization is necessary for the clinical implementation of the algorithms.

Abstract 13124: Better Prognostic Value of Single Time Coronary Artery Calcium Score Over the 30-y Averaged Pooled Cohort Equation in Older Adults: The Atherosclerosis Risk in Communities (ARIC) Study

Background: Cardiovascular disease (CVD) risk prediction in the 75-and-older population is challenging in part because traditional risk factors at older age may not reflect the risk factor profile over the life course. In this regard, coronary artery calcium (CAC) can be considered an integrated biomarker of exposure to CVD risk factors. However, the predictive value of a single time point CAC at older age vs. the cumulative exposure of traditional risk factors over three decades is unknown. Methods: In 1,875 ARIC participants (age 75-94 years) without a history of coronary heart disease (CHD), stroke, and heart failure (HF) at Visit 7 (2018-2019), we assessed the association of Visit 7 CAC vs. a weighted average of Pooled Cohort Equation (PCE) calculated 10-year atherosclerotic CVD (ASCVD) risk from Visit 1 (1987-89) to Visit 7 with the risk of ASCVD (CHD or stroke), HF, and all-cause mortality using adjusted Cox models. Risk prediction improvement was assessed using Harrel’s C-statistics. Results: The median CAC was 221 (IQI 35-743), and the median averaged PCE score was 15.0% (IQI 10.4%-21.2%). Over a median follow-up of 2.1 (IQI 1.7-2.5) years, there were 48 ASCVD events, 36 HF events, and 85 deaths. A higher CAC score was associated with a higher risk of ASCVD and HF, even after adjusting for averaged PCE (adjusted hazard ratio 3.33 [95% CI 1.53, 7.26] and 5.57 [1.95, 15.89] for CAC 1000+ vs. 0-99, respectively), but not all-cause mortality ( Table ). In contrast, averaged PCE was not associated with ASCVD or HF independent of CAC. However, averaged PCE showed robust associations with all-cause mortality. Notably, the addition of CAC to averaged PCE significantly improved risk prediction of HF, whereas adding averaged PCE to CAC did not significantly improve the risk prediction for any adverse outcome. Conclusions: The present study shows that a single time point CAC outperforms 30-y cumulative exposure of PCE for ASCVD and HF prediction in the 75-and-older population.

Serum oxalate concentration is associated with coronary artery calcification and cardiovascular events in Japanese dialysis patients

Coronary artery calcification (CAC) is associated with cardiovascular disease (CVD). CAC might contain calcium oxalate, and a high serum oxalate (SOx) concentration is associated with cardiovascular mortality in dialysis patients. We assessed the associations between SOx and CAC or CVD events in Japanese hemodialysis patients. This cross-sectional and retrospective cohort study was done in 2011. Seventy-seven hemodialysis patients’ Agatston CAC score was measured, and serum samples were collected. SOx concentrations were measured in 2021 by using frozen samples. Also, new-onset CVD events in 2011–2021 were retrospectively recorded. The association between SOx concentration and CAC score ≥ 1000, and new-onset CVD events were examined. Median SOx concentration and CAC score were 266.9 (229.5–318.5) µmol/L and 912.5 (123.7–2944), respectively. CAC score ≥ 1000 was associated with SOx [adjusted odds ratio (OR) 1.01, 95% confidence interval (CI), 1.00–1.02]. The number of new-onset CVD events was significantly higher in patients with SOx ≥ median value [hazard ratio (HR) 2.71, 95% CI 1.26–6.16]. By Cox proportional hazard models, new-onset CVD events was associated with SOx ≥ median value (adjusted HR 2.10, 95% CI 0.90–4.91). SOx was associated with CAC score ≥ 1000 and new-onset CVD events in Japanese hemodialysis patients.

Long-term outcomes of lung cancer screening in males and females

BackgroundThis study explored female and male overall mortality and lung cancer (LC) survival in two LC screening (LCS) populations, focusing on the predictive value of coronary artery calcification (CAC) at baseline low-dose computed tomography (LDCT). MethodsThis retrospective study analysed data of 6495 heavy smokers enrolled in the MILD and BioMILD LCS trials between 2005 and 2016. The primary objective of the study was to assess sex differences in all-cause mortality and LC survival. CAC scores were automatically calculated on LDCT images by a validated artificial intelligence (AI) software. Sex differences in 12-year cause-specific mortality rates were stratified by age, pack-years and CAC score. ResultsThe study included 2368 females and 4127 males. The 12-year all-cause mortality rates were 4.1 % in females and 7.7 % in males (p < 0.0001), and median CAC score was 8.7 vs. 41 respectively (p < 0.0001). All-cause mortality increased with rising CAC scores (log-rank test, p < 0.0001) for both sexes. Although LC incidence was not different between the two sexes, females had lower rates of 12-year LC mortality (1.0 % vs. 1.9 %, p = 0.0052), and better LC survival from diagnosis (72.3 % vs. 51.7 %; p = 0.0005), with a similar proportion of stage I (58.1 % vs. 51.2 %, p = 0.2782). ConclusionsOur findings demonstrate that female LCS participants had lower rates of all-cause mortality at 12 years and better LC survival than their male counterparts, with similar LC incidence rates and stage at diagnosis. The lower CAC burden observed in women at all ages might contribute to explain their lower rates of all-cause mortality and better LC survival.

Association Between Coronary Artery Calcium Score and Left Ventricular Diastolic Dysfunction in Patients with Hypertension

Background: Left ventricular diastolic dysfunction (LVDD) and coronary artery calcium (CAC) are common in patients with hypertension and are strong predictors of cardiovascular events. Aim: This study aims to investigate the association between CAC and LVDD in patients with hypertension without coronary artery disease (CAD). Methods: Consecutive patients with hypertension who underwent echocardiography and non-contrast coronary CT were studied. CAC was quantified using the Agatston score. Patients with a history of CAD, AF or left ventricular ejection fraction (LVEF) &lt;50% were excluded. Characteristics of patients with and without LVDD were compared and the association between LVDD and CAC was evaluated. Univariable and multivariable analyses were performed to determine the predictors of LVDD and high CAC (&gt;median CAC). A p value of &lt;0.05 was considered statistically significant. Results: A total of 250 patients were included, with a mean age of 64.3 ± 10.1 years, 59% women and 26.4% had diabetes. The prevalence of LVDD was 64.8% (grade I LVDD 48%; grade II LVDD 16.8%) and the median CAC score was 58.2 (interquartile range [IQR] 0.7–349.8). Patients with LVDD had a significantly higher median CAC score than those without LVDD (142.8 [IQR 18.8–514.8] versus 5.0 [IQR 0–64.4]; p&lt;0.001). Multivariable analysis showed that the CAC score was independently associated with LVDD (OR 1.003; 95% CI [1.001–1.004]; p&lt;0.001). Left atrial volume index and E-wave deceleration time were independently associated with high CAC (OR 1.05; 95% CI [1.01–1.09]; p=0.008 and OR 1.008; 95% CI [1.002–1.02]; p=0.01), respectively. Conclusion: CAC scoring was associated with LVDD in patients with hypertension.

Coronary artery calcium scoring for cardiovascular risk assessment in patients with inflammatory bowel disease

Inflammatory bowel disease (IBD) is associated with higher incidence of atherosclerotic cardiovascular disease (ASCVD). Data investigating the role of coronary artery calcium (CAC) scoring in identifying subclinical atherosclerotic disease in IBD patients is scarce. Using data obtained from the CLARIFY registry, a prospective study of no-charge coronary artery calcium (CAC) testing at University Hospitals, we reviewed patients with ulcerative colitis (UC) or Crohn's disease (CD) who underwent CAC scoring from 2014 to 2020. We investigated the concordance between CAC risk and 10-year estimated ASCVD risk by AHA/ACC pooled cohort equation using pre-established thresholds for statin prescription (CAC≥100, 10-year ASCVD risk ≥7.5%). We additionally investigated the association between CAC, preventive therapy initiation and Major Adverse Cardiovascular Events (MACE). A total of 369 patients with IBD were included (174 UC, 195 CD), with median age of 60 years. The median CAC score was 14.9 with no significant difference between UC and CD (P=.76). Overall, 151 (41%) had CAC of 0, 108 (29%) had CAC 1-99, 61 (17%) had CAC 100 to 399, and 49 (13%) had CAC ≥400 with no difference in CAC distribution between CD and UC (P=.17). There was no difference in median CAC between IBD or age/sex-matched controls (P=.34). Approximately half of the patients (52%) with IBD had 10-year estimated ASCVD risk of 7.5% or higher. Among patients with ASCVD risk <7.5% (n=163), 29 (18%) had CAC≥100 and among patients with ASCVD risk ≥7.5% (n=178), 102 (57%) had CAC <100. There was no difference between CAC<100 vs CAC≥100 with respect to CRP, use of immunosuppressive or amino-salicylate therapy, IBD severity or complications. CAC score (AUROC 0.67 [0.56-0.78]), but not PCE ASCVD risk (AUROC 0.60 [0.48-0.73]), was predictive of MACE. The best cut-off for CAC score was 76 (sensitivity=60%, specificity=69%), and was associated with 4-fold increase in MACE (Hazard Ratio 4.0 [2.0-8.1], P < .001). Subclinical atherosclerosis, as evaluated by CAC scoring, is prevalent in patients with IBD, and is associated with cardiovascular events. Further studies are needed to understand underlying biological processes of increased atherosclerotic disease risk among adults with IBD.

Coronary Artery Calcium Scores in Older Adults With Diabetes and Their Association With Diabetes-Specific Risk Enhancers (from the Atherosclerosis Risk in Communities Study)

Coronary artery calcium (CAC) is a validated marker of atherosclerotic cardiovascular disease (ASCVD) risk; however, it is not routinely incorporated in ASCVD risk prediction in older adults with diabetes. We sought to assess the CAC distribution among this demographic and its association with "diabetes-specific risk enhancers," which are known to be associated with increased ASCVD risk. We used the ARIC (Atherosclerosis Risk in Communities) study data, including adults aged >75 years with diabetes, who had their CAC measured at ARIC visit 7 (2018 to 2019). The demographic characteristics of participants and their CAC distribution were analyzed using descriptive statistics. Multivariable-adjusted logistic regression models were used to estimate the association between diabetes-specific risk enhancers (duration of diabetes, albuminuria, chronic kidney disease, retinopathy, neuropathy, and ankle-brachial index) and elevated CAC, adjusting for age, gender, race, education level, dyslipidemia, hypertension, physical activity, smoking status, and family history of coronary heart disease. The mean age in our sample was 79.9 (SD 3.97) years, with 56.6% women and 62.1% White. The CAC scores were heterogenous, and the median CAC score was higher in participants with a greater number of diabetes risk enhancers, regardless of gender. In the multivariable-adjusted logistic regression models, participants with ≥2 diabetes-specific risk enhancers had greater odds of elevated CAC than those with <2 (odds ratio 2.31, 95% confidence interval 1.34 to 3.98). In conclusion, the distribution of CAC was heterogeneous among older adults with diabetes, with the CAC burden associated with the number of diabetes risk-enhancing factors present. These data may have implications for prognostication in older patients with diabetes and supports the possible incorporation of CAC in the assessment of cardiovascular disease risk in this population.

The correlation between coronary artery, aortic, and mitral valve calcification in patients with coronary atherosclerosis

BackgroundAtherosclerosis is the underlying process causing coronary artery calcification. Pathophysiology of aortic and mitral valve calcification has several similarities with coronary atherosclerosis, but their correlation has not been clear, especially in patients with coronary atherosclerosis.PurposeThis study aims to investigate the correlation between the calcium score of the coronary arteries, aortic, and mitral valves in patients with coronary atherosclerosis.MethodsThis was a cross-sectional, correlation study. Stratified randomization was done based on the coronary artery calcium score category. The calcium score was calculated using Agatston technique. Statistical tests were done to look for the correlations between the coronary artery and aortic valve calcium score, coronary artery and mitral valve calcium score, as well as coronary artery and aortic + mitral valve calcium score.ResultsThere are ninety-seven subjects (coronary calcium score “mild” 34 subjects, “moderate” 30 subjects, “severe” 33 subjects) with a mean age of 63.85 (± 9.80) years old. The median coronary artery calcium score was 158.7 (Agatston Unit (AU; 1–3917.7), aortic valve 12.6 AU (0–3747), and mitral valve 0.1 AU (0–1247.5 AU). There was a very weak correlation between coronary artery calcium score with aortic, mitral, and aortic + mitral valve calcium score.ConclusionsThere was no statistically significant correlation between the calcium score of the coronary artery and the calcium score of the aortic valve, as well as the calcium score of the mitral valve in patients with coronary atherosclerosis. However, the secondary analysis showed a correlation between them varied depending on the severity of coronary artery calcification, which could shed light on a better understanding of the atherosclerotic process in the coronary artery, aortic, and mitral valve.