Heart Disease and Stroke Statistics—2009 Update

For individuals with a coronary artery calcium (CAC) score of 0, CAC rescans at appropriate timings are recommended, depending on individual risk profiles. Although nonalcoholic fatty liver disease, recently redefined as metabolic-associated fatty liver disease, is a risk factor for atherosclerotic cardiovascular disease events, its relationship with the warranty period of a CAC score of 0 has not been elucidated. A total of 1944 subjects from the MESA (Multi-Ethnic Study of Atherosclerosis) with a baseline CAC score of 0, presence or absence of nonalcoholic hepatic steatosis, and at least 1 follow-up computed tomography scan were included. Nonalcoholic hepatic steatosis was defined using nonenhanced computed tomography and liver/spleen attenuation ratio <1. The association between nonalcoholic hepatic steatosis and new CAC incidence (CAC score >0) was evaluated using a Weibull survival model. Nonalcoholic hepatic steatosis was identified in 268 (14%) participants. Participants with nonalcoholic hepatic steatosis had higher CAC incidence than those without nonalcoholic hepatic steatosis. Nonalcoholic hepatic steatosis was independently associated with new CAC incidence after adjustment for atherosclerotic cardiovascular disease risk factors (hazard ratio, 1.28 [95% CI, 1.05-1.57]; P=0.015). Using a 25% testing yield (25% of participants with zero CAC at baseline would be expected to have developed a CAC score >0), the warranty period of a CAC score of 0 in participants with nonalcoholic hepatic steatosis was shorter than in those without nonalcoholic hepatic steatosis (4.7 and 6.3 years). This association was consistent regardless of sex, race/ethnicity, age, and 10-year atherosclerotic cardiovascular disease risk. Nonalcoholic hepatic steatosis had an impact on the warranty period of a CAC score of 0. The study suggests that the time period until a CAC rescan should be shorter in those with nonalcoholic hepatic steatosis and a CAC score of 0.

Association of Coronary Artery Calcified Plaque With Clinical Coronary Heart Disease in the National Heart, Lung, and Blood Institute’s Family Heart Study

Background: Coronary artery disease (CAD) starts in childhood and progresses to advanced lesions in adult life. The coronary artery calcium (CAC) score is a measure of subclinical CAD that indicates advanced coronary atheroma and independently predicts future clinical events. Our objective was to document the prevalence and amount of subclinical CAD among black and white adults in early adult life. Methods: The Coronary Artery Risk Development in Young Adults (CARDIA) study is a U.S. population-based, prospective, observational study of black and white men and women. Initially 5,115 participants age of 18-30 yrs were recruited in 1985-6. CAC was measured using non-contrast cardiac CT and reported as the Agatston score at three exams 15, 20 &amp; 25 years after the baseline visit. Results: CAC prevalence was 10.1%(309/3046), 18.6%(583/3140) and 28.1%(890/3160) when the returning cohort was between 33-45 yrs, 38-50 yrs, and 43-55 yrs, respectively (see figure). Prevalence of CAC at all time points was greater in men than women and highest in white men. In the most recent exam, black men had a lower prevalence of CAC (34.3% vs 47.7%) compared to white men but similar distribution of CAC amount. Quartiles of CAC among men with any CAC were: black men 10, 48, 183 and white men 14, 42, 173 (Q1, Q2(median) and Q3 respectively). Change in CAC score among participants in the two most recent CT exams was observed in 29.8% (774/2600). Of those participants, 89.3%(691/774) had any increase in CAC score and 66.7%(516/774) an increase of 10 units or greater. Prevalence of CAC was highly correlated with age and no period effect was observed. Conclusions: 28% of adults less than 55 years of age have advanced plaque in their coronary arteries indicating significant subclinical disease burden. Prevalence is highest in white men, followed by black men and then women in these age ranges. Black men, given CAC, have a comparable amount of CAC to white men. Subclinical CAD is prevalent in early adulthood and once initiated appears to progress in the vast majority of adults.

Coronary Artery Calcium Score and Association with Recurrent Nephrolithiasis: The Multi-Ethnic Study of Atherosclerosis

Atherosclerosis and Vascular Biology

Coronary artery calcium score and polygenic risk score have each separately been proposed as novel markers to identify risk of coronary heart disease (CHD), but no prior studies have directly compared these markers in the same cohorts. To evaluate change in CHD risk prediction when a coronary artery calcium score, a polygenic risk score, or both are added to a traditional risk factor-based model. Two observational population-based studies involving individuals aged 45 years through 79 years of European ancestry and free of clinical CHD at baseline: the Multi-Ethnic Study of Atherosclerosis (MESA) study involved 1991 participants at 6 US centers and the Rotterdam Study (RS) involved 1217 in Rotterdam, the Netherlands. Traditional risk factors were used to calculate CHD risk (eg, pooled cohort equations [PCEs]), computed tomography for the coronary artery calcium score, and genotyped samples for a validated polygenic risk score. Model discrimination, calibration, and net reclassification improvement (at the recommended risk threshold of 7.5%) for prediction of incident CHD events were assessed. The median age was 61 years in MESA and 67 years in RS. Both log (coronary artery calcium+1) and polygenic risk score were significantly associated with 10-year risk of incident CHD (hazards ratio per SD, 2.60; 95% CI, 2.08-3.26 and 1.43; 95% CI, 1.20-1.71, respectively), in MESA. The C statistic for the coronary artery calcium score was 0.76 (95% CI, 0.71-0.79) and for the polygenic risk score, 0.69 (95% CI, 0.63-0.71). The change in the C statistic when each was added to the PCEs was 0.09 (95% CI, 0.06-0.13) for the coronary artery calcium score, 0.02 (95% CI, 0.00-0.04) for the polygenic risk score, and 0.10 (95% CI, 0.07-0.14) for both. Overall categorical net reclassification improvement was significant when the coronary artery calcium score (0.19; 95% CI, 0.06-0.28) but was not significant when the polygenic risk score (0.04; 95% CI, -0.05 to 0.10) was added to the PCEs. Calibration of the PCEs and models with coronary artery calcium and/or polygenic risk scores was adequate (all χ2<20). Subgroup analysis stratified by the median age demonstrated similar findings. Similar findings were observed for 10-year risk in RS and in longer-term follow-up in MESA (median, 16.0 years). In 2 cohorts of middle-aged to older adults from the US and the Netherlands, the coronary artery calcium score had better discrimination than the polygenic risk score for risk prediction of CHD. In addition, the coronary artery calcium score but not the polygenic risk score significantly improved risk discrimination and risk reclassification for CHD when added to traditional risk factors.

Factors Associated With Presence and Extent of Coronary Calcium in Those Predicted to Be at Low Risk According to Framingham Risk Score (from the Multi-Ethnic Study of Atherosclerosis)

Reduced estimated glomerular filtration rate (eGFR) is associated with increased risk of cardiovascular disease among people living with HIV (PLWH). It is unclear whether eGFR equations incorporating cystatin C (CysC) measurements are more predictive of preclinical cardiovascular disease than those using only creatinine (Cr). The study aimed to determine which of the 3 Chronic Kidney Disease Epidemiology (CKD-EPI) eGFR equations is most associated with carotid intima media thickness (CIMT) and coronary artery calcium (CAC) score. This cross-sectional analysis of pooled data from 3 large cohorts compared the associations between the 3 CKD-EPI eGFR equations (Cr, CysC, and Cr-CysC) with CIMT and CAC score using multivariable regression analysis. eGFR and CIMT were analyzed as continuous variables. CAC scores were analyzed as a binary variable (detectable calcification versus nondetectable) and as a log10 Agatston score in those with detectable CAC. Thousand four hundred eighty-seven participants were included, and of these 910 (562 HIV+ and 348 HIV-) had CIMT measurements and 366 (296 HIV+ and 70 HIV-) had CAC measurements available. In HIV- participants, GFR estimated by any CKD-EPI equation did not significantly correlate with CIMT or CAC scores. When PLWH were analyzed separately including HIV-specific factors, only GFR estimated using Cr-Cys C correlated with CIMT [β= -0.90, 95% CI: (-1.67 to -0.13) μm; P = 0.023]. Similarly, eGFR correlated with Agatston scores only when using cystatin C-based eGFR [β= -8.63, 95% CI: (-16.49 to -0.77) HU; P = 0.034]. Associations between other eGFR formulas and CAC did not reach statistical significance. In PLWH, preclinical atherosclerosis may be more closely correlated with eGFR using formulae that incorporate CysC measurements than Cr alone.

Objective : The Adult Treatment Panel (ATP) III recommends estimating 10-year risk for cardiovascular disease (CVD), but this strategy identifies few individuals age ≤ 50 years as high risk. Many individuals have a lifetime risk up to 70% despite a low 10-year risk (&lt;10%) for CVD. We hypothesized that individuals with low 10-year/high lifetime risk would have a greater burden of subclinical atherosclerosis compared to individuals with low 10-year/low lifetime risk. Methods : We included individuals age ≤ 50 from two multiethnic NHLBI-sponsored studies designed to assess the importance of risk factors in the development of CVD [2988 from Coronary Artery Risk Development in Young Adults (CARDIA) study;1076 individuals from the Multi-Ethnic Study of Atherosclerosis (MESA)]. The ATP III 10-year risk and lifetime risk for CVD were estimated for each participant, permitting stratification into three groups: low 10-year (&lt;10%)/low lifetime (&lt;39%) risk, low 10-year (&lt;10%)/high lifetime risk (≥ 39%), and high 10-year risk (≥ 10%). Diabetics were considered to have high 10-year (≥ 10%) risk in all analyses. Baseline levels (CAC, IMT) and change in levels of subclinical atherosclerosis (CAC progression) were compared across the 3 risk strata for both cohorts. Results : As expected, those with high 10-year risk (≥ 10%) had the greatest burden of subclinical atherosclerosis in both studies. Among individuals with low 10-year risk (91% of all participants) in CARDIA, individuals with a high lifetime risk had significantly greater carotid IMT, higher CAC prevalence, and greater incidence of CAC progression compared to individuals with low lifetime risk (see table ). A remarkably similar pattern of results was observed in MESA. Conclusions : Individuals with low 10-year but high lifetime risk for CVD have a greater subclinical disease burden and greater incidence of atherosclerotic progression compared to individuals with low 10-year but low lifetime risk. Baseline Carotid Intima-Media Thickness (IMT), Coronary Artery Calcium (CAC) Prevalence and Progression among CARDIA Participants

Implications of C-reactive protein or coronary artery calcium score as an adjunct to global risk assessment for primary prevention of CHD

Background: Cardiovascular diseases (CVDs) remain a leading cause of morbidity and mortality globally, with myocardial ischemia (MI) being one of the most critical manifestations of coronary artery disease (CAD). Myocardial ischemia occurs when there is an insufficient supply of oxygen-rich blood to the heart muscle, typically caused by blockages or narrowing in the coronary arteries due to atherosclerosis. The coronary artery calcium (CAC) score, which quantifies calcium deposits in the coronary arteries, has emerged as a valuable tool in predicting cardiovascular events, including myocardial ischemia. Understanding the relationship between CAC scores and myocardial ischemia, along with other risk factors, could improve patient management and help predict adverse cardiovascular outcomes.Objective: This study aims to evaluate the relationship between CAC scores and the development of myocardial ischemia, as detected through diagnostic imaging methods such as CT angiography and stress echocardiography, and to analyze associated risk factors, including traditional and emerging clinical factors.Methodology: A prospective, cross-sectional observational study was conducted in the Departments of Cardiology and Radiology at Mardan Medical Complex between February 2023 and June 2025. Diagnostic methods such as CT angiography and stress echocardiography were used to assess the presence of myocardial ischemia. Demographic data, clinical characteristics, comorbidities, and CAC scores were collected. Statistical analyses, including two-way analysis of variance (ANOVA), Mann-Whitney U tests, and decision tree modeling, were used to explore the relationship between CAC scores and myocardial ischemia, along with various risk factors such as age, gender, BMI, smoking history, and comorbidities.Results: The study included 129 patients, with 74 (57.36%) diagnosed with myocardial ischemia. A strong correlation was observed between elevated CAC scores and ischemia, with ischemic patients displaying significantly higher CAC scores (671.92 ± 185.82) compared to nonischemic patients (246.36 ± 98.51). The overall CAC scores for individual coronary arteries were 73.57 ± 39.24 for the left main artery (LMA), 196.19 ± 104.63 for the left anterior descending artery (LAD), 122.62 ± 65.40 for the left circumflex artery (LCX), and 98.10 ± 52.32 for the right coronary artery (RCA), while the total CAC score averaged 490.48 ± 261.58. Decision tree analysis identified critical cutoff values for predicting ischemia, including 403.0 for total CAC, 161.2 for LAD, 100.75 for LCX, 80.6 for RCA, and 60.45 for LMA. Additionally, risk factors such as hypertension, diabetes, and smoking were associated with higher CAC scores, particularly among ischemic patients.Conclusion: CAC scoring is an essential tool for evaluating the risk of myocardial ischemia and cardiovascular events, complementing traditional risk factors to improve stratification and enable more focused interventions for patients.

Objectives: Fatty liver disease (FLD) is a well-known risk factor for cardiovascular disease (CVD). However, it is unclear whether FLD per se is an independent risk factor of CVD or combined unfavorable metabolic components with metabolic syndrome (MetS). In this study, we examined the independent impact of FLD on the coronary artery calcification (CAC) score progression. Methods: We examined 1,173 asymptomatic participants who underwent repeated CAC score measurement during routine health examinations. Subjects were categorized into 4 groups according to the presence (+) or absence (-) of FLD and MetS. The CAC score progression was defined as either incident CAC in a population free of CAC at baseline or increase ≥ 2.5 units between the baseline and final square root of CAC scores participants who had detectable CAC at baseline examination. Results: Among the participants, 44.8% (526), 23.2% (272), 8.8% (103) and 23.2% (272) were classified as FLD(-)/MetS(-), FLD(+)/MetS(-), FLD(-)/MetS(+), and FLD(+)/MetS(+), respectively. The proportions of subjects who developed CAC progression was 18.6% (98), 28.3% (77), 29.1% (30) and 32.0% (87) in FLD(-)/Mets(-), FLD(+)/Mets(-), FLD(-)/MetS(+), and FLD(+)/MetS(+), respectively. In logistic regression analysis, FLD(+)/MetS(+) were at significantly higher risk of CAC progression compared to FLD(-)/MetS(-) [multivariate adjusted-odds ratio (OR) 1.76, 95% confidence interval (CI) 1.18-2.62]. FLD(+)/MetS(-) also demonstrated higher risk of CAC progression [multivariate adjusted-OR 1.53, 95% CI 1.05-2.23]. Conclusions: FLD is an independent risk factor for CAC progression irrespective of the presence of metabolic syndrome. Special attention should be paid to subjects with FLD for the prevention of future cardiovascular events, even though MetS does not coexist. Disclosure Y. Cho: None. Y. Kang: None. C. Park: None. S. Park: None. W. Lee: None. J. Park: None. C. Jung: None.

Background Inadequate intake of polyunsaturated fatty acids (PUFAs) is recognized as a modifiable risk factor for atherosclerotic cardiovascular disease (CVD) (1,2). The n-6 PUFA linoleic acid (LA) constitutes the predominant portion of total dietary PUFAs (3). However, whereas cardiometabolic effects of PUFAs belonging to the n-3 series have been studied for decades, less attention has been payed to potential health effects from n-6 PUFAs (4). Further, there has been concern regarding possible proinflammatory properties of several n-6 PUFA related metabolites. Purpose We explored correlations of serum total PUFAs, LA and the n-3 PUFA docosahexaenoic acid (DHA) with the inflammation marker GlycA. Further, we evaluated associations of total PUFAs, LA and DHA with the extension of atherosclerosis, as determined by the Agatston coronary artery calcium (CAC) score (5). Methods The study includes 250 patients who were hospitalized due to acute chest pain and referred to coronary CT angiography (CCTA) during in hospital stay. Exclusion criteria included diagnosis of acute myocardial infarction and/or revascularization within 24 hours after admittance. Serum levels of total PUFAs, LA, DHA and GlycA were analyzed by NMR technology in samples that had been frozen and stored at −80°C. After logarithmic transformation, relations of total PUFA, LA, and DHA with GlycA were evaluated by Pearson correlation analyses. The associations with CAC score were visualized in generalized additive regression plots and further evaluated in linear regression models including age, gender, body mass index, diabetes, hypertension and smoking status as independent covariables. Results Mean (SD) age was 57.6 (12.0) years, and 91 (36.4%) of the patients were women. Median (25th-75th percentiles) serum levels (in mmol/L) were for total PUFA 6.36 (5.76–7.06), LA 5.00 (4.51–5.55), DHA 0.36 (0.31–0.43) and GlycA 1.04 (0.94–1.13). Interestingly, GlycA was strongly, positively correlated with total PUFA (r=0.54). LA (r=0.53) and DHA (r=0.27), all P&amp;lt;0.001. In contrast, total PUFA and LA were inversely associated with CAC score both providing standardized betas of −0.17, P=0.03 after multivariable adjustments. No significant associations were found between CAC score and DHA or GlycA (P≥0.22). Further, the addition of GlycA to the multivariable model did not materially affect the relationship between CAC score and total PUFA or LA, which remained statistically significant (P=0.04). Conclusion In patients undergoing CCTA due to acute chest pain, serum levels of total PUFA and LA were strongly positively correlated with the pro-inflammatory marker GlycA. Still, total PUFA and LA were both inversely associated with the CAC score and the associations remained statistically significant after adjustments for CVD risk factors and GlycA levels. Future studies should further address the diverse effects of n-6 PUFAs on inflammatory pathways, atherogenesis and coronary calcification. Funding Acknowledgement Type of funding sources: Public hospital(s). Main funding source(s): Western Norway Regional Health Authority

BackgroundCT- coronary calcium score, is one of the most studied and widely available modalities in cardiovascular medicine. Coronary artery calcium score (CACS) is an established predictor of coronary artery disease. The ‘standard of care’ diagnostic modality to measure CACS is ECG-gated Cardiac Multi-Detector Computed Tomography. There is convincing evidence of a strong association between CACS and major cardiovascular (CV) events in asymptomatic individuals. Cancer patients (C) may have a higher risk for CV disease than non-cancer patients (NC) related not only to cancer treatments but also to shared biological factors and pathways. Thus, identifying tools for early detection of CV disease in this population is of utmost importance.MethodsA retrospective cohort analysis was performed with patients from Cleveland Clinic Florida and Ohio who had CACS from 2017 to 2021. Patients who had cancer diagnosis prior to CACS were matched to NC for age and sex. CV events after their index CACS events were compared between C and NC, and matched control and propensity analysis were conducted.ResultsTen thousand seven hundred forty-two patients had CACS; 703 cancer patients had CACS and were eligible. Extensive CACS (> 400) were significantly higher in cancer, 94 (13.37%) vs non-cancer patients, 76 (10.83%), P = 0.011. Furthermore, after propensity matched analysis, CACS > 400 was 14.8% in C vs 9.6% in NC, P = < 0.05. CV events were similar in both cohorts (p = NS), despite less CV risk factors in cancer patients (P = < 0.05). For the combined moderate (101–400) & extensive (> 400) CACS, the prevalence of stroke and peripheral arterial disease, a marker of systemic atherosclerosis, was significantly higher in patients with cancer (P < 0.01).ConclusionsDespite having fewer CV risk factors in our study, similar CACS in cancer patients are suggestive of a higher prevalence of CV disease independent of traditional risk factors. High CACS and the overall prevalence of vascular events were more frequent in patients with cancer. Higher prevalence of peripheral arterial disease and cerebrovascular accident further suggests the increased atherosclerotic burden in C.

FRI0080 Bone Mineral Density, Sclerostin and Insulin Are Independently Associated with Coronary-Artery Atherosclerosis in Patients with Established Rheumatoid Arthritis