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Metabolically healthy obesity (MHO) is known to have a close association with subclinical coronary atherosclerosis. Despite recent data on the benefit of intensive systolic blood pressure (SBP) control in diverse clinical conditions, little is known regarding the association of normal SBP maintenance (SBPmaintain) with coronary artery calcification (CAC) progression in MHO. This study included 2724 asymptomatic adults (48.8 ± 7.8 years; 77.9% men) who had no metabolic abnormalities except overweight and obesity. Participants with normal weight (44.2%), overweight (31.6%), and obesity (24.2%) were divided into two groups: normal SBPmaintain (follow-up SBP < 120 mm Hg) and ≥elevated SBPmaintain (follow-up SBP ≥ 120 mm Hg). CAC progression was defined using the SQRT method, a difference of ≥2.5 between the square root (√) of the baseline and follow-up coronary artery calcium score. During a mean follow-up of 3.4 years, the proportion of normal SBPmaintain (76.2%, 65.2%, and 59.1%) and the incidence of CAC progression (15.0%, 21.3%, and 23.5%) was different in participants with normal weight, overweight, and obesity (all p < 0.05, respectively). The incidence of CAC progression was lower in the normal SBPmaintain group than in the ≥elevated SBPmaintain group in only participants with obesity (20.8% vs. 27.4%, p = 0.048). In multiple logistic models, compared to participants with normal weight, those with obesity had a higher risk of CAC progression. Normal SBPmaintain was independently associated with the decreased risk of CAC progression in participants with obesity. MHO had a significant association with CAC progression. Normal SBPmaintain reduced the risk of CAC progression in asymptomatic adults with MHO. [ABSTRACT FROM AUTHOR]

Background and aim: Gastroesophageal reflux disease (GERD) typically presents with symptoms of heartburn and acid regurgitation but occasionally manifests as atypical chest pain. Coronary artery disease (CAD) and GERD share some risk factors, such as smoking and obesity. The aims of this study were to evaluate the association between GERD and coronary atherosclerosis and to assess the risk factors for coronary atherosclerosis in GERD patients. Methods: A total of 16616 subjects who underwent upper gastrointestinal endoscopy from 2003 to 2017 and a cardiac computed tomography (CT) scan within one year were included in this study. Coronary atherosclerosis was evaluated by the coronary artery calcium score (CACS). The severity of GERD was evaluated based on endoscopic findings using the Los Angeles classification. Results: The proportion of high CACSs (≥100) increased significantly in subjects with severe GERD (p = 0.008). However, the presence of a high CACS did not increase the risk of GERD (OR = 1.007, 95% CI 0.857–1.182), nor did that of GERD increase the risk of a high CACS (OR = 1.018, 95% CI 0.865–1.198). The risk factors for a high CACS in GERD patients included age (OR = 1.087, 95% CI 1.066–1.109), male sex (OR = 5.645, 95% CI 2.561–12.446), hypertension (OR = 1.800, 95% CI 1.325–2.446), and hypercholesterolemia (OR = 1.684, 95% CI 1.213–2.338). Conclusions: Although the presence of a high CACS did not increase the risk of GERD or vice versa, the proportion of high CACSs was significantly higher in subjects with severe GERD. Therefore, it might be helpful to assess the CACS in GERD patients with multiple risk factors. [ABSTRACT FROM AUTHOR]

Epidemiologic evidence indicates that the prevalence and severity of coronary artery disease vary depending on ethnicity. In this study, a genome-wide association study for coronary artery calcification (CAC) was performed in a Korean population-based sample of 400 subjects without prior coronary artery disease and replicated in another of 1,288 subjects. CAC score, as assessed by multi-detector computed tomography, was evaluated in volunteers for screening purposes as part of a routine health examination. CAC score greater than the 90th percentile across the age in each sex group was considered severe CAC. Single nucleotide polymorphisms (SNPs) associated with severe CAC after adjusting for age, sex, hypertension, and diabetes were investigated using the additive model of logistic regression. One SNP (rs10757272 in the intronic region of the CDKN2B-AS1 gene in chromosome 9p21.3) met Bonferroni correction in the discovery set (p = 7.55E-08) and was also significant in the validation set by TaqMan assay (p = 0.036). Subjects with rs10757272 were found to have an increased odds ratio (OR) of having severe CAC in multivariate logistic regression analysis after adjusting for age, sex, hypertension, and diabetes (adjusted OR 3.24 and 95% CI 2.11–4.97). In conclusion, SNP rs10757272 in chromosome 9p21.3 was associated with severe CAC based on age and sex in an asymptomatic community-based Korean population. Therefore, it was associated with promotion of coronary artery calcification in subclinical state. [ABSTRACT FROM AUTHOR]

Background: Data on the influence of glycemic status on the progression of coronary calcification, an important marker for future adverse cardiovascular events, are limited. Methods: Data from the Korea Initiatives on Coronary Artery Calcification (KOICA) registry on 12,441 asymptomatic Korean adults (52 ± 9 years, 84.2% males) without previous history of coronary artery disease and stroke, who underwent serial coronary artery calcification (CAC) screening examinations, were included in this study. The median inter-scan period was 3.0 (2.0-4.8) years. All participants were categorized into three groups based on their glycemic status: normal (n = 6578), pre-diabetes (n = 4146), and diabetes (n = 1717). CAC progression was defined as a difference ≥ 2.5 between the square roots (√) of the baseline and follow-up CAC scores. Results: The incidence of CAC progression was significantly different between the three groups (normal, 26.3%; pre-diabetes, 30.9%; and diabetes, 46.9%; p < 0.001). In the univariate logistic analysis, the risk of CAC progression was higher in the pre-diabetes (odds ratio [OR] 1.253; 95% confidential interval [CI] 1.150-1.366) and diabetes (OR 2.471; 95% CI 2.215-2.758) groups than in the normal group (p < 0.001, both). In the multivariate logistic analysis, the risk of CAC progression was not significantly different between the normal and pre-diabetes groups but was significantly higher in the diabetes group than in the normal group. Conclusions: In asymptomatic subjects, diabetes had an incremental impact on CAC progression; however, prediabetes did not increase the risk of CAC progression after adjusting for confounding factors. [ABSTRACT FROM AUTHOR]

Abstract: Objective: It is unclear whether visceral adipose tissue (VAT) is responsible for an increased risk of coronary artery calcification (CAC). We evaluated the associations between body mass index (BMI), waist circumference (WC) and abdominal VAT area with the CAC in healthy Korean men. Methods: This is a cross-sectional study of 1336 Korean men free of cardiovascular disease who underwent CAC score (CACS) by multislice computed tomography (CT) and abdominal CT as part of a routine medical examination. VAT area was measured at the level of the umbilicus using CT. Results: Mean BMI, WC, total adipose tissue and VAT area were higher in subjects with moderate-to-severe CAC (CACS>100) compared to subjects with CACS≤100. The subjects in the fourth quartile of VAT had significantly higher CACS and the greater prevalence of CAC presence and moderate-to-severe CAC than those in the first to third quartiles. The highest quartiles of BMI, WC and VAT area were significantly associated with moderate-to-severe CAC in the age- and CVD risk factor-adjusted model (OR [95% CI]=1.56 [1.11–2.19], 1.56 [1.12–2.18] and 1.42 [1.01–1.98] with p <0.05 for all, respectively). Conclusion: The higher levels of general and central measure of obesity and the amount of abdominal visceral fat were related to moderate-to-severe CAC in asymptomatic Korean men with relatively low risk. [Copyright &y& Elsevier]

We aimed to investigate the association between metabolic syndrome (MetS) and coronary artery calcium (CAC) progression in statin-naïve young adults. From the KOrea Initiatives on Coronary Artery calcification registry, we included asymptomatic young adults aged 20–45 years who underwent serial CAC scans for routine health check-ups. The primary endpoint was CAC progression. We estimated the risk of CAC progression based on the presence and burden of MetS. Among participants with MetS, the temporal relationship between changes in metabolic burden and CAC progression was evaluated. Of 2151 young adults (mean age 41.3 ± 3.8 years; male 85.4%), 488 (22.7%) had MetS. The mean CAC score was 10.8 and 81.3% of them had a CAC score of zero at baseline. During follow-up (median, 2.1 years), CAC progression was observed in 325 (15.1%) adults. MetS was associated with an approximately 1.8-fold increased risk of CAC progression (adjusted hazard ratio [aHR] 1.83, p < 0.001). The risk of CAC progression was directly proportional to the metabolic burden. Elevated blood pressure and elevated triglyceride levels were independent components related to CAC progression, with the strongest contribution being made by elevated blood pressure (aHR 2.00, p < 0.001). A reduction in at least two metabolic burdens was associated with a halved risk of CAC progression in young adults having MetS (odds ratio 0.41, p = 0.018). In statin-naïve young adults, the metabolic burden was associated with a risk of CAC progression in a dose-dependent manner. Improvement in metabolic imbalance may have a preventive effect on CAC progression. [Display omitted] • The presence of metabolic syndrome (MetS) increased the risk of coronary artery calcification (CAC) progression with approximately 1.83-fold, and the risk of CAC progression was directly proportional to the metabolic burden. • Among the metabolic components, elevated blood pressure and triglycerides level independently contributed to CAC progression. • A significant reduction in metabolic burdens was associated with a halved risk of CAC progression in young adults having MetS, suggesting optimization of cardiovascular profiles in early adulthood might play a preventive role for CAC progression. [ABSTRACT FROM AUTHOR]

Objective Colorectal adenoma and coronary atherosclerosis have similar risk factors. The aim of this study was to investigate the association between colorectal adenoma and coronary artery calcification (CAC), which is used as a surrogate marker for coronary atherosclerosis. Methods This is a cross-sectional study of 398 Koreans (290 males, mean age of 56.8 ± 8.1 years) who underwent CAC scoring by multi-slice computed tomography and colonoscopy on the same day as the screening examination. The CAC scores were divided into the following three categories according to severity: absent (CAC score = 0), mild (0 < CAC score ≤ 100), and moderate-to-severe CAC (CAC score > 100). Results Colorectal adenoma was detected in 149 (37.4%) subjects and was significantly associated with a CAC score of >0 (OR = 1.66, 95% CI = 1.05–2.64, P = 0.032), including both mild (OR = 1.80, 95% CI = 1.06–3.03, P = 0.029) and moderate-to-severe CAC (OR = 1.95, 95% CI = 1.05–3.63, P = 0.035), in multivariate analysis after adjusting for age, gender and other risk factors. The proportion of subjects with colorectal adenoma and advanced adenoma progressively increased with increasing CAC score (colorectal adenoma 28.9%–54.1%, P for trend < 0.001; advanced adenoma 7.0%–16.4%, P for trend = 0.026). Conclusion Colorectal adenoma is related to coronary artery calcification independent of traditional risk factors for asymptomatic Koreans. The prevalence of advanced adenoma is more common in individuals with severe coronary atherosclerosis. [ABSTRACT FROM AUTHOR]

Introduction: Patients with renal impairment are considered a coronary artery disease (CAD) equivalent. Repeated coronary artery calcium (CAC) scoring has been recognized as a robust tool for tracking progression of atherosclerosis. Further, CAC progression is an important marker of future adverse event. However, the evidence for an independent association of renal function with CAC progression remains unclear. Hypothesis: To examine the cross-sectional association between renal function and CAC progression. Methods: From a 6-center, single ethnicity observational registry, a total of 10,033 asymptomatic adults (mean age: 51.1±8.5 years, 84.9% men) without prior history of CAD and stroke underwent 2 examinations, including CAC screening as part of a broader health study with an average of 3.3±1.9 years between baseline scan and follow-up scan. Estimated glomerular filtration rate (eGFR; mL/min/1.73 m2) was ascertained using the modified MDRD formula, and was categorized as: ≥90 (normal), 60-89 (mildly decreased), and <60 (moderate-to-severely decreased) based on current guidelines. CAC progression was calculated as the difference between the square root of baseline and square root of follow-up CAC score ≥2.5. Results: During an 8.7-year follow-up (IQR, 6.4-10.6 years), CAC progression was found in 766 subjects (7.6%). The patients with more impaired renal function were older, likely to be women and higher prevalence of hypertension, diabetes mellitus, and dyslipidemia. Among patients with normal or mildly decreased renal function, no difference of the proportion was found according to the presence or absence of CAC progression. Yet, patients with moderate-to-severely decreased renal function of eGFR <60 had higher prevalence of CAC progression (7.3% vs. 4.5%) (Figure). Notably, multivariate logistic regression model revealed that impaired renal function was associated with the progression of CAC (Odds ratio [OR]: 1.11, 95% confidence interval [CI]: 1.00-1.33 for eGFR 60-89 and OR: 1.80, 95% CI: 1.31-2.42 for eGFR <60). Conclusions: Impaired renal function evoked a strong relationship with a higher risk of the progression of subclinical atherosclerosis as measured by CAC scoring. [ABSTRACT FROM AUTHOR]