Development Of Coronary Artery Calcification Research Articles

Alterations in the autonomic and haemodynamic response to prolonged high-intensity endurance exercise in individuals with coronary artery calcification.

Endurance exercise is associated with increased life duration and improved life quality. Paradoxically, high exercise intensity is also associated with increased coronary artery calcification (CAC) and a small but significant increased risk of adverse cardiac events during exercise. The mechanisms underlying the development of CAC during prolonged high-intensity endurance exercise are unknown. This study aims to determine if there are differences in cardiovascular haemodynamic measures and heart rate variability (HRV) in individuals with (CAC+) and without CAC (CAC-). Hemodynamic measures from 56 healthy, middle-aged (median [interquartile range] 51 [43-58] years) individuals (41 men/15 women) participating in a 91km [251.2 [217.2-271.6] min] leisure sport mountain bike race were included in this study. Twenty-five participants (20 men/5 women) were classified as CAC+ based on coronary computed tomographic assessment. Haemodynamic measures and HRV were quantified at the top of the hardest hill (THH) during the last quarter of the race. At the top of THH, CAC+ individuals had significantly higher systolic blood pressure (SBP) (235 [225-245] mmHg vs. 220 [193-238] mmHg, P=0.008), higher diastolic blood pressure (DBP) (105 [95-110] mmHg vs. 95 [85-110] mmHg, P=0.006), higher pulse pressure (130 [125-140] mmHg vs. 123 [110-130] mmHg, P=0.039), higher mean rate pressure product (33,882 [30,872-35,053] bpm × mmHg vs. 31,028 [27,392-33,047] bpm × mmHg, P=0.028), and larger increase in DBP from baseline (20 [20-30] mmHg vs. 10 [0-20] mmHg, P=0.001), compared with CAC- individuals. Further, CAC+ participants showed a significant reduction in the low-frequency component of HRV (HRVLF) (6.3 [2.4-11.5] ms2 vs. 12.4 [6.8-20.2] ms2, P=0.044). In multivariable analysis, HRVLF was an independent predictor of the presence of CAC even after adjusting for established risk factors of atherosclerosis: age, sex, body mass index, maximum heart rate, , smoking, resting SBP and resting DBP. CAC+ individuals had significant alterations in haemodynamic measures and HRVLF following prolonged high-intensity endurance exercise compared with individuals without CAC. HRVLF was an independent predictor of CAC, suggesting an adverse autonomic response to high-intensity endurance exercise in individuals with CAC.

Coronary Artery Calcium Scores After Prophylactic Premenopausal Bilateral Salpingo-Oophorectomy.

Premenopausal risk-reducing salpingo-oophorectomy (RRSO) in women at high familial risk ofovarian cancer leads to immediate menopause. Although early natural menopause is associated with increasedcardiovascular disease risk, evidence on long-term cardiovascular disease risk after early surgical menopause is scarce. We sought to determine the long-term influence of the timing of RRSO on the development of coronary artery calcium (CAC), an established marker for cardiovascular disease risk. We conducted a cross-sectional study (N=733) nested in a nationwide cohort of women at high familial risk of ovarian cancer. In women aged 60-70 years (n=328), we compared CAC scores between women with a premenopausal RRSO (age ≤45 years) and women with a postmenopausal RRSO (age≥54 years), using multivariable Poisson analyses. Within the premenopausal RRSO group (n=498), we also examined the effect of age at RRSO. In addition, we compared the premenopausal RRSO group with an external reference cohort (n=5,226). Multivariable analyses showed that the prevalence rates of any CAC (CAC >0), at least moderate CAC (CAC >100), and severe CAC (CAC >400) were comparable between the premenopausal and postmenopausal RRSO groups (relative risk [RR]: 0.93; 95% CI: 0.75-1.15 for any CAC; RR: 0.71; 95% CI: 0.43-1.17 for at least moderate CAC; RR: 0.81; 95% CI: 0.30-2.13 for severe CAC). There was no difference in CAC between the premenopausal RRSO group and a similar aged reference cohort. Timing of premenopausal RRSO (early premenopausal RRSO [<41 years] vs late premenopausal RRSO [41-45 years]) did not affect the outcomes. Our results do not show a long-term adverse effect of surgical menopause on the development of CAC.

Prevalence of coronary artery calcification in patients with end-stage renal disease undergoing dialysis and the association of various risk factors with the development of coronary artery calcification in this patient population

Background: Patients with end-stage renal disease (ESRD) on dialysis exhibit a significantly higher risk of coronary artery calcification (CAC) than age-matched normal individuals, contributing to elevated cardiovascular morbidity and mortality. Aims and Objectives: This study designed to assess the prevalence of CAC in ESRD patients on dialysis and identify associated risk factors. Materials and Methods: Fifty ESRD patients undergoing maintenance dialysis and twenty normal subjects were included in this cross-sectional observational study. Serum calcium, phosphate, and parathyroid hormone were measured in all ESRD patients and normal controls. Multi Row Spiral Computed Tomography was performed to determine CAC scoring (CACS). Results: CACS was significantly higher in ESRD patients compared to normal subjects (mean CACS: 91.4±32.7 vs. 7.75±9.5 Agatston units, P&lt;0.05). Elevated levels of calcium phosphate products, serum leptin, intact parathyroid hormone (iPTH), presence of diabetes mellitus, and longer duration of dialysis were correlated with increased incidence of CACS in ESRD patients, as indicated by higher odd’s ratios ranged from 1.10 to 6.93. Conclusion: CAC is highly prevalent in ESRD patients on dialysis, emphasizing the need for stringent risk factor management. Our findings suggest that controlling calcium phosphate product, serum leptin, age, iPTH levels, and duration of dialysis may reduce CAC burden in this population, potentially mitigating cardiovascular risk and improving outcomes.

Prevalence of coronary artery calcification in patients with end-stage renal disease undergoing dialysis and the association of various risk factors with the development of coronary artery calcification in this patient population

Background: Patients with end-stage renal disease (ESRD) on dialysis exhibit a significantly higher risk of coronary artery calcification (CAC) than age-matched normal individuals, contributing to elevated cardiovascular morbidity and mortality. Aims and Objectives: This study designed to assess the prevalence of CAC in ESRD patients on dialysis and identify associated risk factors. Materials and Methods: Fifty ESRD patients undergoing maintenance dialysis and twenty normal subjects were included in this cross-sectional observational study. Serum calcium, phosphate, and parathyroid hormone were measured in all ESRD patients and normal controls. Multi Row Spiral Computed Tomography was performed to determine CAC scoring (CACS). Results: CACS was significantly higher in ESRD patients compared to normal subjects (mean CACS: 91.4±32.7 vs. 7.75±9.5 Agatston units, P&lt;0.05). Elevated levels of calcium phosphate products, serum leptin, intact parathyroid hormone (iPTH), presence of diabetes mellitus, and longer duration of dialysis were correlated with increased incidence of CACS in ESRD patients, as indicated by higher odd’s ratios ranged from 1.10 to 6.93. Conclusion: CAC is highly prevalent in ESRD patients on dialysis, emphasizing the need for stringent risk factor management. Our findings suggest that controlling calcium phosphate product, serum leptin, age, iPTH levels, and duration of dialysis may reduce CAC burden in this population, potentially mitigating cardiovascular risk and improving outcomes.

The Risk of Coronary Artery Calcification according to Different Lipid Parameters and Average Lipid Parameters

We compared the association between the baseline and average lipid parameters over time and the coronary artery calcification (CAC) risk. Participants who underwent annual (biannual) health examinations and coronary artery computed tomography to measure CAC at least twice between March 2010 and December 2019, with a baseline CAC of 0, were included. The levels of apolipoprotein B (ApoB), Apolipoprotein A-I (ApoA1), ApoB/ApoA1, non-high-density lipoprotein cholesterol (non-HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglycerides (TG), TG/HDL-C, and TC/HDL-C were measured or calculated. The remnant cholesterol (RC) levels were calculated. The average lipid parameters before study entry were calculated using data from 2002 to 2010. The participants were divided into quartiles (Q) according to the parameter values. Cox proportional hazard modeling, adjusted for confounding factors, compared the CAC risk of the highest quartile to the lowest quartile. Among 29,278 participants (mean age, 39.19±5.21; men, 88.27%), 2,779 developed CAC ＞0. The highest quartile of ApoB showed a numerically strong association with CAC risk, compared with the lowest quartile of ApoB (Q1: reference; Q2: HR,1.41, 95% CI,1.25-1.59; Q3: HR,1.97, 95% CI,1.75-2.21; Q4: HR,2.72, 95% CI,2.41-3.07). RC showed a modest association with CAC risk (Q1: reference; Q2: HR,1.13, 95% CI,0.99-1.28; Q3: HR,1.3, 95% CI,1.15-1.47; Q4: HR,1.7, 95% CI,1.51-1.91). The strength of the association was comparable between the parameters at baseline and the average lipid parameters over time. A high ApoB level showed a strong association with CAC risk compared with the lowest ApoB quartile. The baseline lipid parameters can predict CAC development as effectively as the average of multiple measurements can.

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

The relationship between coronary artery calcification and bone metabolic markers in maintenance hemodialysis patients

BackgroundTo study the influencing factors for coronary artery calcification (CAC) in maintenance hemodialysis (MHD) patients and the relationship between CAC and bone metabolism markers and to attempt to find a reliable marker linking vascular calcification and bone metabolism in MHD patients.MethodsA total of 123 patients were enrolled. CAC was assessed by multislice spiral computed tomography (MSCT), and the CAC score (CACS) was evaluated using the Agaston method. Routine laboratory parameters, including triglycerides (TG), total cholesterol (TC), glucose (Glu), calcium (Ca), phosphorus (P), magnesium (Mg), etc., were measured. Serum markers of bone metabolism, such as alkaline phosphatase(ALP), calcitonin (CT), 25-hydroxy vitamin D [25-(OH)D], intact parathyroid hormone (iPTH), total type I procollagen amino-terminal peptide (tPINP), N-terminal mid-fragment of osteocalcin (N-MID OC), and β-type I collagen crosslinked carboxyl-terminal peptide (β-CTX), were also measured.ResultsAmong 123 MHD patients, 37 patients (30.08%) did not have CAC, and 86 patients (69.92%) had CAC, including 41 patients (47.67%) with mild calcification and 45 patients (52.33%) with moderate to severe calcification. Age, Body Mass Index(BMI), the prevalence of hypertension and diabetes mellitus, TC, Glu, P, and Ca×P in the calcification group were higher than those in the noncalcification group, whereas Mg, iPTH, tPINP, N-MID OC, and β-CTX were lower than those in the noncalcified group (P < 0.05). Compared with the mild calcification group (0<CACS<400), P and Ca×P levels were higher in the moderate to severe calcification group (CACS ≥ 400), and ALP, iPTH, N-MID OC, tPINP, and β-CTX concentrations were lower (P < 0.05). Correlation analysis showed that the CACS was positively correlated with TC, LDL-C, P, and Ca×P (P < 0.05) and negatively correlated with N-MID OC and β-CTX (P < 0.05). There was no significant correlation between the CACS and other parameters (P > 0.05). A logistic regression model was used to evaluate the influencing factors for CAC. The results showed that age, BMI, TC, Glu, P, and Ca×P were risk factors for CAC and its severity in MHD patients, whereas diabetes mellitus, Mg, and N-MID OC were protective factors for CAC in MHD patients. In addition, N-MID OC was a protective factor for the severity of CAC. After adjusting for the corresponding confounding factors, the results of the risk factors were consistent, and N-MID OC was still an independent protective factor for CAC and its severity.ConclusionsElevated serum P and Ca×P were independent risk factors for CAC in MHD patients, and serum Mg may be an independent protective factor for CAC. CAC was closely related to abnormal bone metabolism and bone metabolic markers in MHD patients. Relatively low bone turnover can promote the occurrence and development of CAC. N-MID OC may be a reliable bone metabolic marker linking vascular calcification and bone metabolism in MHD patients.

Association of apolipoproteins C-I and C-II truncations with coronary heart disease and progression of coronary artery calcium: Multi-Ethnic Study of Atherosclerosis

Higher truncated-to-native proteoform ratios of apolipoproteins (apo) C-I (C-I'/C-I) and C-II (C-II'/C-II) are associated with less atherogenic lipid profiles. We examined prospective relationships of C-I'/C-II and C-II'/C-II with coronary heart disease (CHD) and coronary artery calcium (CAC). ApoC-I and apoC-II proteoforms were measured by mass spectrometry immunoassay in 5790 MESA baseline plasma samples. CHD events (myocardial infarction, resuscitated cardiac arrest, fatal CHD, n=434) were evaluated for up to 17 years. CAC was measured 1-4 times over 10 years for incident CAC (if baseline CAC=0), and changes (follow-up adjusted for baseline) in CAC score and density (if baseline CAC>0). C-II'/C-II was inversely associated with CHD (n=434 events) after adjusting for non-lipid cardiovascular risk factors (Hazard ratio: 0.89 [95% CI: 0.81-0.98] per SD), however, the association was attenuated after further adjustment for HDL levels (0.93 [0.83-1.03]). There was no association between C-I'/C-I and CHD (0.98 [0.88-1.08]). C-II'/C-II was positively associated with changes in CAC score (3.4% [95%CI: 0.6, 6.3]) and density (6.3% [0.3, 4.2]), while C-I'/C-I was inversely associated with incident CAC (Risk ratio: 0.89 [95% CI: 0.81, 0.98]) in fully adjusted models that included plasma lipids. Total apoC-I and apoC-II concentrations were not associated with CHD, incident CAC or change in CAC score. Increased apoC-II truncation was associated with reduced CHD, possibly explained by differences in lipid metabolism. Increased apoC-I and apoC-II truncations were also associated with less CAC progression and/or development of denser coronary plaques.

Regression of Nonalcoholic Fatty Liver Disease Reduces the Development of Coronary Artery Calcification: A Longitudinal Cohort Study

Regression of Nonalcoholic Fatty Liver Disease Reduces the Development of Coronary Artery Calcification: A Longitudinal Cohort Study

The influence of rivaroxaban compared to vitamin K antagonist treatment upon development of cardiovascular calcification the IRIVASC-trial

Abstract Vitamin K antagonists (VKA) such as warfarin or phenprocoumon are the mainstay of therapy for patients with several specific indications for long-term oral anticoagulant therapy (OAT). Due to interferences with Matrix-Gla protein, an important vitamin K-dependent local calcification inhibitor in cardiovascular structures, VKAs are theoretically linked to the development of increased cardiovascular calcification (CVC). The IRIVASC trial was a multi-center, prospective, controlled, open, randomized, interventional clinical trial and included 192 patients with atrial fibrillation or pulmonary embolism and an indication for oral anticoagulation &amp;gt;12 months. In short, patients with an indication for OAT were randomized to receive either Rivaroxaban (n=96) or VKA (n=96) and followed up over 12 months. MultiSlice CT (MSCT) was performed at baseline and after 12-month follow up. The primary endpoint of the study was the progression of coronary artery and aortic valve (AV) calcification, as determined by MSCT (volume score). Baseline demographic and laboratory values were comparable between the VKA and the Rivaroxaban groups (median age 72 vs 68, 73.6 vs 69.9 male). The main indication for anticoagulation was AF (95.4% vs 96.6%) After 12-month follow-up complete data sets were available for 164 patients (86%) for coronary calcification and 67 patients for valvular calcification (per protocol analysis). Overall, we found no differences in the primary endpoints. Development of coronary artery calcification was similar within the 2 groups as evidenced by similar developments of the coronary agatston score (804.8±1062.3 vs 946.7±1024.4, p=0.38), the coronary volume score (571.9±855.6 ml vs 791.7±820.1 ml, p=0.359) and the coronary mass score (143.2±195.9 mg vs. 172.2±190.8 mg, p=0.335) after 12 month. Similarly, there was no difference in the development of aortic valve calcification (AV) (AV Agatston score 441.6±711.9 vs. 352.6±751.2, p=0.621. AV volume score 388.2±589.0 ml vs 354.3±654.3, ml p=0.824 and AV Mass Score 75.7±135.1 mg vs 60.2±122.9, p=0.626 mg) (Table 1). To our knowledge this is the first multicenter prospective, randomized trial to ever investigate the effects of VKA vs rivaroxaban treatment regarding the development of coronary and valvular calcification. Our findings are clinically relevant as VKA will remain the mainstay of treatment for several conditions including mechanical valve replacement or antiphospholipid syndrome and hence include patients at cardiovascular risk. Our data point towards a comparable risk of overt CVC progression as detectable by CT-scans in patients irrespective of VKA or NOAK treatment. Funding Acknowledgement Type of funding sources: Private company. Main funding source(s): BAYER GmBH

Macronutrient intake is not associated with cardiovascular risk assessed by Coronary Calcium Score, but dietary fiber showed a significantly inverse relationship

Evidence of impact of dietary factors on development of coronary artery calcification remains uncertain. The objective of the study was to evaluate the association between the intake carbohydrates, proteins, total fats, saturated fatty acids (SFA), monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), trans fatty acids (TFA) cholesterol and fiber with cardiovascular risk. Cross-sectional analysis from 181 dyslipidemic patients. The Coronary Calcium Score (CCS) was used to measure cardiovascular risk. 24-hour recalls were applied and the Multiple Source Method was used to adjust dietary variability. The mean values of the cardiovascular risk categories were compared by analysis of variance, using ANOVA and Kruskal-Wallis. Tukey's post-test was used for multiple analyzes. Simple and multiple binary logistic regression, was used as a measure of association between nutrient intake and cardiovascular risk. Age, male gender, comorbidities and drug treatment were significantly prevalent in those with CCS&gt;100. The average total energy intake was 1315.6 kcal. Total energy and macronutrient intake were higher among men (p &lt; 0.05). No significant results were found regarding the association between cardiovascular risk and macronutrient intake. Fiber intake was inversely associated with cardiovascular risk, regardless of confusion factors (OR:0.918; 95% CI:0.845-0.999; p=0.047). The resultes that there was no association between nutrientes analyzed to cardiovascular risk assessed by CCS. However, the increase of dietary fiber intake in 1 g/day has been shown to reduce the of future cardiovascular events in 8.2% among individuals in the highest risk category. Therefore, we strongly recommend that fiber intake be encouraged.

Abstract 466: Fhl5 Enhances Vascular Calcification By Regulating Smooth Muscle Cell Transcriptional Networks

Coronary artery calcium (CAC) is a hallmark of coronary artery disease (CAD) with increased CAC levels associated with increased risk for CAD related morbidity and mortality. The development of CAC is a pathological process driven by the modulation of smooth muscle cells (SMCs) and maladaptive extracellular matrix remodeling. In the most recent multi-ancestry meta-analysis of more than 35,000 individuals, FHL5 (Four-and-a-half LIM domains 5) was prioritized as a novel CAC gene through Bayesian colocalization and epigenomic analyses. scRNA-seq studies of human coronary and carotid arteries revealed high enrichment of FHL5 gene expression in SMC and pericyte populations. These preliminary studies motivate our hypothesis that FHL5 functions as a transcriptional regulator of vascular remodeling pathways associated with increased CAC risk. Following treatment of SMCs with a calcifying cocktail, stable FHL5 overexpression promoted the osteogenic SMC phenotypic transition, characterized by increased levels of osteogenic activators and reduced expression of SMC contractile markers. This osteogenic gene signature correlated with increased SMC calcification, consistent with the direction of effect of the CAC risk allele. To provide insights into the transcriptional program regulated by FHL5 that contributes to the vascular calcification phenotype, we mapped FHL5 binding sites in SMCs using the CUT&amp;RUN method. We identified 17,201 FHL5 binding sites that overlapped the active enhancer mark H3K27ac. FHL5 target genes were enriched in pathways linked to vascular remodeling, such as cell adhesion and extracellular matrix organization. Moreover, risk variants for pulse pressure, a metric of arterial stiffness that is highly correlated with CAC, was enriched in FHL5 binding sites. Lastly, integration with FHL5 trans-eQTL target genes in STARNET arterial tissues revealed a network of CAD-associated candidate genes regulated by FHL5 in vitro and in vivo that impact SMC proliferation, migration, and calcification. Taken together, we provide evidence that FHL5 regulates a network of genes linked to arterial stiffness, which may explain the underlying mechanism of its genetic association with CAC in individuals from the general population.

Abstract 11099: Treml4 , Snps and Regulatory Mirnas in the Diagnosis of Subclinical Atherosclerosis

Considering the multifactorial nature of the development of coronary artery calcificatioN (CAD), and the difficulty in making its early diagnosis, this study sought to investigate the role of the TREML4 in the development of atherosclerotic lesions by genotyping of two main variants associated with this gene (rs2803495 and rs2803496), mRNA expression and identification of its regulatory miRNAs. 329 patients with Subclinical atherosclerosis (AS) were recruited. The results with AS patients stratified according to the Duke score demonstrated an association of the Duke score with increased expression of mRNA of the TREML4 in peripheral blood leukocytes (OR. = 3.173, 95% CI = 1.29-7, 78, p = 0.012). Furthermore, genotyping revealed that the SNP genotype combination rs2803495 (AG + GG) (OR = 9,007, 95% CI = 4.1-19.8, p &lt;0.001) and rs2803496 (CT + CC) ( OR = 11.1, 95% CI = 4.8-25.4, p = 0.011), favor the expression of TREML4 mRNA. Patients with AS and carriers of the SNP G alleles rs2803495 (AG + GG) (OR = 13.31, 95% CI = 5, 79-30.61, p &lt;0.001) and C allele rs2803496 (CT + CC) (OR = 18.99, 95% CI = 7.60-47.44, p &lt;0.001) are more likely to express TREML4 . Once again, the C allele was associated with higher levels of mRNA expression (OR = 3.98, 95% CI = 1.67-9.48, p = 0.002). The rs2803495 (AG + GG) and rs2803496 (CT + CC) variants were not related to the development of type 2 Diabetes Mellitus (DM2; p&gt; 0.05). However, patients who express TREML4 and are DM2 have higher levels of expression of TREML4 when compared to the control group (OR = 2.6, 95% CI = 1.19-5.72, p &lt;0.001). Patients with DM2 and rs2803495 (AG + GG) genotypes are more likely to express TREML4 (OR = 20.77, 95% CI = 2.29-188.41, p = 0.007). In silico analyzes showed that 8 miRNAs (hsa-miR-181a-5p, hsa-miR-200b-3p, hsa-miR-24-3p, hsa-miR-296-5p, hsa-miR-361-5p, hsa-miR- 423-5p, hsa-miR-486-3p and hsa-miR-708-5p) are expected to interact with TREML4 mRNA.The results suggest that mRNA expression of the TREML4 is associated with the presence of SNPs and increased in patients with AS with DM2 and that miRNAs may be involved in the regulation of the TREML4 being directly or indirectly involved in the pathophysiology of CVD being potential circulating biomarkers for early detection and/or individualized treatment of AS and CAD.

Traditional and novel cardiometabolic risk markers across strata of body mass index in young adults.

BackgroundCardiometabolic risk increases with increasing body mass index (BMI). The exact mechanism is poorly understood, and traditional risk assessment of young adults with obesity has shown to be ineffective. Greater knowledge about potential new effective biomarkers and the use of advanced cardiac imaging for risk assessment in young adults is, therefore, necessary.ObjectiveThis study aims to explore traditional and novel cardiometabolic risk markers across strata of BMI in young adults.MethodsParticipants (N = 264, 50% women, age 28–30 years) were invited from an ongoing cohort study, based on BMI and sex. BMI‐strata were: BMI <25, 25–30, >30 kg/m2, representing normal weight (NW), overweight (OW), and obesity (OB). Participants underwent cardiac computed tomography to detect coronary artery calcification, measures of body composition, blood pressure measurements, and a comprehensive panel of circulating cardiometabolic risk markers.ResultsNo significant coronary artery calcifications were detected in this study. Minor differences in median levels of traditional risk markers were detected across BMI‐strata, for example, total cholesterol (men‐ NW: 4.7 (4.3–5.1) and OB: 4.8 (4.2–5.6) mmol/L, p = 0.58; women‐ NW: 4.3 (3.9–4.8) and OB: 4.7 (4.2–5.3) mmol/L, p = 0.016), whereas substantial differences were seen in markers of inflammation and glucose metabolism, for example, high sensitive CRP (men‐ NW: 0.6 (0.3–1.1) and OB: 2.8 (1.5–4.0) mg/L, p < 0.001; women‐ NW: 0.7 (0.3–1.7) and OB: 4.0 (2.2–7.8) mg/L, p < 0.001) and insulin (men‐ NW: 47.0 (35.0–59.0) and OB: 113.5 (72.0–151.0) pmol/L, p < 0.001; women‐ NW: 44.0 (35.0–60.0) and OB: 84.5 (60.0–126.0) pmol/L, p < 0.001).ConclusionIn young adults, obesity is associated with an early onset insulin resistance and inflammatory response prior to development of coronary artery calcification and deterioration of lipid profiles.

Mitochondria and traffic-related air pollution linked coronary artery calcification: exploring the missing link.

The continuing increase in the exposure to Traffic-related air pollution (TRAP) in the general population is predicted to result in a higher incidence of non-communicable diseases like cardiovascular disease. The chronic exposure of air particulate matter from TRAP upon the vascular system leads to the enhancement of deposition of calcium in the vasculature leading to coronary artery calcification (CAC), triggered by inflammatory reactions and endothelial dysfunction. This calcification forms within the intimal and medial layers of vasculature and the underlying mechanism that connects the trigger from TRAP is not well explored. Several local and systemic factors participate in this active process including inflammatory response, hyperlipidemia, presence of self-programmed death bodies and high calcium-phosphate concentrations. These factors along with the loss of molecules that inhibit calcification and circulating nucleation complexes influence the development of calcification in the vasculature. The loss of defense to prevent osteogenic transition linked to micro organelle dysfunction that includes deteriorated mitochondria, elevated mitochondrial oxidative stress, and defective mitophagy. In this review, we examine the contributory role of mitochondria involved in the mechanism of TRAP linked CAC development. Further we examine whether TRAP is an inducer or trigger for the enhanced progression of CAC.

Presepsin Level Correlates with the Development of Moderate Coronary Artery Calcifications in Hemodialysis Patients: A Preliminary Cross-Section Design Study.

PurposeEnd-stage renal disease patients have a high mortality rate linked to cardiovascular complications, and one of these complications is vascular calcification. This study was performed to test if presepsin, an inflammatory marker, is a predictor of coronary artery calcification (CAC) in hemodialysis (HD) patients.Patients and MethodsThis study was a cross-sectional design involving 48 HD patients and 13 control subjects. Coronary artery calcification score (CACs) was evaluated by a high resolution, ECG synchronized computed tomography of the heart using a CT calcium scoring. Presepsin and other laboratory analyses were performed on blood samples drawn before HD.ResultsPresepsin levels in HD patients were 14 times higher than healthy controls (P<0.01). Also, all laboratory tests except for vitamin D were significantly different than controls. Presepsin, phosphorus levels, and calcium-phosphate product were positively correlated with increasing CACs within groups of zero to moderate calcifications (p<0.05, R=0.459 and <0.01, R=0.591, respectively). These correlations were not seen with eGFR, PTH, calcium, vitamin D, CRP, or ESR levels. Furthermore, the log-transformed data of presepsin correlated with 1–15 months of HD vintage (p<0.05, R=0.482), whereas CACs data correlated with 1–20 months of HD vintage (p<0.05, R=0.425).ConclusionAlthough this study is preliminary and has a limited number of patients, it shows that presepsin, as an inflammatory marker, correlates with the development of moderate CAC in HD patients and may predict CAC development. Therefore, measuring presepsin and managing inflammation before and during the early phases of HD may lower coronary calcification development. However, more clinical studies in this direction are essential.

Gender-based Differences In The Contribution Of Traditional Cardiovascular Risk Factors To The Development Of Coronary Artery Calcification

Introduction: Gender has been shown to be an independent predictor for the development of coronary atherosclerosis. Despite increased interest in the pathophysiology of CAD in women, there is limited data on how traditional atherosclerotic risk factors affect calcification development differently based upon gender, especially in symptomatic patients.

Association of psychosocial traits with coronary artery calcium development and progression: The Multi-Ethnic Study of Atherosclerosis

Coronary artery calcium (CAC) is a well-established quantifiable risk factor for cardiovascular disease (CVD). We examined the association of anger, hostility, anxiety, and depression with the development and progression of CAC. We studied the association of these psychosocial traits with CAC among participants in the Multi-Ethnic Study of Atherosclerosis (MESA). Anger was measured using the Spielberger Trait Anger questionnaire, hostility using a modified Cook-Medley Hostility questionnaire, anxiety using the Spielberger Trait Scale, and depression using the Center for Epidemiological Studies Depression Scale (CES-D). Among the subsample of participants with CAC=0at the beginning of the study period, Poisson regression models were used to determine the relative risk of developing CAC>0 over the study period. In the subsample that developed CAC>0, we used linear regression models to estimate the average increase in CAC associated with a unit increase in psychosocial trait. Median time of follow-up was 9.4 years (range 8.0-11.4 years). Cross-sectional analyses at baseline revealed no association of any of the psychosocial traits with the presence or magnitude of CAC (anger: RR 0.98, p<0.01; hostility: RR 1.01, p=0.25; anxiety: RR 0.99, p<0.01; depression: RR 0.99, p<0.01 [not statistically significant after adjustment for covariates]). No association was detected between the traits and development of CAC (anger: RR 0.99, p=0.23; hostility: RR 1.01, p=0.68, anxiety: RR 1.00, p=0.49; depression: RR 1.00, p=0.51). We also found no association between any of the traits and progression of CAC (anger: beta -3.21, p=0.08; hostility: beta 2.28, p=0.43; anxiety: 3.45, p=0.02 [not statistically significant after adjustment for covariates]; depression: beta -1.46, p=0.11). We found no association between anger, hostility, anxiety, or depression and CAC, suggesting these personality traits are not independent risk factors for CVD.

Heart dose and coronary artery calcification in patients receiving thoracic irradiation for lung cancer.

BackgroundThoracic irradiation (TIR) is associated with an increased risk of coronary artery disease (CAD) and coronary-related death. Lung cancer patients receive considerable doses of TIR, making them a high-risk population that may benefit from post-therapy surveillance. Coronary artery calcium (CAC) is a known biomarker of CAD development and may serve as a useful indicator of disease progression in this population. We hypothesized greater CAC progression in lung cancer patients subjected to higher whole heart radiation doses.MethodsCAC progression (pre- and >2 years post-TIR) from chest CT scans of lung cancer patients were evaluated. A 2:1 matched control population was established controlling for age, gender, race, and CT scan interval. Vessel-specific CAC presence, progression, and extension in pre- and post-interval CT studies was evaluated by two blinded reviewers using the ordinal method. Dosimetric treatment files were restored and contours of the whole heart and proximal left anterior descending artery (LAD) were created within existing plans to compute radiation doses (Pinnacle Treatment Planning Software). Binary logistic regression analysis identified factors predictive for CAC development. Multiple logistic regression analysis with hierarchal method was used to assess covariates.ResultsThirty-five patients and 65 controls (50% female) were evaluated; mean age 57 years, mean follow-up post-radiation 4.9±2.2 years. Average mean and maximum left anterior descending coronary artery (LAD) radiation doses were 19.9 Gy (95% CI, 14.1–25.7) and 30.7 Gy (95% CI, 23.8–37.5), respectively; 91.6% inter-observer variability. There was greater incidence of coronary calcification in irradiated patients (48.6% vs. 24.6%; P=0.01). In interval CT scans, a greater proportion of radiated patients demonstrated new coronary calcification (P=0.007) and extension within the LAD (P=0.003). Radiation exposure was the only independent predictor of new calcification (OR 3.1; 95% CI: 1.09–9.2).ConclusionsWe identified both an increase in the development and progression of CAC in lung cancer patients receiving TIR. Future studies utilizing alternative cancer populations and larger sample sizes are necessary to further correlate radiographic and dosimetric observations to cardiovascular events.

The association between hyperuricemia and coronary artery calcification development: A systematic review and meta-analysis.

Hyperuricemia coincides with coronary artery calcification (CAC) development, but the role of serum uric acid (SUA) as a risk factor for CAC remains unclear. The objective of this study was to gain an insight into the association between SUA and CAC in adults by performing a meta‐analysis. MEDLINE, EMBASE, the Cochrane Library, and EBSCO (CINAHL) were searched for relevant observational studies published until 2 June 2019. Studies were included only if they reported data on CAC presence (Agatston score > 0) or progression related to hyperuricemia in subclinical adult patients. The pooled estimates of crude and adjusted odds ratios (ORs) and 95% confidence interval (CI) were calculated to evaluate the association between CAC presence or progression and hyperuricemia. A total of 11 studies were identified involving 11 108 adults. The pooled OR based on the frequency of CAC presence showed that patients in the high SUA group had 1.806‐fold risk for developing CAC (95% CI: 1.491‐2.186) under the minimal threshold of hyperuricemia (more than 6 mg/dL or 357 μmoL/L). When SUA levels were analyzed as categorical variables, the pooled estimate of adjusted ORs was 1.48 (95% CI: 1.23‐1.79) for CAC presence. Additionally, for each increase of 1 mg/dL of SUA level, the risk of CAC progression was increased by 31% (95% CI: 1.15‐1.49) with an average follow‐up duration ranged from 4.6 to 6.1 years. Hyperuricemia is closely associated with increased risk of CAC development and CAC progression in asymptomatic patients.