Progression Of Coronary Artery Calcification Research Articles

THU-558 - Impact of visceral adiposity for coronary artery calcification progression in patients with metabolic dysfunction-associated fatty liver disease; multicenter cohort study

THU-558 - Impact of visceral adiposity for coronary artery calcification progression in patients with metabolic dysfunction-associated fatty liver disease; multicenter cohort study

Assessment of Normal Systolic Blood Pressure Maintenance with the Risk of Coronary Artery Calcification Progression in Asymptomatic Metabolically Healthy Korean Adults with Normal Weight, Overweight, and Obesity.

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.

Progression of coronary artery calcification after radiation therapy for esophageal cancer.

Advances in cancer treatment have resulted in increased attention toward potential cardiac complications, especially following treatment for esophageal cancer, which is associated with a risk of coronary artery disease. As the heart is directly irradiated during radiotherapy, coronary artery calcification (CAC) may progress in the short term. Therefore, we aimed to investigate the characteristics of patients with esophageal cancer that predispose them to coronary artery disease, CAC progression on PET-computed tomography and the associated factors, and the impact of CAC progression on clinical outcomes. We retrospectively screened 517 consecutive patients who received radiation therapy for esophageal cancer from our institutional cancer treatment database between May 2007 and August 2019. CAC scores were analyzed clinically for 187 patients who remained by exclusion criteria. A significant increase in the Agatston score was observed in all patients (1 year: P = 0.001*, 2 years: P < 0.001*). Specifically for patients receiving middle-lower chest irradiation (1 year: P = 0.001*, 2 years: P < 0.001*) and those with CAC at baseline (1 year: P = 0.001*, 2 years: P < 0.001*), a significant increase in the Agatston score was observed. There was a trend for a difference in all-cause mortality between patients who had irradiation of the middle-lower chest ( P = 0.053) and those who did not. CAC can progress within 2 years after the initiation of radiotherapy to the middle or lower chest for esophageal cancer, particularly in patients with detectable CAC before radiotherapy initiation.

Lung Function Decline in Young Adulthood and Coronary Artery Calcium Progression in Midlife

BackgroundReduced lung function has been linked to cardiovascular disease, but population-based evidence on the relationship between lung function decline and coronary artery calcium (CAC) progression is rare. MethodsA total of 2694 participants (44.7% men) with a mean ± standard deviation age of 40.4 ± 3.6 years from the Coronary Artery Risk Development in Young Adults (CARDIA) were included. The rates of decline in forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) over a 20-year period were calculated for each participant and categorized into quartiles. The primary outcome was CAC progression. ResultsDuring a mean follow-up of 8.9 years, 455 (16.9%) participants had CAC progression. After adjusting for traditional cardiovascular risk factors, the hazard ratios (95% confidence intervals [CIs]) for CAC progression were higher for participants in the 2nd (Q2), 3rd (Q3), and highest quartiles (Q4) of FVC decline compared with those in the lowest quartile (Q1): 1.366 (1.003-1.861), 1.412 (1.035-1.927), and 1.789 (1.318-2.428), respectively. Similar trends were observed for the association between FEV1 and CAC progression. The association remained robust across a series of sensitivity analyses and all subgroups. ConclusionsA faster decline in FVC or FEV1 during young adulthood is independently associated with an increased risk of CAC progression in midlife. Maintaining optimal lung function during young adulthood may improve future cardiovascular health.

Computational clustering reveals differentiated coronary artery calcium progression at prevalent levels of pulse wave velocity by classifying high-risk patients.

Many studies found that increased arterial stiffness is significantly associated with the presence and progression of Coronary Calcium Score (CCS). However, none so far have used machine learning algorithms to improve their value. Therefore, this study aims to evaluate the association between carotid-femoral Pulse Wave Velocity (cfPWV) and CCS score through computational clustering. We conducted a retrospective cross-sectional study using data from a cardiovascular risk screening program that included 377 participants. We used an unsupervised clustering algorithm using age, weight, height, blood pressure, heart rate, and cfPWV as input variables. Differences between cluster groups were analyzed through Chi-square and T-student tests. The association between (i) cfPWV and age groups, (ii) log (CCS) and age groups, and (iii) cfPWV and log(CCS) were addressed through linear regression analysis. Clusters were labeled post hoc based on cardiovascular risk. A "higher-risk group" had significantly higher left (0.76 vs. 0.70 mm, P < 0.001) and right (0.71 vs. 0.66 mm, P = 0.003) intima-media thickness, CCS (42 vs. 4 Agatston units, P = 0.012), and ascending (3.40 vs. 3.20 cm, P < 0.001) and descending (2.60 vs. 2.37 cm, P < 0.001) aorta diameters. Association with age appeared linear for cfPWV and exponential for log (CCS). The progression of the log (CCS) and cfPWV through age groups was steeper in the "higher-risk group" than in the "lower-risk group". cfPWV strongly correlated with CCS, and CCS progression over cfPWV differed among clusters. This finding could improve PWV as a "gate-keeper" of CCS testing and potentially enhance cardiovascular risk stratification.

Longitudinal Associations of Healthy Dietary Pattern Scores with Coronary Artery Calcification and Pericardial Adiposity in United States Adults with and without Type 1 Diabetes

BackgroundPericardial adipose tissue volume (PAT) and coronary artery calcification (CAC) are prognostic indicators for future cardiovascular events; however, no studies have assessed the long-term associations of adherence to dietary patterns (DPs) with PAT and CAC in adults with and without type 1 diabetes (T1D). ObjectivesWe investigated the longitudinal associations of the Mediterranean Diet (MedDiet) and Dietary Approaches to Stop Hypertension (DASH) diet with PAT and CAC progression in adults with and without T1D. MethodsThe Coronary Artery Calcification in Type 1 Diabetes (CACTI) study is a population-based, prospective study of 652 T1D and 764 nondiabetic mellitus (nonDM) (19–56 y) participants that began in 2000–2002 with follow-up visits in 2003–2004 and 2006–2007. At each visit, food frequency questionnaires were collected and used to develop adherence scores for the MedDiet and DASH diets. PAT and CAC were measured at each visit using electron beam computed tomography. CAC progression was defined as a ≥2.5 mm square root-transformed volume. Mixed effect models were used to conduct statistical analyses. ResultsCombined models found a significant–0.09 cm3 (95% CI: −0.14, −0.03; P = 0.0027) inverse association in PAT for every 1-point increase in the MedDiet score and a significant–0.26 cm3 (95% CI: −0.38, −0.14; P < 0.0001) inverse association in PAT for every 1-point increase in the DASH score. In combined models, the DPs were not significantly associated with lower odds of CAC progression; however, both DPs had significant interactions by diabetes status for CAC. Only the DASH diet was associated with lower odds of CAC progression in the nonDM group (OR: 0.96; 95% CI: 0.93, 0.99; P = 0.0224). ConclusionsThese data suggest that the DPs are associated with lower PAT, which may reduce future cardiovascular events. The DASH diet may be beneficial for lower odds of CAC progression in those without T1D.

Association between triglyceride glucose index and arterial stiffness and coronary artery calcification: a systematic review and exposure-effect meta-analysis

BackgroundThe triglyceride and glucose (TyG) index has been linked to various cardiovascular diseases. However, it's still unclear whether the TyG index is associated with arterial stiffness and coronary artery calcification (CAC).MethodsWe conducted a systematic review and meta-analysis of relevant studies until September 2022 in the PubMed, Cochrane Library, and Embase databases. We used a random-effects model to calculate the pooled effect estimate and the robust error meta-regression method to summarize the exposure-effect relationship.ResultsTwenty-six observational studies involving 87,307 participants were included. In the category analysis, the TyG index was associated with the risk of arterial stiffness (odds ratio [OR]: 1.83; 95% CI 1.55–2.17, I2 = 68%) and CAC (OR: 1.66; 95% CI 1.51–1.82, I2 = 0). The per 1-unit increment in the TyG index was also associated with an increased risk of arterial stiffness (OR: 1.51, 95% CI 1.35–1.69, I2 = 82%) and CAC (OR: 1.73, 95% CI 1.36–2.20, I2 = 51%). Moreover, a higher TyG index was shown to be a risk factor for the progression of CAC (OR = 1.66, 95% CI 1.21–2.27, I2 = 0, in category analysis, OR = 1.47, 95% CI 1.29–1.68, I2 = 41% in continuity analysis). There was a positive nonlinear association between the TyG index and the risk of arterial stiffness (Pnonlinearity < 0.001).ConclusionAn elevated TyG index is associated with an increased risk of arterial stiffness and CAC. Prospective studies are needed to assess causality.Graphical

Metabolically healthy non-alcoholic fatty liver disease and progression of coronary artery calcification: A 15 year longitudinal study

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Study protocol of the InterVitaminK trial: a Danish population-based randomised double-blinded placebo-controlled trial of the effects of vitamin K (menaquinone-7) supplementation on cardiovascular, metabolic and bone health

IntroductionVitamin K has been suggested to have protective effects against progression of vascular calcification and development of cardiovascular disease (CVD). However, few well-powered randomised controlled trials have examined whether vitamin...

Progression of Vascular Calcification and Clinical Outcomes in Patients Receiving Maintenance Dialysis

Baseline findings from the China Dialysis Calcification Study (CDCS) revealed a high prevalence of vascular calcification (VC) among patients with end-stage kidney disease; however, data on VC progression were limited. To understand the progression of VC at different anatomical sites, identify risk factors for VC progression, and assess the association of VC progression with the risk of cardiovascular events and death among patients receiving maintenance dialysis. This cohort study was a 4-year follow-up assessment of participants in the CDCS, a nationwide multicenter prospective cohort study involving patients aged 18 to 74 years who were undergoing hemodialysis or peritoneal dialysis. Participants were recruited from 24 centers across China between May 1, 2014, and April 30, 2015, and followed up for 4 years. A total of 1489 patients receiving maintenance dialysis were included in the current analysis. Data were analyzed from September 1 to December 31, 2021. Patient demographic characteristics and medical history; high-sensitivity C-reactive protein laboratory values; serum calcium, phosphorus, and intact parathyroid hormone (iPTH) values; and previous or concomitant use of medications. The primary outcome was progression of VC at 3 different anatomical sites (coronary artery, abdominal aorta, and cardiac valves) and identification of risk factors for VC progression. Participants received assessments of coronary artery calcification (CAC), abdominal aortic calcification (AAC), and cardiac valve calcification (CVC) at baseline, 24 months, 36 months, and 48 months. Secondary outcomes included (1) the association between VC progression and the risk of all-cause death, cardiovascular (CV)-related death, and a composite of all-cause death and nonfatal CV events and (2) the association between achievement of serum calcium, phosphorus, and iPTH target levels and the risk of VC progression. Among 1489 patients, the median (IQR) age was 51.0 (41.0-60.0) years; 59.5% of patients were male. By the end of 4-year follow-up, progression of total VC was observed in 86.5% of patients; 69.6% of patients had CAC progression, 72.4% had AAC progression, and 33.4% had CVC progression. Common risk factors for VC progression at the 3 different anatomical sites were older age and higher fibroblast growth factor 23 levels. Progression of CAC was associated with a higher risk of all-cause death (model 1 [adjusted for age, sex, and body mass index]: hazard ratio [HR], 1.97 [95% CI, 1.16-3.33]; model 2 [adjusted for all factors in model 1 plus smoking status, history of diabetes, and mean arterial pressure]: HR, 1.89 [95% CI, 1.11-3.21]; model 3 [adjusted for all factors in model 2 plus calcium, phosphorus, intact parathyroid hormone, and fibroblast growth factor 23 levels and calcium-based phosphate binder use]: HR, 1.92 [95% CI, 1.11-3.31]) and the composite of all-cause death and nonfatal CV events (model 1: HR, 1.98 [95% CI, 1.19-3.31]; model 2: HR, 1.91 [95% CI, 1.14-3.21]; model 3: HR, 1.95 [95% CI, 1.14-3.33]) after adjusting for all confounding factors except the presence of baseline calcification. Among the 3 targets of calcium, phosphorus, and iPTH, patients who achieved no target levels (model 1: odds ratio [OR], 4.75 [95% CI, 2.65-8.52]; model 2: OR, 4.81 [95% CI, 2.67-8.66]; model 3 [for this analysis, adjusted for all factors in model 2 plus fibroblast growth factor 23 level and calcium-based phosphate binder use]: OR, 2.76 [95% CI, 1.48-5.16]), 1 target level (model 1: OR, 3.71 [95% CI, 2.35-5.88]; model 2: OR, 3.62 [95% CI, 2.26-5.78]; model 3: OR, 2.19 [95% CI, 1.33-3.61]), or 2 target levels (model 1: OR, 2.73 [95% CI, 1.74-4.26]; model 2: OR, 2.69 [95% CI, 1.71-4.25]; model 3: OR, 1.72 [95% CI, 1.06-2.79]) had higher odds of CAC progression compared with patients who achieved all 3 target levels. In this study, VC progressed rapidly in patients undergoing dialysis, with different VC types associated with different rates of prevalence and progression. Consistent achievement of serum calcium, phosphorus, and iPTH target levels was associated with a lower risk of CAC progression. These results may be useful for increasing patient awareness and developing appropriate strategies to improve the management of chronic kidney disease-mineral and bone disorder among patients undergoing dialysis.

Coronary artery calcium progression and all-cause mortality.

Coronary artery calcium (CAC) has been demonstrated as a noninvasive, low-cost means of assessing atherosclerotic burden and risk of major cardiovascular events. While it has been previously shown that CAC progression predicts all-cause mortality, we sought to quantify this association by examining a large cohort over a follow-up period of 1-22 years. We studied 3260 persons aged 30-89 years referred by their primary physician for CAC measurement, with a follow-up scan at least 12 months from the initial scan. Receiver operator characteristic (ROC) curves assessed a level of annualized CAC progression that predicted all-cause mortality. Multivariate analyses using Cox proportional hazards models were used to compute hazard ratios and 95% confidence intervals (CIs) for the association between annualized CAC progression and death after adjusting for relevant cardiovascular risk factors. The average time between scans was 4.7 ± 3.2 years with an additional average of 9.1 ± 4.0 years of follow-up time. The average age of the cohort was 58.1 ± 10.5 years, 70% being male, and 164 deaths occurred. Annualized CAC progression of 20 units optimized sensitivity (58%) and specificity (82%) in ROC curve analysis. Annualized CAC progression of 20 units was significantly associated with mortality while adjusting for age, sex, race, diabetes, hypertension, hyperlipidemia, smoking, baseline CAC level, family history, and time between scans, hazard ratio 1.84 (95% CI, 1.28-2.64) P = 0.001. Annualized CAC progression of greater than 20 units per year significantly predicts all-cause mortality. This may add clinical value in encouraging close surveillance and aggressive treatment of individuals within this range.

Association between urinary chloride excretion and progression of coronary artery calcification in patients with nondialysis chronic kidney disease: results from the KNOW-CKD study.

Urine chloride has recently been suggested as a biomarker of renal tubule function in patients with nondialysis chronic kidney disease (CKD), as low urinary chloride concentration is associated with an increased risk of CKD progression. We investigate the association between urinary chloride excretion and the progression of coronary artery calcification (CAC). A total of 1,065 patients with nondialysis CKD were divided into tertiles by spot urine chloride-to-creatinine ratios. The 1st, 2nd, and 3rd tertiles were defined as low, moderate, and high urinary chloride excretion, respectively. The study outcome was CAC progression, which was defined as an increase in coronary artery calcium score of more than 200 Agatston units during the 4-year follow-up period. Compared to moderate urinary chloride excretion, high urinary chloride excretion was associated with decreased risk of CAC progression (adjusted odds ratio, 0.379; 95% confidence interval, 0.190-0.757), whereas low urinary chloride excretion was not associated with risk of CAC progression. Restricted cubic spine depicted an inverted J-shaped curve, with a significant reduction in the risk of CAC progression in subjects with high spot urine chloride-to-creatinine ratios. High urinary chloride excretion is associated with decreased risk of CAC progression in patients with nondialysis CKD.

Abstract P614: The Association Between Dietary Patterns and Coronary Artery Calcium Score: A Systematic Review

Background and Objective: Coronary artery calcium (CAC) score is an early indicator of CVD. Diet is an established primary prevention strategy for CVD, but limited research has systematically evaluated the relationship between diet and CAC. The current study sought to review longitudinal studies evaluating the association between dietary intake and CAC score. Methods: Five databases were searched from inception to October 2022. We included prospective studies that included terms to capture food, diet, and nutrient intake in disease-free adults with CAC score measured by computed tomography. Two authors developed the search strategies and screened articles for inclusion. Results: Of 58 articles on dietary intake and CAC score, nine assessed the relationship between dietary intake at baseline and CAC score at follow up. Sample size was moderate to large across the nine studies, ranging from 861 to 15,368 participants. Seven studies used a food frequency questionnaire, one used a semi-quantitative interview, and one used a single-item question to assess diet intake. One study was conducted in Germany, while eight were conducted in the US. Three studies derived data from the CARDIA study, a cohort of young adults aged 18-30 at baseline. Two studies used the MESA study, a prospective study of adults aged 45-84 at baseline. Four studies found an association between dietary pattern intake and CAC score, with studies finding that higher fruit and vegetable intake and Mediterranean-like diet associated with lower risk of CAC progression, and low carbohydrate diet and starchy vegetable, meat and alcohol intake associated with increased risk of CAC presence. Conclusions: Studies suggested that there is a relationship between diet intake and CAC presence and progression, with research reflecting positive effects associated with patterns rich in fruits and vegetables alongside deleterious effects associated with high saturated fat and low dietary fiber intake. Finding reflect the strong influence of diet on clinical indicators of CVD.

Relationship between left main trifurcation angulation, calcium score, and the onset of plaque formation.

It has been suggested that a wider left main (LM) bifurcation angle is associated with the development of atherosclerosis. However, the relationship between LM trifurcation angulation and atherosclerosis has not been investigated. We aimed to investigate the relationship between LM trifurcation angulation and the presence of calcifications in the left coronary artery (LCA) using coronary computed tomography angiography (CCTA). Furthermore, we assessed the relationship between LM trifurcation angulation and the age at which calcification originated. The LM trifurcation angle and coronary artery calcium (CAC) score in the LCA were measured. Based on observational studies, we assumed that CAC progression is 25% per year on average. Then, we calculated the age at which LCA CAC scores were lower than 0.1 Agatston units. Of 266 patients, 52 patients (mean age of [standard deviation, SD] 61 [6] years; 28 men) with LM trifurcation were included in the study. Calcified plaques occurred in the LCA in 36 patients (69.2%). The mean LM trifurcation angle in patients with a diseased LCA was wider than that in patients with a normal LCA (108° [33°] vs. 91° [28°]; P = 0.04). Pearson correlation coefficient showed that the wider the LM trifurcation angle was, the earlier the calcification in the LCA may be expected (r = -0.34; P = 0.04 with outliers; r = -0.43; P = 0.009 without outliers). A wider LM trifurcation angle is associated with a higher LCA CAC score. Moreover, the LM trifurcation angle has a significant impact on the earlier onset of atherosclerosis.

Malnutrition leads to the progression of coronary artery calcification in hemodialysis patients.

Malnutrition is considered a risk factor for cardiovascular disease in patients with chronic kidney disease. However, no in vivo studies have reported on using optical coherence tomography to evaluate the effect of nutritional status on coronary atherosclerosis in hemodialysis patients. We aimed to conduct a detailed analysis of the effect of nutritional status on the coronary arteries in hemodialysis patients. Among 64 hemodialysis patients who underwent percutaneous coronary interventions, 41 that underwent optical coherence tomography imaging were included in this study. And, among them, 24 patients that could also be evaluated using OCT also at the 6-month follow-up were included in this study. The patients were divided into two groups based on nutritional evaluation using the geriatric nutritional risk index. Culprit and non-culprit lesions were evaluated at baseline and after 6 months. In the culprit lesions at baseline, the length of the lipid plaque was significantly smaller in the malnutrition group. In contrast, the thickness and length of the calcified plaque and the angle of the calcified nodule were significantly larger (each p < 0.01). In the non-culprit lesions, the 6-month change in the angle of the calcified plaque was significantly greater in the malnutrition group (p = 0.02). The significant factors that affected the change in the angle of calcification were "malnutrition at geriatric nutritional risk index" [odds ratio, 8.17; 95% confidence interval, 1.79 to 37.33; p < 0.01] and "serum phosphorus level" (odds ratio, 3.73; 95% confidence interval, 1.42 to 9.81; p < 0.01). Appropriate management of nutritional status is crucial for suppressing the progression of coronary artery disease in hemodialysis patients.

Persistence or regression of prediabetes and coronary artery calcification among adults without diabetes

The effect of changes in glycemic status on subclinical atherosclerosis is uncertain. We assessed the association of persistence, regression, or progression of prediabetes with coronary artery calcium score (CACS) as a measure of subclinical atherosclerosis. A cross-sectional study, comprising 126 765 adults, and longitudinal sub-study, comprising 40 622 adults (with baseline and at least 1 follow-up computed tomography scan to assess changes in CACS), were undertaken. Changes in glycemic status over 1.5 years (interquartile range, 1.0-2.0) before the first CACS assessment were categorized according to 6 groups: persistent normoglycemia (reference), normoglycemia to prediabetes, normoglycemia to diabetes, prediabetes to normoglycemia, persistent prediabetes, and prediabetes to diabetes. Logistic regression was used to calculate the odds ratios (ORs) and 95% CIs for prevalent coronary artery calcification (CAC). Mixed models with random intercepts and random slopes were used to estimate 5-year CAC progression rates. Mean (SD) age was 41.3 (7.0) years (74.7% male) (n = 126 765). Multivariable-adjusted OR for prevalent CAC was 1.13 (95% CI, 1.08-1.18) for persistent prediabetes, 1.05 (0.98-1.12) for regression to normoglycemia, and 1.46 (95% CI, 1.27-1.67) for progression from prediabetes to diabetes, compared with persistent normoglycemia. Coronary artery calcification progression increased significantly in all prediabetes groups. Multivariable-adjusted ratio of 5-year CAC progression rates was 1.19 (95% CI, 1.16-1.22) (persistent prediabetes), 1.11 (1.07-1.14) (regression to normoglycemia), and 1.63 (95% CI, 1.26-2.10) (progression from prediabetes to diabetes). Unfavorable changes in glycemic status, including persistence of prediabetes or progression to diabetes from prediabetes, were associated with increased risk of CAC.

High- vs. Low-Intensity Statin Therapy and Changes in Coronary Artery Calcification Density after One Year.

Statin therapy promotes the progression of coronary artery calcification (CAC). Comparing patients on high (HIST) vs. low-to-intermediate intensity statin therapy (LIST), randomized controlled trials with a one-year follow-up failed to document a relevant difference in the Agatston score and CAC volume. We evaluated whether statin intensity modifies CAC density at one year. We performed a pooled analysis of two randomized-controlled trials (BELLES, EBEAT), comparing the effects of HIST (Atorvastatin 80 mg) vs. LIST (Pravastatin 40 mg, Atorvastatin 10 mg) on CAC measures after one year. The differences in CAC density and its change were compared using the two-sided t-test. Data from 852 patients (66.7% female) with available baseline and follow-up CT were evaluated from both trials. HIST vs. LIST more effectively reduced LDL-cholesterol (annualized change: -45.8 ± 38.5 vs. -72.9 ± 46.0 mg/dL, p &lt; 0.001). Mean CAC density increased from 228.8 ± 35.4 HU to 232.6 ± 37.0 HU (p &lt; 0.0001) at one-year follow-up. Comparing patients on HIST vs. LIST, CAC density at follow-up (HIST: 231.9 ± 36.1 HU vs. LIST: 233.3 ± 37.7 HU, p = 0.59) and its change from baseline (HIST: 4.0 ± 19.1 HU vs. LIST: 3.6 ± 19.6 HU, p = 0.73) did not differ. Subgroup analyses, stratifying by LDL reduction (&lt;median: 2.0 ± 24.3 HU, ≥median: 3.6 ± 21.9 HU, p = 0.34), Agatston score at baseline (&lt;100: 2.6 ± 22.5 HU vs. 3.2 ± 25.6 HU, p = 0.82; ≥100: 4.8 ± 17.0 HU vs. 3.8 ± 16.6 HU, p = 0.44, for HIST vs. LIST; respectively), and equal number of lesions in both CT scans (3.7 ± 20.3 HU vs. 7.0 ± 22.2 HU, p = 0.24) showed similar results. HIST vs. LIST leads to a higher reduction in cholesterol levels, which does not translate into relevant differences in the change of CAC density at one-year follow-up.

Exercise Volume Versus Intensity and the Progression of Coronary Atherosclerosis in Middle-Aged and Older Athletes: Findings From the MARC-2 Study.

Physical activity and exercise training are associated with a lower risk for coronary events. However, cross-sectional studies in middle-aged and older male athletes revealed increased coronary artery calcification (CAC) and atherosclerotic plaques, which were related to the amount and intensity of lifelong exercise. We examined the longitudinal relationship between exercise training characteristics and coronary atherosclerosis. Middle-aged and older men from the MARC-1 (Measuring Athlete's Risk of Cardiovascular Events 1) study were invited for follow-up in MARC-2 (Measuring Athlete's Risk of Cardiovascular Events 2) study. The prevalence and severity of CAC and plaques were determined by coronary computed tomography angiography. The volume (metabolic equivalent of task [MET] hours/week) and intensity (moderate [3 to 6 MET hours/week]; vigorous [6 to 9 MET hours/week]; and very vigorous [≥9 MET hours/week]) of exercise training were quantified during follow-up. Linear and logistic regression analyses were performed to determine the association between exercise volume/intensity and markers of coronary atherosclerosis. We included 289 (age, 54 [50 to 60] years [median (Q1 to Q3)]) of the original 318 MARC-1 participants with a follow-up of 6.3±0.5 years (mean±SD). Participants exercised for 41 (25 to 57) MET hours/week during follow-up, of which 0% (0 to 19%) was at moderate intensity, 44% (0 to 84%) was at vigorous intensity, and 34% (0 to 80%) was at very vigorous intensity. Prevalence of CAC and the median CAC score increased from 52% to 71% and 1 (0 to 32) to 31 (0 to 132), respectively. Exercise volume during follow-up was not associated with changes in CAC or plaque. Vigorous intensity exercise (per 10% increase) was associated with a lesser increase in CAC score (β, -0.05 [-0.09 to -0.01]; P=0.02), whereas very vigorous intensity exercise was associated with a greater increase in CAC score (β, 0.05 [0.01 to 0.09] per 10%; P=0.01). Very vigorous exercise was also associated with increased odds of dichotomized plaque progression (adjusted odds ratio [aOR], 1.09 [1.01 to 1.18] per 10%; aOR, 2.04 [0.93 to 4.15] for highest versus lowest very vigorous intensity tertiles, respectively), and specifically with increased calcified plaques (aOR, 1.07 [1.00 to 1.15] per 10%; aOR, 2.09 [1.09 to 4.00] for highest versus lowest tertile, respectively). Exercise intensity but not volume was associated with progression of coronary atherosclerosis during 6-year follow-up. It is intriguing that very vigorous intensity exercise was associated with greater CAC and calcified plaque progression, whereas vigorous intensity exercise was associated with less CAC progression.

Coronary artery calcification progression over two years in breast cancer patients treated with radiation therapy: Findings from BACCARAT study

Coronary artery calcification progression over two years in breast cancer patients treated with radiation therapy: Findings from BACCARAT study

New look at the power of zero coronary artery calcium (CAC) in Asian population: a systemic review and meta-analysis.

Numerous studies have validated a 5-year warranty period for heart health in Western populations with a coronary artery calcium (CAC) score of zero. While the calcium score is a crucial cardiovascular risk indicator, its interpretation in Asian populations remains unclear. This meta-analysis aimed to clarify the uncertainty surrounding the prevalence, warranty period, and prognostic implications of zero CAC scores in Asian populations. It also examined the impact of sex on subclinical CAC progression. While the calcium score is a crucial cardiovascular risk indicator, its interpretation in Asian populations remains unclear. The study aimed to shed light on these issues by exploring the specificities of subclinical CAC progression in the Asian context. Our systematic literature search, from the study's inception to October 2023, targeted studies on subclinical CAC progression in the Asian population with a zero CAC score. We searched the Cochrane Library, and PubMed. The search terms included "zero score", "coronary calcification", "zero CAC score", and "CAC scan". We evaluated seven published studies through a meta-analysis and assessed the risk of bias using the Newcastle-Ottawa Scale (NOS). In this meta-analysis of three observational studies addressing zero CAC prevalence (n=7,661), the pooled prevalence of zero CAC scores in the Asian population was 18.2% [95% confidence interval (CI): 12.5-25.9%]. A significant difference in follow-up warranty period was observed between the CAC zero group and subclinical CAC progression group (mean difference, 1.26 years; 95% CI: 0.94-1.58; P<0.001). Furthermore, the conversion rate of subclinical CAC progression differed significantly between males and females (risk ratio, 2.37; 95% CI: 1.98-2.84; P<0.001). Analysis of four studies revealed a notable discrepancy in the major adverse cardiovascular event (MACE) rate between the CAC (-) and CAC (+) groups (risk ratio, 4.78; 95% CI: 2.21-10.36; P<0.001). The meta-analysis of zero CAC scores in Asian populations suggested an 18.2% prevalence. A 5-year warranty period was noted, with heightened subclinical CAC progression likelihood after this duration. Additionally, sex-based differences were observed in subclinical CAC progression rates. These findings will provide clinical cardiovascular risk stratification for guiding gender-specific clinical decision-making in asymptomatic in Asian individuals.