Risk Of Coronary Artery Calcification Progression Research Articles

Abstract MP25: Physical Activity And The Progression Of Coronary Artery Calcification

Introduction: High volume endurance physical activity (PA) has been shown to associate with increased clinically relevant coronary artery calcification (CAC) but not mortality. A key issue is whether active individuals with CAC have progression of atherosclerosis in the setting of sustained high levels of PA. Hypothesis: We hypothesized that changes in CAC are not related to corresponding changes in PA volume. Further, we hypothesized the rate of CAC progression to ≥100 Agatston units (AU) does not depend on baseline PA level. Methods: The study included 6,525 men and 2,056 women with ≥2 assessments of PA and CAC (EBT scans (1997-2007) or MDCT scans (2007-2019)). All individuals had at least one follow-up visit (mean=1.8). We used mixed linear regression to relate within-person changes in square-root CAC to changes in PA volume, controlling for between-person effects. We used interval-censored proportional hazards regression to test if progression to CAC≥100 AU was related to baseline PA level: ≥3000, 1500-2999, and <1500 MET·minutes/week (MET·min/wk). Covariates included age, smoking, BMI, glucose, cholesterol, systolic blood pressure, and statin use. In addition, the longitudinal analysis was adjusted for time since baseline, while the time-to-CAC-threshold analysis was adjusted for baseline CAC. Results: Mean baseline age was 50 years in men/51 years in women. Mean time to first follow-up was 4.5 years in men/5.1 years in women. PA levels increased by 100 MET·min/wk in men but were stable in women. Cardiorespiratory fitness was stable between visits. Within person changes in CAC were not associated with changes in PA volume (Table). At baseline, 5285 men and 1948 women had CAC<100 AU; at follow-up, 1127 men and 136 women progressed to CAC≥100 AU. Neither PA ≥3000 nor 1500-2999 MET·min/wk exhibited significant risk of CAC progression versus <1500 MET·min/wk. Estimated hazard ratios were ≤1 for both men and women. Conclusions: These results show no apparent risk of increasing CAC with sustained PA in active individuals.

Clinical and biochemical markers of coronary artery calcification progression after elective coronary artery bypass grafting

Aim. To assess the relationship of various clinical and biological markers of bone metabolism with the progression of coronary artery calcification (CAC) in patients with stable coronary artery disease (CAD) within 5 years after coronary artery bypass grafting (CABG).Material and methods. This single-center prospective observational study included 111 men with CAD who were hospitalized for elective CABG. In the preoperative period, all patients underwent duplex ultrasound of extracranial arteries (ECA) and multislice computed tomography (MSCT) to assess CAC severity using the Agatston score, as well as densitometry with determination of bone mineral density in the femoral neck, lumbar spine and T-score for them, In all participants, the following bone metabolism biomarkers were studied: calcium, phosphorus, calcitonin, osteopontin, osteocalcin, osteoprotegerin (OPG), alkaline phosphatase, parathyroid hormone. Five years after CABG, ECA duplex ultrasound, MSCT coronary angiography and bone metabolism tests were repeated. Depending on CAC progression (>100 Agatston units (AU)), patients were divided into two groups to identify significant biomarkers and clinical risk factors associated with CAC progression.Results. For 5 years after CABG, contact with 16 (14,4%) patients was not possible; however, their vital status was assessed (they were alive). Death was recorded in 4 (3,6%) cases (3 — due to myocardial infarction, 1 — due to stroke). In 18 (19,7%) cases, non-fatal endpoints were revealed: angina recurrence after CABG — 16 patients, myocardial infarction — 1 patient, emergency stenting for unstable angina — 1 patient. There were no differences in the incidence of events between the groups with and without CAC progression. According to MSCT 5 years after CABG (n=91 (81,9%)), CAC progression was detected in 60 (65,9%) patients. Multivariate analysis allowed to create a model for predicting the risk of CAC progression, which included following parameters: cathepsin K <16,75 pmol/L (p=0,003) and bone mineral density <0,95 g/cm3 according to femoral neck densitometry before CABG (p=0,016); OPG <3,58 pg/ml (p=0,016) in the postoperative period 5 years after CABG.Conclusion. Within 5 years after CABG, 65,9% of male patients with stable coronary artery disease have CAC progression, the main predictors of which are low preoperative cathepsin K level (<16,75 pmol/L) and low bone mineral density (<0,95 g/cm3) according to femoral neck densitometry, as well as a low OPG level (<3,58 pg/ml) 5 years after CABG.

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.

The Impact of Fatty Liver Disease and Metabolic Syndrome on the Progression of Coronary Artery Calcification

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.

Evaluation of the impact of glycemic status on the progression of coronary artery calcification in asymptomatic individuals

BackgroundData on the influence of glycemic status on the progression of coronary calcification, an important marker for future adverse cardiovascular events, are limited.MethodsData 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.ResultsThe 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.ConclusionsIn asymptomatic subjects, diabetes had an incremental impact on CAC progression; however, pre-diabetes did not increase the risk of CAC progression after adjusting for confounding factors.

Aged Garlic Extract with Supplement is Associated with Beneficial Effect on Bone Mineral Density and Predicts Lack of Progression of Atherosclerosis: A Prospective Double Blinded Randomized Trial

Aged Garlic Extract with Supplement is Associated with Beneficial Effect on Bone Mineral Density and Predicts Lack of Progression of Atherosclerosis: A Prospective Double Blinded Randomized Trial Low levels of bone-mineral-density (BMD) are independently associated with the presence and severity of coronary-arterycalcium (CAC). This study evaluates the beneficial-effects of aged-garlic-extract therapy with-supplements (AGE-S) on levels of BMD, vascular-function, inflammation and CAC. Sixty subjects, randomized to four daily capsules of placebo vs. AGE-S inclusive of aged garlic extract (1000 mg) plus VitaminB12 (400 mcg or µg), folic-acid (1200 mcg or µg), Vitamin-B6 (50 mg) and L-arginine (400 mg) underwent CAC, thoracicBMD (mg/cc), lipid-profile, lipoprotein a (Lp-a), homocysteine and vascular-function measurement at baseline and 12- months. The postcuff-deflation temperature-rebound (TR), digital-thermal-monitoring index of vascular-function was assessed using a reactive-hyperemia-procedure. At 1-year, the mean increase in CAC and decrease in BMD was significantly lower in the AGE-S as compared to the placebo (p<0.05). After adjustment for risk-factors, the risk of CAC progression and reduced BMD was 65% and 68% less in AGE-S as compared to placebo (P<0.05). From baseline to 12 months, a significant correlation was noted between increase in CAC and decreases in BMD. Similarly, a significant correlation was noted between increase in TR and decrease in homocysteine as well as increase in Lp-a with lack of decrease in BMD. The maximum beneficial effect of AGE-S was noted with increase in TR, lack of decrease in BMD and lack of progression of CAC. In conclusion, this study demonstrates AGE-S is independently associated with favorable effect on A strong direct relation between increases in vascular-function, decrease in inflammation with lack of lowering in BMD levels as well as lack of CAC-progression in response to AGE-S was noted.