Progression Of Coronary Calcification Research Articles

Association between cumulative intake of sugar-sweetened and artificially sweetened beverages and progression of coronary calcification: Insights from the CARDIA study

Background and aimsThis study investigates the relationship between the cumulative intake of artificially sweetened beverages (ASBs) and sugar-sweetened beverages (SSBs) during young adulthood and the progression of coronary artery calcium (CAC) by midlife, using data from the Coronary Artery Risk Development in Young Adults study. Methods and resultsWe included 2,466 participants with CAC measurement via computed tomography at the 15th, 20th, and 25th year follow-ups. Dietary intake was assessed using the CARDIA Diet History at baseline and years 7. Cumulative average beverage intake was calculated and categorized. Multivariable Cox regression models adjusted for demographic, lifestyle, and cardiovascular risk factors assessed associations between beverages consumption and CAC progression. Among the included participants, 1107 (44.9 %) were male, 1439 (58.4 %) were white, and the average age was 40.4 years with a standard deviation of 3.5 years. Over a 9.2±1.8-year follow-up, CAC progression was recorded in 715 participants. Higher cumulative ASBs intake was associated with increased CAC progression risk, with hazard ratios (95%CI, P-value) for low and high ASBs consumption being 1.35 (1.14, 1.60; P < 0.001) and 1.54 (1.15, 2.07; P < 0.001) compared to non-consumers. Participants consuming >2 servings/day of SSBs had a 37 % higher CAC progression risk (HR 1.37, 95 % CI 1.14–1.64, P < 0.001). However, no significant association was found between SSB consumption and CAC progression after adjusting for confounders. ConclusionsProlonged consumption of beverages, especially ASBs, in young adults is linked to an increased risk of CAC progression.

Rivaroxaban versus vitamin K antagonist treatment on the progression of coronary calcification: the IRIVASC-trial

Vitamin K antagonists (VKA) remain the only option of anticoagulation for people with mechanical valve replacement and due to their wider availability and lower acquisition costs, VKA’s remain widely used in low- and middle-income countries. It has been suggested that prolonged use of VKAs can increase the development of vascular and valvular calcification, though this effect has not been examined in larger randomized prospective trials. This investigator-initiated multicenter, prospective, randomized, open-label interventional trial randomized patients with baseline coronary or valvular calcification and an indication for prolonged oral anticoagulation therapy to Marcumar or Rivaroxaban. Patients were followed-up through repeat coronary computed tomographies to measure the progression of coronary and valvular calcification for up to 24 months. 192 patients were randomized between 2013 and 2018 to receive either Rivaroxaban or Marcumar and followed for up to 24 months. Coronary calcification significantly increased over time although there was no significant difference in progression between the groups after 12 and 24 months as measured by the Agatston score [360.7 (90.2; 1075.3) vs 380.4 (136.4; 1546.9) p = 0.69], the volume score [295.8 (93.0; 995.3) vs 335.5 (128.7; 1316.9) p = 0.95] and the mass score [58.5 (15.9; 172.0) vs 71.1 (24.8; 257.3) p = 0.5]. Dephosphorylated, uncarboxylated matrix Gla Protein (Dp-ucMGP) significantly decreased in the VKA group [Δ dp-uc MGP – 95.2 (− 554.1; 156.0) vs 231.3 (− 59.7; 388.1) p < 0.001]. There does not appear to be a relevant effect of vitamin K inhibition by the vitamin K antagonist marcumar upon coronary calcification.

The association of lipoprotein(a) and coronary artery calcium in asymptomatic patients: a systematic review and meta-analysis.

Lipoprotein(a) [Lp(a)] is an atherogenic lipid particle associated with increased risk for coronary heart disease (CHD) events. Coronary artery calcium (CAC) score is a tool to diagnose subclinical atherosclerosis and guide clinical decision-making for primary prevention of CHD. Studies show conflicting results concerning the relationship between Lp(a) and CAC in asymptomatic populations. We conducted a meta-analysis to evaluate the association of Lp(a) and CAC in asymptomatic patients. We systematically searched PubMed, Embase, and Cochrane until April 2023 for studies evaluating the association between Lp(a) and CAC in asymptomatic patients. We evaluated CAC > 0 Agatston units, and CAC ≥ 100. Lp(a) was analysed as a continuous or dichotomous variable. We assessed the association between Lp(a) and CAC with pooled odds ratios (OR) adopting a random-effects model. A total of 23 105 patients from 18 studies were included in the meta-analysis with a mean age of 55.9 years, 46.4% female. Elevated Lp(a) increased the odds of CAC > 0 [OR 1.31; 95% confidence intervals (CI) 1.05-1.64; P = 0.02], CAC ≥100 (OR 1.29; 95% CI 1.01-1.65; P = 0.04; ), and CAC progression (OR 1.43; 95% CI 1.20-1.70; P < 0.01; ). For each increment of 1 mg/dL in Lp(a) there was a 1% in the odds of CAC > 0 (OR 1.01; 95% CI 1.01-1.01; P < 0.01). Our findings of this meta-analysis suggest that Lp(a) is positively associated with a higher likelihood of CAC. Higher Lp(a) levels increased the odds of CAC >0. These data support the concept that Lp(a) is atherogenic, although with high heterogeneity and a low level of certainty. CRD42023422034. Asymptomatic patients with elevated Lp(a) had 31% higher chances of having any coronary calcification (CAC > 0) and 29% higher chances of having more advanced calcification (CAC > 100). It increased the chances of having progression of coronary calcification over time by 43%. For each 1 mg/dL of Lp(a) there was an increment of 1% chance of having coronary calcification.

Serial longitudinal changes of coronary calcified plaques with clear outer borders under intensive lipid management: insights from optical coherence tomography.

Percutaneous coronary intervention (PCI) for calcified lesions is one of the most challenging procedures related to worse clinical outcomes. To stabilize vulnerable plaques, intensive lipid management is recommended; however, the serial changes of calcified plaques under intensive lipid management are unknown. A total of 31 patients (mean age, 63 ± 10years; men, 29 patients) who underwent PCI with intensive lipid management were retrospectively studied. We evaluated the serial longitudinal changes of calcified plaques with clear outer borders using optical coherence tomography (OCT) at two time points: at the time of PCI (baseline) and the chronic phase. The median interval from PCI to chronic phase was 287 (233-429) days. Twenty-eight patients (90.3%) had increased calcium volume at the chronic phase compared with those at baseline (2.6 [1.3-5.1] vs. 1.8 [0.7-4.3] mm2, p < 0.05), and the median increase rate of calcium volume was 27.4% at the chronic phase. According to the median increase rate of calcium volume (27.4%), patients were divided into the following two groups: rapid progression (≥ 27.4%, RP group) and non-rapid progression (< 27.4%, non-RP group). The RP group had more patients with diabetes, and diabetes was independently associated with rapid progression by multivariate analysis. Furthermore, patients with diabetes had significantly higher changes in calcium index and volume from the baseline to the chronic phase than those without diabetes. Coronary calcification progression during relatively short intervals was observed using OCT even under intensive lipid management. Diabetes was an independent predictor for rapid coronary calcification progression.

#3724 CHANGES IN CARDIOVASCULAR CALCIFICATION AFTER PARATHYROIDECTOMY IN DIALYSIS-DEPENDENT PATIENTS

Abstract Background and Aims Vascular calcification (VC) is common in patients with end stage kidney disease on dialysis and with secondary hyperparathyroidism (SHPT). There is a lack of knowledge regarding dynamics of VC after surgical treatment of SHPT. We aimed to evaluate evolution of coronary artery calcification (CAC) and abdominal aortic calcification (AAC) after parathyroidectomy (PTx) in dialysis patients with SHPT. Method The prospective cohort study included 33 dialysis-dependent patients (mean age of 50±13 years) with severe SHPT who underwent subtotal (n = 16) or total PTx with autotransplantation of parathyroid tissue (n = 17). Cardiac computed tomography scan (quantification of coronary calcium by Agatston method) and lateral lumbar X-ray (semi-quantitative Kauppila score) were used to assess prevalence of VC before and 18 months after surgery. Levels of serum total calcium, phosphorus, parathyroid hormone (PTH), and alkaline phosphatase (AP) before and 18 months after surgery were also evaluated. Results In our cohort median dialysis vintage before surgery was 71 [Q1-Q3: 29; 136] months, total serum Ca was 2.47±0.23 mmol/l, median PTH was 139 [Q1-Q3: 90; 161] pg/ml. Prevalence of CAC before PTx was 79% (n = 26), and 61% (n = 20) of patients had AAC. Of note, 54.5% of the patients had severe coronary calcification (&amp;gt;400 AU), while only 12% were considered to have severe calcification using Kauppila score (&amp;gt;12). We observed moderate positive correlation between CAC and AAC scores (Spearman's ρ = 0.699 [95% CI: 0.48; 0.84], р&amp;lt;0.0001). Both CAC and AAC scores correlated moderately with age of the patients (ρ = 0.57 [95% CI: 0.3; 0.76], р = 0.0002, and ρ = 0.64 [95% CI: 0.39; 0.8], р&amp;lt;0.0001, respectively), AAC had weak correlation with their dialysis vintage (ρ = 0.45 [95% CI: 0.14; 0.68], р = 0.005. Median of baseline CAC was 458 [Q1-Q3: 23; 1585] AU, after 18 months - 491 [Q1-Q3: 58; 1956] AU, no statistically significant differences were observed (p = 0.91, Wilcoxon test). We did not find statistically significant differences between median of Kauppila scores before and after PTx as well: 3 [Q1-Q3: 0; 10] and 2 [Q1-Q3: 0; 10], correspondingly, p = 0.17 (Wilcoxon test) – Fig. 1. As it can be seen from Fig. 1, dynamics of both CAC and AAC values before and after PTx varied markedly across subjects. To investigate the factors that can promote VC we divided patients into 2 groups based on dynamics of САС (as the most accurate assessment method) 18 months after surgery: group 1 with CAC progression of more than 50 AU (n = 9) and group 2 with regression or progression less than 50 AU (n = 24). Patients who had progression of coronary calcification by the end of the follow-up had higher age (59±11 vs 46±12 years in 2nd group, p = 0.0128) higher serum calcium levels (2.57±0.24 vs 2.29±0.32 mmol/l in 2nd group, p = 0.0267), and higher AP levels at follow-up (69.8 [Q1-Q3: 62.8, 96.0] vs 51.7 [Q1-Q3: 41.4; 57.1] U/ml in 2nd group, p = 0.003). Univariate analysis showed no significant differences between groups comparing dialysis vintage (p = 0.53), phosphate levels (p = 0.54), PTH levels (p = 0.32). In addition, CAC progression risk was not associated with type of surgery (total vs subtotal PTx RR = 1.11 [95% CI: 0.71; 1.8], OR = 1.48 [95% CI: 0.3; 5.7], p = 0.708). Conclusion Prevalence of vascular calcification in dialysis-dependent patients with severe SHPT is high. Progression of CAC by 18 months after PTx was associated with higher age of the patients, higher follow-up levels of serum total Ca and AP.

Visceral adipose tissue is an independent predictor and mediator of the progression of coronary calcification: a prospective sub-analysis of the GEA study

BackgroundCoronary artery calcium (CAC) improves cardiovascular event prediction. Visceral adipose tissue (VAT) is a cardiometabolic risk factor that may directly or through its related comorbidities determine the obesity-related risk. A clinical VAT estimator could allow an efficient evaluation of obesity-related risk. We aimed to analyze the effect of VAT and its related cardiometabolic risk factors on CAC progression.MethodsCAC was quantified at baseline and after 5 years by computed tomography (CT), determining its progression. VAT and pericardial fat were measured by CT and estimated by a clinical surrogate (METS-VF). Considered cardiometabolic risk factors were: peripheral insulin resistance (IR), HOMA-IR, adipose tissue IR (ADIPO-IR), and adiponectin. Factors independently associated to CAC progression were analyzed by adjusted Cox proportional hazard models, including statin use and ASCVD risk score as covariates. We performed interaction and mediation models to propose possible pathways for CAC progression.ResultsThe study included 862 adults (53 ± 9 years, 53% women), incidence CAC progression rate: 30.2 (95% CI 25.3–35.8)/1000 person-years. VAT (HR: 1.004, 95% CI 1.001–1.007, p < 0.01) and METS-VF (HR: 1.001, 95% CI 1.0–1.001, p < 0.05) independently predicted CAC progression. VAT-associated CAC progression risk was evident among low-risk ASCVD subjects, and attenuated among medium–high-risk subjects, suggesting that traditional risk factors overcome adiposity in the latter. VAT mediates 51.8% (95% CI 44.5–58.8%) of the effect attributable to IR together with adipose tissue dysfunction on CAC progression.ConclusionsThis study supports the hypothesis that VAT is a mediator of the risk conferred by subcutaneous adipose tissue dysfunction. METS-VF is an efficient clinical surrogate that could facilitate the identification of at-risk adiposity subjects in daily clinical practice.

Statin Intolerance and Noncompliance: An Empiric Approach

Statin Intolerance and Noncompliance: An Empiric Approach

Coronary artery calcification progression and long-term cardiovascular outcomes in renal transplant recipients: an analysis by the joint model.

ABSTRACTBackground Compared with the general population, the risk of death is substantially higher in renal transplant recipients than in age- and sex-matched individuals in the general population. In the general population, coronary artery calcification (CAC) predicts all-cause and cardiovascular mortality. In this study we aimed to analyse these relationships in renal transplant recipients.MethodsWe examined 178 renal transplant patients in this prospective observational cohort study. We measured CAC with multidetector spiral computed tomography using the Agatston score at multiple time points. Overall, 411 scans were performed in 178 patients over an average 12.8 years follow-up. The clinical endpoint was a composite including all-cause death and non-fatal cardiovascular events. Data analysis was performed by the joint model.ResultsDuring a follow-up of 12.8 ± 2.4 years, coronary calcification progressed over time (P < 0.001) and the clinical endpoint occurred in 54 patients. In the analysis by the joint model, both the baseline CAC score and the CAC score progression were strongly associated with the incidence rate of the composite event [hazard ratio 1.261 (95% confidence interval 1.119–1.420), P = 0.0001].ConclusionsCAC at baseline and coronary calcification progression robustly predict the risk of death and cardiovascular events in renal transplant recipients. These findings support the hypothesis that the link between the calcifying arteriopathy of renal transplant patients and clinical end points in these patients is causal in nature.

Predictors for Rapid Progression of Coronary Calcification: An Optical Coherence Tomography Study.

BackgroundThe role of coronary calcification in cardiovascular events and plaque stabilization is still being debated, and factors involved in the progression of coronary calcification are not fully understood. This study aimed to identify the predictors for rapid progression of coronary calcification.Methods and ResultsPatients with serial optical coherence tomography imaging at baseline and at 6 months were selected. Changes in the calcification index and predictors for progression of calcification were studied. Calcification index was defined as the product of the mean calcification arc and calcification length. Rapid progression of calcification was defined as an increase in the calcification index above the median value. Among 187 patients who had serial optical coherence tomography imaging, 235 calcified plaques were identified in 105 patients (56.1%) at baseline. After 6 months, the calcification index increased in 95.3% of calcified plaques from 132.0 to 178.2 (P<0.001). In multivariable analysis, diabetes mellitus (odds ratio [OR], 3.911; P<0.001), chronic kidney disease (OR, 2.432; P=0.037), lipid‐rich plaque (OR, 2.698; P=0.034), and macrophages (OR, 6.782; P<0.001) were found to be independent predictors for rapid progression of coronary calcification. Interestingly, rapid progression of calcification was associated with a significant reduction of inflammatory features (thin‐cap fibroatheroma; from 21.2% to 11.9%, P=0.003; macrophages; from 74.6% to 61.0%, P=0.001).ConclusionsDiabetes mellitus, chronic kidney disease, lipid‐rich plaque, and macrophages were independent predictors for rapid progression of coronary calcification. Baseline vascular inflammation and subsequent stabilization may be related to rapid progression of calcification.RegistrationURL: https://www.clinicaltrials.gov; Unique identifier: NCT01110538.

Coronary 18F-Fluoride Uptake and Progression of Coronary Artery Calcification.

Background Positron emission tomography (PET) using 18F-sodium fluoride (18F-fluoride) to detect microcalcification may provide insight into disease activity in coronary atherosclerosis. This study aimed to investigate the relationship between 18F-fluoride uptake and progression of coronary calcification in patients with clinically stable coronary artery disease. Methods Patients with established multivessel coronary atherosclerosis underwent 18F-fluoride PET-computed tomography angiography and computed tomography calcium scoring, with repeat computed tomography angiography and calcium scoring at one year. Coronary PET uptake was analyzed qualitatively and semiquantitatively in diseased vessels by measuring maximum tissue-to-background ratio. Coronary calcification was quantified by measuring calcium score, mass, and volume. Results In a total of 183 participants (median age 66 years, 80% male), 116 (63%) patients had increased 18F-fluoride uptake in at least one vessel. Individuals with increased 18F-fluoride uptake demonstrated more rapid progression of calcification compared with those without uptake (change in calcium score, 97 [39-166] versus 35 [7-93] AU; P<0.0001). Indeed, the calcium score only increased in coronary segments with 18F-fluoride uptake (from 95 [30-209] to 148 [61-289] AU; P<0.001) and remained unchanged in segments without 18F-fluoride uptake (from 46 [16-113] to 49 [20-115] AU; P=0.329). Baseline coronary 18F-fluoride maximum tissue-to-background ratio correlated with 1-year change in calcium score, calcium volume, and calcium mass (Spearman ρ=0.37, 0.38, and 0.46, respectively; P<0.0001 for all). At the segmental level, baseline 18F-fluoride activity was an independent predictor of calcium score at 12 months (P<0.001). However, at the patient level, this was not independent of age, sex, and baseline calcium score (P=0.50). Conclusions Coronary 18F-fluoride uptake identifies both patients and individual coronary segments with more rapid progression of coronary calcification, providing important insights into disease activity within the coronary circulation. At the individual patient level, total calcium score remains an important marker of disease burden and progression. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02110303.

Predictors for rapid progression of coronary calcification: an optical coherence tomography (OCT) study

Abstract Background The natural progression of coronary calcification has not been systematically studied. In vivo coronary calcium can be evaluated by OCT. Purpose To identify the incidence and predictors for rapid progression of coronary calcification. Methods Patients with serial OCT imaging at baseline and at 6 months were selected from our database. Changes in calcium index during 6-month follow-up and predictors for progression of calcification were studied. Calcium index was defined as the product of the mean calcium arc and calcium length. Rapid progression of calcification was defined as an increase in calcium index above the median value. Results Among 187 patients who had serial OCT imaging, 235 calcified plaques were identified in 108 patients (57.8%) at baseline with median calcium index of 132.0 (Interquartile range 58.5–281.2). After 6 months, the calcium index increased in 95.3% of calcified plaques from 132.0 to 178.2 (p&amp;lt;0.001). In multivariable analysis, diabetes mellitus (DM), chronic kidney disease (CKD), lipid-rich plaque, and macrophages were found to be independent predictors for rapid progression of coronary calcification (table). Interestingly, rapid progression of calcification was associated with a significant reduction of inflammatory features (thin-cap fibroatheroma [TCFA]; baseline 21.2% vs. follow-up 11.9%, p=0.003, macrophages; baseline 74.6% vs. follow-up 61.0%, p=0.001). Conclusions This study demonstrated that DM, CKD, lipid-rich plaque, and macrophages were independent predictors for rapid progression of coronary calcification. High level of vascular inflammation may stimulate rapid progression of calcification. Funding Acknowledgement Type of funding source: None

172Coronary 18F-sodium fluoride uptake predicts progression of coronary arterial calcification

Abstract Background Combined positron emission tomography and computed tomography (PET-CT) using 18F-sodium fluoride (18F-NaF) to detect microcalcification provides the opportunity to gain important insights into disease activity in coronary atherosclerosis. However, the relationship between 18F-NaF uptake and progression of coronary calcification has not been determined. Purpose To determine the relationship between 18F-NaF uptake and progression of coronary calcification in patients with clinically stable coronary artery disease (CAD). Methods Patients with established, multivessel CAD underwent 18F-NaF PET-CT and CT coronary calcium scoring at baseline, with repeat CT calcium scoring at one year. Coronary arterial PET uptake was analysed qualitatively and semi-quantitatively in diseased vessels by measuring maximum tissue-to-background ratio (TBRmax) – defined as the maximum standardised uptake value in a plaque divided by mean blood pool activity measured in the right atrium. Coronary calcification was quantified by measuring calcium mass, volume, average calcium density and total Agatston score (AU). Results In total, 185 patients underwent baseline and repeat imaging (median age 66 years, 80% men), and 118 (64%) had increased 18F-NaF uptake in at least one vessel. Median total calcium score, volume, mass and average density were higher in patients with compared to those without increased 18F-NaF uptake (Table 1). At one year, patients with evidence of increased 18F-NaF uptake demonstrated more rapid progression of coronary calcification (97 [39–166] AU) versus those without uptake (35 [7–93] AU; p&lt;0.0001). Amongst 18F-NaF-positive patients, the calcium score increased only in coronary segments with 18F-NaF uptake (baseline 90.5 [27.5–202] AU versus one year 135.5 [59.3–281.8] AU; p&lt;0.0001) and not in 18F-NaF-negative segments (baseline 44.5 [16–110.5] AU versus one year 46.5 [18.25–114] AU; p=0.446). There was a moderate correlation between TBRmax and change in total calcium score, volume and mass at 1 year (Spearman's Rho = 0.37, 0.38, 0.46 respectively; p&lt;0.0001 for all). Coronary calcification at baseline in PET-negative and PET-positive patients All patients (n=185) 18F-NaF Positive (n=118) 18F-NaF Negative (n=67) P value Agatston Score (AU) 381 [107–892] 541 [245–1130] 136 [55–361] p&lt;0.0001 Calcium Volume (mm3) 358 [131–787] 506 [251–1014] 131 [64–343] p&lt;0.0001 Calcium Mass (mg) 71 [23–155] 100 [48–222] 24 [11–69] p&lt;0.0001 Average Density (mg/mm3) 0.19 [0.17–0.22] 0.20 [0.18–0.23] 0.18 [0.16–0.20] p&lt;0.0001 Conclusions Coronary 18F-NaF uptake identifies both patients and individual coronary segments with greater disease and more rapid progression of coronary calcification over one year. Acknowledgement/Funding AstraZeneca (unrestricted educational grant). British Heart Foundation (CH/09/002, RE/13/3/30183, FS/17/79/33226) Wellcome Trust (WT103782AIA).

Dynamics of Coronary Calcification and Its Association with the Clinical Course of Ischemic Heart Disease and Osteopenic Syndrome

to study the relationship between degree of calcification of coronary arteries, osteopenic syndrome, and clinical courseof ischemic heart disease (IHD) during 3-5 years of follow-up in men after coronary artery bypass grafting (CABG). Materials andmethods. We included in this prospective study 111 men admitted for CABG under cardiopulmonary bypass. All patients underwentcolor duplex scanning (CDS) of brachiocephalic arteries (BCA), coronary angiography, multislice computed tomography (MSCT)of coronary arteries (CAs) to assess the degree of calcification, densitometry of femoral neck. Cardiac calcium score of the vessels wasassessed by the Agatston method. After 3-5 (mean 4.2) years we assessed dead or alive status of 111 patients. Mortality during followupwas 11.7 % (n=13). In 59 of 98 survived patients we repeated CDS of BCA and MSCT of CAs with calculation of CA calcificationscores. Significant CA calcification prior to CABG was detected in more than half of the patients (57.6 %). Among all clinicaland anamnestic factors only one risk factor - smoking was associated with mortality (odds ratio [OR] 9.8, 95 % confidence interval[CI] 1.2-78.1, χ2=6.6, р=0.01). There were no association of mortality with index of CA calcification, Syntax score, osteopenicsyndrome and BCA involvement. In the group of patients with baseline coronary calcification index &gt;400 there were more smokers(р=0.026) and patients with lesions in &gt;3 CAs (р=0.037) compared with the group with values ≤400. At the preoperative stage werevealed associations of CAs calcification index with T-test characterizing presence of the osteopenic syndrome (r= -0.24, р=0.06),Syntax score (r=0.26, р=0.041), and number of affected CAs (r=0.25, р=0.048). At repeated examination 3-5 years after CABG a mediumpositive correlation was detected between the severity of CA calcification and the severity of BCA stenoses (r=0.28, р=0.029).Linear regression analysis with stepwise selection identified baseline (prior to CABG) higher values of T-test evaluated at femoralbone as the only significant predictor of calcium score increase during 3-5 years of follow-up. Dynamics of calcificationof CAs in men with IHD during 3-5 years of follow-up after CABG was multidirectional, but in most cases (66 %) it was progressive.There was correlation between coronary calcification and smoking status and decreased T-test assessed at femoral bone priorto CABG. In the long-term follow-up period the correlation between severity of BCA lesion and severity of coronary calcification wasfound. Negative correlation was detected between progression of coronary calcification and baseline impairment of mineral densityof femoral bone.

Non-traditional risk factors for coronary calcification and its progression in patients with type 2 diabetes: The impact of postprandial glycemia and fetuin-A.

ObjectiveThis study was performed to assess the impact of risk factors on the presence and progression of coronary calcification in patients with type 2 diabetes.MethodsWe prospectively enrolled 45 patients without cardiovascular or kidney disease. Coronary calcification was measured with multidetector computed tomography at baseline and 18 months. We also measured blood pressure; body mass index; serum levels of calcium, phosphate, and 25-hydroxyvitamin D; mineral bone density; and levels of alkaline phosphatase, parathormone, fetuin-A, high-sensitivity C-reactive protein, fibrinogen, albumin, homocysteine, lipids, HbA1c, and average preprandial and postprandial blood glucose at 18 months. Information about severe hypoglycemia and smoking was recorded. Spearman’s correlation coefficients were calculated. Multiple linear regression was used for the multivariate analysis.ResultsThe median baseline calcium score was 63, and that at 18 months was 100. In the univariate analysis, albumin was significantly correlated with the baseline calcium score. Fetuin-A and postprandial glycemia were correlated with calcium score progression. In the multivariate model, postprandial glycemia and fetuin-A were independently associated with calcium score progression.ConclusionsFetuin-A and postprandial glycemia influence coronary calcification progression in patients with type 2 diabetes. The absence of some correlations could be due to pharmacological treatments for cardiovascular risk reduction.

Effect of spironolactone on the progression of coronary calcification in peritoneal dialysis patients: a pilot study.

ABSTRACTIntroduction:There is evidence that aldosterone plays a role in the pathogenesis of vascular calcification. The aim of this study was to evaluate the effect of spironolactone, a mineralocorticoid receptor antagonist, on the progression of coronary calcification (CC) in peritoneal dialysis patients and to identify the factors involved in this progression.Methods:Thirty-three patients with a coronary calcium score (CCS) ≥ 30, detected through multi-detector computed tomography (MDCT) and expressed in Agatston units, were randomly assigned to a group receiving 25mg spironolactone per day for 12 months (spironolactone group) and a control group not receiving this drug. The primary outcome was a percentage change in CCS from baseline to end of the study (relative progression), when a further MDCT was conducted. Patients who had progression of CC were compared with those who did not progress.Results:Sixteen patients, seven in the spironolactone group and nine in the control group, concluded the study. The relative progression of the CCS was similar in both groups, 17.2% and 27.5% in the spironolactone and control groups respectively. Fifty-seven percent of the treated patients and 67% of those in the control group presented progression in the CC scores (p = 0.697). Progressor patients differed from non-progressors because they presented higher levels of calcium and low-density lipoprotein cholesterol and lower levels of albumin.Conclusion: In peritoneal dialysis patients, spironolactone did not attenuate the progression of CC. However, large-scale studies are needed to confirm this observation. Disorders of mineral metabolism and dyslipidemia are involved in the progression of CC.

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.

A Double-Blind Randomised Placebo Controlled 2 × 2 Factorial Trial of the Effect of Vitamin K and Colchicine on Vascular Calcification Activity in Subjects With Diabetes Mellitus: The Rationale and Design of the Vikcovac Diabetes Trial

Introduction: Cardiovascular disease is the leading cause of death in the Western world. Diabetes mellitus confers a doubling in risk of cardiovascular disease. Computed tomographic (CT) coronary calcium scoring (CCS) is an effective method for cardiovascular risk stratification in asymptomatic individuals. The rate of progression of coronary calcium on consecutive CT scans provides further cardiovascular disease-risk stratification capabilities. Patients with no progression of their CCS are at low risk of cardiovascular disease events [ [1] Budoff M. et al. J Am Coll Cardiol. 2013; 61: 1231-1239 Crossref PubMed Scopus (268) Google Scholar ]. There are no known therapies that prevent vascular calcification (VC). 18F-Sodium Fluoride Positron Emission Tomography is a novel molecular imaging modality that identifies regions of vascular calcification activity that subsequently develop into established macrocalcifications, allowing a unique approach for clinical trials studying potential modifiers of CCS [ [2] Irkle A. et al. Nature Commun. 2015; 6: 7495 Crossref PubMed Scopus (314) Google Scholar ].

Differential Impact of Chronic Kidney Disease on Coronary Calcification and Atherosclerosis in Asymptomatic Individuals with or without Diabetes: Analysis from a Coronary Computed Tomographic Angiography Registry

Aim: The aim of this study was to assess the combined effects of chronic kidney disease (CKD) and diabetes on the extent and developmental pattern of coronary artery disease (CAD). Methods: A total of 3,017 self-referred asymptomatic individuals without known CAD who underwent 64-channel dual-source coronary computed tomography angiography between 2006 and 2010 were enrolled. The patients were divided into six groups based on their diabetes status (nondiabetic or diabetic) and estimated glomerular filtration rate (eGFR) (eGFR > 90 mL/min/1.73 m², normal renal function; eGFR 60–89, mild CKD; or eGFR 30–59, moderate CKD). We compared the coronary artery calcium score (CACS), segment stenosis score (SSS), and ≥50% obstructive CAD among the groups. Results: In nondiabetics, whereas SSS and ≥50% obstructive CAD were not different as renal function deteriorated, after adjusting for cardiovascular risk factors, CACS showed a unique developmental pattern: no CACS increase until mild CKD, but abrupt increase from the stage of moderate CKD (moderate vs. normal renal function, adjusted OR 5.118, 95% CI 1.293–20.262, p = 0.020). In diabetics, patients from the stage of mild CKD were more likely to have ≥50% obstructive CAD (p = 0.004), higher CACS (p = 0.020), and SSS (p = 0.001) in multivariable analysis. Conclusions: The presence of CKD did not have a significant impact on the development of coronary atherosclerosis, but affected the progression of coronary calcification more markedly from the stage of moderate CKD in nondiabetics. However, in diabetics, the deterioration of renal function was significantly associated with the development of coronary atherosclerosis and calcification from the stage of mild CKD.

Serial Assessment of Tissue Precursors and Progression of Coronary Calcification Analyzed by Fusion of IVUS and OCT: 5-Year Follow-Up of Scaffolded and Nonscaffolded Arteries

ObjectivesThe aim of this study was to assess calcium growth with fused grayscale intravascular ultrasound (IVUS), IVUS–virtual histology, and optical coherence tomography (OCT) from baseline to 5-year follow-up in patients treated with bioresorbable vascular scaffolds. BackgroundIVUS and OCT have individual strengths in assessing plaque composition and volume. Fusion of images obtained using these methods could potentially aid in coronary plaque assessment. MethodsAnatomic landmarks and endoluminal radiopaque markers were used to fuse OCT and IVUS images and match baseline and follow-up. ResultsSeventy-two IVUS–virtual histology and OCT paired matched cross-sectional in- and out-scaffold segments were fused at baseline and follow-up. In total, 46 calcified plaques at follow-up were detected using the fusion method (33 in-scaffold, 13 out-scaffold), showing either calcium progression (52.2%) or de novo calcifications (47.8%). On OCT, calcification volume increased from baseline to follow-up by 2.3 ± 2.4 mm3 (p = 0.001). The baseline virtual histologic tissue precursors of dense calcium at follow-up were necrotic core in 73.9% and fibrous or fibrofatty plaque in 10.9%. In 15.2%, calcium was already present at baseline. Precursors on OCT were lipid pool in 71.2%, fibrous plaque in 4.3%, and fibrocalcific plaque in 23.9%. ConclusionsThe use of OCT and IVUS fusion imaging shows similar calcium growth in- and out-scaffold segments. Necrotic core is the most frequent precursor of calcification. The scaffold resorption process creates a tissue layer that re-caps the calcified plaques. (Absorb Clinical Investigation, Cohort B [ABSORB B]; NCT00856856)

Left ventricular function at two-year follow-up in treatment-naive rheumatoid arthritis patients is associated with anti-cyclic citrullinated peptide antibody status: a cohort study

Objectives: In rheumatoid arthritis (RA), the role of autoimmunity, especially anti-cyclic citrullinated peptide antibody (anti-CCP) level, and the time-course of left ventricular (LV) function is unknown. The objective was to assess LV function and the amount of coronary calcium in relation to anti-CCP levels in a cohort of treatment-naive RA patients, and to assess changes in these parameters during a 2 year follow-up period.Method: Sixty-six steroid- and disease-modifying anti-rheumatic drug-naive RA patients were treated with methotrexate according to the Danish national guidelines. We assessed LV function by conventional echocardiography and speckle-tracking echocardiography. We estimated the amount and progression of coronary calcium by coronary computed tomography. Patients were examined at the time of diagnosis and after 2 years.Results: Patients with elevated anti-CCP at baseline and after 2 years, compared to those with non-persistently elevated anti-CCP, had significantly less improvement in S´ (1 ± 1.4 cm/s vs 0.2 ± 0.9 cm/s; p = 0.04) and a worsening in global longitudinal systolic strain (GLS) (0.6 ± 1.8% vs −1 ± 2.8%; p = 0.04). There was a significant correlation between ΔGLS over 2 years and anti-CCP at 2 year follow-up (r = 0.36; p = 0.006). We observed a small progression of coronary calcium score during the 2 year follow-up period. No differences in progression were found between patients with high anti-CCP titres at baseline and 2 year follow-up (n = 12) and patients with normal/low anti-CCP titres (n = 32) (23.8 ± 40.3 vs 22.6 ± 68.9; p = 0.96).Conclusions: Deformation analysis by speckle-tracking echocardiography is a valuable tool to detect early development of myocardial dysfunction despite normal ejection fraction in RA.