Progression Of Noncalcified Plaque Research Articles

Effects of high- versus low-intensity lipid-lowering treatment in patients undergoing serial coronary computed tomography angiography: results of the multi-center LOCATE study.

To evaluate the effects of lipid-lowering medications of different intensities on total, calcified, and non-calcified plaque volumes in patients undergoing serial cardiac computed tomography angiography (CCTA). Individuals with chronic coronary syndromes from 11 centers were included in a retrospective registry. Total, calcified, and non-calcified plaque volumes were quantified and the relative difference in plaque volumes between baseline and follow-up CCTA was calculated. The intensity of lipid-lowering treatment was designated as low, moderate, or high, based on current recommendations. Of 216 patients (mean age 63.1 ± 9.7years), undergoing serial CCTA (median timespan = 824.5 [IQR = 463.0-1323.0] days), 89 (41.2%) received no or low-intensity lipid-lowering medications, and 80 (37.0%) and 47 (21.8%) moderate- and high-intensity lipid-lowering agents, respectively. Progression of total and non-calcified plaque was attenuated in patients on moderate-/high- versus those on no/low-intensity treatment and arrested in patients treated with high-intensity statins or PCSK9 inhibitors (p < 0.001). Halted increase of non-calcified plaque was associated with LDL-cholesterol reduction (p < 0.001), whereas calcified plaque mass and Agatston score increased irrespective of the lipid-lowering treatment (p = NS). The intensity of lipid-lowering therapy robustly predicted attenuation of non-calcified plaque progression as a function of the time duration between the two CCTA scans, and this was independent of age and cardiovascular risk factors (HR = 3.83, 95% CI = 1.81-8.05, p < 0.001). The LOCATE multi-center observational study shows that progression of non-calcified plaques, which have been previously described as precursors of acute coronary syndromes, can be attenuated with moderate-intensity, and arrested with high-intensity lipid-lowering therapy. DRKS00031954.

Longitudinal assessment of coronary plaque regression related to sodium–glucose cotransporter-2 inhibitor using coronary computed tomography angiography

BackgroundSodium–Glucose Cotransporter-2 Inhibitor (SGLT2i) is a novel oral drug for treating type 2 diabetes mellitus (T2DM) with demonstrated cardiovascular benefits. Previous studies in apolipoprotein E knockout mice have shown that SGLT2i is associated with attenuated progression of atherosclerosis. However, whether this effect extends to T2DM patients with coronary atherosclerosis in real-world settings remains unknown.MethodsIn this longitudinal cohort study using coronary computed tomography angiography (CCTA), T2DM patients who underwent ≥ 2 CCTA examinations at our center between 2019 and 2022 were screened. Eligible patients had multiple study plaques, defined as non-obstructive stenosis at baseline and not intervened during serial CCTAs. Exclusion criteria included a CCTA time interval < 12 months, prior SGLT2i treatment, or initiation/discontinuation of SGLT2i during serial CCTAs. Plaque volume (PV) and percent atheroma volume (PAV) were measured for each study plaque using CCTA plaque analysis software. Patients and plaques were categorized based on SGLT2i therapy and compared using a 1:1 propensity score matching (PSM) analysis.ResultsThe study included 236 patients (mean age 60.5 ± 9.5 years; 69.1% male) with 435 study plaques (diameter stenosis ≥ 50%, 31.7%). Following SGLT2i treatment for a median duration of 14.6 (interquartile range: 13.0, 20.0) months, overall, non-calcified, and low-attenuation PV and PAV were significantly decreased, while calcified PV and PAV were increased (all p < 0.001). Meanwhile, reductions in overall PV, non-calcified PV, overall PAV, and non-calcified PAV were significantly greater in SGLT2i-treated compared to non-SGLT2i-treated plaques (all p < 0.001). PSM analysis showed that SGLT2i treatment was associated with higher reductions in overall PV (− 11.77 mm3 vs. 4.33 mm3, p = 0.005), non-calcified PV (− 16.96 mm3 vs. − 1.81 mm3, p = 0.017), overall PAV (− 2.83% vs. 3.36%, p < 0.001), and non-calcified PAV (− 4.60% vs. 0.70%, p = 0.003). These findings remained consistent when assessing annual changes in overall and compositional PV and PAV. Multivariate regression models demonstrated that SGLT2i therapy was associated with attenuated progression of overall or non-calcified PV or PAV, even after adjusting for cardiovascular risk factors, medications, and baseline overall or non-calcified PV or PAV, respectively (all p < 0.05). The effect of SGLT2i on attenuating non-calcified plaque progression was consistent across subgroups (all p for interaction > 0.05).ConclusionsIn this longitudinal CCTA cohort of T2DM patients, SGLT2i therapy markedly regressed coronary overall PV and PAV, mainly result from a significant reduction in non-calcified plaque.Graphical abstract

Effects of Pitavastatin on Coronary Artery Disease and Inflammatory Biomarkers in HIV: Mechanistic Substudy of the REPRIEVE Randomized Clinical Trial.

Cardiovascular disease (CVD) is increased in people with HIV (PWH) and is characterized by premature noncalcified coronary plaque. In the Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE), pitavastatin reduced major adverse cardiovascular events (MACE) by 35% over a median of 5.1 years. To investigate the effects of pitavastatin on noncalcified coronary artery plaque by coronary computed tomography angiography (CTA) and on inflammatory biomarkers as potential mechanisms for MACE prevention. This double-blind, placebo-controlled randomized clinical trial enrolled participants from April 2015 to February 2018 at 31 US clinical research sites. PWH without known CVD who were taking antiretroviral therapy and had low to moderate 10-year CVD risk were included. Data were analyzed from April to November 2023. Oral pitavastatin calcium, 4 mg per day. Coronary CTA and inflammatory biomarkers at baseline and 24 months. The primary outcomes were change in noncalcified coronary plaque volume and progression of noncalcified plaque. Of 804 enrolled persons, 774 had at least 1 evaluable CTA. Plaque changes were assessed in 611 who completed both CT scans. Of 611 analyzed participants, 513 (84.0%) were male, the mean (SD) age was 51 (6) years, and the median (IQR) 10-year CVD risk was 4.5% (2.6-7.0). A total of 302 were included in the pitavastatin arm and 309 in the placebo arm. The mean noncalcified plaque volume decreased with pitavastatin compared with placebo (mean [SD] change, -1.7 [25.2] mm3 vs 2.6 [27.1] mm3; baseline adjusted difference, -4.3 mm3; 95% CI, -8.6 to -0.1; P = .04; 7% [95% CI, 1-12] greater reduction relative to placebo). A larger effect size was seen among the subgroup with plaque at baseline (-8.8 mm3 [95% CI, -17.9 to 0.4]). Progression of noncalcified plaque was 33% less likely with pitavastatin compared with placebo (relative risk, 0.67; 95% CI, 0.52-0.88; P = .003). Compared with placebo, the mean low-density lipoprotein cholesterol decreased with pitavastatin (mean change: pitavastatin, -28.5 mg/dL; 95% CI, -31.9 to -25.1; placebo, -0.8; 95% CI, -3.8 to 2.2). The pitavastatin arm had a reduction in both oxidized low-density lipoprotein (-29% [95% CI, -32 to -26] vs -13% [95% CI, -17 to -9]; P < .001) and lipoprotein-associated phospholipase A2 (-7% [95% CI, -11 to -4] vs 14% [95% CI, 10-18]; P < .001) compared with placebo at 24 months. In PWH at low to moderate CVD risk, 24 months of pitavastatin reduced noncalcified plaque volume and progression as well as markers of lipid oxidation and arterial inflammation. These changes may contribute to the observed MACE reduction in REPRIEVE. ClinicalTrials.gov Identifier: NCT02344290.

Eicosapentaenoic and docosahexaenoic acid supplementation and coronary artery calcium progression in patients with coronary artery disease: A secondary analysis of a randomized trial

Background and aimsWe previously reported that an omega-3 fatty acid index ≥4% with high-dose eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) prevented progression of noncalcified plaque. Higher coronary artery calcium (CAC) scores and progression of CAC are associated with increased cardiovascular events and mortality. We examined the effect of EPA + DHA on CAC score. MethodsA total of 242 patients with coronary artery disease (CAD) on statin therapy were randomized to 1.86 g EPA and 1.5 g DHA daily or none (control) for 30 months. The CAC score was measured at baseline and 30-months with non-contrast, cardiac computed tomography. ResultsBoth EPA + DHA and control groups had significant progression in CAC scores over 30 months (median change:183.5 vs 221.0, respectively, p < 0.001) despite a 13.6% reduction in triglyceride level with EPA + DHA. No significant difference was observed between groups for the total group, by baseline CAC scores of <100, 100–399, 400–999 and ≥1000 or quartiles of achieved levels of EPA, DHA and the omega-3 fatty acid index. Similar rates of CAC progression were noted in those on high-intensity statin compared to low- and moderate-intensity statin. ConclusionsEPA and DHA added to statin resulted in similar CAC progression over 30 months regardless of baseline CAC categories, statin intensity and achieved levels of EPA, DHA and the omega-3 fatty acid index.

Effects of renin-angiotensin-aldosterone-system inhibitors on coronary atherosclerotic plaques: The PARADIGM registry

Background and aimsInhibition of Renin-Angiotensin-Aldosterone-System (RAAS) has been hypothesized to improve endothelial function and reduce plaque inflammation, however, their impact on the progression of coronary atherosclerosis is unclear. We aim to study the effects of RAAS inhibitor on plaque progression and composition assessed by serial coronary CT angiography (CCTA). MethodsWe performed a prospective, multinational study consisting of a registry of patients without history of CAD, who underwent serial CCTAs. Patients using RAAS inhibitors were propensity matched to RAAS inhibitor naïve patients based on clinical and CCTA characteristics at baseline. Atherosclerotic plaques in CCTAs were quantitatively analyzed for percent atheroma volume (PAV) according to plaque composition. Interactions between RAAS inhibitor use and baseline PAV on plaque progression were assessed in the unmatched cohort using a multivariate linear regression model. ResultsOf 1248 patients from the registry, 299 RAAS inhibitor taking patients were matched to 299 RAAS inhibitor naïve patients. Over a mean interval of 3.9 years, there was no significant difference in annual progression of total PAV between RAAS inhibitor naïve vs taking patients (0.75 vs 0.79%/year, p = 0.66). With interaction testing in the unmatched cohort, however, RAAS inhibitor use was significantly associated with lower non-calcified plaque progression (Beta coefficient −0.100, adjusted p = 0.038) with higher levels of baseline PAV. ConclusionsThe use of RAAS inhibitors over a period of nearly 4 years did not significantly impact on total atherosclerotic plaque progression or various plaque components. However, interaction testing to assess the differential effect of RAAS inhibition based on baseline PAV suggested a significant decrease in progression of non-calcified plaque in patients with a higher burden of baseline atherosclerosis, which should be considered hypothesis generating.

Impact of immune checkpoint inhibitors on atherosclerosis progression in patients with lung cancer

BackgroundPatients with lung cancer face a heightened risk of atherosclerosis-related cardiovascular events. Despite the strong scientific rationale, there is currently a lack of clinical evidence examining the impact of immune...

Abstract 13889: Effect of Eicosapentaenoic and Docosahexaenoic Acid Supplementation on Noncalcified Coronary Plaque and Coronary Artery Calcium Score in Subjects With Coronary Artery Disease According to Hypertension Status

Introduction: Higher amounts of noncalcified plaque and higher coronary artery calcium (CAC) scores are associated with increased cardiovascular events and mortality. The effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on noncalcified coronary plaque and more advanced calcified plaque as measured by the CAC score according to hypertensive (HTN) status is unknown. Methods: A total of 242 subjects with coronary artery disease (CAD) on statin were randomized to 3.36 g of EPA+DHA or none (control) for 30 months. Coronary plaque composition and CAC scores were measured with computed tomographic coronary angiography at baseline and 30-month follow-up. Results: Mean (SD) age was 63.1 years (7.7); mean (SD) LDL-C: 77.8 mg/dL (27.3) and median [IQR] triglyceride (TG): 117.5 mg/dL [81.3,166.8]. Despite a significantly higher CAC score at baseline in HTN subjects, both HTN and normotensive (NTN) subjects had similar CAC progression over 30 months with no difference between EPA+DHA and control groups (Figure B). NTN subjects on EPA+DHA had a 20.7% reduction in TG level and 36.6% lower neutrophil count, a marker of inflammation, and lack of progression of noncalcified plaque compared to control who had progression (median % change: -7.6 vs 13.2 mm 3 /mm, P=0.008) (Figure A). In contrast, HTN subjects on EPA+DHA and control had progression of noncalcified coronary plaque with no significant difference between the two groups (Figure A) Conclusions: EPA+DHA prevented progression of noncalcified plaque in NTN subjects but not HTN subjects with no effect on more advanced plaque which has calcified in the setting of low LDL-C and TG levels. The benefit of EPA+DHA in CAD patients on statin therapy appears limited to noncalcified coronary plaque in NTN subjects. Whether this benefit is related to more favorable effects on inflammation based on blood pressure status should be examined further.

Progression of whole-heart Atherosclerosis by coronary CT and major adverse cardiovascular events

BackgroundThe current study aimed to examine the independent prognostic value of whole-heart atherosclerosis progression by serial coronary computed tomography angiography (CCTA) for major adverse cardiovascular events (MACE). MethodsThe multi-center PARADIGM study includes patients undergoing serial CCTA for symptomatic reasons, ≥2 years apart. Whole-heart atherosclerosis was characterized on a segmental level, with co-registration of baseline and follow-up CCTA, and summed to per-patient level. The independent prognostic significance of atherosclerosis progression for MACE (non-fatal myocardial infarction [MI], death, unplanned coronary revascularization) was examined. Patients experiencing interval MACE were not omitted. ResultsThe study population comprised 1166 patients (age 60.5 ​± ​9.5 years, 54.7% male) who experienced 139 MACE events during 8.2 (IQR 6.2, 9.5) years of follow up (15 death, 5 non-fatal MI, 119 unplanned revascularizations). Whole-heart percent atheroma volume (PAV) increased from 2.32% at baseline to 4.04% at follow-up. Adjusted for baseline PAV, the annualized increase in PAV was independently associated with MACE: OR 1.23 (95% CI 1.08, 1.39) per 1 standard deviation increase, which was consistent in multiple subpopulations. When categorized by composition, only non-calcified plaque progression associated independently with MACE, while calcified plaque did not. Restricting to patients without events before follow-up CCTA, those with future MACE showed an annualized increase in PAV of 0.93% (IQR 0.34, 1.96) vs 0.32% (IQR 0.02, 0.90), P ​< ​0.001. ConclusionsWhole-heart atherosclerosis progression examined by serial CCTA is independently associated with MACE, with a prognostic threshold of 1.0% increase in PAV per year.

Impact of Clinical Characteristics and Statins on Coronary Plaque Progression by Serial Computed Tomography Angiography.

Background Progression of coronary artery disease using serial coronary computed tomography angiography (CTA) is of clinical interest. Our primary aim was to prospectively assess the impact of clinical characteristics and statin use on quantitatively assessed coronary plaque progression in a low-risk study population during long-term follow-up. Methods Patients who previously underwent coronary CTA for suspected coronary artery disease were prospectively included to undergo follow-up coronary CTA. The primary end point was coronary artery disease progression, defined as the absolute annual increase in total, calcified, and noncalcified plaque volume by quantitative CTA analysis. Results In total, 202 patients underwent serial coronary CTA with a mean interscan period of 6.2±1.4 years. On a per-plaque basis, increasing age (β=0.070; P=0.058) and hypertension (β=1.380; P=0.075) were nonsignificantly associated with annual total plaque progression. Male sex (β=1.676; P=0.009), diabetes mellitus (β=1.725; P=0.012), and statin use (β=1.498; P=0.046) showed an independent association with annual progression of calcified plaque. While hypertension (β=2.259; P=0.015) was an independent determinant of noncalcified plaque progression, statin use (β=-2.178; P=0.050) was borderline significantly associated with a reduced progression of noncalcified plaque. Conclusions Statin use was associated with an increased progression of calcified coronary plaque and a reduced progression of noncalcified coronary plaque, potentially reflecting calcification of the noncalcified plaque component. Whereas hypertension was the only modifiable risk factor predictive of noncalcified plaque progression, diabetes mellitus mainly led to an increase in calcified plaque. These findings could yield the need for intensified preventive treatment of patients with diabetes mellitus and hypertension to slow and stabilize coronary artery disease progression and improve clinical outcome.

Biomarkers and Noncalcified Coronary Artery Plaque Progression in Older Men Treated With Testosterone.

Recent results from the Cardiovascular Trial of the Testosterone Trials showed that testosterone treatment of older men with low testosterone was associated with greater progression of noncalcified plaque (NCP). We evaluated the effect of anthropometric measures and cardiovascular biomarkers on plaque progression in individuals in the Testosterone Trial. The Cardiovascular part of the trial included 170 men aged 65 years or older with low testosterone. Participants received testosterone gel or placebo gel for 12 months. The primary outcome was change in NCP volume from baseline to 12 months, as determined by coronary computed tomography angiography (CCTA). We assayed several markers of cardiovascular risk and analyzed each marker individually in a model as predictive variables and change in NCP as the dependent variable. Of 170 enrollees, 138 (73 testosterone, 65 placebo) completed the study and were available for the primary analysis. Of 10 markers evaluated, none showed a significant association with the change in NCP volume, but a significant interaction between treatment assignment and waist-hip ratio (WHR) (P = 0.0014) indicated that this variable impacted the testosterone effect on NCP volume. The statistical model indicated that for every 0.1 change in the WHR, the testosterone-induced 12-month change in NCP volume increased by 26.96 mm3 (95% confidence interval, 7.72-46.20). Among older men with low testosterone treated for 1 year, greater WHR was associated with greater NCP progression, as measured by CCTA. Other biomarkers and anthropometric measures did not show statistically significant association with plaque progression.

Coronary Artery Calcium Progression Is Associated With Coronary Plaque Volume Progression: Results From a Quantitative Semiautomated Coronary Artery Plaque Analysis

ObjectivesThe aim of this study was to determine whether coronary artery calcium (CAC) progression was associated with coronary plaque progression on coronary computed tomographic angiography. BackgroundCAC progression and coronary plaque characteristics are associated with incident coronary heart disease. However, natural history of coronary atherosclerosis has not been well described to date, and the understanding of the association between CAC progression and coronary plaque subtypes such as noncalcified plaque progression remains unclear. MethodsConsecutive patients who were referred to our clinic for evaluation and had serial coronary computed tomography angiography scans performed were included in the study. Coronary artery plaque (total, fibrous, fibrous-fatty, low-attenuation, densely calcified) volumes were calculated using semiautomated plaque analysis software. ResultsA total of 211 patients (61.3 ± 12.7 years of age, 75.4% men) were included in the analysis. The mean interval between baseline and follow-up scans was 3.3 ± 1.7 years. CAC progression was associated with a significant linear increase in all types of coronary plaque and no plaque progression was observed in subjects without CAC progression. In multivariate analysis, annualized and normalized total plaque (β = 0.38; p < 0.001), noncalcified plaque (β = 0.35; p = 0.001), fibrous plaque (β = 0.56; p < 0.001), and calcified plaque (β = 0.63; p = 0.001) volume progression, but not fibrous-fatty (β = 0.03; p = 0.28) or low-attenuation plaque (β = 0.11; p = 0.1) progression, were independently associated with CAC progression. Plaque progression did not differ between the sexes. A significantly increased total and calcified plaque progression was observed in statin users. ConclusionsIn a clinical practice setting, progression of CAC was significantly associated with an increase in both calcified and noncalcified plaque volume, except fibrous-fatty and low-attenuation plaque. Serial CAC measurements may be helpful in determining the need for intensification of preventive treatment.

Coronary Plaque Progression and Regression in Asymptomatic African American Chronic Cocaine Users With Obstructive Coronary Stenoses: A Preliminary Study.

Although rapid progression of coronary atherosclerosis was observed in chronic cocaine users, it is unknown whether reduced cocaine use retards the progression of atherosclerosis. We investigated whether reduced cocaine use over a 12-month period was associated with coronary plaque regression in cocaine users. Fifteen African American chronic cocaine users with previously coronary computed tomography angiography (CCTA)-confirmed >50% coronary stenosis in Baltimore, Maryland, were enrolled in a study to investigate whether reduced cocaine use is associated with changes in coronary plaque burden over a 12-month period of cash-based incentive intervention, which was implemented to systematically reinforce cocaine abstinence. In addition to previous CCTA (preintervention), CCTA was performed at the intervention baseline and at postintervention. Plaque analyses were performed to determine the trajectory of plaque changes in the absence of intervention by comparing the preintervention with the intervention baseline studies; the trajectory of plaque changes associated with the intervention by comparing the intervention baseline with the postintervention studies; and (3) whether reduced cocaine use was independently associated with changes in coronary plaque burden. During the 12-month cash-based incentive intervention period, cocaine use in participants was lower. The medians of noncalcified plaque indices were 37.8 (interquartile range [IQR] 29.3-44.0), 43.1 (IQR 38.3-49.0), and 38.7 (IQR 31.2-46.8) mm at preintervention, intervention baseline, and postintervention, respectively. Multivariable generalized estimating equation analysis showed that both total plaque and noncalcified plaque indices at preintervention were significantly lowered as compared with intervention baseline levels; both total plaque and noncalcified plaque indices after intervention were significantly lowered as compared with intervention baseline levels; and reduced cocaine use was independently associated with lower total plaque volume index (P < 0.0001) and noncalcified plaque volume index (P = 0.010). Our findings suggest that continued cocaine use may be associated with noncalcified plaque progression, whereas reduced cocaine use may be associated with noncalcified plaque regression. Larger studies are needed to confirm these findings.

Effect of Targeting Inflammation With Salsalate: The TINSAL-CVD Randomized Clinical Trial on Progression of Coronary Plaque in Overweight and Obese Patients Using Statins.

Inflammation may contribute to pathological associations among obesity, diabetes mellitus, and cardiovascular disease. To determine whether targeting inflammation using salsalate compared with placebo reduces progression of noncalcified coronary artery plaque. In the Targeting Inflammation Using Salsalate in Cardiovascular Disease (TINSAL-CVD) trial participants were randomly assigned between September 23, 2008, and July 5, 2012, to 30 months of salsalate or placebo in addition to standard, guideline-based therapies. Randomization was computerized and centrally allocated, with patients, health care professionals, and researchers masked to treatment assignment. Participants were overweight and obese statin-using patients with established, stable coronary heart disease. Salsalate (3.5 g/d) or placebo orally over 30 months. The primary outcome was progression of noncalcified coronary artery plaque assessed by multidetector computed tomographic angiography. Secondary outcomes were other measures of safety and efficacy. Two hundred fifty-seven participants were randomized to salsalate (n = 129) or placebo (n = 128). Their mean (SD) age was 60.8 (7.0) years, and 94.0% (236 of 251) were male. One hundred ninety participants (89 in the salsalate group and 101 in the placebo group) completed the study. Compared with baseline, there was no increase in noncalcified plaque volume in the placebo-treated patients and no difference in change between the salsalate and placebo groups (mean difference, -1 mm3; 95% CI, -11 to 9 mm3; P = .87). Salsalate treatment decreased total white blood cell, lymphocyte, monocyte, and neutrophil counts and increased adiponectin levels without change in C-reactive protein levels. Fasting glucose, triglycerides, uric acid, and bilirubin levels were decreased in the salsalate group compared with the placebo group, while hemoglobin levels were increased. Urinary albumin levels increased, with tinnitus and atrial arrhythmias more common, in the salsalate group compared with the placebo group. Salsalate when added to current therapies that include a statin does not reduce progression of noncalcified coronary plaque volume assessed by multidetector computed tomographic angiography in statin-using patients with established, stable coronary heart disease. The absence of progression of noncalcified plaque volume in the placebo group may limit interpretation of the trial results. clinicaltrials.gov Identifier: NCT00624923.

Abstract 19494: 3D Volumetric Assessment of Coronary Plaque Change in Asymptomatic Subjects in Response to Therapy Using CT Angiography

Introduction: Studies using intravascular ultrasound have demonstrated that plaque can regress after statin treatment. However, due to the invasive nature of this method data on asymptomatic individuals is scarce. CT angiography (CTA) data on change in plaque volume has shown variable success and has been evaluated mainly in high risk individuals. The aim of this study was to determine the change in coronary plaque in asymptomatic subjects undergoing statin treatment. Methods: Study subjects were recruited from an ongoing study (‘Randomized Trial of Imaging Versus Risk Factor-Based Therapy for Plaque Regression’). CTA (320-slice) was performed at baseline and after 2 years using a consistent protocol (kVp 120 or 100 kVp, iodine dose base on body weight). Plaque lesions (n = 100) were measured at baseline and follow up using customized tools to align coronary datasets based on anatomic landmarks. Plaque components were assessed by stratification of change in plaque volume by age. Results: The mean subject age was 64 years (81 % male). The mean Framingham risk was 11%. The median statin dose was 40 mg simvastatin or equivalent. Plaque characterization showed that younger subjects had a significantly higher proportion of non-calcified plaque subcomponents compared with older subjects (86% vs 62% respectively, p ≤ 0.01). The median change in total and non-calcified plaque volume was +2.9% and -5.9% respectively (not statistically significant from 0). Overall 36% of the lesions showed progression of non-calcified plaque while 64% showed regression. Of note, older subjects (over 65y) showed progression of total plaque volume while younger subjects showed no significant change. Younger subjects experienced more reduction in non-calcified plaque volume compared with older subjects (median -12.1% vs -2% respectively, p=0.02). Conclusions: Approximately 2/3 of the lesions showed plaque regression with 40 mg equivalent simvastatin dose over two years. Younger subjects (≤ 65 years) had larger percentages of soft plaque than older subjects, and showed significantly more regression of non-calcified plaque in relationship to statin therapy. Change in plaque using 3D volumetric registration of CTA data appears feasible and may help determine response to therapy.

The impact of central obesity on accelerated progression of noncalcified coronary plaque assessed by coronary CT angiography: a 4-year-follow-up study

Purpose: Although excess visceral adipose tissue (VAT) is more strongly associated with risk factors of coronary artery disease (CAD) than body mass index (BMI) or waist circumference, an association between VAT and CAD progression has not been fully evaluated. The aim of this study was to investigate whether adding VAT measurements to CAD risk factors provides better risk assessment for progression of calcified and noncalcified coronary plaque on coronary CT angiography. Methods: This prospective cohort study comprised 553 CAD patients with calcified and noncalcified coronary plaque with ≤ 50% coronary stenosis as assessed by coronary CT angiography. Quantification of VAT area was performed using abdominal CT scanning. Results: After a mean 55±8 month follow-up, 332 patients underwent repeated CT scans for worsening angina symptoms without findings of positive ischemia. Increased segments of noncalcified plaque were seen in 161 (48%) and increases above the median calcium score were seen in 168 (51%) patients. The risk for progression of noncalcified plaque increased steadily with higher VAT quartiles, independent of CAD risk factors. Patients in the higher VAT quartiles were at increased risk of progression of noncalcified plaque (quartiles IV OR 5.5; 95% CI 2.8-11.0, p-value < 0.001). In contrast, increases above the median calcium score showed no independent correlation to VAT. Progression of noncalcified plaque showed no phased increase with either higher waist circumference or BMI quartiles. Conclusions: Excess VAT was positively associated with progression of noncalcified coronary plaque, but not of calcified plaque. This suggests that risk assessment of progression of noncalcified plaque can be improved by combining VAT measurements and CAD risk factors.

Visceral abdominal fat accumulation predicts the progression of noncalcified coronary plaque

BackgroundExcess visceral abdominal tissue (VAT) is more strongly associated with risk factors of coronary artery disease (CAD) than body mass index (BMI) or waist circumference. However, whether adding VAT measurements to CAD risk factors provides better risk assessment for CAD progression has not been fully evaluated. Methods and resultsThis prospective cohort study comprised 553 CAD patients with coronary plaque with ≤50% coronary stenosis as assessed by computed tomography (CT) angiography. Quantification of VAT area was performed together with CT angiography using abdominal CT scanning. After a mean 38±8months follow-up, 320 patients underwent repeated CT scans for worsening angina symptoms without findings of positive ischemia. Increased segments of noncalcified plaque were seen in 152 (48%) and an increased calcium score was seen in 261 (82%) patients. The risk for progression of noncalcified plaque increased steadily with higher VAT quartiles, independent of CAD risk factors. Patients in the higher quartiles were at increased risk of progression of noncalcified plaque (quartiles IV OR 4.7; 95% CI 2.3–9.4, p-value<0.001). In contrast, increases above the median calcium score showed no independent correlation to VAT. Compared to VAT, progression of noncalcified plaque showed no phased increase with higher waist circumference and weaker increase with higher BMI quartiles. ConclusionVAT accumulation was positively associated with progression of coronary noncalcified plaque, but not of calcified plaque. This suggests that risk assessment of progression of noncalcified plaque can be improved by combining VAT measurements and CAD risk factors.