Cardiovascular events, including myocardial infarction and stroke, are the primary causes of mortality in both type 1 and type 2 diabetes. Affected patients frequently have asymptomatic coronary artery disease. Studies have shown heterogeneity in cardiovascular risk among patients with diabetes. Imaging can help categorize risk of future cardiovascular events by identifying those patients with atherosclerosis, rather than relying on risk prediction based on population-based studies. In this article, we will review the evidence regarding use of atherosclerosis imaging in patients with diabetes to predict risk of coronary heart disease and mortality.

Vitamin K antagonists (VKAs) are known to increase vascular calcification, suggesting increased cardiovascular disease events. Apixaban is an oral direct factor Xa inhibitor superior to warfarin at preventing stroke or systemic embolism and may stabilize coronary atherosclerosis. The potential benefits of avoiding VKA therapy and the favorable effects of factor Xa inhibitors could contribute to cardiovascular disease event reduction. We hypothesized that apixaban inhibits vascular calcification and coronary atherosclerosis progression compared with warfarin in patients with atrial fibrillation (AF). This study is a single-center, prospective, randomized, open-label study. From May 2014 to December 2015, 66 patients with nonvalvular AF who experienced VKA therapy were enrolled. Patients were randomized into either warfarin or apixaban cohorts and followed for 52 weeks. The primary objective is to compare the rate of change in coronary artery calcification (CAC) from baseline to follow-up in apixaban vs warfarin cohorts. The key secondary objective is to compare the rate of incident plaques and quantitative changes in plaque types between patients randomized to either warfarin or apixaban cohorts using serial coronary computed tomography angiography. Expert readers will blindly assess CAC and coronary artery plaques. It is thought that this trial will result in significant differences in CAC and coronary artery plaque progression between the VKA and apixaban. The results are anticipated to provide a novel insight into treatment selection for AF patients. The study is registered at http://www.clinicaltrials.gov (NCT 02090075).

HIV infection has been associated with diastolic heart failure and atrial fibrillation. The purpose of this study is to determine whether HIV infection is associated with differences in left ventricular mass (LVM), left ventricular end-diastolic volume (LVEDV), and left atrial volume (LAV) indexed to body surface area (left ventricular mass index, left ventricular end-diastolic volume index [LVEDVI], and left atrial volume index [LAVI], respectively). Cross-sectional study of 721 men [425 HIV-infected (HIV+), 296 HIV-uninfected (HIV-) enrolled in the cardiovascular substudy of the Multicenter AIDS Cohort Study (MACS). Participants underwent cardiac computed tomography imaging. A blinded reader measured LVM, LVEDV, and LAV. We used multivariable linear regression models to evaluate whether LVEDVI, left ventricular mass index (LVMI), and LAVI differed by HIV serostatus, adjusting for demographics and cardiovascular disease risk factors. LVMI was significantly greater in HIV+ compared with HIV- men, with adjusted difference of 2.65 g/m² (95% confidence interval 0.53-4.77, p < .001). Left ventricular end-diastolic index and LAVI did not differ significantly between the two groups. HIV-related factors (nadir CD4 count, clinical AIDS diagnosis, cumulative antiretroviral therapy use, and cumulative protease inhibitor use) were not significantly associated with LVMI, LVEDVI, or LAVI. LVM was significantly higher in HIV+ than HIV- men, which may contribute to the observed increased risk for diastolic heart failure associated with HIV infection. Although HIV infection has been associated with an increased risk for atrial fibrillation, we did not find any difference in LAV by HIV serostatus.

Background and aims

We aimed at investigating whether diabetes is associated with progression in coronary plaque components.

Methods

We identified 142 study subjects undergoing serial coronary computed tomography angiography. The resulting propensity score was applied 1:1 to match diabetic patients to non-diabetic patients for clinical risk factors, prior coronary stenting, coronary artery calcium (CAC) score and the serial scan interval, resulting in the 71 diabetes and 71 non-diabetes patients. Coronary plaque (total, calcified, non-calcified including fibrous, fibrous-fatty and low attenuation plaque [LAP]) volume normalized by total coronary artery length was measured using semi-automated plaque software and its change overtime between diabetic and non-diabetic patients was evaluated.

Results

The matching was successful without significant differences between the two groups in all matched variables. The baseline volumes in each plaque also did not differ. During a mean scan interval of 3.4 ± 1.8 years, diabetic patients showed a 2-fold greater progression in normalized total plaque volume (TPV) than non-diabetes patients (52.8 mm³vs. 118.3 mm³, p = 0.005). Multivariable linear regression model revealed that diabetes was associated with normalized TPV progression (β 72.3, 95%CI 24.3-120.3). A similar trend was observed for the non-calcified components, but not calcified plaque (β 3.8, 95%CI -27.0-34.7). Higher baseline CAC score was found to be associated with total, non-calcified and calcified plaque progression. However, baseline non-calcified volume but not CAC score was associated with LAP progression.

Conclusions

The current study among matched patients indicates diabetes is associated with a greater plaque progression. Our results show the need for strict adherence of diabetic patients to the current preventive guidelines.

Objectives

The aim of this study was to determine whether coronary artery calcium (CAC) progression was associated with coronary plaque progression on coronary computed tomographic angiography.

Background

CAC 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.

Methods

Consecutive 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.

Results

A 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.

Conclusions

In 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.

Background and aims

The association between minimally elevated coronary artery calcification (CAC) and cerebrovascular disease is not well known. We assessed whether individuals with minimal CAC (Agatston scores of 1-10) have higher ischemic stroke or transient ischemic attack (TIA) frequencies compared with those with no CAC. We also investigated the relative prevalence of carotid atherosclerosis in these two groups.

Methods

A total of 3924 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) without previous cardiovascular events, including stroke, and with baseline CAC scores of 0-10 were followed for the occurrence of incident ischemic stroke/TIA. We used carotid ultrasound to detect carotid artery plaques and to measure the intima-media thickness (IMT).

Results

During a median follow-up of 13.2 years, 130 participants developed incident ischemic stroke/TIA. There was no significant difference in the ischemic stroke/TIA incidence between those with minimal CAC and no CAC (3.7 versus 2.7 per 1000 person-years). In participants with minimal CAC, we observed a significant association of the condition with an internal carotid artery (ICA) that had a greater-than-average IMT (ICA-IMT; β = 0.071, p = 0.001) and a higher odds ratio (OR) for carotid artery plaques (OR 1.46; with a 95% confidence interval [CI] of 1.18-1.80; p < 0.001).

Conclusions

A CAC score of 0-10 is associated with a low rate of ischemic stroke/TIA, and thus a minimal CAC score is not a valuable predictive marker for ischemic stroke/TIA. A minimal CAC score may, however, provide an early and asymptomatic sign of carotid artery disease.

Current risk stratification strategies do not fully explain cardiovascular disease (CVD) risk. We aimed to evaluate the association of low-density lipoprotein (LDL-P) and high-density lipoprotein (HDL-P) particles with progression of coronary artery calcium and carotid wall injury. All participants in the Multi-Ethnic Study Atherosclerosis (MESA) with LDL-P and HDL-P measured by ion mobility, coronary artery calcium score (CAC), carotid intima-media thickness (IMT), and carotid plaque data available at Exam 1 and 5 were included in the study. CAC progression was annualized and treated as a categorical or continuous variable. Carotid IMT and plaque progression were treated as continuous variables. Fully adjusted regression models included established CVD risk factors, as well as traditional lipids. Mean (±SD) follow-up duration was 9.6 ± 0.6 years. All LDL-P subclasses as well as large HDL-P at baseline were positively and significantly associated with annualized CAC progression, however, after adjustment for established risk factors and traditional lipids, only the association with medium and very small LDL-P remained significant (β -0.02, p = 0.019 and β 0.01, p = 0.003, per 1 nmol/l increase, respectively). Carotid plaque score progression was positively associated with small and very small LDL-P (p <0.01 for all) and non-HDL-P (p = 0.013). Only the association with very small LDL-P remained significant in a fully adjusted model (p = 0.035). Mean IMT progression was not associated with any of the lipid particles. In conclusion, in the MESA cohort, LDL-P measured by ion mobility was significantly associated with CAC progression as well as carotid plaque progression beyond the effect of traditional lipids.

Background

The purpose of this study is to determine if a new score calculated with coronary artery calcium (CAC) density and volume is associated with total coronary artery plaque burden and composition on coronary CT angiography (CCTA) compared to the Agatston score (AS).

Methods

We identified 347 men enrolled in the Multicenter AIDS cohort study who underwent contrast and non-contrast CCTs, and had CAC>0. CAC densities (mean Hounsfield Units [HU]) per plaque) and volumes on non-contrast CCT were measured. A Density-Volume Calcium score was calculated by multiplying the plaque volume by a factor based on the mean HU of the plaque (4, 3, 2 and 1 for 130-199, 200-299, 300-399, and ≥400HU). Total Density-Volume Calcium score was determined by the sum of these individual scores. The semi-quantitative partially calcified and total plaque scores (PCPS and TPS) on CCTA were calculated. The associations between Density-Volume Calcium score, PCPS and TPS were examined.

Results

Overall, 2879 CAC plaques were assessed. Multivariable linear regression models demonstrated a stronger association between the log Density-Volume Calcium score and both the PCPS (β 0.99, 95%CI 0.80-1.19) and TPS (β 2.15, 95%CI 1.88-2.42) compared to the log of AS (PCPS: β 0.77, 95%CI 0.61-0.94; TPS: β 1.70, 95%CI 1.48-1.94). Similar results were observed for numbers of PC or TP segments.

Conclusion

The new CAC score weighted towards lower density demonstrated improved correlation with semi-quantitative PC and TP burden on CCTA compared to the traditional AS, which suggests it has utility as an alternative measure of atherosclerotic burden.