Computed tomography angiography (CTA) has validated the use of pericoronary adipose tissue (PCAT) attenuation as a credible indicator of coronary inflammation, playing a crucial role in coronary artery disease (CAD). This study aimed to evaluate the long-term effects of high-dose statins on PCAT attenuation at coronary lesion sites and changes in plaque distribution. Our prospective observational study included 52 patients (mean age 60.43) with chest pain, a low-to-intermediate likelihood of CAD, who had documented atheromatous plaque through CTA, performed approximately 1 year and 3 years after inclusion. We utilized the advanced features of the CaRi-Heart^® and syngo.via Frontier^® systems to assess coronary plaques and changes in PCAT attenuation. The investigation of changes in plaque morphology revealed significant alterations. Notably, in mixed plaques, calcified portions increased (p < 0.0001), while non-calcified plaque volume (NCPV) decreased (p = 0.0209). PCAT attenuation generally decreased after one year and remained low, indicating reduced inflammation in the following arteries: left anterior descending artery (LAD) (p = 0.0142), left circumflex artery (LCX) (p = 0.0513), and right coronary artery (RCA) (p = 0.1249). The CaRi-Heart^® risk also decreased significantly (p = 0.0041). Linear regression analysis demonstrated a correlation between increased PCAT attenuation and higher volumes of NCPV (p < 0.0001, r = 0.3032) and lipid-rich plaque volume (p < 0.0001, r = 0.3281). Our study provides evidence that high-dose statin therapy significantly reduces CAD risk factors, inflammation, and plaque vulnerability, as evidenced by the notable decrease in PCAT attenuation, a critical indicator of plaque progression.

Background: Coronary artery calcium (CAC) scores are a widely used surrogate marker for atherosclerotic burden, but they do not fully reflect plaque vulnerability or coronary inflammation. This study aimed to evaluate the relationship between CACs, coronary plaque characteristics, and perivascular inflammatory activity using advanced CCTA and CaRi-Heart^® analysis. Methods: A total of 250 patients with no prior cardiovascular disease were retrospectively evaluated and stratified by CACs into three groups: 0 (n = 28), 1–100 (n = 121), and >100 (n = 101). Coronary plaque morphology, high-risk plaque (HRP) features, CAD-RADS scores, and AI-derived fat attenuation index (FAI) centiles were assessed. Results: Significant differences across CAC categories were observed for several key parameters. The number of diseased coronary segments increased markedly (from 1.39 ± 1.10 vs. 2.97 ± 1.57 vs. 3.94 ± 2.10; p < 0.0001, one-way ANOVA). A similar upward trend was seen for segment involvement scores, HRP prevalence, and the proportions of mixed and calcified plaque components. Regression analysis demonstrated that CACs correlated significantly with segment burden (r² = 0.2520), CAD-RADS (r² = 0.1352), and the FAI score centile (r² = 0.0568). Conclusions: This study highlights the limitations of CACs as a standalone risk stratification tool. Vulnerable and inflamed plaques may already be present in patients with low or zero CACs. Integrating CCTA with perivascular FAI mapping enables earlier detection of biologically active atherosclerosis and supports more precise clinical decision-making.

Introduction: The pericoronary fat attenuation index (FAI) is an emerging computed tomography-derived marker for measuring vascular inflammation at coronary vessels. It holds prognostic significance for major cardiovascular events and enhances cardiac risk assessment, complementing traditional risk factors and coronary artery calcium scores. However, the impact of local coronary circulation factors on pericoronary inflammation development in right versus left coronary arteries has not been clearly understood. Objective: This study aimed to investigate the regional differences in inflammation levels between the right and left coronary arteries in four clinical scenarios: acute coronary event in the follow-up period, post-COVID patients, recent percutaneous intervention, and unstable angina with significant lesions on native coronary arteries. Methods: The study included 153 patients (mean age 62 years, 70.5% male) who underwent clinically indicated coronary computed tomography angiography (CCTA). Vulnerable plaque features were analyzed to identify high-risk plaques. FAI and the FAI score, a score integrating risk factors and age, were calculated for each case at the left anterior descending artery (LAD), circumflex artery (LCX), and right coronary artery (RCA). Results: A total of 459 coronary arteries were analyzed. Both FAI and FAI scores were higher in the RCA (15.23 ± 11.97) compared to the LAD (10.55 ± 6.78) and (11.48 ± 6.5) LCX (p = 0.02). FAI values showed a significantly higher level at the RCA (−71.25 ± 7.47 HU) compared to the LCX (−76 ± 7.68 HU) and the LAD (−73.04 ± 8.9 HU, p <0.0001). This trend persisted across all subgroups, including post-COVID CT scans (−75.49 ± 7.62 HU for RCA vs. −72.89 ± 9.40 HU for the LCX vs. −71.28 ± 7.82 HU for the LAD, p = 0.01) and patients with high-risk plaques (20.98 ± 16.29 for the RCA vs. 11.77 ± 7.68 for the LCX vs. 12.83 ± 6.47 for the LAD, p = 0.03). Conclusion: Plaques in different coronary areas show varied vulnerability and inflammation levels. The RCA, in particular, demonstrates greater inflammation susceptibility, with higher inflammation scores in areas surrounding the coronary plaques.

Background and Objectives: The modified Duke index derived from coronary computed tomography angiography (CCTA) was designed to predict cardiovascular outcomes based on the severity of coronary stenosis. However, it does not take into consideration the presence or severity of peri-coronary inflammation. The peri-coronary fat attenuation index (FAI) is a novel imaging marker determined by CCTA which reflects the degree of inflammation in the coronary tree in patients with coronary artery disease. To assess the association between the modified Duke index assessed by CCTA, cardiovascular risk factors, and peri-coronary inflammation in the coronary arteries of patients with coronary artery disease. Materials and Methods: One hundred seventy-two patients who underwent CCTA for typical angina were assigned into two groups based on the modified Duke index: group 1—patients with low index, ≤3 (n = 107), and group 2—patients with high index, >3 (n = 65). Demographic, clinical, and CCTA data were collected for all patients, and FAI analysis of coronary inflammation was performed. Results: Patients with increased values of the modified Duke index were significantly older compared to those with a low index (61.83 ± 9.89 vs. 64.78 ± 8.9; p = 0.002). No differences were found between the two groups in terms of gender distribution, hypertension, hypercholesterolemia, or smoking history (all p > 0.5). The FAI score was significantly higher in patients from group 2, who presented a significantly higher score of inflammation compared to the patients in group 1, especially at the level of the right coronary artery (FAI score, 20.85 ± 15.80 vs. 14.61 ± 16.66; p = 0.01 for the right coronary artery, 13.85 ± 8.04 vs. 10.91 ± 6.5; p = 0.01 for the circumflex artery, 13.26 ± 10.18 vs. 11.37 ± 8.84; p = 0.2 for the left anterior descending artery). CaRi-Heart^® analysis identified a significantly higher risk of future events among patients with a high modified Duke index (34.84% ± 25.86% vs. 16.87% ± 15.80%; p < 0.0001). ROC analysis identified a cut-off value of 12.1% of the CaRi-Heart^® risk score for predicting a high severity of coronary lesions, with an AUC of 0.69. Conclusions: The CT-derived modified Duke index correlates well with local perilesional inflammation as assessed using the FAI score at different levels of the coronary circulation.

(1) Background: CTA has validated the use of pericoronary adipose tissue (PCAT) attenuation as a credible indicator of coronary inflammation and plays a crucial role in coronary artery disease (CAD). This study aimed to evaluate the long-term effects of high-dose statins on PCAT attenuation at coronary lesion sites and changes in plaque distribution; (2) Methods: Our prospective observational study included 52 patients (mean age 60.43) with typical chest pain, a low-to-intermediate likelihood of CAD, and documented atheromatous plaque through CCT. We utilized advanced features of the CaRi-Heart® and syngo.via Frontier® systems to assess coronary plaques and changes in PCAT attenuation; (3) Results: Changes in plaque morphology were investigated, revealing significant alterations. Notably, in mixed plaques, calcified portions increased (p < 0.0001), while non-calcified plaque volume (NCPV) decreased (p = 0.0209). PCAT attenuation generally decreased after one year and remained low, indicating reduced inflammation in the following arteries: LAD (p = 0.0142), LCX (p = 0.0513), and RCA (p = 0.1249). The CaRi-Heart® risk also decreased significantly (p = 0.0041). Linear regression analysis demonstrated a correlation between increased PCAT attenuation and higher volumes of NCPV (p < 0.0001, r = 0.3032) and lipid-rich plaque volume (p < 0.0001, r = 0.3281); (4) Conclusions: Our study provides evidence that high-dose statin therapy significantly reduces CAD risk factors, inflammation, and plaque vulnerability, as evidenced by the notable decrease in PCAT attenuation, a critical indicator of plaque progression.

(1) The link between periodontal disease (PD) and acute coronary syndromes (ACSs) is predominantly attributed to the atherosclerotic process, mediated by systemic inflammation. However, the correlation between the severity of PD, characterized by the presence of periodontal pathogens, and systemic inflammation in patients with ACS remains inadequately clarified. (2) This study aims to assess the association between the severity of PD and systemic inflammatory biomarkers, along with lipid profiles, in patients with ACS. (3) In total, 42 patients with ACS and concomitant PD were divided into two groups based on the presence of periodontal pathogens belonging to the red or red-orange complexes. Group 1–29 patients displayed pathogens from the red complex (RC) and group 2–13 patients displayed pathogens from the red-orange complex (ROC). All participants underwent a comprehensive dental examination, including DNA sampling from the periodontal pockets for pathogen detection. Systemic inflammation was evaluated alongside assessments of lipid profiles. (4) Inflammatory markers were more pronounced in the RC group compared with the ROC group. Moreover, patients in the RC group showed significantly higher monocyte-to-lymphocyte ratios (0.41 ± 0.20 vs. 0.28 ± 0.12; p = 0.002), platelet-to-lymphocyte ratios (139.50 ± 33.85 vs. 100.90 ± 8.84; p = 0.02), serum C-reactive protein levels (9.34 ± 1.08 mg/L vs. 5.46 ± 1.03 mg/L; p = 0.03), and serum uric acid levels (6.9 ± 0.49 mg/dL vs. 5.4 ± 0.26 mg/dL; p = 0.006). Concerning lipid profiles, the RC group exhibited significantly higher low-density lipoprotein cholesterol (LDL) levels (169.60 ± 12.63 mg/dL vs. 106.70 ± 9.34 mg/dL; p = 0.0007) and significantly lower high-density lipoprotein cholesterol (HDL) levels (29.29 ± 3.50 mg/dL vs. 39.56 ± 2.07 mg/dL; p = 0.002). (5) The severity of PD, indicated by the concomitant presence of pathogens from the red and orange complexes, is associated with an unfavorable lipid profile and elevated inflammatory biomarkers. These findings highlight the potential importance of periodontal intervention in the prevention of ACS.