Search Results (1,185)

Background/Objectives: The triglyceride-to-High-density lipoprotein cholesterol (TG/HDL) ratio is an established marker of atherogenic dyslipidaemia and insulin resistance. Although its association with subclinical atherosclerosis has been reported, the relative contributions of long-term TG/HDL burden and visit-to-visit variability to carotid intima media thickness (CIMT) remain unclear. This study aimed to evaluate the differential associations of the longitudinal mean and temporal variability of the TG/HDL ratio with CIMT. Methods: This retrospective single-center observational cohort study included 260 adult patients with at least three years of longitudinal lipid measurements and a standardized carotid ultrasonography assessment. The longitudinal mean TG/HDL ratio and variability indices, including standard deviation, coefficient of variation, average real variability and variability independent of the mean, were calculated. CIMT was measured using B-mode ultrasonography. Associations were assessed using correlation analyses, multivariable linear regression, joint category analyses and stratified analyses according to statin therapy. Results: The longitudinal mean TG/HDL ratio was independently associated with increased CIMT after adjustment for traditional cardiovascular risk factors. In contrast, TG/HDL variability indices showed no independent association with CIMT and did not improve model performance beyond the mean TG/HDL ratio. Restricted cubic spline analysis demonstrated a significant non-linear association between TG/HDL mean and CIMT, suggesting a threshold-dependent relationship. Joint category analyses demonstrated higher CIMT values in groups with elevated TG/HDL mean regardless of variability status. A significant interaction was observed between TG/HDL variability and statin therapy (p for interaction = 0.011). Conclusions: These findings indicate that cumulative exposure to atherogenic dyslipidaemia, reflected by the long-term mean TG/HDL ratio, is more strongly associated with subclinical carotid atherosclerosis than short-term lipid fluctuations. Full article

Carotid atherosclerosis remains one of the primary etiological factors underlying ischemic stroke, contributing to adult neurological disability and mortality. In recent years, non-coding RNAs (ncRNAs) have emerged as key regulators of gene expression, actively modulating molecular pathways involved in atherogenesis. This systematic review, the first to be exclusively focused on carotid atherosclerosis, aimed at synthesizing current findings on the differential expression of ncRNAs throughout the natural history of the disease, thus providing the first comprehensive attempt to delineate a stage-specific ncRNA expression profile in carotid disease. A comprehensive literature search was conducted in PubMed and Scopus databases in January 2025, following PRISMA guidelines. Original studies involving human subjects with carotid atherosclerosis, evaluating the expression of intracellular or circulating ncRNAs, were included and then categorized according to their association with cardiovascular risk factors, carotid intima-media thickness (cIMT), presence of atherosclerotic plaques, plaque vulnerability, clinical symptoms, and ischemic stroke. Out of 148 articles initially identified, 49 met the inclusion criteria and were analyzed in depth. Among the different classes of ncRNAs, microRNAs (miRNAs) were the most frequently reported as dysregulated, followed by circular RNAs (circRNAs) and long non-coding RNAs (lncRNAs). Notably, the majority of identified ncRNAs were implicated in key pathogenic mechanisms such as inflammatory signaling, vascular smooth muscle cell (VSMC) phenotypic modulation, and ABCA1-mediated cholesterol efflux. Collectively, the evidence underscores the association and possible involvement of ncRNAs in the initiation and progression of carotid atherosclerosis and its cerebrovascular complications. Their relative stability in biological fluids and cell-specific expression profiles highlight their strong potential as minimally invasive biomarkers and—possibly—novel therapeutic targets. Full article

Background/Objectives: Cardiovascular (CV) and cerebrovascular diseases, primarily attributed to atherosclerosis, stand as leading global causes of morbidity and mortality. This study aims to evaluate the impact of preclinical atherosclerosis parameters, including intima-media thickness (IMT) and arterial stiffness, in a seven-year follow-up of 100 patients with CV risk factors but no known history of CV or cerebrovascular diseases. Methods: Between April 2014 and December 2015, 100 patients presenting with suspected ischemic heart disease were enrolled. The study integrates the color Doppler examination of the supra-aortic trunks with the evaluation of preclinical parameters of atherosclerosis, such as intima-media thickness (IMT), βeta index, and pulse wave velocity (PWV), as well as echocardiographic evaluations, including global longitudinal strain (GLS). CV risk factors, metabolic syndrome, and insulin resistance were assessed and measured for each patient using the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Two- and seven-year follow-ups assessed various CV events. Results: The study population comprised 67% males and 33% females. Metabolic syndrome, impaired fasting glycemia and hypertension were prevalent. The mean value of IMT was 1.21 ± 0.26 mm, and PWV was 8.47 ± 2.14 m/s. The 7-year follow-up identified IMT, PWV, and HOMA-IR as strong positive predictors of cardiovascular events, with PWV emerging as a particularly sensitive indicator of early events. Conclusions: Insulin resistance and cardiovascular risk factors may contribute to early alterations in myocardial and vascular function, even in the absence of overt disease. PWV, as a recognized surrogate marker of arterial stiffness, may serve as a sensitive tool for the early prediction of cardiovascular events. A comprehensive screening, including the assessment of markers indicating subclinical vascular alterations, along with the implementation of preventive interventions, is crucial for populations at risk. Full article

Atherosclerosis (AS) is a disease characterized by chronic vascular wall inflammation and lipid deposition. Although lipid-lowering drugs such as statins have significantly reduced cardiovascular event rates, “residual inflammatory risk” remains a key factor driving disease progression and plaque rupture. As a central regulator of the inflammatory response, the nuclear factor-κappaB (NF-κB) signaling network comprises both canonical pro-inflammatory pathways and functionally more complex non-canonical pathways. Increasing evidence in recent years indicates that abnormal and sustained activation of the non-canonical NF-κB signaling pathway plays a pivotal role in driving plaque rupture. This review first elaborates on the shift in AS strategies from “lipid-lowering” to “anti-inflammatory” approaches, followed by an in-depth analysis of the molecular activation mechanisms of the NF-κB signaling pathway and its distinctiveness in the AS pathological process, along with its epigenetic regulation. It emphasizes how this pathway drives pathological angiogenesis and regulates vascular smooth muscle cell (VSMC) phenotypic switching and macrophage function, thereby forming a vicious cycle that amplifies inflammation and structural damage, ultimately leading to acute cardiovascular events. Finally, we systematically summarize current progress and challenges in drug development targeting the NF-κB pathway (e.g., targeting key kinases like NIK and IKKα), aiming to provide theoretical foundations and future directions for novel therapeutic strategies to stabilize coronary plaques and prevent acute coronary syndromes. Full article

Background and Objectives: Whole Blood Viscosity (WBV), estimated using the De Simone formula, is a key hemodynamic parameter linked to endothelial dysfunction and atherosclerosis. Its association with significant coronary calcification, defined as a high Coronary Artery Calcium Score (CACS ≥ 100), remains unclear. This study investigated whether calculated WBV predicts high CACS. Materials and Methods: In this single-center, retrospective, cross-sectional study, 403 patients undergoing coronary computed tomography angiography for suspected stable coronary artery disease were included. Participants were stratified into CACS < 100 (n = 258) and CACS ≥ 100 (n = 145). WBV was calculated at High Shear Rate (HSR) and Low Shear Rate (LSR) using the De Simone formula. Multivariate binomial logistic regression adjusted for conventional cardiovascular risk factors was used to identify independent predictors of high CACS. Results: Patients with CACS ≥ 100 were older, more frequently male, and had a higher prevalence of diabetes and hypertension (all p < 0.01). Mean WBV did not differ significantly between groups: WBV-HSR, 4.3 ± 0.5 cP vs. 4.4 ± 0.5 cP (p = 0.456); WBV-LSR, 29.9 ± 8.0 cP vs. 30.4 ± 8.6 cP (p = 0.505). In multivariate models, neither WBV-HSR (OR: 0.489; p = 0.462) nor WBV-LSR (OR: 0.987; p = 0.520) independently predicted high CACS. Age and sex were the strongest independent predictors (p < 0.001). Conclusions: No independent association was found between calculated WBV and high CACS in this cross-sectional study. Full article

Background: Cardiovascular risk models, such as the Framingham and atherosclerotic cardiovascular disease (ASCVD) calculators, have improved risk prediction but often fail to identify individuals who experience ASCVD events despite low or intermediate predicted risk. This suggests that underrecognized, non-traditional risk factors may contribute significantly to the development of atherosclerosis. Objective: This narrative review synthesizes and summarizes recent evidence on high-yield non-traditional risk factors for atherosclerosis, with a focus on clinically significant, emerging, and applicable contributors beyond conventional frameworks. This review is distinct in that it aggregates a wide array of non-traditional risk factors while also consolidating recent data on ASCVD in more vulnerable populations. Unlike the existing literature, this manuscript integrates in a single comprehensive review various domains of non-traditional atherosclerotic risk factors, including inflammatory, metabolic, behavioral, environmental, and physical pathways. An additional unique highlight in the same manuscript is the discussion of non-traditional risk factors for atherosclerosis in more vulnerable populations, specifically South Asians. We also focus on clinically actionable factors that can guide treatment decisions for clinicians. Results: Key non-traditional risk factors identified include inflammation and biomarker-based risk factors such as C-reactive protein or interleukin-6 levels, metabolic and microbial risk factors, behavioral factors such as E-cigarette use, and environmental or infectious risk factors such as air and noise pollution. We explore certain physical exam findings associated with atherosclerotic burden, such as Frank’s sign and Achilles tendon thickness. Conclusions: Atherosclerosis is a multifactorial process influenced by diverse and often overlooked factors. Integrating non-traditional risks into clinical assessment may improve early detection, guide prevention and personalize care. Future risk prediction models should incorporate molecular, behavioral, and environmental data to reflect the complex nature of cardiovascular disease. Full article

Background and Objectives: Obesity, heart failure (HF), and atherosclerosis have common pathways, including chronic inflammation, immune cells activation, and metabolic disturbances. These pathways often coexist and overlap, increasing cardiometabolic risk. Growth differentiation factor 15 (GDF-15) is an emerging cytokine linked to inflammation, oxidative stress, and metabolic dysregulation, which are common pathways between heart failure, obesity and atherosclerosis. Beyond its established prognostic value in cardiovascular diseases (CVD) and HF, recent evidence suggests that GDF-15 may also reflect subclinical atherosclerosis, potentially improving early risk stratification in obese and HF populations. The aim of this review is to synthesize current evidence on the association between GDF-15 and markers of subclinical atherosclerosis, and to evaluate whether GDF-15 may serve as an integrative biomarker reflecting shared cardiometabolic pathways. Materials and Methods: We conducted a systematic review following PRISMA recommendations registered by CRD420251267457 number on PROSPERO. PubMed, Embase, Scopus, and Web of Science were searched for human studies evaluating the correlation between markers of subclinical atherosclerosis and GDF-15 concentration. We excluded the studies not published in English, not involving human participants, and not meeting the inclusion criteria. We assessed the risk of bias using the Joanna Briggs Institute appraisal tool. Due to the heterogeneity of studies, a narrative synthesis was performed. Result: The review included 18 studies, which evaluated the association between GDF-15 and subclinical atherosclerosis markers, such as intima media thickness, coronary artery calcium score, ankle-brachial index, and atherosclerotic plaques. Studies included patients with metabolic disorders, chronic inflammatory diseases, HIV cohorts, and general population samples. Most of the studies reported that GDF-15 levels were associated with greater atherosclerotic burden; however, results were frequently influenced by confounders. Methodological limitations, such as limited or highly specified samples, cross-sectional designs, variability in atherosclerotic-imaging technique, and inconsistent adjustment for confounders, restrict generalization of the results. Conclusions: Current evidence supports GDF-15 as a biomarker integrating inflammatory and metabolic stress signals, indirectly linking obesity, HF and subclinical atherosclerosis. While current data supports its prognostic relevance, further studies are needed to confirm its clinical utility in routine assessment and preventive cardiovascular care. Full article

Growth Differentiation Factor-15 (GDF-15) is a stress-responsive cytokine belonging to the Transforming Growth Factor-beta (TGF-β) superfamily. Initially identified as macrophage inhibitory cytokine-1 (MIC-1), GDF-15 is expressed in various tissues and markedly upregulated under pathological conditions involving inflammation, oxidative stress, and tissue injury. Notably, GDF-15 upregulation has been associated with several cardiovascular events, such as heart failure, atrial fibrillation, atherosclerosis, coronary artery disease, and stroke. Furthermore, it has been observed that GDF-15, either alone or in combination with other cardiac biomarkers, can provide valuable complementary information enhancing risk assessment, early detection of cardiovascular events, and prediction of adverse outcomes. GDF-15 can be measured in various body fluids, using different methods. Immunoassays are widely employed and offer good sensitivity and reproducibility; however, variability between methods and potential interference from genetic variants highlight the need for standardization. This review summarizes current insights into GDF-15, with emphasis on its quantification methods, biological functions in cardiovascular diseases, and its emerging role as a diagnostic and prognostic biomarker. Full article

Background/Objectives: Clinical observations linking primary snoring (PS) to early markers of vascular dysfunction suggest a possible contribution to subclinical atherosclerosis. This study aimed to evaluate carotid and femoral intima–media thickness (cIMT and fIMT) in patients with atherosclerosis with or without PS, and to identify potential determinants of increased cIMT. Methods: In this cross-sectional study, 140 patients with atherosclerosis enrolled. Participants were divided into two groups based on polysomnography results: patients with PS (n = 95) and patients without snoring (n = 45). Demographic data and anthropometric measurements were recorded for all patients. High-resolution B-mode ultrasound was used to measure cIMT and fIMT. Group comparisons, correlation analyses, and multiple linear regressions were performed to evaluate the relationship between IMT and anthropometric parameters. Results: Patients with PS had significantly higher cIMT than patients without PS (0.90 ± 0.15 mm vs. 0.65 ± 0.10 mm, p < 0.001, Cohen’s d = −1.83), whereas fIMT did not differ between groups (p = 0.185). Carotid IMT was positively correlated with age, body mass index (BMI), waist circumference, and neck circumference (all p < 0.001). Multivariate analysis identified age, waist circumference, and neck circumference as independent predictors of increased cIMT (adjusted R² = 0.31, p < 0.001). Within the PS group, no significant difference was observed between cIMT and fIMT (p = 0.33). Conclusions: PS is strongly associated with increased carotid intima–media thickness in patients with atherosclerosis, independent of obstructive sleep apnea. The absence of a similar effect in the femoral artery supports the hypothesis that mechanical vibrations caused by snoring may cause local vascular damage in the carotid wall. These findings suggest that PS may represent an independent risk factor and an early marker of carotid atherosclerosis. Full article

Background: Several cohort studies have demonstrated a link between subclinical carotid atherosclerosis and obstructive chronic airflow limitation. These conditions exhibit common risk factors associated with unhealthy lifestyles, as well as analogous pathophysiological mechanisms, including chronic low-degree systemic inflammation. Purpose: The aim of this study was to investigate the association between airflow obstruction and carotid intima–media thickness (c-IMT), together with the influence of inflammatory biomarkers on this relationship, in patients diagnosed with chronic obstructive pulmonary disease (COPD). Methods and Patients: This study is cross-sectional and includes 106 patients with stable COPD. All patients underwent evaluation through spirometry, carotid ultrasound, and assessment of inflammatory biomarkers, including C-reactive protein, fibrinogen, and erythrocyte sedimentation rate. The relationship between carotid subclinical atherosclerosis and the Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage of COPD was assessed. Additionally, we compared patients with two positive biomarkers of inflammation with those who had no positive inflammatory biomarkers. Results: Significant statistical differences were observed in carotid intima–media thickness values associated with the severity of airflow obstruction, with measurements of 1.03 mm in COPD stage 1–2 GOLD, 1.07 mm in COPD GOLD 3, and 0.96 mm in GOLD 4 (p = 0.04). However, no direct correlation with forced expiratory volume in the first second (FEV1) was identified. The post hoc analysis revealed a notable increase in carotid wall thickness for the early stages of COPD. C-IMT demonstrated a significant association with inflammation parameters, muscle dysfunction, body composition, and lipid profile. The comparison of groups exhibiting two positive inflammatory biomarkers with those with no positive inflammatory markers revealed significant differences in age, c-IMT, exercise tolerance, and COPD symptoms. Conclusions: Subclinical carotid atherosclerosis is evident from the early stages of obstructive airflow limitation. Carotid intima–media thickness is significantly higher in patients with positive inflammatory biomarkers. Full article

Clonal hematopoiesis of indeterminate potential (CHIP) is defined by the expansion of hematopoietic stem cells harboring leukemogenic mutations in the absence of overt malignancy. Strongly associated with advancing age, CHIP is detected by next-generation sequencing of peripheral blood in more than 20% of individuals over 80, most commonly through mutations in DNMT3A, TET2, ASXL1, and PPM1D. While CHIP confers over a four-fold increased risk of hematologic malignancy, it has recently emerged as a key determinant of cardiometabolic health. Epidemiological data indicated a 40% higher cardiovascular disease (CVD) risk events and a 34% increase in all-cause mortality among CHIP carriers, with specific mutations and larger clone sizes conferring greater cardiovascular burden. Preclinical studies have shown that macrophages deficient in TET2 or DNMT3A drive interleukin (IL)-1β/IL-6 inflammasome activation, thereby promoting atherosclerosis and metabolic dysfunction, whereas the JAK2V617F mutation accelerates thrombosis. CHIP integrates into a broader network of dysregulation encompassing adiposity and inflammaging, which underlies its association with diverse comorbidities, including type 2 diabetes (T2D), chronic kidney disease (CKD), and chronic obstructive pulmonary disease (COPD). Multi-omics approaches have identified epigenetic and proteomic signatures correlated with CHIP expansion, providing potential biomarkers for risk stratification. Despite growing evidence of its systemic impact, CHIP screening remains limited to research settings. Emerging therapeutic strategies, including inflammasome inhibition, STING modulation, and epigenetic restoration, highlight its potential as a modifiable risk factor. This narrative review synthesizes current epidemiological, mechanistic, and translational insights, framing CHIP as an emerging causal factor in cardiometabolic disease and as a promising target for precision medicine in aging populations. Full article

Background: Coronary artery disease (CAD) is a multifactorial atherosclerotic disorder. Silicon (Si) is a trace mineral with potential antioxidant, anti-inflammatory, and lipid-modulating effects, but its clinical relevance in cardiovascular disease remains unclear. This study evaluated whether hair Si concentration—reflecting long-term exposure—is associated with CAD severity, clinical phenotype, risk factors, and systemic inflammation. Methods: A total of 130 patients with angiographically confirmed CAD (N = 36, 28% women) who met the inclusion criteria were enrolled. Disease severity was quantified using the Coronary Artery Surgery Study Score (CASSS) and SYNTAX score. Hair Si concentration was determined by inductively coupled plasma optical emission spectrometry (ICP-OES). Associations with demographic, clinical, biochemical, and inflammatory parameters were analyzed using non-parametric tests and multivariable ordinal logistic regression. Results: Median hair Si concentration was 21.3 ppm (range: 0.7–211.0). Hair Si levels showed no significant differences across CAD severity assessed by CASSS (H = 2.51; p = 0.47) or SYNTAX score (r = 0.079; p = 0.37). Similarly, no differences were observed between patients with stable angina and those presenting with acute coronary syndrome (p = 0.57) or between individuals with and without prior myocardial infarction. Hair Si concentration was unrelated to age, BMI, cardiovascular risk factors, lipid profile, or systemic inflammatory indices (all p > 0.2). Conclusions: Hair silicon concentration was not associated with CAD severity, phenotype, or systemic inflammation, suggesting that long-term Si exposure is metabolically neutral in advanced atherosclerosis. Unlike other minerals, silicon appears unlikely to serve as a diagnostic or prognostic biomarker in CAD, although its relevance may be confined to early vascular remodeling and primary prevention. Full article

Background: Interleukin-6 (IL-6) is a key inflammatory cytokine implicated in atherosclerotic plaque progression and carotid vulnerability. Although elevated IL-6 levels have been linked to cerebrovascular risk, its prognostic value in patients undergoing carotid endarterectomy (CEA) remains undefined. This systematic review aimed to investigate the available evidence on the relationship between IL-6 levels, surgical outcomes and mechanistic evidence in CEA patients. Materials and Methods: The review followed the PRISMA statement and AMSTAR-2 critical appraisal guidelines, with the protocol registered on PROSPERO (CRD420251120023). PubMed/MEDLINE, Scopus, and Web of Science were systematically searched up to July 2025 using the terms “interleukin-6” and “carotid endarterectomy”. Original studies in humans assessing IL-6 in relation to clinical outcomes after CEA or mechanistic evidence were included without language or date restrictions. Study quality was evaluated using the Cochrane Risk of Bias 2 and NHLBI tools, and evidence certainty was appraised using the GRADE framework. Given the heterogeneity of studies, only a qualitative synthesis was performed. Results: From 1232 records identified, 13 studies encompassing 1396 patients met the inclusion criteria. Most were prospective observational cohorts, with a mean participant age of 68.52 years and 81.16% male predominance. Perioperative stroke and mortality rates were uniformly low (≤2%), consistent with contemporary registry data. Across studies, elevated IL-6 levels—whether systemic or plaque-derived—were consistently associated with symptomatic carotid disease, plaque vulnerability, and adverse long-term outcomes. However, not all studies presented quantitative data on IL-6 levels, limiting the ability to draw definitive prognostic conclusions. Conclusions: Current evidence supports a mechanistic link between IL-6–mediated inflammation and carotid plaque instability, yet robust clinical validation in surgical populations is lacking. Future large-scale, prospective studies incorporating IL-6 measurement are warranted to establish its prognostic utility, guide anti-inflammatory therapeutic strategies, and refine postoperative risk stratification in patients undergoing CEA. Full article

Coronary artery disease remains a significant global health challenge, driven by a multifactorial pathophysiology, including immunological activation. The identification and management of potential risk factors are crucial for improving prevention opportunities. In this study, the role of novel, innate immune system response markers, such as podoplanin 38, in atherosclerosis was investigated. A total of 150 consecutive patients (87 (58%) male; median age of 68 (61–76) years) with chronic coronary symptoms (anginal equivalent, e.g., exertional dyspnea) who underwent clinical evaluation and de novo coronary angiography for a prospective single-center analysis were included. Demographic and clinical data, combined with echocardiographic and coronary angiography results, were analyzed in conjunction with laboratory results from admission, including serum podoplanin (PDPN) concentrations. Serum PDPN concentrations were significantly lower in the coronary artery disease group (238 (174–360) pg/mL) compared to the control group (428 (207–1381) pg/mL, p = 0.002). A negative correlation was observed between PDPN and the number of involved coronary arteries in the atherosclerotic process (R = −0.27, p < 0.01). In diabetic populations, glycemic hemoglobin (Hb1Ac) is correlated with the podoplanin concentration (r = −0.51, p = 0.001). A correlation between PDPN and the left ventricular ejection fraction was noted in both the control (r = 0.33, p < 0.01) and CAD groups (r = 0.37, p < 0.001). Podoplanin (PDPN) can be considered a novel marker for coronary atherosclerosis. Low serum podoplanin concentrations characterized patients with coronary artery disease. Full article

Background: Cardiovascular disease (CVD), driven primarily by atherosclerosis, is a major cause of morbidity and mortality among cancer patients. This study aims to evaluate the diagnostic value of [⁶⁸Ga]Ga-FAPI-PET as a novel molecular imaging tool for atherosclerosis, compared with established, non-specific [¹⁸F]FDG. Methods: We retrospectively analyzed twenty patients with bladder cancer who underwent [⁶⁸Ga]Ga-FAPI positron-emission tomography/magnetic resonance (PET/MR) and [¹⁸F]FDG positron emission tomography/computed tomography (PET/CT) at staging. The target-to-background ratio (TBRs) of both tracers were assessed along six arterial segments, and uptake patterns were compared between the two radiotracers. Additionally, associations between the intensity of PET-active lesions and certain CVD risk factors, as well as the intake of acetylsalicylic acid (ASA), were evaluated. Results: [⁶⁸Ga]Ga-FAPI detects significantly more active arterial PET lesions and shows significantly higher uptake than [¹⁸F]FDG in the per-lesion analysis (TBR_FAPI: 1.7 ± 0.5 vs. TBR_FDG: 1.4 ± 0.2; difference 19%; p < 0.001) and in the patient-based analysis (TBR_FAPI: 1.7 ± 0.4 vs. TBR_FDG: 1.4 ± 0.2; difference 19%; p = 0.018). Arterial hypertension (p < 0.001), dyslipidemia (p < 0.001), and particularly type 2 diabetes mellitus (p < 0.001; difference 34%), were significantly associated with elevated [⁶⁸Ga]Ga-FAPI expression compared to [¹⁸F]FDG uptake. ASA therapy was associated with a significant reduction in arterial [⁶⁸Ga]Ga-FAPI expression than [¹⁸F]FDG (p = 0.02). Conclusions: [⁶⁸Ga]Ga-FAPI-PET imaging, demonstrating superior detection of atherosclerotic activity compared to [¹⁸F]FDG, might be a promising molecular imaging marker for atherosclerosis. Full article