Perivascular Adipose Tissue Research Articles

Perivascular Adipose Tissue and Perivascular Adipose Tissue-Derived Extracellular Vesicles: New Insights in Vascular Disease.

Perivascular adipose tissue (PVAT) is a special deposit of fat tissue surrounding the vasculature. Previous studies suggest that PVAT modulates the vasculature function in physiological conditions and is implicated in the pathogenesis of vascular diseases. Understanding how PVAT influences vasculature function and vascular disease progression is important. Extracellular vesicles (EVs) are novel mediators of intercellular communication. EVs encapsulate molecular cargo such as proteins, lipids, and nucleic acids. EVs can influence cellular functions by transferring the carried bioactive molecules. Emerging evidence indicates that PVAT-derived EVs play an important role in vascular functions under health and disease conditions. This review will focus on the roles of PVAT and PVAT-EVs in obesity, diabetic, and metabolic syndrome-related vascular diseases, offering novel insights into therapeutic targets for vascular diseases.

Improving cardiovascular risk prediction with machine learning: a focus on perivascular adipose tissue characteristics

BackgroundTimely prevention of major adverse cardiovascular events (MACEs) is imperative for reducing cardiovascular diseases-related mortality. Perivascular adipose tissue (PVAT), the adipose tissue surrounding coronary arteries, has attracted increased amounts of attention. Developing a model for predicting the incidence of MACE utilizing machine learning (ML) integrating clinical and PVAT features may facilitate targeted preventive interventions and improve patient outcomes.MethodsFrom January 2017 to December 2019, we analyzed a cohort of 1077 individuals who underwent coronary CT scanning at our facility. Clinical features were collected alongside imaging features, such as coronary artery calcium (CAC) scores and perivascular adipose tissue (PVAT) characteristics. Logistic regression (LR), Framingham Risk Score, and ML algorithms were employed for MACE prediction.ResultsWe screened seven critical features to improve the practicability of the model. MACE patients tended to be older, smokers, and hypertensive. Imaging biomarkers such as CAC scores and PVAT characteristics differed significantly between patients with and without a 3-year MACE risk in a population that did not exhibit disparities in laboratory results. The ensemble model, which leverages multiple ML algorithms, demonstrated superior predictive performance compared with the other models. Finally, the ensemble model was used for risk stratification prediction to explore its clinical application value.ConclusionsThe developed ensemble model effectively predicted MACE incidence based on clinical and imaging features, highlighting the potential of ML algorithms in cardiovascular risk prediction and personalized medicine. Early identification of high-risk patients may facilitate targeted preventive interventions and improve patient outcomes.

Propagermanium as a Novel Therapeutic Approach for the Treatment of Endothelial Dysfunction in Type 2 Diabetes.

Propagermanium (PG) has immune modulating activity and anti-inflammatory properties. This work aimed to study the therapeutic efficacy of PG on endothelial and perivascular dysfunction associated with type 2 diabetes. Non-obese type 2 diabetic Goto-Kakizaki (GK) rats were divided into four groups: (1) the control group; (2) the group treated with 50 mg/kg PG; (3) the group fed a high-fat diet (GKHFD); and (4) the group of GKHFD treated with 50 mg/kg PG. PG was given orally for 3 months. Several in vivo parameters and endothelial function were studied in aortas with perivascular adipose tissue PVAT (+) or without PVAT (-). We also determined the vascular inflammation and levels of CD36 in PVAT. In diabetic GK rats, PG did not affect the lipid profile or the results of the intraperitoneal glucose tolerance test. Instead, it improved the fasting glucose levels (18%, p < 0.01), insulin resistance (32%, p < 0.05), endothelial function (33 and 25% in aortas mounted with (+) or without PVAT (-), p < 0.05), and restored the anticontractile effect of the perivascular adipose tissue by reducing its inflammation (56%, p < 0.05) and oxidative stress profile (55%, p < 0.05). Due to its anti-inflammatory characteristics, PG likely improved endothelial dysfunction and restored the perivascular adipose tissue's anticontractile properties.

Renal denervation alleviates vascular remodeling in spontaneously hypertensive rats by regulating perivascular adipose tissue.

Vascular remodeling is the main pathological process that causes the damage of the target organ of hypertension. Perivascular adipose tissue (PVAT) surrounds blood vessels and plays a key role in the pathogenesis of various cardiovascular diseases. This study aimed to investigate the effects of renal denervation (RDN) on hypertensive vascular remodeling and to elucidate the role of PVAT in this process. Male spontaneously hypertensive rat (SHR) and Wistar-Kyoto (WKY) rat were selected. Aortic vascular remodeling was evaluated using hematoxylin and eosin (H&E) staining and Masson's trichrome staining. Morphological changes in the PVAT were observed through H&E and Oil Red O staining. Dihydroethidium was used to measure oxidative stress levels in PVAT, while western blot analysis was used to determine the expression levels of proteins associated with vascular remodeling. The results showed that the aortic medial thickness, media thickness/lumen diameter, collagen volume fraction, and reactive oxygen species (ROS) level in PVAT were significantly higher in the SHR group than in the WKY group. The indexes mentioned above were lower in the SHR-RDN group than in the SHR group. H&E staining revealed that fat droplets in PVAT in the SHR-RDN group became smaller and browning occurred. Moreover, the protein expression of uncoupling protein-1 (UCP-1) and neuregulin 4 (Nrg4) was significantly increased in the SHR-RDN group. In addition, the expression of adiponectin increased and the expression of leptin decreased in the SHR-RDN group compared to the SHR group. In conclusion, RDN can relieve hypertensive vascular remodeling, which may be associated with PVAT.

Peritoneal Dialysis Aggravates and Accelerates Atherosclerosis in Uremic ApoE-/- Mice.

Atherosclerosis is highly prevalent in people with chronic kidney disease (CKD), including those receiving peritoneal dialysis (PD). Although it is lifesaving, PD induces profound systemic inflammation, which may aggravate atherosclerosis. Therefore, the hypothesis is that this PD-induced inflammation aggravates atherosclerosis via immune cell activation. ApoE-/- mice were subjected to a 5/6 nephrectomy to induce CKD. Three weeks later, mice were fed a high-cholesterol diet. Half of the nephrectomized mice then received daily peritoneal infusions of 3.86% Physioneal for 67 further days (CKD+PD) until the end of the experiment, and were compared with mice without CKD. Sham operated and PD-only mice were additional controls. CKD+PD mice displayed more severe atherosclerotic disease than control mice. Plaque area increased, and plaques were more advanced with a vulnerable phenotype typified by decreased collagen content and decreased fibrous cap thickness. Increased CD3+ T-cell numbers were present in plaques and perivascular adipose tissue of CKD and CKD+PD mice. Plaques of CKD+PD mice contained more iNOS+ immune cells. Spleens of CKD+PD mice showed more CD4+ central memory, terminally differentiated type 1 T-helper (Th1), Th17, and CX3C motif chemokine receptor 1+ (CX3CR1) CD4+ T-cells with less regulatory and effector T-cells. PD-fluid exposure in uremic mice potentiates systemic and vascular T-cell-driven inflammation and aggravates atherosclerosis. PD polarized CD4+ T-cells toward an inflammatory Th1/Th17 phenotype, and increased CX3CR1+ CD4+ T-cells, which are associated with vascular homing in CKD-associated atherosclerosis. Targeting CD4+ T-cell activation and CX3CR1+ polarization has the potential to attenuate atherosclerosis in PD patients.

30-Day Risk Score for Mortality and Stroke in Patients with Carotid Artery Stenosis Using Artificial Intelligence Based Carotid Plaque Morphology

The gold standard for determining carotid artery stenosis intervention is based on a combination of percent stenosis and symptomatic status. Few studies have assessed plaque morphology as an additive tool for stroke prediction. Our goal was to create a predictive model and risk score for 30-day stroke and death inclusive of plaque morphology. Patients with a computed tomographic angiography head/neck between 2010 and 2021 at a single institution and a diagnosis of carotid artery stenosis were included in our analysis. Each computed tomography was used to create a three-dimensional image of carotid plaque based off image recognition software. A stepwise backward regression was used to select variables for inclusion in our prediction models. Model discrimination was assessed with area under the receiver operating characteristic curves (AUCs). Additionally, calibration was performed and the model with the least Akaike Information Criterion (AIC) was selected. The risk score was modeled from the Framingham Study. Primary outcome was mortality/stroke. We created 3 models to predict mortality/stroke from 366 patients: model A using only clinical variables, model B using only plaque morphology and model C using both clinical and plaque morphology variables. Model A used age, sex, peripheral arterial disease, hyperlipidemia, body mass index (BMI), chronic obstructive pulmonary disease (COPD), and history of transient ischemia attack (TIA)/stroke and had an AUC of 0.737 and AIC of 285.4. Model B used perivascular adipose tissue (PVAT) volume, lumen area, calcified volume, and target lesion length and had an AUC of 0.644 and AIC of 304.8. Finally, model C combined both clinical and software variables of age, sex, matrix volume, history of TIA/stroke, BMI, PVAT, lipid rich necrotic core, COPD and hyperlipidemia and had an AUC of 0.759 and an AIC of 277.6. Model C was the most predictive because it had the highest AUC and lowest AIC. Our study demonstrates that combining both clinical factors and plaque morphology creates the best predication of a patient's risk for all-cause mortality or stroke from carotid artery stenosis. Additionally, we found that for patients with even 3 points in our risk score model has a 20% chance of stroke/death. Further prospective studies are needed to validate our findings.

Statin Therapy Mitigates Oxidative Stress in Epicardial and Perivascular Adipose Tissue: A Pilot Study in Cardiac Surgery Patients

Epicardial and perivascular adipose tissues have gained significant attention in the past decade due to their involvement in complex metabolic shifts and inflammatory changes in cardiovascular diseases. Statins, the cornerstone of lipid-lowering therapy, have pleiotropic effects, including the potential of alleviating epicardial adipose dysfunction and inflammation, although their impact on local oxidative stress has received less scrutiny. This study was purported to assess the production of reactive oxygen species (ROS) in epicardial and perivascular fat samples harvested from patients undergoing elective cardiac surgery and who were treated or not with statins. Here, we report that patients chronically treated with statins (atorvastatin and rosuvastatin) exhibited significantly lower levels of ROS in their epicardial and perivascular adipose tissues. Additionally, a positive correlation was observed between adipose tissue oxidative stress and the diameter of the right ventricle. Larger studies are required to provide mechanistic insights regarding the sources of epicardial ROS and signal transduction pathways activated by statins.

Correlation between perivascular adipose tissue surrounding coronary arteries measured on coronary artery CT Angiography and the presence and severity of CAD

Correlation between perivascular adipose tissue surrounding coronary arteries measured on coronary artery CT Angiography and the presence and severity of CAD

Indicators Of Increased CT Attenuation Of Perivascular Adipose Tissue In Abdominal Aortic Aneurysms

Indicators Of Increased CT Attenuation Of Perivascular Adipose Tissue In Abdominal Aortic Aneurysms

Correction to: Leptin-Dependent and Leptin-Independent Paracrine Effects of Perivascular Adipose Tissue on Neointima Formation.

Correction to: Leptin-Dependent and Leptin-Independent Paracrine Effects of Perivascular Adipose Tissue on Neointima Formation.

Ghrelin Expression in Atherosclerotic Plaques and Perivascular Adipose Tissue: Implications for Vascular Inflammation in Peripheral Artery Disease.

Atherosclerosis, a leading cause of peripheral artery disease (PAD), is driven by lipid accumulation and chronic inflammation within arterial walls. Objectives: This study investigates the expression of ghrelin, an anti-inflammatory peptide hormone, in plaque morphology and inflammation in patients with PAD, highlighting its potential role in age-related vascular diseases and metabolic syndrome. Methods: The analysis specifically focused on the immunohistochemical expression of ghrelin in atherosclerotic plaques and perivascular adipose tissue (PVAT) from 28 PAD patients. Detailed immunohistochemical staining was performed to identify ghrelin within these tissues, comparing its presence in various plaque types and assessing its association with markers of inflammation and macrophage polarization. Results: Significant results showed a higher prevalence of calcification in fibro-lipid plaques (63.1%) compared to fibrous plaques, with a notable difference in inflammatory infiltration between the two plaque types (p = 0.027). Complicated plaques exhibited increased ghrelin expression, suggesting a modulatory effect on inflammatory processes, although this did not reach statistical significance. The correlation between ghrelin levels and macrophage presence, especially the pro-inflammatory M1 phenotype, indicates ghrelin's involvement in the inflammatory dynamics of atherosclerosis. Conclusions: The findings propose that ghrelin may influence plaque stability and vascular inflammation, pointing to its therapeutic potential in managing atherosclerosis. The study underlines the necessity for further research to clarify ghrelin's impact on vascular health, particularly in the context of metabolic syndrome and age-related vascular alterations.

Early Methylglyoxal Exposure Leads to Worsened Cardiovascular Function in Young Rats.

Though maternal diabetes effects are well described in the literature, the effects of maternal diabetes in postnatal phases are often overlooked. Diabetic individuals have higher levels of circulating glycotoxins, and there is a positive correlation between maternal-derived glycotoxins and circulating glycotoxins in their progeny. Previous studies evaluated the metabolic effects of high glycotoxin exposure during lactation in adult animals. However, here we focus on the cardiovascular system of juvenile rats. For this, we used two experimental models: 1. High Methylglyoxal (MG) environment: pregnant Wistar rats were injected with PBS (VEH group) or Methylglyoxal (MG group; 60 mg/kg/day; orally, postnatal day (PND) 3 to PND14). 2. GLO-1 inhibition: pregnant Wistar rats were injected with dimethyl sulfoxide (VEH group) or a GLO-1 inhibitor (BBGC group; 5 mg/kg/day; subcutaneously, PND1-PND5). The offspring were evaluated at PND45. MG offspring presented cardiac dysfunction and subtly worsened vasomotor responses in the presence of perivascular adipose tissue, without morphological alterations. In addition, an endogenous increase in maternal glycotoxins impacts offspring vasomotricity due to impaired redox status. Our data suggest that early glycotoxin exposure led to cardiac and vascular impairments, which may increase the risk for developing cardiovascular diseases later in life.

Egg white hydrolysate modulates the renin-angiotensin system in mesenteric perivascular adipose tissue in doca-salt hypertensive rats and restores its anticontractile ability

Perivascular adipose tissue (PVAT) regulates vascular tonus with an anticontractile effect, which may be dysfunctional in hypertension. An Egg White Hydrolysate (EWH), a bioactive food, restores endothelium dysfunction and reduces blood pressure levels in malignant hypertension. We aimed to evaluate whether dietary supplementation with EWH interferes with the PVAT function in the mesenteric resistance arteries (MRA) of DOCA-salt hypertensive animals and the mechanisms involved. Male rats were divided into 4 groups and treated for 8 weeks. For 4 weeks, DOCA-salt or vehicle-treated rats (SHAM) were induced, and after that, some rats were co-treated with DOCA-salt or vehicle plus EWH (1 g/kg/day) for 4 weeks more. MRA and/or their PVAT (mPVAT) were used for functional, molecular, and biochemical analysis. The anticontractile effect of mPVAT in response to norepinephrine (NE) was observed only in MRA rings with PVAT of the SHAM group, while this effect was abolished in DOCA-salt rings. The EWH treatment did not change the anticontractile effect of mPVAT in SHAM but partially restored it in DOCA-salt rats. Acute aliskiren incubation reduced NE-induced contraction only in MRA with PVAT of DOCA-salt rats. EWH prevented the overactivation of the renin levels and ACE activity in mPVAT of DOCA-salt rats; while did not change AT1R expression, but increased AT2R expression. In mPVAT, EWH blocked the increase of MDA, ROS and pro-inflammatory cytokines observed in DOCA-salt rats. EWH improved PVAT dysfunction in MRA of severe hypertension. This beneficial effect could be mediated by an ameliorated redox balance, inflammatory state, and RAS axis.

Interleukin-10 deficiency induces thoracic perivascular adipose tissue whitening and vascular remodeling.

Perivascular adipose tissue (PVAT) is an adipose layer, surrounding blood vessels, with a local modulatory role. Interleukin-10 (IL-10) has been shown to modulate vascular tissue. This study aimed to characterize the endogenous role of IL-10 in vascular remodeling, and PVAT phenotyping. Thoracic aortic segments from control (C57BL/6J) and IL-10 knockout (IL-10-/-) male mice were used. Analyzes of aorta/PVAT morphometry, and elastin, collagen and reticulin deposition were performed. Tissue uncoupling protein 1 (UCP1) was accessed by Western blotting. Endogenous absence of IL-10 reduced total PVAT area (p = 0.0310), and wall/lumen ratio (p = 0.0024), whereas increased vascular area and thickness (p < 0.0001). Total collagen deposition was augmented in IL-10-/-, but under polarized light, the reduction of collagen-I (p = 0.0075) and the increase of collagen-III (p = 0.0055) was found, simultaneously with reduced elastic fibers deposition (p = 0.0282) and increased deposition of reticular fibers (p < 0.0001). Adipocyte area was augmented in the IL-10 absence (p = 0.0225), and UCP1 expression was reduced (p = 0.0420). Moreover, relative frequency of white adipose cells and connective tissue was augmented in IL-10-/- (p < 0.0001), added to a reduction in brown adipose cells (p < 0.0001). Altogether, these data characterize aorta PVAT from IL-10-/- as a white-like adipocyte phenotype. Endogenous IL-10 prevents vascular remodeling and favors a brown-like adipocyte phenotype, suggesting a modulatory role for IL-10 in PVAT plasticity.

Sex-Specific Effects of Cholesteryl Ester Transfer Protein (CETP) on the Perivascular Adipose Tissue.

Cholesteryl ester transfer protein (CETP) increases the atherosclerosis risk by lowering HDL-cholesterol levels. It also exhibits tissue-specific effects independent of HDL. However, sexual dimorphism of CETP effects remains largely unexplored. Here, we hypothesized that CETP impacts the perivascular adipose tissue (PVAT) phenotype and function in a sex-specific manner. PVAT function, gene and protein expression, and morphology were examined in male and female transgenic mice expressing human or simian CETP and their non-transgenic counterparts (NTg). PVAT exerted its anticontractile effect in aortas from NTg males, NTg females, and CETP females, but not in CETP males. CETP male PVAT had reduced NO levels, decreased eNOS and phospho-eNOS levels, oxidative stress, increased NOX1 and 2, and decreased SOD2 and 3 expressions. In contrast, CETP-expressing female PVAT displayed increased NO and phospho-eNOS levels with unchanged NOX expression. NOX inhibition and the antioxidant tempol restored PVAT anticontractile function in CETP males. Ex vivo estrogen treatment also restored PVAT function in CETP males. Moreover, CETP males, but not female PVAT, show increased inflammatory markers. PVAT lipid content increased in CETP males but decreased in CETP females, while PVAT cholesterol content increased in CETP females. CETP male PVAT exhibited elevated leptin and reduced Prdm16 (brown adipocyte marker) expression. These findings highlight CETP sex-specific impact on PVAT. In males, CETP impaired PVAT anticontractile function, accompanied by oxidative stress, inflammation, and whitening. Conversely, in females, CETP expression increased NO levels, induced an anti-inflammatory phenotype, and preserved the anticontractile function. This study reveals sex-specific vascular dysfunction mediated by CETP.

Deciphering Abdominal Aortic Diseases Through T-Cell Clonal Repertoire of Perivascular Adipose Tissue.

Recent studies suggest that immune-mediated inflammation of perivascular adipose tissue of abdominal aortic aneurysms (AAAs) contributes to disease development and progression. Whether the perivascular adipose tissue of AAA is characterized by a specific adaptive immune signature remains unknown. To investigate this hypothesis, we sequenced the T-cell receptor β-chain in the perivascular adipose tissue of patients with AAA and compared it with patients with aortic occlusive disease, who share the former anatomical site of the lesion and risk factors but differ in pathogenic mechanisms. Our results demonstrate that patients with AAA have a lower repertoire diversity than those with aortic occlusive disease and significant differences in variable/joining gene segment usage. Furthermore, we identified a set of 7 public T-cell receptor β-chain clonotypes that distinguished AAA and aortic occlusive disease with very high accuracy. We also found that the T-cell receptor β-chain repertoire differentially characterizes small and large AAAs (aortic diameter<55 mm and ≥55 mm, respectively). This work supports the hypothesis that T cell-mediated immunity is fundamental in AAA pathogenesis and opens up new clinical perspectives.

The role of adipose tissue cell elements in the regulation of the nitroxidergic system and possible ways of pharmacological modulation

Endothelial dysfunction is characterized by a decrease in the bioavailability of the vasodilator – nitric oxide (NO), and an increase in the level of vasoconstrictor substances. This imbalance leads to vasoconstriction, leukocyte attachment and inflammatory reactions in the vascular wall, atherosclerosis and thrombosis. The aim: to evaluate the role of adipose tissue elements in the regulation of parameters of the nitroxidergic system under hypoxia conditions. Materials and methods. The studies were carried out on 30 adult white male Wistar rats. All animals were randomly assigned and divided into groups: a control group (15 rats), type 2 diabetes mellitus (T2DM) was induced in the animals of the second group (15 rats). Isolated fragments of the popliteal arteries (PA) and intrapulmonary artery (IPA) were cleared of perivascular adipose tissue (PVAT-) or left uncleaned (PVAT+) and cut into rings. The simulation of acute hypoxia with further study of medical agents were performed. Results. The PA and IPA with PVAT responded to acute hypoxia with vasoconstriction – an increase in the amplitude of contraction in the first and second phases, and after removing PVAT, they responded with a decrease in the maximum amplitude of contraction by 3.4 times in the 1st phase and an increase in amplitude by 1.8 times in the 2nd phase. Perfusion with Angiolin reduced 2nd phase of HV of the PA and IPA. Adding a combination of Thiotriazoline and L-arginine (1:4) to a solution for perfusion of fragments of arteries of animals with T2DM, causes a significant increase in constrictor reactions in both the 1st and 2nd phases of HV, regardless of presence of perivascular adipose tissue. Conclusions. The presence of PVAT affects the HV of arteries, both in normal and in T2DM. The possibilities of ways of pharmacological modulation of the nitroxidergic system depending on the state of PVAT were determined.

Level of Perivascular Inflammation Is Significantly Lower Around the Left Internal Mammary Artery Than Around Native Coronary Arteries.

The left internal mammary artery (LIMA) is protected from developing atherosclerosis. Perivascular inflammation, which is closely associated with atherosclerosis, can be measured by perivascular adipose tissue attenuation on computed tomography angiography. Whether the absence of atherosclerosis in LIMA is related to the lower level of perivascular inflammation is unknown. This study was performed to compare the level of perivascular inflammation between LIMA insitu and native coronary arteries in patients with coronary artery disease. A total of 573 patients who underwent both computed tomography angiography and optical coherence tomography imaging were included. The level of perivascular adipose tissue attenuation between LIMA insitu and coronary arteries was compared. Perivascular adipose tissue attenuation around LIMA insitu was significantly lower around the 3 coronary arteries (-82.9 [-87.3 to -78.0] versus -70.8 [-75.9 to -65.9]; P<0.001), irrespective of the level of pericoronary inflammation or the number of vulnerable features on optical coherence tomography. When patients were divided into high and low pericoronary inflammation groups, those in the high inflammation group had more target vessel failure (hazard ratio, 2.97 [95% CI, 1.16-7.59]; P=0.017). The current study demonstrated that perivascular adipose tissue attenuation was significantly lower around LIMA insitu than around native coronary arteries. The lower level of perivascular inflammation may be related to the low prevalence of atherosclerosis in LIMA. URL: https://www.clinicaltrials.gov; Unique Identifier: NCT04523194.

Radiomics of pericoronary adipose tissue on computed tomography angiography predicts coronary heart disease in patients with type 2 diabetes mellitus

BackgroundDiabetes is a common chronic metabolic disease. The progression of the disease promotes vascular inflammation and the formation of atherosclerosis, leading to cardiovascular disease. The coronary artery perivascular adipose tissue attenuation index based on CCTA is a new noninvasive imaging biomarker that reflects the spatial changes in perivascular adipose tissue attenuation in CCTA images and the inflammation around the coronary arteries. In this study, a radiomics approach is proposed to extract a large number of image features from CCTA in a high-throughput manner and combined with clinical diagnostic data to explore the predictive ability of vascular perivascular adipose imaging data based on CCTA for coronary heart disease in diabetic patients.MethodsR language was used for statistical analysis to screen the variables with significant differences. A presegmentation model was used for CCTA vessel segmentation, and the pericoronary adipose region was screened out. PyRadiomics was used to calculate the radiomics features of pericoronary adipose tissue, and SVM, DT and RF were used to model and analyze the clinical data and radiomics data. Model performance was evaluated using indicators such as PPV, FPR, AAC, and ROC.ResultsThe results indicate that there are significant differences in age, blood pressure, and some biochemical indicators between diabetes patients with and without coronary heart disease. Among 1037 calculated radiomic parameters, 18.3% showed significant differences in imaging omics features. Three modeling methods were used to analyze different combinations of clinical information, internal vascular radiomics information and pericoronary vascular fat radiomics information. The results showed that the dataset of full data had the highest ACC values under different machine learning models. The support vector machine method showed the best specificity, sensitivity, and accuracy for this dataset.ConclusionsIn this study, the clinical data and pericoronary radiomics data of CCTA were fused to predict the occurrence of coronary heart disease in diabetic patients. This provides information for the early detection of coronary heart disease in patients with diabetes and allows for timely intervention and treatment.

Perivascular Adipose Tissue Density and Stenosis Plaque Degree in Lower Limb Peripheral Arteries in CT

Background: Perivascular adipose tissue (PVAT) attenuation has emerged as a novel biomarker for identifying high-risk arterial plaques due to its association with inflammation. Recognizing the systemic nature of atherosclerosis and its link with major cardiovascular events in coronary disease, this study evaluated PVAT attenuation in the peripheral arteries using CT imaging to expand the understanding of its diagnostic and prognostic potential. Methods: a retrospective analysis of 53 consecutive patients who underwent CT angiography, examining PVAT density across five primary peripheral arterial segments. A 5 mm region of interest adjacent to the vascular wall was analyzed by two blinded readers, with reproducibility coefficients calculated to determine the reliability of the measurements. For the statistical analyses, mean values were derived from these measurements. The patients were stratified into four groups based on the degree of arterial stenosis: &lt;25%, 25–50%, 50–70%, and &gt;70%. PVAT density comparisons between these groups were performed using the Kruskal–Wallis test and the pairwise Mann–Whitney U test with Holm–Bonferroni correction for multiple comparisons. Results: the Kruskal–Wallis test revealed statistically significant disparities in PVAT density across the categorically differentiated stenosis groups (p &lt; 0.001), indicating an association between PVAT density and arterial stenosis severity. This association was especially pronounced in the external iliac, common femoral, superficial femoral, and popliteal arteries, where the p-values were consistently below 0.05. Subsequent pairwise analyses utilizing the Mann–Whitney U test with Holm–Bonferroni correction affirmed these findings, in particular for the external iliac, common femoral, superficial femoral and popliteal arteries (p &lt; 0.05). Conclusions: our findings reinforce the correlation between increased PVAT density and the degree of arterial stenosis, supporting the clinical value of PVAT as a non-invasive biomarker for cardiovascular risk stratification and potentially guiding therapeutic interventions.