Plaque Group Research Articles

Quantification of patient-specific coronary material properties and their correlations with plaque morphological characteristics: An in vivo IVUS study

BackgroundA method using in vivo Cine IVUS and VH-IVUS data has been proposed to quantify material properties of coronary plaques. However, correlations between plaque morphological characteristics and mechanical properties have not been studied in vivo.Method: In vivo Cine IVUS and VH-IVUS data were acquired at 32 plaque cross-sections from 19 patients. Six morphological factors were extracted for each plaque. These samples were categorized into healthy vessel, fibrous plaque, lipid-rich plaque and calcified plaque for comparisons. Three-dimensional thin-slice models were constructed using VH-IVUS data to quantify in vivo plaque material properties following a finite element updating approach by matching Cine IVUS data. Effective Young's moduli were calculated to represent plaque stiffness for easy comparison. Spearman's rank correlation analysis was performed to identify correlations between plaque stiffness and morphological factor. Kruskal-Wallis test with Bonferroni correction was used to determine whether significant differences in plaque stiffness exist among four plaque groups. ResultOur results show that lumen circumference change has a significantly negative correlation with plaque stiffness (r = −0.7807, p = 0.0001). Plaque burden and calcification percent also had significant positive correlations with plaque stiffness (r = 0.5105, p < 0.0272 and r = 0.5312, p < 0.0193) respectively. Among the four categorized groups, calcified plaques had highest stiffness while healthy segments had the lowest. ConclusionThere is a close link between plaque morphological characteristics and mechanical properties in vivo. Plaque stiffness tends to be higher as coronary atherosclerosis advances, indicating the potential to assess plaque mechanical properties in vivo based on plaque compositions.

Correlation analysis between D-dimer-to-fibrinogen-ratio and carotid plaque in young patients aged 18–45 with acute cerebral infarction

BackgroundD-Dimer and fibrinogen were commonly used to detect the coagulation and fibrinolytic function, but D-dimer to fibrinogen ratio (DFR) in carotid plaque in young patients aged 18–45 with acute cerebral infarction (ACI) has not been used clinically. In this work, we focused on the evaluation of the DFR value of this group of patients and analyzed its possible correlation. MethodsA total of 164 patients with ACI patients aged 18–45 were selected as research subjects after their first admission. They had undergone carotid plaque contrast-enhanced ultrasound (CEUS) and were divided into two groups with carotid plaque (n = 97) and with no carotid plaque (n = 67). According to NIHSS score and carotid plaque grade, the clinical symptoms of patients were judged. Univariate and multivariate analyses were conducted to compare the risk factors of carotid plaque in ACI patients. ResultsThe DFR value of patients in the carotid plaque group (103.41 ± 20.81) was significantly higher than that of the no carotid plaque control group (88.9 ± 26.51). We also identified DFR X103 was the only independent risk factor (β = 0.53; 95% CI, 0.914–0.984; P = 0.05). DFR X103 was increased with the severity of the disorder and with the CEUS grades. The area under the DFR curve was 0.673 (95% CI 0.584～0.762). ConclusionThe value of the DFR is positively correlated with CEUS carotid plaque grading and NIHSS score, which can predict the severity of carotid plaque in ACI patients aged 18–45. Therefore it is worthy of clinical application.

High systemic immune-inflammation index is associated with carotid plaque vulnerability: New findings based on carotid ultrasound imaging in patients with acute ischemic stroke.

Vulnerable carotid plaque is closely related to the occurrence of Ischemic stroke. Therefore, accurate and rapid identification of the nature of carotid plaques is essential. AS is a chronic immune inflammatory process. Systemic immune-inflammation index (SII) is a novel index of immune inflammation obtained from routine whole blood cell count analysis, which comprehensively reflects the state of inflammation and immune balance in the body. This study sought to explore the relationship between SII level and carotid plaque vulnerability, plaque composition characteristics, and acute ischemic stroke (AIS) severity. A total of 131 patients diagnosed with AIS presenting with a carotid atherosclerotic plaque were enrolled in this study. Using carotid ultrasound (CDU) to assess the carotid-responsible plaque properties, we divided the patients into stable plaques group and vulnerable plaques group, and analyzed the correlation between SII levels and plaque vulnerability. And we further analyzed to evaluate the correlation between high SII levels and plaque characteristics and AIS severity. In addition, Cohen's Kappa statistics was used to detect the consistency of Carotid ultrasound (US) and cervical High-resolution magnetic resonance imaging (HRMRI) in evaluating plaque vulnerability. The findings showed that the vulnerable group had higher levels of SII compared with the stable group. The high SII group had more vulnerable plaques and a high frequency of plaque fibrous cap rupture compared with the low SII group. Logistic analysis showed that a high SII level was an independent risk factor for vulnerable plaques (odds ratio [OR] = 2.242) and plaque fibrous cap rupture (OR=3.462). The results also showed a high consistency between Carotid US and HRMRI methods in the assessment of plaque vulnerability [Cohen's kappa value was 0.89 (95% CI = 0.78–0.97)] and the level of SII was positively associated with NIHSS score (r = 0.473, P < 0.001). Our study suggests that elevated levels of SII may have adverse effects on the vulnerability of carotid plaques, especially in stroke patients with vulnerable plaques with ruptured fibrous caps, which may aggravate the severity of AIS.

Features of non-stenotic carotid plaque on computed tomographic angiography in patients with embolic stroke of undetermined source.

PurposeEmbolic stroke of undetermined source (ESUS) is a subset of cryptogenic stroke constituting a large proportion of acute ischemic strokes. This study aimed to assess the features of non-stenotic carotid plaque (<50%) on computed tomographic angiography (CTA) and to evaluate the association between non-stenotic carotid plaque and ESUS.MethodsFrom January 1 to December 31, 2019, a total of 60 consecutive patients with primary unilateral ESUS and <50% carotid artery stenosis, as determined using screening ultrasonography, were hospitalized in the Department of Neurology of our hospital. All enrolled patients underwent CTA to determine the composition and morphological features of non-stenotic carotid plaques using consecutive sections in both carotid arteries. The features of these plaques with and without ipsilateral stroke in patients with ESUS were compared.ResultsSixty ESUS images were included in the study, with 85 plaques. Forty-five (52.9%) of these plaques were ipsilateral and 40 (47.1%) were contralateral to the stroke. Compared to that of the contralateral plaque group, the maximum carotid plaque thickness and plaque length of the ipsilateral group were greater (2.1 mm vs. 1.5 mm, p = 0.03; 20.8 mm vs. 12.1 mm, p = 0.02); however, there were no significant differences in the degree of luminal stenosis, presence of soft plaque and calcified plaque, and the number of ulcers on the plaque surface between the two groups. Similarly, the number of plaques with thickness >3 mm in the ipsilateral group was greater than in the contralateral group (30 vs. 13, p = 0.01). A lipid core was more common in individuals with ipsilateral strokes than in those with contralateral strokes (19 vs. 7, p = 0.02). Regression analysis showed that plaque lipid core area was an independent risk factor for ESUS (odds ratio, 1.92; 95% confidence interval, 1.22–3.04; p = 0.03).ConclusionsNon-stenotic carotid plaques could be an etiology of acute ischemic strokes classified as ESUS. The presence of a lipid core was a risk factor in individuals with non-stenotic carotid plaques.

Association between circulating asprosin levels and carotid atherosclerotic plaque in patients with type 2 diabetes

BackgroundCarotid plaque is one of the typical manifestations and precursors of diabetic cardiovascular complications. As a new adipokine, asprosin participates in the development of diabetes and cardiovascular diseases, and is considered to be closely related to insulin resistance and glucolipid metabolism. This study aimed to analyze the relationship between serum asprosin level and carotid plaque in patients with type 2 diabetes mellitus (T2DM). MethodsA total of 180 patients with T2DM were selected. The basic parameters and biochemical indexes of the subjects were measured, and the serum asprosin concentration of the subjects was detected by ELISA. The carotid plaque was evaluated by color Doppler ultrasound. ResultsThe level of serum asprosin in the T2DM with carotid plaque group was significantly higher than that in T2DM without carotid plaque group [2.53(1.73–3.21) vs 1.72(1.23–2.34) ng/mL, P < 0.05]. The incidence of carotid plaque in the low, middle and high quartiles was 31.7 %, 48.3 % and 70 % respectively. Correlation analysis showed that serum asprosin was positively correlated with BMI, WHR, SBP, DBP, FIns, LDL-C, HOMA-IR, and HOMA-β (P < 0.05). Linear regression analysis showed that WHR, DBP, FIns, and LDL-C were independent influencing factors of asprosin. Logistic regression analysis showed that serum asprosin was still significantly correlated with carotid plaque in T2DM patients after adjusting for multiple confounding factors. The area under receiver-operating curve (ROC) of asprosin predicting carotid plaque was 0.701 (0.625–0.777) in T2DM. ConclusionThe level of serum asprosin in T2DM patients with carotid plaques is significantly higher, suggesting that asprosin may play a role in the occurrence and development of carotid plaques in T2DM. Detection of this index can provide new clinical evidence for the prevention and treatment of diabetic cardiovascular disease.

Early Diagnosis and Treatment of Coronary Heart Disease with Image Features of Optical Coherence Tomography under Adaptive Segmentation Algorithm.

This research was aimed at exploring the application value of optical coherence tomography (OCT) images under adaptive segmentation algorithm in the early diagnosis of coronary heart disease (CHD). Eighty-two patients with CHD were included, who were to undergo coronary angiography (CAG) to confirm their condition. According to the diagnostic criteria of CHD in the American Coronary Artery Surgery Study (CASS), the patients were divided into the stable plaque group (41 cases) and unstable plaque group (41 cases). Besides, 20 healthy volunteers were selected as the control group, and all of them underwent OCT scans. On the basis of a fourth-order partial differential equation (PDE) and active contour (AC) model, a novel adaptive image segmentation algorithm PDE-AC was constructed and used for OCT image processing. No significant difference was found in general clinical data and serological indicators in the control group compared to the other two groups (P > 0.05). The lipid plaque length, degree of stenosis, and lipid pool angle, macrophages and intimal erosion, and plaque fissure in the unstable plaque group were highly greater than those in the stable plaque group. The fibrous cap thickness (FCT) was significantly thinner than that in the stable plaque group (P < 0.05). The diagnostic sensitivity, specificity, and accuracy of OCT under PDE-AC algorithm for CHD (91.53%, 84.08%, and 95.38%) were markedly higher than those of single OCT (83.46%, 75.11%, and 88.02%) (P < 0.05). In summary, OCT images under PDE-AC algorithm did better than simple OCT images in the diagnosis of CHD. Lipid plaque length, degree of stenosis, and lipid pool angle, macrophage and intimal erosion, plaque fissure, and FCT were important indicators for judging plaque stability, having the better clinical application value.

Brain alterations of regional homogeneity, degree centrality, and functional connectivity in vulnerable carotid plaque patients with neither clinical symptoms nor routine MRI lesions: A resting-state fMRI study.

AimsBased on resting-state functional MRI (fMRI), we preliminarily explored brain alterations in asymptomatic patients with vulnerable carotid plaques, but carotid stenosis was < 50%.MethodsA total of 58 asymptomatic patients with vulnerable carotid plaques (stenosis <50%) and 38 healthy controls were recruited. Between-group differences in regional homogeneity (ReHo), degree centrality (DC), and functional connectivity (FC) were analyzed. Correlation analysis was performed between the ReHo or DC values in altered brain regions as well as voxel-wise abnormal FC and scores on neuropsychiatric scales, serum interleukin-6 (IL-6), and C-reactive protein (CRP).ResultsBoth ReHo and DC values on the left superior occipital gyrus (SOG.L) of the asymptomatic vulnerable carotid plaque group reduced, regardless of plaque location (left, right, or bilateral). Functional connections weakened between the SOG.L and right lingual gyrus (LING.R)/right inferior occipital gyrus (IOG.R), right middle frontal gyrus (MFG.R)/orbital part of superior frontal gyrus (ORBsup.R)/orbital part of middle frontal gyrus (ORBmid.R), left precentral gyrus (PreCG.L)/postcentral gyrus (PoCG.L), left supplementary motor area (SMA.L), right paracentral lobule (PCL.R), left precuneus (PCUN.L), and right postcentral gyrus (PoCG.R)/PCL.R. In ReHo-altered brain regions, ReHo values were positively correlated with Hamilton Rating Scale for Depression (HAMD) scores, and the setting region of abnormal ReHo as seed points, voxel-wise FC between the SOG.L and PreCG.L was negatively correlated with CRP.ConclusionsCerebral alterations of neuronal synchronization, activity, and connectivity properties in the asymptomatic vulnerable carotid plaque group were independent of the laterality of vulnerable carotid plaques. Significant relation between ReHo values on the SOG.L and HAMD indicated that even when there were neither clinical symptoms nor lesions on routine MRI, brain function might have changed already at an early stage of carotid atherosclerosis. Inflammation might play a role in linking vulnerable carotid plaques and changes of resting-state functional connectivity.

Cluster of Differentiation 147 (CD147) serves as a promoter of atherosclerosis in patients with cerebral infarction.

The aim of this study was to investigate the correlations of cluster of differentiation 147 (CD147) with plaque stability of carotid atherosclerosis (AS), degree of stenosis, inflammatory factors, matrix metalloproteinase-9 (MMP-9) expression and vascular endothelial function in patients with cerebral infarction. A total of 50 patients diagnosed with cerebral infarction (cerebral infarction group), 70 patients diagnosed with AS plaque (plaque group, with no infarction but plaques only) and 30 healthy people receiving physical examination (control group) in our hospital from March 2018 to July 2019 were collected. The levels of biochemical indexes, CD147, MMP-9, vascular endothelial function indexes [endothelin-1 (ET-1) and C-reactive protein (CRP)] and inflammatory factors [interleukin-10 (IL-10), IL-16 and tumor necrosis factor-alpha (TNF-α)] in the blood of each group of patients were detected via radioimmunoassay and enzyme-linked immunosorbent assay (ELISA). Moreover, ultrasonic examination and Gensini score system were applied to score the degree of carotid stenosis in cerebral infarction group. Finally, the differences in various parameters were compared among the three groups, and the correlations of CD147 with different indexes were evaluated using Spearman method. Compared with those in control group, the levels of CD147, MMP-9, hemoglobin, platelets, total cholesterol, triglyceride, low-density lipoprotein (LDL), high-density lipoprotein (HDL), apolipoprotein A, apolipoprotein B, IL-10, IL-13 and TNF-α in the blood were remarkably elevated in cerebral infarction group and plaque group (p<0.05). Cerebral infarction group had notably higher levels of CD147, hemoglobin, triglyceride, apolipoprotein B, IL-10, IL-13 and TNF-α in the blood than plaque group (p<0.05). The plaque score was markedly higher in cerebral infarction group than that in plaque group [(3.27±2.86) points vs. (0.93±1.44) points] (p<0.05). In comparison with control group, plaque group and cerebral infarction group exhibited evidently raised levels of blood ET-1 and CRP (p<0.05). The serum CD147 level was significantly associated with MMP-9 (p=0.003, r=0.616), Gensini score (p=0.006, r=0.656), plaque score (p=0.027, r=0.396), IL-10 (p=0.004, r=0.603), TNF-α (p=0.001, r=0.746) and CRP (p=0.037, r=0.450) in cerebral infarction group. CD147 level is prominently increased in carotid AS and closely related to inflammatory responses, and CD147 may become a new reference for the prediction and treatment of AS and cerebral infarction.

Serum sulfatide as a biomarker of carotid atherosclerosis in patients with rheumatoid arthritis

PurposeRheumatoid arthritis (RA) patients have accelerated atherosclerosis (AS) leading to excess cardiovascular morbidity and mortality, but traditional risk factors for cardiovascular disease (CVD) are invalid to explain the problem. Sulfatides, as major components of serum lipoproteins, are synthesized in the liver. These molecules are reported to play an important role in the development of AS, thrombogenesis, and inflammation. However, it is unclear whether sulfatides are responsible for such issue. To elucidate the possible association between serum sulfatide and the accelerated progress of AS, evaluated by carotid intima-media thickness (CIMT), and ascertain the related mechanism underlying the correlation in RA cases. MethodsWe performed an observational study of 144 patients with RA and 120 sex and age-matched controls. Meanwhile, 107 patients (of the 144 RA patients enrolled at baseline) were invited to undergo a second measurement after 12 months. Serum sulfatide levels of all the enrolled subjects were quantified by mass spectrometry after they were converted into lysosulfatides (LS), and then calculated as the sum of the levels of seven LS molecular species. Serum oxidative stress marker, malondialdehyde (MDA) was detected by ELISA. We subsequently statistically analyzed the causalities between carotid AS and clinical parameters, and the association of serum sulfatide with other variables. Multivariable logistic regression analysis was finally employed by taking all factors to identify independent determinant for carotid atherosclerotic plaque and serum sulfatide level. ResultsA gradual declined trend in serum sulfatide levels was observed in control subjects, non-plaque group, and the plaque group (8.56 ± 1.37 nmol/mL, 5.63 ± 1.57 nmol/mL, 3.18 ± 1.32 nmol/mL, respectively, p < 0.01), along with an increased value of CIMT (0.63 ± 0.07 mm, 0.92 ± 0.14 mm, 1.43 ± 0.22 mm, respectively, p < 0.01). Meanwhile, a negative linear correlation between CIMT and serum sulfatide was further confirmed by Spearman’s analysis (r = -0.622, p < 0.01). Eventually, multivariate logistic regression analysis identified serum MDA as the only independent factor for the abnormal level of serum sulfatide, and serum sulfatide was detected as a significant protective factor for the occurrence of carotid plaques in RA cases (p < 0.01), which was confirmed repeatedly by our cross-sectional and longitudinal studies. ConclusionExcessive abnormal levels of oxidative stress decreased serum sulfatide levels, followed by a high occurrence of AS in RA patients. Serum sulfatide level might be useful as a predictor (biomarker) for the progression of AS in RA cases.

Follow-up assessment of atherosclerotic plaques in acute ischemic stroke patients using high-resolution vessel wall MR imaging.

Data on evolution of intracranial plaques in acute ischemic stroke patients after receiving medical therapy is still limited. We aimed to investigate the plaque features associated with culprit lesions and to explore the plaque longitudinal changes during treatment using high-resolution vessel wall MR imaging (VW-MRI). Twenty-three patients (16 men; mean age, 51.4years ± 11.1) with acute ischemic stroke underwent 3-T VW-MRI for intracranial atherosclerosis and were taken follow-up assessments. Each identified plaque was retrospectively classified as culprit, probably culprit, or nonculprit. Plaque features were analyzed at both baseline and follow-up and were compared using paired t-test, paired Wilcoxon test, or McNemar's test. A total of 87 intracranial plaques were identified (23 [26.4%] culprit, 10 [11.5%] probably culprit, and 54 [62.1%] nonculprit plaques). The median time interval between initial and follow-up MRI scans was 8.0months. In the multiple ordinal logistic regression analysis, plaque contrast ratio (CR) (OR, 1.037; 95% CI, 1.013-1.062; P = 0.002) and surface irregularity (OR, 4.768; 95% CI, 1.064-21.349; P = 0.041) were independently associated with culprit plaques. During follow-up, plaque length, maximum thickness, normalized wall index (NWI), stenosis degree, and CR significantly decreased (all P-values < 0.05) in the culprit plaque group. The plaque NWI and CR dropped in the probably culprit plaques (P = 0.041, 0.026, respectively). In the nonculprit plaque group, only plaque NWI and stenosis degree showed significant decrement (P = 0.017, 0.037, respectively). Follow-up VW-MRI may contribute to plaque risk stratification and may provide valuable insights into the evolution of different plaques in vivo.

Genomic DNA Methylation in Diabetic Chronic Complications in Patients With Type 2 Diabetes Mellitus.

AimTo explore the relationship between genomic DNA methylation and diabetic chronic complications.Methods299 patients with type 2 diabetes mellitus (T2DM) hospitalized in the Second Affiliated Hospital of Soochow University were enrolled. We divided the patients into different complications groups and corresponding non-complication groups. Clinical and biochemical parameters were compared between the two groups. The level of genomic DNA methylation in leukocytes was determined by high-performance liquid chromatography-tandem mass spectrometry.Results(1) Age, duration of diabetes, creatinine (Cr), blood urea nitrogen (BUN), genomic DNA methylation, 24- hour urine total protein (24-hUTP), and intima-media thickness (IMT) were significantly higher in the carotid plaque (CP) group. Waist-to-hip ratio (WHR), body mass index (BMI), estimated glomerular- filtration rate (eGFR), and albumin (Alb) were significantly lower in the CP group. Gender, age and BMI were the influencing factors of CP. (2) Age, duration, Cr, BUN, urinary microalbumin creatinine ratio (UACR), systolic blood pressure (SBP), TCSS, and 24- hUTP were significantly higher in the diabetic retinopathy (DR) group. eGFR, 2h postprandial C- peptide, and Alb were lower in the DR group. Age, duration, Cr, Alb, SBP, and the presence of DN were the influencing factors of DR. (3) Age, duration, HbA1c, BUN, TCSS, SBP, and IMT(R) were significantly higher in the diabetic nephropathy (DN) group. 2h postprandial C-peptide, and Alb were lower in the DN group. HbA1c, BUN, DR, and HBP were the influencing factors of DN. (4) Age, duration, total cholesterol (TC), low-density lipoprotein (LDL-C), triglyceride (TG), Cr, BUN, uric acid (UA), and SBP were significantly higher in the diabetic peripheral neuropathy (DPN) group. The level of genomic DNA methylation and eGFR were significantly lower in the DPN group. Age, duration, LDL-C, UA, the presence of DR, and the genomic DNA methylation level were the influencing factors for DPN. Incorporating the level of genomic DNA methylation into the prediction model could improve the ability to predict DPN on the basis of conventional risk factors.ConclusionLow level of genomic DNA methylation is a relatively specific risk factor for DPN in patients with T2DM and not a contributing factor to the other chronic complications.

The Profile of Circulating Blood microRNAs in Outpatients with Vulnerable and Stable Atherosclerotic Plaques: Associations with Cardiovascular Risks.

Non-coding RNAs reflect many biological processes in the human body, including athero-sclerosis. In a cardiology outpatient department cohort (N = 83), we aimed to compare the levels of circulating microRNAs in groups with vulnerable plaques (N = 22), stable plaques (N = 23) and plaque-free (N = 17) depending on coronary computed tomography angiography and to evaluate associations of microRNA levels with calculated cardiovascular risks (CVR), based on the SCORE2 (+OP), ACC/AHA, ATP-III and MESA scales. Coronary computed tomography was performed on a 640-slice computed tomography scanner. Relative plasma levels of microRNA were assessed via a real-time polymerase chain reaction. We found significant differences in miR-143-3p levels (p = 0.0046 in plaque-free vs. vulnerable plaque groups) and miR-181b-5p (p = 0.0179 in stable vs. vulnerable plaques groups). Analysis of microRNA associations with CVR did not show significant differences for SCORE2 (+OP) and ATPIII scales. MiR-126-5p and miR-150-5p levels were significantly higher (p < 0.05) in patients with ACC/AHA risk >10% and miR-145-5p had linear relationships with ACC/AHA score (adjusted p = 0.0164). The relative plasma level of miR-195 was higher (p < 0.05) in patients with MESA risk > 7.5% and higher (p < 0.05) in patients with zero coronary calcium index (p = 0.036). A linear relationship with coronary calcium was observed for miR-126-3p (adjusted p = 0.0484). A positive correlation with high coronary calcium levels (> 100 Agatson units) was found for miR-181-5p (p = 0.036). Analyzing the biological pathways of these microRNAs, we suggest that miR-143-3p and miR-181-5p can be potential markers of the atherosclerosis process. Other miRNAs (miR-126-3p, 126-5p, 145-5p, 150-5p, 195-5p) can be considered as potential cardiovascular risk modifiers, but it is necessary to validate our results in a large prospective trial.

Measurement of epicardial adipose tissue using non-contrast routine chest-CT: a consideration of threshold adjustment for fatty attenuation

BackgroundEpicardial adipose tissue (EAT) is known as an important imaging indicator for cardiovascular risk stratification. The present study aimed to determine whether the EAT volume (EV) and mean EAT attenuation (mEA) measured by non-contrast routine chest CT (RCCT) could be more consistent with those measured by coronary CT angiography (CCTA) by adjusting the threshold of fatty attenuation.MethodsIn total, 83 subjects who simultaneously underwent CCTA and RCCT were enrolled. EV and mEA were quantified by CCTA using a threshold of (N30) (− 190 HU, − 30 HU) as a reference and measured by RCCT using thresholds of N30, N40 (− 190 HU, − 40 HU), and N45 (− 190 HU, − 45 HU). The correlation and agreement of EAT metrics between the two imaging modalities and differences between patients with coronary plaques (plaque ( +)) and without plaques (plaque ( −)) were analyzed.ResultsEV obtained from RCCT showed very strong correlation with the reference (r = 0.974, 0.976, 0.972 (N30, N40, N45), P < 0.001), whereas mEA showed a moderate correlation (r = 0.516, 0.500, 0.477 (N30, N40, N45), P < 0.001). Threshold adjustment was able to reduce the bias of EV, while increase the bias of mEA. Data obtained by CCTA and RCCT both demonstrated a significantly larger EV in the plaque ( +) group than in the plaque ( −) group (P < 0.05). A significant difference in mEA was shown only by RCCT using a threshold of N30 (plaque ( +) vs ( −): − 80.0 ± 4.4 HU vs − 78.0 ± 4.0 HU, P = 0.030). The mEA measured on RCCT using threshold of N40 and N45 showed no significant statistical difference between the two groups (P = 0.092 and 0.075), which was consistent with the result obtained on CCTA (P = 0.204).ConclusionApplying more negative threshold, the consistency of EV measurements between the two techniques improves and a consistent result can be obtained when comparing EF measurements between groups, although the bias of mEA increases. Threshold adjustment is necessary when measuring EF with non-contrast RCCT.

CT angiography-based radiomics as a tool for carotid plaque characterization: a pilot study.

Radiomics is a quantitative method able to analyze a high-throughput extraction of minable imaging features. Herein, we aim to develop a CT angiography-based radiomics analysis and machine learning model for carotid plaques to discriminate vulnerable from no vulnerable plaques. Thirty consecutive patients with carotid atherosclerosis were enrolled in this pilot study. At surgery, a binary classification of plaques was adopted ("hard" vs "soft"). Feature extraction was performed using the R software package Moddicom. Pairwise feature interdependencies were evaluated using the Spearman rank correlation coefficient. A univariate analysis was performed to assess the association between each feature and the plaque classification and chose top-ranked features. The feature predictive value was investigated using binary logistic regression. A stepwise backward elimination procedure was performed to minimize the Akaike information criterion (AIC). The final significant features were used to build the models for binary classification of carotid plaques, including logistic regression (LR), support vector machine (SVM), and classification and regression tree analysis (CART). All models were cross-validated using fivefold cross validation. Class-specific accuracy, precision, recall and F-measure evaluation metrics were used to quantify classifier output quality. A total of 230 radiomics features were extracted from each plaque. Pairwise Spearman correlation between features reported a high level of correlations, with more than 80% correlating with at least one other feature at |ρ|> 0.8. After a stepwise backward elimination procedure, the entropy and volume features were found to be the most significantly associated with the two plaque groups (p < 0.001), with AUCs of 0.92 and 0.96, respectively. The best performance was registered by the SVM classifier with the RBF kernel, with accuracy, precision, recall and F-score equal to 86.7, 92.9, 81.3 and 86.7%, respectively. The CART classification tree model for the entropy and volume features model achieved 86.7% well-classified plaques and an AUC of 0.987. This pilot study highlighted the potential of CTA-based radiomics and machine learning to discriminate plaque composition. This new approach has the potential to provide a reliable method to improve risk stratification in patients with carotid atherosclerosis.

Microbiota analysis of peri-implant mucositis in patients with periodontitis history

ObjectivesTo investigate the bacterial diversity in peri-implant plaques and the effect of periodontitis history on the occurrence of peri-implant mucositis.Materials and methodsThree groups of subgingival plaques were collected from peri-implant sulci in the first molar area. The three groups included healthy implants in patients without periodontitis (NH implant), healthy implants in patients with periodontitis history (PH implant), and peri-implant mucositis implants in patients with periodontitis history (PM implant). Subgingival plaques in periodontal pockets of contralateral natural first molars were also collected. Bacterial DNA was extracted and the V4 region of the 16S rDNA sequence was amplified and sequenced on an Illumina HiSeq platform. The operational taxonomic units obtained from amplicon sequencing were used to analyze the prevalence and identity of bacteria based on public databases and advanced techniques.ResultsAnalysis of similarities indicated a significant difference in bacterial structures between the NH implant and PM implant groups. Additionally, a significantly higher relative abundance of the genera Actinomyces and Streptococcus was found in the samples of the NH implant group. The genera Fusobacterium and Prevotella could be considered as potential biomarkers for peri-implant mucositis. Moreover, more gram-negative anaerobic bacteria (Porphyromonas and Prevotella) were detected in the samples from patients with periodontitis history.ConclusionsThe increased accumulation of Fusobacterium and Prevotella is associated with a higher risk of peri-implant mucositis. In addition, patients with periodontal history may be more likely to develop peri-implant mucositis.Clinical relevanceThe increase in periodontal pathogens and the decrease in health-associated bacteria in patients with periodontitis history may be more likely to develop peri-implant mucositis. These results provide a bacteriological basis for the prevention and treatment of peri-implant mucositis in patients with periodontitis history.

ASSOCIATION OF SERUM URIC ACID LEVELS AND ATHEROMATOSIS OF CAROTID ARTERIES IN HYPERTENSIVE PATIENTS

Objective: The aim of this study was to investigate a possible association between the serum uric acid levels with the atheromatosis of the carotid arteries of hypertensive patients and the possible role of fibrinogen in this status. Design and method: We studied 1296 hypertensive patients (45,2% female), treated or newly diagnosed untreated, of mean age: 60,2 ± 5,3 years, without any known cardiovascular disease and with mean office systolic/diastolic arterial blood pressure (S/DBPo): 145,9 ± 12.6/89.7 ± 5,3 mmHg, mean office heart rate (HRo): 74,3 ± 9,9 bpm, average body mass index (BMI): 28.3 ± 5,3 kg/m2and average waist circumference (WC) 96.1 ± 12.9 cm. The levels of serum uric acid (SUA), fibrinogen, urea and creatinine, were recorded. eGFR was calculated according Cockcroft-Gault Equation. All studied patients underwent triplex –Doppler ultrasound of carotids and intima -media thickness was measured (IMT) and the presence or not of atheromatous plaque was investigated. The study population was separated in two groups, according the IMT value and the existence or not of atheromatous plaque. Group A: IMT &gt; 0.9 mm or/and existence of atheromatous plaque Group B: IMT &lt; 0.9 mm and without any atheromatous plaque (t-test between the two groups p &lt; = 0.001). By using the ANOVA statistic method we registered the SUA levels values in both groups as well as fibrinogen levels. Using Pearson correlation method we correlated SUA with fibrinogen serum levels Results: Table 1: Differences of serum uric acid levels between group A and group B Table 2. Correlation between serum uric acid levels with fibrinogen levels SUA: serum uric acid Conclusions: In hypertensive patients treated or not, the existence of increased thickness or atheromatous plaques in carotids was associated with significantly higher serum uric acid levels and fibrinogen levels, possibly indicating their importance in the atheromatous status of hypertensive patients while a significant positive correlation exists between SUA and fibrinogen levels in this population

Inflammation Progresses to Normal Tissue in Patients with Anthracosis after Discontinuation of Exposure to Fossil Fuel.

Exposure to toxic materials predisposes the lungs to infectious agents and inflammatory responses. The present study was performed on patients with anthracosis caused by exposure to fossil fuels in previous years, and histopathological features of airways' normal-appearing tissue were compared with histopathological features of anthracotic plaques in these patients. Bronchoscopic evaluations were performed on bakery workers who were directly in contact with fossil fuels. Samples were taken from anthracotic plaques (Group A) or seemingly intact tissues at their periphery (Group B). Pathological evaluations were done after hematoxylin and eosin staining. Then, microbiological cultures were performed for the diagnosis of Mycobacterium tuberculosis. Data obtained from bronchoscopy, pathology, and cultures were compared between anthracotic and normal-appearing peripheral tissues using chi-square and analysis of variances (ANOVA) at a 95% confidence level. Sixty-eight patients were diagnosed with anthracotic plaques. The mean ± SD of the patients' age was 72.12 ± 13.74 years. Females comprised 58.8% of the sample, and 85.3% of the patients were Iranian. The frequency rates of disseminated plaques and obstructive types were 86.8% and 48.5%, respectively. Ten patients (14.70%) were diagnosed with tuberculosis, and 4.41% (3 of 68) had granuloma, which was detectable only in samples gathered from Group A. Fibrosis was more common in Group A (10.3%, p = 0.03), and most of the evaluated samples in both groups exhibited inflammatory features. Inflammatory changes and tissue damage can be seen in anthracotic plaques and the surrounding normal-appearing tissue, even after removing the triggering factors. So, it is suggested to take a biopsy from seemingly intact tissue at the periphery of the anthracotic plaque when a biopsy is needed in a patient with anthracosis to reduce the risk of bleeding. Besides, medical treatment should be done to control inflammation.

Serum Homocysteine Level Predictive Capability for Severity of Restenosis Post Percutaneous Coronary Intervention

Background: In stent restenosis (ISR) is one of the major complications after stent implantation. Thus, there is a growing interest in identifying a biomarker for the onset of ISR. High levels of serum homocysteine (Hcy) have been associated with the progression of cardiovascular disease. Therefore, the study was carried out to quantify the correlation between serum Hcy and ISR severity. Compared with coronary angiography (CAG), Hcy levels provided a significantly better clinical detection of ISR severity after PCI. Methods: A total of 155 patients were recruited from Shanxi Bethune hospital, from 6 months to 2 years post PCI. Serum Hcy levels and postoperative angiography results were used to differentiate the patients into two experimental groups: ISR (>50% diametrical stenosis), and non-ISR. The non-ISR included two subgroups: intimal hyperplasia (10–50% diametrical stenosis), and recovery (<10% diametrical stenosis). In addition, a group of 80 healthy individuals was used as a negative control. The correlation between homocysteine level and ISR severity t was analyzed for all groups. In addition, the correlation between serum Hcy level and the severity of ISR in the experimental group was analyzed by the Pearson correlation test. Results: The serum Hcy level in the experimental group and control group was determined to be (20.21 ± 11.42) μmol/L and (15.11 ± 10.25) μmol/L respectively. The level of serum Hcy in the experimental group was significantly higher than in the control group (t-value of 2.385; p-value of 0.019). The serum Hcy level in the restenosis and the intimal hyperplasia group was (25.72 ± 13.71) μmol/L and (17.35 ± 7.70) μmol/L respectively. The serum Hcy level in the restenosis group was significantly higher than in the intimal hyperplasia group (t-value of 2.215; p-value of 0.033). The level of serum Hcy in the group without a plaque in the stent was (16.30 ± 6.08) μmol/L, whereas in the control group was (15.11 ± 10.25) μmol/L. The no plaque group had a slightly higher serum Hcy level than the control group (t-value of 0.634; p-value of 0.528). All included patients were divided into four quartiles based on the serum Hcy concentration: quartile 1 (8.90–13.20 μmol/L), quartile 2 (13.30–16.45 μmol/L), quartile 3 (16.60–24.25 μmol/L) and quartile 4 (24.30-65.30 μ mol/L). The incidence of ISR was 5, 6.25, 7.5 and 15%, in the 1,2,3 and four quartiles respectively. The serum Hcy level in the experimental group was (20.21 ± 11.42) μmol/L, the severity of in-stent restenosis was (0.25 ± 0.31), (R-value was 0.234; p-value was 0.037), indicating a correlation between serum Hcy and the severity of restenosis (p < 0.05). Taking coronary angiography as the gold standard, a ROC curve analysis was performed on the serum Hcy levels for the experimental group. The area under the curve (AUC) was 0.718 (95% CI 0.585-0.854, p < 0.001), indicating that the serum Hcy concentration could predict ISR. On the ROC curve, the best critical value of serum Hcy concentration for predicting ISR was 20.05 μmol/L, with a sensitivity of 45% and specificity of 88.1%. Conclusion: A positive correlation was observed between homocysteine and the severity of restenosis after PCI, The level of Hcy could serve as a predictive biomarker for the severity of ISR.

Association between carotid atherosclerosis and brain activation patterns during the Stroop task in older adults: An fNIRS investigation

There is an increasing body of evidence suggesting that vascular disease could contribute to cognitive decline and overt dementia. Of particular interest is atherosclerosis, as it is not only associated with dementia, but could be a potential mechanism through which cardiovascular disease directly impacts brain health. In this work, we evaluated the differences in functional near infrared spectroscopy (fNIRS)-based measures of brain activation, task performance, and the change in central hemodynamics (mean arterial pressure (MAP) and heart rate (HR)) during a Stroop color-word task in individuals with atherosclerosis, defined as bilateral carotid plaques (n = 33) and healthy age-matched controls (n = 33). In the healthy control group, the left prefrontal cortex (LPFC) was the only region showing evidence of activation when comparing the incongruous with the nominal Stroop test. A smaller extent of brain activation was observed in the Plaque group compared with the healthy controls (1) globally, as measured by oxygenated hemoglobin (p = 0.036) and (2) in the LPFC (p = 0.02) and left sensorimotor cortices (LMC)(p = 0.008) as measured by deoxygenated hemoglobin. There were no significant differences in HR, MAP, or task performance (both in terms of the time required to complete the task and number of errors made) between Plaque and control groups. These results suggest that carotid atherosclerosis is associated with altered functional brain activation patterns despite no evidence of impaired performance of the Stroop task or central hemodynamic changes.

Relationship of the Low-Density Lipoprotein Cholesterol/High-Density Lipoprotein Cholesterol Ratio with a Vulnerable Plaque in Patients with Severe Carotid Artery Stenosis: A Case-Control Study in the Han Chinese Population.

Carotid plaque is often an important factor in ischemic stroke after it changes from stable to vulnerable, and low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) are associated with plaque vulnerability. We aimed to investigate whether the LDL-c/HDL-c ratio, an easily available and novel biomarker, is associated with vulnerable plaques and enhances the warning effect on vulnerability compared to LDL-c or HDL-c alone. We conducted a retrospective study of 187 patients with severe CAS admitted to the Department of Vascular Surgery at the Nanjing Drum Tower Hospital from January 2019 to July 2021. They were divided into a stable plaque group and a vulnerable plaque group according to carotid ultrasonography, carotid angiography (CTA), and plaque pathology. Baseline information was collected and compared between the two groups. Correlation analysis was used to determine the degree of correlation between clinical variables. Univariate and multifactor logistic regression analyses were used to examine independent risk factors for vulnerable plaque in patients with severe CAS. Receiver operating characteristic (ROC) curves were used to assess the capacity of LDL-c/HDL-c to predict the occurrence of vulnerable plaque. The age of the vulnerable plaque group was 68.12 ± 8.90 years, with 85 males (89.91%); the age of the stable plaque group was 68.77 ± 8.43 years, with 70 males (89.74%). Multivariate logistic regression analysis showed that LDL-c/HDL-c, smoking and diabetes were independent risk factors for vulnerable plaque (all P <0.05). The risk of vulnerable plaque was 4.78-fold greater in the highest LDL-c/HDL-c quartile (≥ 2.63) than in the lowest quartile (≤ 1.31) (P-trend <0.001), and the area under the ROC curve for LDL-c/HDL-c (AUC=0.681, P <0.001) was higher than that for LDL-c and HDL-c. LDL-c/HDL-c, smoking and diabetes were independent risk factors for vulnerable plaque in patients with severe CAS, and LDL-c/HDL-c had a higher predictive value for the presence of vulnerable plaque compared with other lipid parameters.