RESUMEN

Background/Objectives: The underlying mechanism of the potential involvement of inflammatory crosstalk between pericarotid fat and vascular layers in atherosclerosis pathogenesis is unclear. We investigated the association between pericarotid fat density and positive remodeling and inflammatory markers in carotid stenosis. We hypothesized that pericarotid fat density might serve as a marker of plaque inflammation in a clinical setting. Methods: We evaluated the stenosis degree and pericarotid fat density in 258 patients with carotid plaques. Plaque composition was examined, and the correlation between pericarotid fat density and expansive remodeling was investigated. Pearson's product-moment correlation coefficient was used to examine the relationship between pericarotid fat density and the expansive remodeling ratio. We also evaluated the relationship of pericarotid fat density with plaque composition, degree of stenosis, and macrophage and microvessel counts by. The subgroup analysis compared these factors between symptomatic mild carotid stenosis. Results: The pericarotid fat density was -63.0 ± 11.1 HU. The carotid fat densities were -56.8 ± 10.4 HU in symptomatic and -69.2 ± 11.4 HU in asymptomatic lesions. The pericarotid fat density values in intraplaque hemorrhage, lipid-rich necrotic core, and fibrous plaque were -51.6 ± 10.4, -59.4 ± 12.8, and -74.2 ± 8.4 HU, respectively. Therefore, the expansive remodeling ratio was 1.64 ± 0.4. Carotid fat density and expansive remodeling ratio were correlated. Immunohistochemistry showed high macrophage and microvessel levels (143.5 ± 61.3/field and 121.2 ± 27.7/field, respectively). In symptomatic mild carotid stenosis, pericarotid fat density was correlated with other inflammatory factors. The pericarotid fat density and expansive remodeling ratio (2.08 ± 0.21) were high in mild stenosis (-50.1 ± 8.4 HU). Conclusions: Pericarotid fat and intraplaque components were well correlated. Carotid fat density may be a marker of plaque inflammation in carotid plaques.

RESUMEN

BACKGROUND: Positive remodeling is an integral part of the vascular adaptation process during the development of atherosclerosis, which can be detected by coronary computed tomography angiography (CTA). METHODS: A total of 426 patients who underwent both coronary CTA and optical coherence tomography (OCT) were included. Four machine learning (ML) models, gradient boosting machine (GBM), random forest (RF), deep learning (DL), and support vector machine (SVM), were employed to detect specific plaque features. A total of 15 plaque features assessed by OCT were analyzed. The variable importance ranking was used to identify the features most closely associated with positive remodeling. RESULTS: In the variable importance ranking, lipid index and maximal calcification arc were consistently ranked high across all four ML models. Lipid index and maximal calcification arc were correlated with positive remodeling, showing pronounced influence at the lower range and diminishing influence at the higher range. Patients with more plaques with positive remodeling throughout their entire coronary trees had higher low-density lipoprotein cholesterol levels and were associated with a higher incidence of cardiovascular events during 5-year follow-up (Hazard ratio 2.10 [1.26-3.48], P â€‹= â€‹0.004). CONCLUSION: Greater lipid accumulation and less calcium burden were important features associated with positive remodeling in the coronary arteries. The number of coronary plaques with positive remodeling was associated with a higher incidence of cardiovascular events.

Asunto(s)

RESUMEN

Background: Insulin resistance (IR) is associated with atherosclerotic plaque progression and the occurrence of stroke, with the triglyceride-glucose (TyG) index serving as a surrogate indicator. The present study aimed to investigate the association between TyG index levels and intracranial arterial remodeling in patients with acute ischemic stroke (AIS). Methods: Patients with AIS who visited the Neurology Department of the Second Hospital of Hebei Medical University and underwent high-resolution magnetic resonance imaging (HR-MRI) between September 2018 and October 2021 were enrolled. A total of 123 patients were finally included in the study, with 81 excluded. The TyG index levels were measured, and the characteristics of intracranial atherosclerotic stenosis (ICAS) plaques were evaluated using HR-MRI. A logistic regression model was employed to analyze the relationship between TyG index levels and remodeling mode. Patients were divided into two groups, positive remodeling (PR) and non-positive remodeling (non-PR), based on the remodeling index (RI). Results: Patients in the PR group had a higher TyG index than those in the non-PR group {median [interquartile range (IQR)]: 9.11 (8.82-9.51) vs. 8.72 (8.30-9.23), P<0.001}. After adjusting factors such as age and gender, the TyG index was found to be significantly correlated with intracranial arterial PR [odds ratio (OR): 3.169, 95% confidence interval (CI): 1.327-7.569, P=0.009]. In non-diabetes mellitus (DM) patients, the TyG index level in the PR group was significantly higher than that in the non-PR group (8.95±0.42 vs. 8.50±0.45, P<0.001), whereas there was no such difference in patients with DM. Conclusions: TyG index was correlated with intracranial vessel PR, indicating that the TyG index level may be a useful marker for predicting intracranial vessel PR.

RESUMEN

Inflammation has been considered to promote atheroma instability. Coronary computed tomography angiography (CCTA) visualizes pericoronary adipose tissue (PCAT) attenuation, which reflects coronary artery inflammation. While PCAT attenuation has been reported to predict future coronary events, plaque phenotypes exhibiting high PCAT attenuation remains to be fully elucidated. The current study aims to characterize coronary atheroma with a greater vascular inflammation. We retrospectively analyzed culprit lesions in 69 CAD patients receiving PCI from the REASSURE-NIRS registry (NCT04864171). Culprit lesions were evaluated by both CCTA and near-infrared spectroscopy/intravascular ultrasound (NIRS/IVUS) imaging prior to PCI. PCAT attenuation at proximal RCA (PCATRCA) and NIRS/IVUS-derived plaque measures were compared in patients with PCATRCA attenuation ≥ and < -78.3 HU (median). Lesions with PCATRCA attenuation ≥ -78.3 HU exhibited a greater frequency of maxLCBI4mm ≥ 400 (66% vs. 26%, p < 0.01), plaque burden ≥ 70% (94% vs. 74%, p = 0.02) and spotty calcification (49% vs. 6%, p < 0.01). Whereas positive remodeling (63% vs. 41%, p = 0.07) did not differ between two groups. On multivariable analysis, maxLCBI4mm ≥ 400 (OR = 4.07; 95%CI 1.12-14.74, p = 0.03), plaque burden ≥ 70% (OR = 7.87; 95%CI 1.01-61.26, p = 0.04), and spotty calcification (OR = 14.33; 95%CI 2.37-86.73, p < 0.01) independently predicted high PCATRCA attenuation. Of note, while the presence of only one plaque feature did not necessarily elevate PCATRCA attenuation (p = 0.22), lesions harboring two or more features were significantly associated with higher PCATRCA attenuation. More vulnerable plaque phenotypes were observed in patients with high PCATRCA attenuation. Our findings suggest PCATRCA attenuation as the presence of profound disease substrate, which potentially benefits from anti-inflammatory agents.

RESUMEN

OBJECTIVES: Both vascular positive remodeling and apolipoprotein B/apolipoprotein AI (apoB/AI) are important risk factors for ischemic stroke. However, it is unclear whether apoB/AI level plays a role in vascular positive remodeling. This study aimed to investigate the association between apoB/AI and intracranial vascular positive remodeling. MATERIALS AND METHODS: Symptomatic patients with intracranial artery 30-99% stenosis were recruited and underwent high-resolution magnetic resonance (MR) imaging. The levels of apolipoprotein B (apoB), apolipoprotein AI (apoAI) and apoB/AI were tested. Intracranial vascular remodeling index (RI) defined as the wall area ratio between maximal luminal narrowing and reference site was evaluated on MR images. Positive remodeling was defined as RI ≥1.05. The association between apoB/AI level and positive remodeling was respectively determined in anterior and posterior circulation. RESULTS: Of 65 recruited patients (mean age: 58.5 ± 10.6 years; 36 males), 25 (38.5%) had positive remodeling, of which 24 (36.9%) were in the posterior circulation group. Patients with positive remodeling had significantly higher apoB (1.0 ± 0.3 g/L vs. 0.8 ± 0.3 g/L, P = 0.003) and apoB/AI (1.0 ± 0.3 vs. 0.8 ± 0.2, P = 0.008) than those without. Univariate logistic regression showed that apoB/AI (OR: 2.302, 95%CI: 1.229-4.321, P = 0.009) was significantly associated with positive remodeling. After adjusted for confounders, the association of apoB/AI (OR: 2.935, 95%CI: 1.061-8.123, P = 0.038) with positive remodeling remained significant. ApoB/AI (OR: 76.110, 95%CI: 1.169-4953.287, P = 0.042) was significantly associated with positive remodeling in posterior circulation but not in anterior circulation. CONCLUSION: ApoB/AI is a potential indicator for intracranial vulnerable atherosclerosis characterized by positive remodeling, especially in posterior circulation.

Asunto(s)

RESUMEN

Objective:To investigate the association between plaque vulnerability characteristics and infarction sub-types in patients with acute unilateral anterior circulation cerebral infarction due to intracranial atherosclerotic disease.Methods:A total of 58 eligible patients who underwent intracranial high-resolution magnetic resonance imaging (HRMRI) were finally enrolled in the retrospective study from December 2018 to December 2020. In the current study, all patients were classified into the group with artery-to-artery (A-to-A) embolic infarction ( n=32) and the group without ( n=26), according to infarction sub-types on diffusion-weighted imaging. Baseline information, the presence/absence of hyperintense plaque, irregular plaque surface, remodeling pattern and quadrant distribution by HRMRI were collected and evaluated. Multivariate Logistic regression analysis was performed to determine the relationship between plaque vulnerability and infarction sub-types. Furthermore, the analysis of interaction between hyperintense plaque and positive remodeling in response to A-to-A embolism was visualized by Sankey diagram. Results:The presence of hyperintense plaque ( OR=3.90, 95% CI 1.21-12.59, P=0.023) and arterial remodeling patterns (positive remodeling vs intermediate state, OR=4.32, 95% CI 0.86-21.49, P for trend=0.027) were the strong independent predictors for A-to-A embolism. Importantly, a significantly positive synergy between the remodeling pattern and hyperintense plaque in response to infarction sub-types was found by Sankey diagram ( Wald=10.044, P for interaction=0.007). Similarly, in receiver operating characteristic curve analysis, the discrimination of hyperintense plaque combined with positive remodeling for A-to-A embolism was significantly superior to that of either biomarker alone (area under the curve=0.710, 95% CI 0.576-0.845, P=0.006). Conclusion:A synergistic effect between positive remodeling and hyperintense plaque can promote plaque vulnerability, suggesting a potential target sub-population may benefit from stroke prevention with intensive antithrombotic therapy, although this must be confirmed in future.

Asunto(s)

RESUMEN

Previous optical coherence tomography (OCT) study reported that irregular protrusion (IP) post drug-eluting stent (DES) implantation was an independent predictor of clinical outcome; however, the relationship between IP and the presence of subsequent in-stent neoatherosclerosis remains unclear. This study aimed to assess the relationship between IP and in-stent neoatheroscrerosis formation using OCT. We evaluated 83 patients (101 lesions) who underwent second-generation DES implantation and 8-month follow-up (8M-FU) using OCT. Lesions were divided into two groups in presence of IP (IP: n = 43, non-IP: n = 58). At prepercutaneous coronary intervention (pre-PCI), lipid-rich plaque, lesions with positive remodeling, and in-stent thrombus formation were more frequent in IP than in non-IP. On multivariate analysis, the thrombus at pre-PCI and the lesions with positive remodeling were independent predictors of IP. At 8M-FU, heterogeneous neointima, microvessel, lipid-laden neointima, and thin-cap fibro-atheroma like neointima were more frequent in IP than in non-IP (respectively, P < 0.05). On multivariate analysis, IP was associated with heterogeneous neointima. Binary restenosis was more frequent and late lumen loss tended to be larger in IP than in non-IP (19% versus 5%, P = 0.04; 1.25 ± 1.24 mm versus 0.91 ± 0.63 mm, P = 0.09); however, the target lesion revascularization rate was similar in both groups at 8M-FU. In conclusion, our study suggested that poststent IP was associated with subsequent neoatherosclerosis formation at 8M-FU after the second-generation DES implantation.

Asunto(s)

RESUMEN

AIMS: Although several antihypertensive agents reduced the carotid intima-media thickness (IMT), it remains unclear whether those agents affect the interadventitial diameter (IAD). We aimed to examine whether cilnidipine, an L/N-type calcium channel blocker, reduced the common carotid IMT or IAD in post-stroke hypertensive patients. METHODS: The common carotid IMT and IAD were measured at the start of cilnidipine treatment and 12 months from that. The changes in the mean max-IMT or IAD between baseline and the 12-month follow-up were evaluated and compared between the thick group (max-IMT ≥1.1 mm) and the normal group (max-IMT ＜1.1 mm). RESULTS: A total of 603 post-stroke hypertensive subjects (mean age=69.3 yr, 378 males) were included in the analysis. At baseline, IAD was increased stepwise according to the value of max-IMT (p for trend ＜0.001). Among them, 326 subjects were followed up for 12 months. The mean max-IMT from baseline to 12 months did not change in the normal group (－0.01 mm, 95% confidence interval [CI] －0.03 to 0.01, n=170), whereas a significant reduction was observed in the thick group (－0.09 mm, 95% CI －0.13 to －0.05, n=156). The mean IAD was significantly reduced during the study period in the normal group (－0.14 mm, 95% CI －0.22 to －0.05) as well as in the thick group (－0.12 mm, 95% CI －0.21 to －0.03). CONCLUSIONS: Cilnidipine promoted the regression of common carotid IMT in post-stroke hypertensive patients, especially in the thick group. Cilnidipine also reduced the IAD in both normal and thick groups.

Asunto(s)

RESUMEN

OBJECTIVES: Current clinical models predict the pre-test probability of obstructive coronary artery disease, but these models do not predict the presence of high-risk plaques. Thus the objective of this study was to propose a model to predict high-risk plaque assessed by coronary computed tomography (CT) angiography. METHODS: This study was a retrospective cross-sectional study. A clinical model was derived from 2392 patients and verified by 733 patients who underwent coronary CT suspected of coronary artery disease. High-risk plaque was defined as a plaque with positive remodeling (remodeling index>1.1), low attenuation (<30Hounsfield units) and napkin-ring sign. The risk score was calculated from the following 6 variables with a maximum of 24 points: age, sex, hemoglobin A1c, systolic blood pressure, high-density lipoprotein and smoking status. RESULTS: The proportion of patients with high-risk plaque was 11% and 17% in the derivation and validation cohort, respectively. The area under the receiver operation characteristic curve was 0.71 (95% confidence interval (CI): 0.68 to 0.74) in the derivation cohort and 0.75 (95% CI: 0.70 to 0.79) in the validation cohort. The frequency of high-risk plaques was 4% in the low-risk group (≤8 points) while it was 53% in the high-risk group (≥17 points) of the derivation cohort. CONCLUSIONS: We propose a scoring system to detect high-risk plaque assessed by coronary CT. Patients in the high-risk group have a high prevalence of high-risk plaque and might benefit from lipid lowering therapy.

Asunto(s)

RESUMEN

AIM: To investigate the relationship between coronary calcium score (CCS) and vulnerable plaque/significant stenosis using coronary computed tomographic angiography (CCTA). METHODS: CCTA was performed in 651 patients and these patients were divided into the four groups (CCS 0, 1-100, 101-400 and > 400). We studied the incidence of high-risk plaque, including positive remodeling, low attenuation plaque, spotty calcification, and napkin-ring sign, and significant stenosis in each group. RESULTS: High-risk plaque was found in 1.3%, 10.1%, 13.3% and 13.4% of patients with CCS 0, 1-100, 101-400 and > 400, respectively (P < 0.001). The difference was only significant for patients with zero CCS. The incidence of significant stenosis was 0.6%, 7.6%, 13.3% and 26.9% for each patient group, respectively (P < 0.001), which represented a significant stepwise increase as CCS increased. The combined incidence of high-risk plaque and significant stenosis was 1.9%, 17.7%, 26.9% and 40.3% in each patient group, respectively (P < 0.001), again representing a significant stepwise increase with CCS. The rate of major coronary event was 0%, 4.0%, 7.9% and 17.2% in each patient group, respectively (P < 0.001), another significant stepwise increase as CCS increased. CONCLUSION: Stepwise increased risk of coronary events associated with increasing CCS is caused by increasing incidence of significant stenosis, while that of high-risk plaque remains the same.

RESUMEN

We studied the dynamic change of high-risk plaque detected by coronary computed tomographic angiography (CCTA) in patients with subclinical coronary artery disease. We analyzed paired CCTA findings in 103 patients. The follow-up period was 1.37 ± 0.49 years. We studied the prevalence and change of high-risk plaque (HRP) defined as positive remodeling, low attenuation plaque, spotty calcification, or napkin-ring sign. Of 413 plaques detected by CCTA, thirty-seven patients had 47 HRP at baseline. At follow-up, eight patients showed disappearance of HRP. Sixty-six patients had no HRP at baseline. At follow-up, new HRP was detected in 12 patients. As a whole, 20 patients (19.4 %) showed appearance or disappearance of HRP. For 29 patients with persistent HRP, five of twenty-one patients with one HRP at baseline showed two HRP at follow-up. Five of eight patients with two HRP at baseline showed one HRP at follow-up. As a whole, in 27 % of patients with persistent HRP, the number of HRP changed. These changes were neither associated with statin use nor location of the HRP. Our results showed that about 20 % of patients showed appearance or disappearance of HRP 1 year later. In addition, in 27 % of patients with persistent HRP, the number of HRP increased or decreased. These results suggest a dynamic nature of HRP.

Asunto(s)

Asunto(s)

RESUMEN

Studies in human and non-human primates have confirmed the compensatory enlargement or positive remodeling (Glagov phenomenon) of coronary vessels in the presence of focal stenosis. To our knowledge, this is the first study to document arterial enlargement in a metabolic syndrome animal model with diffuse coronary artery disease (DCAD) in the absence of severe focal stenosis. Two different groups of Ossabaw miniature pigs were fed a high fat atherogenic diet for 4 months (Group I) and 12 months (Group II), respectively. Group I (6 pigs) underwent contrast enhanced computed tomographic angiography (CCTA) and intravascular ultrasound (IVUS) at baseline and after 4 months of high fat diet, whereas Group II (7 pigs) underwent only IVUS at 12 months of high fat diet. IVUS measurements of the left anterior descending (LAD), left circumflex (LCX) and right coronary (RCA) arteries in Group I showed an average increase in their lumen cross-sectional areas (CSA) of 25.8%, 11.4%, and 43.4%, respectively, as compared to baseline. The lumen CSA values of LAD in Group II were found to be between the baseline and 4 months values in Group I. IVUS and CCTA measurements showed a similar trend and positive correlation. Fractional flow reserve (FFR) was 0.91±0.07 at baseline and 0.93±0.05 at 4 months with only 2.2%, 1.6% and 1% stenosis in the LAD, LCX and RCA, respectively. The relation between percent stenosis and lumen CSA shows a classical Glagov phenomenon in this animal model of DCAD.

RESUMEN

BACKGROUND: The ability of coronary CT angiography (CTA) findings such as plaque characteristics to predict future coronary events remains controversial. OBJECTIVE: We investigated whether noncalcified atherosclerotic lesions (NCALs) detected by coronary CTA were predictive of future coronary events. METHODS: A total of 511 patients who underwent coronary CTA were followed for cardiovascular events over a period of 3.3 ± 1.2 years. The primary end point was defined as hard events, including cardiac death, nonfatal myocardial infarction, or unstable angina that required urgent hospitalization. Early elective coronary revascularizations (n = 58) were excluded. The relationship between features of NCALs and outcomes is described. RESULTS: A total of 15 hard events (2 cardiac deaths, 7 myocardial infarctions, 6 cases of unstable angina that required urgent hospitalization) were documented in the remaining 453 patients with modest risks during a follow-up period of 3.3 ± 1.2 years. For these hard events, a univariate Cox proportional hazard model showed that the hazard ratio for the presence of >50% stenosis was 7.27 (95% CI, 2.62-21.7; P = .0002). Although the presence of NCAL by itself was not statistically significant, NCALs with low attenuation and positive remodeling (low-attenuation plaque [LAP] and positive remodeling [PR]; plaque CT number ≤ 34 HU and remodeling index ≥ 1.20) showed an adjusted hazard ratio of 11.2 (95% CI, 3.71-36.7; P < .0001). With C-statistics analysis, when both LAP and PR and >50% stenosis were added, the C-statistic was significantly improved compared with the basal model adjusted for age, sex, and log2 (Agatston score +1) (0.900 vs 0.704; P = .0018). CONCLUSIONS: Identification of NCALs with LAP and PR characteristics by coronary CTA provides additional prognostic information to coronary stenosis for the prediction of future coronary events.

Asunto(s)

RESUMEN

BACKGROUND: This study aimed to evaluate the efficacy of assessing positive remodeling for predicting future stroke events in the internal carotid artery. We therefore assessed narrowing of the carotid artery lumen using multidetector-row computer tomography (MDCT) angiography and carotid plaque characteristics using black-blood (BB) magnetic resonance (MR). METHODS: We retrospectively selected 17 symptomatic and 11 asymptomatic lesions with luminal narrowing >50%. We compared remodeling parameters of luminal stenosis (remodeling ratio, RR/remodeling index, RI) using MDCT and MR intensities of atherosclerotic plaque contents using the BB technique (relative signal intensity, rSI). We also confirmed the validity of the relationship between MR intensity and atherosclerotic plaque contents by histology. The levels of biological markers related to vessel atherosclerosis were measured. RESULTS: Plaque lesions with positive remodeling in carotid arteries were associated with a significantly higher prevalence of stroke compared with plaques with negative remodeling (p < 0.05). Radiologic and histologic analyses determined that plaques with positive remodeling had higher signal intensities (with respect to their lipid-rich content or to hemorrhage) compared with negative remodeling (correlation coefficients: RI and rSI, r = 0.41, p < 0.05; RR and rSI, r = 0.50, p < 0.05). Levels of biological markers, including high-sensitivity C-reactive protein, hemoglobin A1C, total cholesterol, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol, were not useful for predicting stroke events. CONCLUSIONS: The results of this study suggest that the combined analysis of RR, RI and rSI could potentially help to predict future stroke events.