Artery Atherosclerotic Plaques Research Articles

The Hypothesis of Trace Elements Involvement in the Coronary Arteries Atherosclerotic Plaques' Location.

Background: Coronary artery disease (CAD) is a chronic inflammatory disease with multiple well-known risk factors. Although epidemiological studies report improvements in classical CAD risk-factor control, except for diabetes and obesity, cardiovascular diseases remain the leading causes of morbidity and mortality in the current population. The question regarding the atherosclerotic plaque location in particular arteries remains unanswered. Research on novel possible aspects that could help to properly understand atherosclerosis pathophysiology is essential. This study was based on a body trace-elements analysis, measured in scalp hair samples, as possible co-factors of various enzymes that may be crucial for CAD development. Methods: A total of 133 consecutive male patients with a median age of 71 (65-75) years, who presented with anginal symptoms of CCS class 2.0 (0.3) without previous heart-related interventions, were included in the analysis. The results of the cine-angiography were compared with the demographical, clinical, and laboratory results, followed by scalp-hair trace analysis. The possible predictors for coronary disease locations in the left descending artery (LAD), the circumflex artery (Cx), and the right coronary artery (RCA) were the subjects of this study. Results: Statistically significant differences in the scalp-hair trace elements concentration between the CAD and normal angiogram groups were noticed for magnesium (p = 0.003), calcium (p < 0.001), chromium (p = 0.011), and copper (p = 0.043). The multivariable analysis for epicardial atherosclerotic disease revealed the co-existence of diabetes mellitus (OR: 2.94, 95% CI: 1.27-6.79, p = 0.012) as a possible causative factor for the LAD location. The multivariable analysis for the atherosclerosis location in the Cx artery presented scalp-hair magnesium as a possible predictive factor (OR: 0.98, 95% CI: 0.96-1.00, p = 0.024). The multivariable model for the RCA location of atherosclerotic plaque indicated scalp-hair Zn concentration (0.99, 95% CI: 0.98-1.00, p = 0.002) and serum HDL (OR: 0.61, 95% CI: 0.04-0.09, p = 0.016). Conclusions: Possible hypothetical distinctive pathomechanisms, in particular, coronary artery involvement, in atherosclerosis processes are presented in the male group. Diabetes mellitus was found to be the primary factor for left descending artery disease. The low scalp-hair magnesium concentration was found to be a possible risk factor involved in the circumflex artery atherosclerotic plaque location. The inverse relation between serum high-density lipoprotein, the scalp hair zinc concentration, and right coronary disease was noticed.

Ultrasound-based prevalence of polyvascular disease and its association with adverse outcome in patients undergoing coronary artery bypass grafting.

Objective: Polyvascular disease (polyVD) often coexists with coronary artery disease (CAD). We aim to investigate the prevalence of polyVD using the method of ultrasound and find its association with adverse outcomes in coronary artery bypass grafting (CABG) patients. Methods: This retrospective and cross-sectional study included 1344 patients with a mean age of 61.4 years. Presence of peripheral artery atherosclerotic plaque and stenosis was assessed using the method of ultrasound. Receiver operating characteristic (ROC) analysis and multivariate logistic regression analysis were performed to investigate the association of polyVD with in-hospital all-cause death. Results: 52.1% of the patients had polyVD and among which 31.9% had one additional arterial bed involvement and 20.2% had two or three additional arterial beds involvement. Patients with two or three involved arterial beds had worse baseline characteristics. In-hospital all-cause death rate increased with the number of involved arterial beds (1.1% in patients with only CAD vs 3.7% in patients with two or three involved arterial beds), and this trend was more prominent in elderly patients. Multivariate logistic regression analysis confirmed that polyVD patients with two or three involved arterial beds had about three times the risk for all-cause death. Conclusions: Prevalence of polyVD assessed by ultrasound was high in CABG patients and it was significantly associated with in-hospital all-cause death. Our study may provide additive information for preoperative risk stratification in CABG patients.

Development and approval of a mobile test bench for the study of the mechanical properties of biological tissues

The determination of the mechanical properties of vessel walls and atherosclerotic plaques is a recurring issue in the numerical modelling of vessel sections. Testing machines are usually located in specialised laboratories outside medical facilities, and transporting samples from the clinic is difficult. Therefore, the task of developing mobile testing devices that can be installed directly in the clinic to perform tests immediately after surgery is relevant. This paper presents the results of the development and validation of a mobile test bench for performing mechanical experiments on uniaxial compression and tension of biological tissues. The purpose of the work is to perform mechanical tests on tissues in the clinic, avoiding their transport to the laboratory and/or freezing. Arduino UNO hardware platform is used as the control element of the test bench, which controls the main elements (motor, load cell), records data on SD card and displays information about the experiment on the computer screen. Structurally, the test bench is an analogue of a two-column testing machine. All mechanisms are assembled in a portable case, the control module is in the form of a remote plastic box. Verification of the test bench was carried out using an Instron 3342 universal testing machine with a 500 N load cell. A total of 121 soft tissue tests (including arterial wall and atherosclerotic plaque) were performed on the bench. The Young's modulus and ultimate strength values obtained are summarised in a table. The mean Young's modulus for the wall of the internal carotid artery was 0.32 ± 0.24 MPa, for soft plaque 0.30 ± 0.17 MPa, and for hard plaque 0.85 ± 0.39 MPa; a tensile strength of 1.12 ± 0.67 MPa was also determined for hard plaques in carotid arteries. The result is a unique database of tissue Young's moduli obtained from freshly collected material. The methodology and its implementation on the mobile test bench show good agreement with literature data.

Tudor-SN exacerbates pathological vascular remodeling by promoting the polyubiquitination of PTEN via NEDD4-1

BackgroundDysregulation of vascular homeostasis can induce cardiovascular diseases and increase global mortality rates. Although lineage tracing studies have confirmed the pivotal role of modulated vascular smooth muscle cells (VSMCs) in the progression of pathological vascular remodeling, the underlying mechanisms are still unclear.MethodsThe expression of Tudor-SN was determined in VSMCs of artery stenosis, PDGF-BB-treated VSMCs and atherosclerotic plaque. Loss- and gain-of-function approaches were used to explore the role of Tudor-SN in the modulation of VSMCs phenotype both in vivo and in vitro.ResultsIn this study, we demonstrate that Tudor-SN expression is significantly elevated in injury-induced arteries, atherosclerotic plaques, and PDGF-BB-stimulated VSMCs. Tudor-SN deficiency attenuates, but overexpression aggravates the synthetic phenotypic switching of VSMCs and pathological vascular remodeling. Loss of Tudor-SN also reduces atherosclerotic plaque formation and increases plaque stability. Mechanistically, PTEN, the major regulator of the MAPK and PI3K-AKT signaling pathways, plays a vital role in Tudor-SN-mediated regulation on proliferation and migration of VSMCs. Tudor-SN facilitates the polyubiquitination and degradation of PTEN via NEDD4-1, thus exacerbating vascular remodeling under pathological conditions. BpV (HOpic), a specific inhibitor of PTEN, not only counteracts the protective effect of Tudor-SN deficiency on proliferation and migration of VSMCs, but also abrogates the negative effect of carotid artery injury-induced vascular remodeling in mice.ConclusionsOur findings reveal that Tudor-SN deficiency significantly ameliorated pathological vascular remodeling by reducing NEDD4-1-dependent PTEN polyubiquitination, suggesting that Tudor-SN may be a novel target for preventing vascular diseases.

A cross-sectional study comparing the expression of DNA repair molecules in subjects with and without atherosclerotic plaques.

Atherosclerosis, serving as the primary pathological mechanism at the core of cardiovascular disease, is now widely acknowledged to be associated with DNA damage and repair, contributing to atherosclerotic plaque formation. Therefore, molecules involved in the DNA repair process may play an important role in the progression of atherosclerosis. Our research endeavors to explore the contributions of specific and interrelated molecules involved in DNA repair (APE1, BRCA1, ERCC2, miR-221-3p, miR-145-5p, and miR-155-5p) to the development of atherosclerotic plaque and their interactions with each other. Gene expression study was conducted using the real-time polymerase chain reaction (qRT-PCR) method on samples from carotid artery atherosclerotic plaques and nonatherosclerotic internal mammary arteries obtained from 50 patients diagnosed with coronary artery disease and carotid artery disease. Additionally, 50 healthy controls were included for the determination of 8-hydroxy-2'-deoxyguanosine (8-OHdG). Although no difference was observed in mRNA gene expressions, we noted a decrease in miR-155-5p gene expression (p = 0.003) and an increase in miR-221-3p gene expression (p = 0.015) in plaque samples, while miR-145-5p gene expression remained unchanged (p = 0.57). Regarding serum 8-OHdG levels, patients exhibited significantly higher levels (1111.82 ± 28.64) compared to controls (636.23 ± 24.23) (p < 0.0001). In our study demonstrating the role of miR-155-5p and miR-221-3p in atherosclerosis, we propose that these molecules are potential biomarkers and therapeutic targets for coronary artery diseases and carotid artery disease.

Hypertension-Mediated Organ Damage in Relation to Severity of Chronic Low Back Pain in Hypertensive Patients.

Chronic pain triggers a stress response, which results in increased blood pressure (BP). We investigated whether chronic low back pain (cLBP) in hypertensive patients is associated with an increased risk of hypertension-related organ damage. We studied 85 consecutive hypertensive patients with a median age of 62 years (55-67), who suffered from cLBP, the severity of which was evaluated according to the Oswestry Disability Index (ODI). Patients underwent transthoracic echocardiography, arterial ultrasonography and vascular tonometry. We assessed carotid artery atherosclerotic plaques, along with carotid-femoral pulse wave velocity (cf-PWV) and left ventricular mass index (LVMI). An equal to or higher than median (16 points) ODI score in 48 subjects (56.5%) was associated with the presence of carotid artery plaques (p = 0.014). In multivariate analysis, after adjusting for covariates, the presence of carotid artery plaques remained independently associated with an ODI score equal to or higher than the median (OR, 3.71; 95% CI, 1.04-13.25; p = 0.044). None of the other analyzed parameters of hypertension-related organ damage demonstrated a significant relationship with the ODI score. We observed that more severe cLBP is associated with a higher prevalence of carotid artery atherosclerotic plaques among hypertensive patients.

Are Hair Scalp Trace Elements Correlated with Atherosclerosis Location in Coronary Artery Disease?

Coronary artery disease is among the leading current epidemiological challenges. The genetic, clinical, and lifestyle-related risk factors are well documented. The reason for specific epicardial artery locations remains unsolved. The coronary artery topography and blood flow characteristics may induce local inflammatory activation. The atherosclerotic plaque formation is believed to represent inflammatory response involving enzymatic processes co-factored by trace elements. The possible relation between trace elements and coronary artery disease location was the subject of the study. There were 175 patients (107 (61) men and 68 (39) females) in a median (Q1-3) age of 71years (65-76) admitted for coronary angiography due to chronic coronary syndrome. The angiographic results focused on the percentage of lumen stenosis in certain arteries and were compared with the results for hair scalp trace elements. The correlation between left main coronary artery atherosclerotic plaques and nickel (Ni), zinc (Zn), and antimony (Sb) hair scalp concentration was noted. The analysis revealed a positive relation between left descending artery disease and chromium (Cr), sodium (Na), arsenic (As), and molybdenum (Mo) and a negative correlation with strontium (Sr). The atherosclerotic lesion in the circumflex artery revealed correlations in our analysis with sodium (Na), potassium (K), chromium (Cr), nickel (Ni), arsenic (As), and negative with strontium (Sr) (r) hair scalp concentrations. The negative correlations between right coronary artery disease and magnesium (Mg) and strontium (Sr) concentrations were noted. The possible explanation of different epicardial artery involvement and severity by atherosclerotic processes may lay in their topography and blood rheological characteristics that induce different inflammatory reactions co0factored by specific trace elements. The trace element concentration in the hair scalp may correlate with a particular coronary atherosclerotic involvement, including the severity of lumen reduction. This may indicate the missing link between the pathophysiological processes of atherosclerosis development and its location in coronary arteries.

Plasma NOTCH3 and the risk of cardiovascular recurrence in patients with ischemic stroke.

Ischemic stroke patients are more prone to developing another cardiovascular event. This study aims to examine potential biological predispositions to cardiovascular recurrence in patients with ischemic stroke. Human and preclinical studies. Quantitative proteomic analysis, animal stroke, atherosclerosis models and circulating endothelial cells (CECs) were employed to examine candidate biomarkers derived from an ischemic stroke cohort in Singapore. Proteomic analysis of pooled microvesicles of "Event" (n = 24) and without "Event" (n = 24) samples identified NOTCH3 as a candidate marker; plasma NOTCH3 were shown to be elevated in "Event" patients compared to those without "Events" and age-matched controls. In a validation cohort comprising 431 prospectively recruited ischemic stroke patients (mean age 59.1 years; median follow-up 3.5 years), men with plasma NOTCH3 (>1600pg/ml) harbored increased risk of cardiovascular recurrence (adjusted hazards ratio 2.29, 95% CI 1.10-4.77); no significant association was observed in women. Chronic renal failure, peripheral artery disease and NT-pro-brain natriuretic peptide were significant predictors of plasma NOTCH3 in men without ischemic stroke (adjusted r2=0.43). Following middle cerebral artery occlusion, NOTCH3 expression in mouse sera increased and peaked at 24 hrs, persisting thereafter for at least 72 hours. In Apoe-/- atherosclerotic mice, NOTCH3 stained the endothelium of defective arterial lining and atherosclerotic plaques. Analysis of CECs isolated from stroke patients revealed increased gene expression of NOTCH3, further supporting endothelial damage underpinning NOTCH3-mediated atherosclerosis. Findings from this study suggests that NOTCH3 could be important in cardiovascular recurrence following an ischemic stroke.

The hemodynamic and geometric characteristics of carotid artery atherosclerotic plaque formation.

Ischemic stroke, which has a high incidence, disability, and mortality rate, is mainly caused by carotid atherosclerotic plaque. The difference in the geometric structures of the carotid arteries inevitably leads to the variability in the local hemodynamics, which plays a key role in the formation of carotid atherosclerosis. At present, the combined mechanisms of hemodynamic and geometric in the formation of carotid atherosclerotic plaque are not clear. Thus, this study characterized the geometric and hemodynamic characteristics of carotid atherosclerotic plaque formation using four-dimensional (4D) flow magnetic resonance imaging (MRI). Ultimately, 122 carotid arteries from 61 patients were examined in this study. According to the presence of plaques at the bifurcation of the carotid artery on cervical vascular ultrasound (US), carotid arteries were placed into a plaque group (N=69) and nonplaque group (N=53). The ratio of the maximum internal carotid artery (ICA) inner diameter to the maximum common carotid artery (CCA) inner diameter (ICA-CCA diameter ratio), bifurcation angle, and tortuosity were measured using neck three-dimensional time-of-flight magnetic resonance angiography (3D TOF-MRA). Meanwhile, 4D flow MRI was used to obtain the following hemodynamic parameters of the carotid arteries: volume flow rate, velocity, wall shear stress (WSS), and pressure gradient (PG). Independent sample t-tests were used to compare carotid artery geometry and hemodynamic changes between the plaque group and nonplaque group. The ICA-CCA diameter ratio between the plaque group and the nonplaque group was not significantly different (P=0.124), while there were significant differences in the bifurcation angle (P=0.005) and tortuosity (P=0.032). The bifurcation angle of the plaque group was greater than that of the nonplaque group (60.70°±20.75° vs. 49.32°±22.90°), and the tortuosity was smaller than that of the nonplaque group (1.07±0.04 vs. 1.09±0.05). There were no significant differences between the two groups in terms of volume flow rate (P=0.351) and the maximum value of velocity (velocitymax) (P=0.388), but the axial, circumferential, and 3D WSS values were all significantly different, including their mean values (all P values <0.001) and the maximum value of 3D WSS (P<0.001), with the mean axial, circumferential, 3D WSS values, along with the maximum 3D WSS value, being lower in the plaque group. The two groups also differed significantly in terms of maximum PG value (P=0.030) and mean PG value (P=0.026), with these values being greater in the nonplaque group than in the plaque group. A large bifurcation angle and a low tortuosity of the carotid artery are geometric risk factors for plaque formation in this area. Low WSS and low PG values are associated with carotid atherosclerotic plaque formation.

The frequency of coronary artery atherosclerotic plaques in patients with newly diagnosed type 2 diabetes mellitus

The frequency of coronary artery atherosclerotic plaques in patients with newly diagnosed type 2 diabetes mellitus

Evaluation of the effect on stroke mechanism, stroke recurrence and clinical outcome in stroke patients with basilar artery atherosclerosis: A single centre retrospective observational study.

Basilar artery atherosclerotic plaque is the predominant cause of stroke in the posterior circulation. İscheamic stroke caused basilar artery atherosclerosis faces a high risk of recurrence despite optimal medical treatment, which might lie in the less than ideal recognition of underlying stroke mechanism and lack of individualized treatment for strokes of different mechanisms. We aim in this study to investigate the effect on stroke mechanism, stroke recurrence and clinical outcome in stroke patients with basilar artery atherosclerosis. In this study, 107 ischaemic stroke patients with atherosclerotic stenosis in the BA who were followed up in Uludag University Faculty of Medicine between 1 January 2019 and 1 January 2022. The study was conducted retrospectively and observationally. According to the results of our study, the degree of stenosis in atherosclerotic stenosis of the symptomatic basilar artery was found to be an independent risk factor for stroke recurrence. Independent risk factors for unfavourable clinical outcomes in these patients were determined as female gender, stenosis being in the proximal segment, stroke mechanism being from artery to artery embolism, and congestive heart failure. The most striking result of our study is that clinical outcome was found to be closely related to the female gender, the stroke mechanism being artery-to-artery embolism, and the stenosis is in the proximal segment. If stroke mechanisms were evaluated more clearly, it would likely help provide individualised treatments.

The Complex Mechanisms and the Potential Effects of Statins on Vascular Calcification: A Narrative Review.

Vascular calcification (VC) is a complex process of calcium deposition on the arterial wall and atherosclerotic plaques and involves interaction between vascular smooth muscle cells, inflammatory and VC mediators. The latter are independent predictors of cardiovascular morbidity and mortality and potential targets of pharmaceutical therapy. This paper is a narrative review of the complex mechanisms of VC development and in this context the potential anti-atherosclerotic effects of statins. At the initial stages of atherosclerosis VC correlates with atherosclerosis burden and in the long-term with cardiovascular morbidity and mortality. A plethora of animal and clinical studies have proposed statins as the cornerstone of primary and secondary prevention of atherosclerotic cardiovascular disease. Based on coronary computed tomography data, high doses of statins may have negligible or even positive effects on the progression of coronary artery calcification. Growing data support an increase in atherosclerotic plaque calcification in peripheral arteries (e.g., carotids), after long-term, statin-therapy. Despite the paradox of increasing VC, those effects of statins have been associated with higher plaque stability, reducing the risk of consequent adverse events. Statins seem to promote a "favorable" atherosclerotic calcification, suppressing atherosclerotic lesion expansion and their vulnerability. More studies are required to clarify the underlying mechanisms.

Conditional deletion of Ccl2 in smooth muscle cells does not reduce early atherosclerosis in mice

Background and aimsC–C motif chemokine ligand 2 (CCL2) is a pro-inflammatory chemokine important for monocyte recruitment to the arterial wall and atherosclerotic plaques. Global knockout of Ccl2 reduces plaque formation and macrophage content in mice, but the importance of different plaque cell types in mediating this effect has not been resolved. Smooth muscle cells (SMCs) can adopt a potentially pro-inflammatory function with expression of CCL2. The present study aimed to test the hypothesis that SMC-secreted CCL2 is involved in early atherogenesis in mice. MethodsSMC-restricted Cre recombinase was activated at 6 weeks of age in mice with homozygous floxed or wildtype Ccl2 alleles. Separate experiments in mice lacking the Cre recombinase transgene were conducted to control for genetic background effects. Hypercholesterolemia and atherosclerosis were induced by a tail vein injection of recombinant adeno-associated virus (rAAV) encoding proprotein convertase subtilisin/kexin type 9 (PCSK9) and a high-fat diet for 12 weeks. ResultsUnexpectedly, mice with SMC-specific Ccl2 deletion developed higher levels of plasma cholesterol and larger atherosclerotic plaques with more macrophages compared with wild-type littermates. When total cholesterol levels were incorporated into the statistical analysis, none of the effects on plaque development between groups remained significant. Importantly, changes in plasma cholesterol and atherosclerosis remained in mice lacking Cre recombinase indicating that they were not caused by SMC-specific CCL2 deletion but by effects of the floxed allele or passenger genes. ConclusionsSMC-specific deficiency of Ccl2 does not significantly affect early plaque development in hypercholesterolemic mice.

A Race Against Time: Coronary Computed Tomography Angiography Discovers a Highly Inflamed Plaque in 49-Year-Old Right Before STEMI

Abstract In the modern management of coronary artery disease (CAD), cardiac computed tomography angiography (CCTA) has emerged as a pivotal diagnostic tool, offering detailed visualization of coronary artery lumens and atherosclerotic plaques. We present the case of a 49-year-old woman, with no prior cardiovascular history but with several risk factors, in whom CCTA identified a highly inflamed atherosclerotic plaque, which led immediately to an acute myocardial infarction. Significantly, this case spotlights the vital role of perivascular inflammation mapping in CCTA, crucial for identifying high-risk plaques. The case emphasizes the necessity for a comprehensive, multifaceted diagnostic approach in the evaluation and management of CAD, incorporating advanced techniques like perivascular inflammation mapping for a more accurate and predictive assessment.

Extracranial carotid artery atherosclerotic plaque and APOE polymorphisms: a systematic review and meta-analysis.

Carotid atherosclerotic plaque is an important independent risk factor for stroke. Apolipoprotein E (APOE) influences cholesterol levels and certain isoforms are associated with increased carotid atherosclerosis, though the exact association between APOE and carotid plaque is uncertain. The study aimed to evaluate the association between APOE and carotid plaque. A systematic review was performed to retrieve all studies which examined the association between carotid plaque and APOE. This study was conducted in accordance with the PRISMA guidelines. Independent readers extracted the relevant data from each study including the type of imaging assessment, plaque definition, frequency of APOE E4 carrier status and type of genotyping. Meta-analyses with an assessment of study heterogeneity and publication bias were performed. Results were presented in a forest plot and summarized using a random-effects model. After screening 838 studies, 17 studies were included for systematic review. A meta-analysis of 5 published studies showed a significant association between ε4 homozygosity and carotid plaque [odds ratio (OR), 1.53; 95% CI, 1.16, 2.02; p = .003]. Additionally, there was a significant association between patients possessing at least one ε4 allele, heterozygotes or homozygotes, and carotid plaque (OR, 1.25; 95% CI, 1.03, 1.52; p = .03). Lastly, there was no association between ε4 heterozygosity and carotid plaque (OR, 1.08; 95% CI, 0.93, 1.26; p = .30). APOE ε4 allele is significantly associated with extracranial carotid atherosclerotic plaque, especially for homozygous individuals.

Association between visceral adiposity index and coronary artery calcification score and atherosclerotic plaque morphology.

The relationship between the visceral adipose index (VAI), a surrogate marker of visceral adipose tissue dysfunction, and coronary atherosclerotic plaque (CAP) morphology remains unclear. This study aimed to investigate the relationships between the VAI and the coronary artery calcification (CAC) score and CAP morphology in asymptomatic patients. We retrospectively assessed 782 patients between January 2012 and January 2020. CAC scores were determined at the threshold of 130 Hounsfield units according to the Agatston technique using 64-slice computed tomography. Patients were assigned to groups with no plaque (NP), fatty plaque (FP), calcified plaque (CP), and mixed plaque (MP). The median VAI levels were significantly different in each group (NP: 1.2 vs. FP: 1.7 vs. CP: 2.3 vs. MP: 2.8; P <0.001). An increased VAI level was an independent predictor of the CAC score. The threshold value of the VAI exhibited a gradual increase in predicting CAP morphology. VAI threshold values were >1.6 for the FP group (vs. the NP group), >2.1 for the CP group (vs. the FP group), and >2.6 for the MP group (vs. the CP group). High VAI levels independently predict an increased CAC score and CAP morphology. The VAI exhibits superior diagnostic performance in distinguishing the presence and morphology of CAP in asymptomatic patients and offers gradual cut-off values. Therefore, the VAI may be a potential screening tool for risk stratification and diagnosing CAP morphology in patients with suspected coronary artery disease.

Correlation of the middle cerebral artery atherosclerotic plaque characteristics with ischemic stroke recurrence: a vessel wall magnetic resonance imaging study.

This study aims to analyze the imaging features of atherosclerotic plaques in the middle cerebral artery (MCA) of patients with recurrent ischemic stroke using vessel wall magnetic resonance imaging (VWMRI) and investigate the correlation between these imaging features and the recurrence of ischemic stroke. Consecutive patients with ischemic stroke caused by atherosclerotic stenosis of the MCA were collected. The patients were divided into recurrent and non-recurrent ischemic stroke groups. We obtained VWMRI images of MCA plaques using 3.0T MRI by black-blood sequences, and the differences in VWMRI characteristics and clinical information between the two groups were compared. A binary Logistic regression model was used to analyze the VWMRI characteristics and clinical information related to ischemic stroke recurrence. 179 patients were collected from August 2018 to May 2020, and 81 patients were included in the study. The recurrent ischemic stroke group patients had a higher stenosis rate (0.69 vs 0.64). Meanwhile, the rate of centripetal wall thickening was significantly higher in patients with recurrent ischemic stroke (33.3% vs 11.7%). Binary Logistic regression analysis showed that sex (P=0.036, OR:2.983, CI:1.075-8.279), stenosis rate (P=0.038, OR:148.565, CI:1.331-16583.631), and vessel wall thickening pattern (P=0.012, OR:0.171, CI:0.043-0.678) were related to ischemic stroke recurrence. The patients with ischemic stroke caused by atherosclerotic stenosis of MCA, female patients, and those with concentric wall thickening and a high degree of stenosis have a higher risk of recurrence. Our results suggest that VWMRI is a valuable tool for predicting the risk of ischemic stroke recurrence in patients with MCA plaques.

Familial Hypercholesterolaemia in Children and Adolescents: Current and Future Perspectives.

Familial hypercholesterolemia (FH) is a genetic disease, the underlying cause of which is represented by mutations capable of influencing the metabolism of low-density lipoproteins (LDL). The distinguishing characteristic of FH has increased LDL cholesterol blood levels since birth, triggering early development of atherosclerosis-related diseases. Diagnosis of FH is frequently either missed or made with a considerable delay. Prompt identification of the disease is pivotal in implementing early prevention measures. Safe and effective drugs have been approved for use in children and adolescents, with statins, with or without ezetimibe, representing first-line therapy. At times, however, these medications may not be sufficient to achieve the therapeutic target, particularly in homozygous FH patients. Lipoprotein apheresis, which has proved safe and efficient, is strongly suggested in such cases. New drugs still at the investigational stage may represent a promising and personalised therapy. Lowering cholesterol levels in childhood hampers the formation of arterial atherosclerotic plaques, thus reducing cardiovascular events later in life. Accordingly, early detection, diagnosis, and therapy in FH subjects are priority aims.

Fluid-structure interaction study of hemodynamics and its biomechanical influence on carotid artery atherosclerotic plaque deposits

Atherosclerotic plaque deposits are common causes of blood flow disruption in the carotid artery bifurcation and the associated fluid mechanics has been extensively studied using Computational Fluid Dynamics (CFD) and Fluid Structure Interaction (FSI). However, the elastic responses of plaques to hemodynamics in the carotid artery bifurcation has not been deeply studied using either of the above-mentioned numerical techniques. In this study, a two-way FSI study was coupled with CFD technique, using Arbitrary-Lagrangian-Eulerian method, to study the biomechanics of blood flow on nonlinear and hyperelastic calcified plaque deposits in a realistic geometry of the carotid sinus. FSI parameters such as total mesh displacement and von Misses stress on the plaque, as well as flow velocity and blood pressure around the plaques, were analyzed and compared to variables such as velocity streamline, pressure and wall shear stress obtained from CFD simulation in a healthy model. The blood flow simulations reveal complete reversed blood flow behavior in the internal carotid artery, ICAs and external carotid artery, ECAs for both cases. In particular, this study suggests that plaques, irrespective of the masses, possess a high yielding response to hemodynamic forces at the attaching edges, while the surfaces are vulnerable to rupture.

Carotid atherosclerotic plaque segmentation in multi-weighted MRI using a two-stage neural network: advantages of training with high-resolution imaging and histology.

A reliable and automated method to segment and classify carotid artery atherosclerotic plaque components is needed to efficiently analyze multi-weighted magnetic resonance (MR) images to allow their integration into patient risk assessment for ischemic stroke. Certain plaque components such as lipid-rich necrotic core (LRNC) with hemorrhage suggest a greater likelihood of plaque rupture and stroke event. Assessment for presence and extent of LRNC could assist in directing treatment with impact upon patient outcomes. To address the need to accurately determine the presence and extent of plaque components on carotid plaque MRI, we proposed a two-staged deep-learning-based approach that consists of a convolutional neural network (CNN), followed by a Bayesian neural network (BNN). The rationale for the two-stage network approach is to account for the class imbalance of vessel wall and background by providing an attention mask to the BNN. A unique feature of the network training was to use ground truth defined by both high-resolution ex vivo MRI data and histopathology. More specifically, standard resolution 1.5 T in vivo MR image sets with corresponding high resolution 3.0 T ex vivo MR image sets and histopathology image sets were used to define ground-truth segmentations. Of these, data from 7 patients was used for training and from the remaining two was used for testing the proposed method. Next, to evaluate the generalizability of the method, we tested the method with an additional standard resolution 3.0 T in vivo data set of 23 patients obtained from a different scanner. Our results show that the proposed method yielded accurate segmentation of carotid atherosclerotic plaque and outperforms not only manual segmentation by trained readers, who did not have access to the ex vivo or histopathology data, but also three state-of-the-art deep-learning-based segmentation methods. Further, the proposed approach outperformed a strategy where the ground truth was generated without access to the high resolution ex vivo MRI and histopathology. The accurate performance of this method was also observed in the additional 23-patient dataset from a different scanner. In conclusion, the proposed method provides a mechanism to perform accurate segmentation of the carotid atherosclerotic plaque in multi-weighted MRI. Further, our study shows the advantages of using high-resolution imaging and histology to define ground truth for training deep-learning-based segmentation methods.