Search

AbstractWe investigated serum concentrations of specific inflammatory parameters in patients with significant carotid artery stenosis (CAS) of 50–99%, with an additional focus on patients with moderate stenosis (50–69%), in terms of both symptomatic status and plaque morphology, to determine whether there are certain parameters that can be associated with plaque instability before the progression of CAS to a high degree. The study included 119 CAS patients, 29 of whom had moderate stenosis, and 46 controls. Ultrasonography of the carotid arteries was performed using color flow Doppler and B-mode duplex ultrasound, and serum inflammatory parameters were measured using commercially available enzyme immunoassays. When comparing patients with 50–99% stenosis, only serum amyloid A (SAA) was higher in symptomatic patients, while in the group of patients with 50–69% stenosis, myeloperoxidase (MPO) was higher and pentraxin-3 (PTX-3) was lower in symptomatic compared to asymptomatic patients, and soluble urokinase plasminogen activator receptor (suPAR) was higher in patients with carotid plaque of unstable compared to stable morphology. Our results suggest that the importance of different inflammatory parameters in patients with moderate CAS is not the same as in CAS patients in general, and therefore their separate investigation in patients with high and moderate stenosis may be beneficial. SAA has the potential to be further considered in research to predict CAS symptom risk. There is a possibility that MPO and PTX-3 play a role in the development of CAS symptoms originating from less stenotic plaques and that suPAR is involved in the destabilisation of such plaques. [ABSTRACT FROM AUTHOR]

Introduction: Apolipoprotein (apo)C-III, a key regulator of plasma triglyceride (TG) levels, is a prime candidate for the treatment of hypertriglyceridemia (HTG), prevention of acute pancreatitis, and reduction of future atherosclerotic cardiovascular disease (ASCVD) events. Areas covered: We discuss the role of apoC-III as a therapeutic target for HTG, describe the pharmacodynamics, pharmacokinetics, and metabolism of olezarsen, as well as report on the findings of recent clinical trials with this liver-directed APOC3 antisense oligonucleotide (ASO). Expert opinion: Olezarsen, a GalNac-conjugated ASO targeting apoC-III, can reduce TG levels by ~ 50% in patients with extreme HTG due to familial chylomicronemia syndrome, as well as in patients with moderate HTG. Attention is now focused on whether olezarsen reduces ASCVD risk in patients with moderate and severe HTG. While olezarsen does cause elevations in liver enzymes, these changes are not clinically meaningful, and are not associated with thrombocytopenia, an issue with its predecessor, volanesorsen. The need for 4-weekly administration puts olezarsen at a disadvantage to competing injectables. Results from the CORE, CORE2, and ESSENCE phase III clinical trials in patients with severe HTG, expected in the second half of 2025, will help determine the requirement for a larger cardiovascular outcomes trial. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a severe cardiovascular disease followed by the accumulation of atherosclerotic plaques within the lumen of blood vessels resulting in reduced blood flow thus initiating a series of events. Conventional therapies for atherosclerosis encounter multiple challenges, especially difficulty in precisely concentrating in certain affected regions and the potential for unwanted side effects. Consequently, scientists are focused on developing nanoformulations for atherosclerosis diagnosis and therapy. Peptide-based nanomedicines improve conventional therapies by offering improved structural and therapeutic stability and enabling target-specific delivery. Their inherent biocompatibility and biodegradability additionally render them desirable materials intended for in vivo use. This review manuscript aims to provide an in-depth overview of peptide-based nanomedicines for atherosclerosis, focusing on targeted cells like endothelial cells, macrophages, and monocytes and their interaction with different plaque components. Moreover, the manuscript also highlights the latest progress in multimodal techniques and provides a comprehensive overview of limitations associated with their practical implementation. [ABSTRACT FROM AUTHOR]

The mortality rates due to cardiovascular diseases are on a rise globally. One of the major cardiovascular diseases is stroke which occurs due to atherosclerotic plaques build-up in the carotid artery. The common carotid artery (CCA) bifurcates into the internal carotid artery (ICA) and external carotid artery (ECA). Sinus present at ICA is an ellipsoidal-shaped dilated region acting as a pressure receptor and blood flow regulator. Dimensions of the sinus vary from person to person, affecting the hemodynamics of the carotid artery. The current numerical study manifests a 3D flow analysis by varying the sinus length to investigate its local and global effects on the hemodynamics of the carotid artery using various biomechanical risk analysis parameters of atherosclerosis. User-defined function (UDF) dictates the pulsatile flow velocity profile imposed at the inlet. Near the outer wall (OW) of the sinus, the blood flow velocities are lower and recirculation zones are more. Though the recirculation zones for shorter sinus will be close to the inner wall (IW), interestingly, with an increase in the sinus length, the recirculation zones shift toward the OW with higher strength. These significantly decrease the x-wall shear stress (x-WSS) and time-averaged wall shear stress (TAWSS) values on the OW of the longer sinus. The other risk analysis parameters, like oscillatory shear index (OSI) and relative residence time (RRT), support the described consequences. These results reveal that sinus of increased length is more prone to developing atherosclerotic plaque. [ABSTRACT FROM AUTHOR]

We wanted to evaluate if optical coherence tomography angiography OCTA findings could predict the functional outcome in extracranial carotid artery atherosclerotic disease (ECAD) associated stroke. This exploratory study was performed on adults with acute ischaemic stroke due to ECAD at 3–6 weeks following stroke onset with risk factor matched controls without carotid artery stenosis. Twenty-three stroke patients (cases) and 23 controls were enrolled. There was significant difference between cases and controls in deep vessel density at the macula (p =.0007) and in radial peripapillary capillary perfusion density (RPCPD) at the optic nerve head (ONH) (p =.0007). Statistically significant difference was noted in the total superficial vessel density (SVD) at the macula (SVD within 1 standard deviation [SD] versus SVD beyond 1 SD of control data) in the ipsilateral eye and functional outcome at 3 months (poor versus very good outcome, modified Rankin scale [mRS] 0–1 versus mRS 2–6, respectively; p =.0361). There was statistically insignificant correlation between the RPCPD at the ONH and the National Institutes of Health Stroke Scale score at admission, mRS at discharge, and mRS at 3 months following stroke onset (r =.33, r =.35, r =.39; p =.11, p =.09, p =.06, respectively). The findings of this exploratory study suggested that OCTA findings may predict 3 month outcomes in cases of ECAD-related stroke and could be useful in decision making in future intervention studies as to whether intervene or not in patients having critical or non-critical ECAD for preventing stroke. [ABSTRACT FROM AUTHOR]

AbstractObjective: To analyze the diagnostic value of HR-VWI in intracranial arterial stenosis and occlusion and compare it with DSA. Methods: A retrospective analysis of clinical data of 59 patients with intracranial arterial stenosis in our hospital was conducted to compare the diagnostic results of the two methods for different degrees of intracranial stenosis and various morphological plaques. Results: The diagnosis of stenosis and occlusion by both methods showed no significant difference (P > 0.05). Comparison of plaque morphology detected by HR-VWI with pathological examination results showed no significant difference (P > 0.05); however, there was a significant difference between plaque morphology detected by DSA and pathological examination results (P < 0.05). Additionally, there was a significant difference between plaque morphology detected by HR-VWI and DSA (P < 0.05). Conclusion: HR-VWI technique is comparable to DSA technique in diagnosing intracranial arterial stenosis and occlusion, but it is superior to DSA in plaque morphology diagnosis. [ABSTRACT FROM AUTHOR]

Atherosclerosis (AS) is considered to be one of the major causes of cardiovascular disease. Its pathological microenvironment is characterised by increased production of reactive oxygen species, lipid oxides, and excessive inflammatory factors, which accumulate at the monolayer endothelial cells in the vascular wall to form AS plaques. Therefore, intervention in the pathological microenvironment would be beneficial in delaying AS. Researchers have designed biomimetic nanomedicines with excellent biocompatibility and the ability to avoid being cleared by the immune system through different therapeutic strategies to achieve better therapeutic effects for the characteristics of AS. Biomimetic nanomedicines can further enhance delivery efficiency and improve treatment efficacy due to their good biocompatibility and ability to evade clearance by the immune system. Biomimetic nanomedicines based on therapeutic strategies such as neutralising inflammatory factors, ROS scavengers, lipid clearance and integration of diagnosis and treatment are versatile approaches for effective treatment of AS. The review firstly summarises the targeting therapeutic strategy of biomimetic nanomedicine for AS in recent 5 years. Biomimetic nanomedicines using cell membranes, proteins, and extracellular vesicles as carriers have been developed for AS. [ABSTRACT FROM AUTHOR]

Backgound: Alzheimer disease (AD) is a disastrous disease characterized by accretion of amyloid-beta plaques, neurofibrillary tangles inducing oxidative stress, loss of neuronal functions and continuous progression of cognitive impairment leading to severe dementia. Material and Methods: The newly synthesized benzimidazole derivative 4-chloro-3-(2-phenyl-1H-benzimidazole-1-sulfonyl) benzoic acid (CB) was evaluated for its anti-Alzheimer activity using in silico, in vivo, in vitro and molecular techniques (ELISA, WB & IHC). Results:In-silico studies revealed that CB has atomic contact energy values of −3.9 to −8.9 kcal/mol against selected targets. In vitro assay showed that CB caused acetylcholinesterase (AChE) and diphenyl-1-picrylhydrazyl inhibition. In-vivo findings revealed improvement in dementia as observed in the morris water maze test and Ymaze test. Amyloid-beta disaggregation, increased level of anti-oxidants, decreased expressions of inflammatory markers and enhanced cellular architecture were found in the cortex and hippocampus of treated rats in the histopathological examination, immunohistochemistry analysis, enzyme-linked immunosorbent assay and western blot analysis. Conclusions: This study revealed that CB possess different binding affinities with the Alzheimer-related targets and it possess anti-Alzheimer activity, mediated via AChE and amyloid-beta inhibition, anti-oxidant and anti-inflammatory pathways. [ABSTRACT FROM AUTHOR]

Plaque psoriasis, a chronic immune-mediated skin disorder, is characterized by well-demarcated erythematous plaques with silvery scales. This condition stems from complex interactions between genetic predisposition, immune dysregulation, and environmental triggers. Tapinarof downregulates the cytokine IL-17, diminishes the inflammatory infiltrate, and provides antioxidant properties while enhancing the expression of skin barrier proteins. This review begins by assessing tapinarof's mechanism in treating plaque psoriasis. Subsequently, it examines the effectiveness and safety of tapinarof 1% cream in adult patients. Tapinarof 1% cream, which works by activating the aryl hydrocarbon receptor, is an FDA-approved treatment for adult plaque psoriasis. This therapy introduces a novel, nonsteroidal method for addressing inflammation and skin barrier issues, potentially serving as an alternative to conventional treatments. The once-daily, convenient cream formulation and favorable safety profile may enhance patient adherence, which is often poor with topical treatments. Tapinarof also maintains disease clearance for a mean of 4 months after treatment cessation. [ABSTRACT FROM AUTHOR]

AbstractThe presence of macrophage cells inside plaque can lead to a change in plaque temperature, which can be measured by using arterial wall thermographic techniques to predict the severity of stenosis in the vessel without complicated surgery. This study aims to analyze the effect of plaque symmetricity with a similar degree of stenosis (DOS) on plaque surface temperature and blood heat transfer in a straight vessel. This analysis aims towards predicting the severity of stenosis in a straight blood vessel through plaque temperature as an indicator. Two cases are being analyzed here; case 1 and case 2 refer to having similar vessel dimensions and an overall degree of stenosis (DOS) of 70%, with the exception of case 1 having a symmetrically developed plaque while case 2 refers to an asymmetrically developed plaque. Euler-Euler multiphase method with the application of the granular model is being applied in this study. At peak systole (0.2 s into the 10th cardiac cycle) in a cardiac cycle, the increase in plaque surface temperature at exit is higher in case of a symmetrically developed stenosis compared to an asymmetric one but the reverse situation happens during end systole (0.5 s into the 10th cardiac cycle). Although the population of macrophages in a plaque is a deciding factor of the thermal signature of a plaque, the symmetricity variation also needs to be taken into consideration while plaque progression is being diagnosed through thermographic technique. [ABSTRACT FROM AUTHOR]

Macrophages are the most abundant cell group in atherosclerosis (AS) lesions and play a vital role in all stages of AS progression. Recent research has shown that reactive oxygen species (ROS) generation from photodynamic therapy (PDT) induces macrophage autophagy to improve abnormal lipid metabolism and inflammatory environment. Especially in macrophage-derived foam cells, which has become a potential strategy for the treatment of AS. In this study, we prepared the conjugate (DB) of dextran (DEX) and bovine serum albumin (BSA). The DB was used as the emulsifier to prepare nanoemulsion loaded with upconversion nanoparticles (UCNPs) and chlorin e6 (Ce6) (UCNPs-Ce6@DB). The DEX modified on the surface of the nanoemulsion can recognise and bind to the scavenger receptor class A (SR-A) highly expressed on macrophages and promote the uptake of macrophage-derived foam cells in AS plates through SR-A-mediated endocytosis. In addition, UCNPs-Ce6@DB-mediated PDT enhanced ROS generation and induced autophagy in macrophage-derived foam cells, enhanced the expression of ABCA 1, a protein closely related to cholesterol efflux, and inhibited the secretion of pro-inflammatory cytokines. Ultimately, UCNPs-Ce6@DB was shown to inhibit plaque formation in mouse models of AS. In conclusion, UCNPs-Ce6@DB offers a promising treatment for AS. [ABSTRACT FROM AUTHOR]

Background: As one of the essential hypertension (EH)-mediated target organ damage, carotid plaque is a crucial subclinical precursor for cardiovascular events. Therefore, it is vital to identify the risk factors and pathogenesis for EH with carotid plaque. Methods: Based on our previous microarray analysis, we selected four circRNAs as the candidate circRNAs and detected their expression levels in blood of 192 subjects (64 healthy controls, 64 EH patients, and 64 EH patients with carotid plaque) by qRT-PCR analysis. The regulatory mechanism of circRNAs involved in carotid plaque was predicted by bioinformatics analysis. Results: The level of hsa_circ_0124782 increased significantly and the levels of hsa_circ_0131618 and hsa_circ_0127342 decreased significantly in the EH group and EH with carotid plaque group compared with the control group (P < .05). Functional enrichment analysis showed that three circRNAs might be implicated in pathogenesis for carotid plaque. Conclusion: Our study revealed the relationship between three circRNAs and carotid plaque, suggesting that they may serve as potential biomarkers for EH with carotid plaque. [ABSTRACT FROM AUTHOR]

This article discusses the need for new cardiovascular tools to reclassify stroke risk. It highlights that a significant proportion of strokes are of undetermined origin and that current risk factors do not fully explain the risk of stroke. The article explores the potential use of novel assessment tools such as circadian rhythm of blood pressure, arterial stiffness, and atrial cardiopathy in improving stroke risk assessment. It also suggests that reclassifying strokes into different types based on factors like carotid plaque characteristics can help guide treatment decisions. Overall, the article emphasizes the importance of understanding the underlying causes of strokes to improve prevention and treatment strategies. [Extracted from the article]

Ferroptosis may play an essential role in lipid peroxidation and endothelial dysfunction of aortic endothelial cells (ECs) in type 2 diabetes mellitus (T2DM) with atherosclerosis (AS). Hydroxysafflor yellow A (HSYA) has shown substantial antioxidant stress and anti-ferroptosis. This study confirms whether HSYA improves symptoms in a mouse model of T2DM/AS and elucidates the underlying mechanisms. ApoE-/- mice were fed with high fat combined with 30 mg/kg streptozotocin to establish a T2DM/AS model. Then mice were treated with intraperitoneal injections of 2.25 mg/kg HSYA for 12 weeks. Human Umbilical Vein Endothelial cells (HUVEC) induced by 33.3 mM d-glucose +100 μg/mL ox-LDL were used to construct a high lipid and high glucose cell model treated with 25 μM HSYA. The changes in oxidative stress- and ferroptosis-related markers were detected, and the regulatory effect of HSYA on the miR-429/SLC7A11 was also verified. Normal ApoE-/- mice or HUVEC cells were used as the control group. HSYA effectively reduced atherosclerotic plaque formation in the T2DM/AS mouse model and inhibited HUVEC ferroptosis, such as upregulating GSH-Px, SLC7A11 and GPX4, but inhibited ACSL4. Furthermore, HSYA also downregulated the expression of miR-429, which further regulated SLC7A11 expression. After miR-429 mimic or SLC7A11 siRNA transfection in the HUVEC, the antioxidative stress and anti-ferroptosis effects of HSYA were significantly abolished. HSYA is expected to become an important health drug to prevent the occurrence and development of T2DM/AS. [ABSTRACT FROM AUTHOR]

Previously, we found Alisma orientalis beverage (AOB), a classic traditional Chinese medicine (TCM) formulation, had the potential effect of treating atherosclerosis (AS). The underlying mechanism was still unclear. As an extention of our previous work, to investigate the underlying mechanism of action of AOB in the treatment for AS. Network pharmacology was conducted using SwissTargetPrediction, GeneCards, DrugBank, Metascape, etc., to construct component-target-pathway networks. In vivo, AS models were induced by a high-fat diet (HFD) for 8 consecutive weeks in APOE−/− mice. After the administration of AOB (3.8 g/kg, i.g.) for 8 weeks, we assessed the aortic plaque, four indicators of blood lipids, and expression of the PI3K/AKT/SREBP-1 pathway in liver. Network pharmacology showed that PI3K/AKT/SREBP-1 played a role in AOB's treatment for AS (PI3K: degree = 18; AKT: degree = 17). Moreover, we found that the arterial plaque area and four indicators of blood lipids were all significantly reversed by AOB treatment in APOE−/− mice fed with HFD (plaque area reduced by about 37.75%). In addition, phosphorylated expression of PI3K/AKT and expression of SREBP-1 were obviously increased in APOE−/− mice fed with HFD, which were all improved by AOB (PI3K: 51.6%; AKT: 23.6%; SREBP-1: 40.0%). AOB had therapeutic effects for AS by improving blood lipids and inhibition of the PI3K/AKT/SERBP-1 pathway in the liver. This study provides new ideas for the treatment of AS, as well as new evidence for the clinical application of AOB. [ABSTRACT FROM AUTHOR]

Bile acids play crucial roles in various metabolisms, as well as Lactobacillus in the intestine. But studies on their roles in acute coronary syndrome (ACS) are still insufficient. The aim of this study was to investigate their role and potential association with the severity of coronary lesions and the prognosis of ACS. Three hundred and sixty ACS patients were selected. Detection of gut Lactobacillus levels was done through 16S rDNA sequence analysis. Evaluation of the extent of lesions was done using the SYNTAX (SS) score. Mediation analysis was used to assess the relationship between serum total bile acid (TBA), Lactobacillus, atherosclerotic lesions and prognosis of ACS. Logistic regressive analysis disclosed that serum TBA and Lactobacillus were independent predictors of coronary lesions (high vs. low SS: serum TBA adjusted odds ratio (aOR) = 0.8, 95% confidence interval (CI): 0.6–0.9, p <.01; Lactobacillus: aOR = 0.9, 95% CI: 0.9–1.0, p =.03). According to multivariate Cox regression analysis, they were negatively correlated with the overall risk of all-cause death (serum TBA: adjusted hazard ratio (aHR) = 0.1, 95% CI: 0.0–0.6, p =.02; Lactobacillus: aHR = 0.6, 95% CI: 0.4–0.9, p =.01), especially in acute myocardial infarction (AMI) but not in unstable angina pectoris (UAP). Ulteriorly, mediation analysis showed that serum TBA played an important role as a mediation effect in the following aspects: Lactobacillus (17.0%, p <.05) → SS association (per 1 standard deviation (SD) increase), Lactobacillus (43.0%, p <.05) → all-cause death (per 1 SD increase) and Lactobacillus (45.4%, p <.05) → cardiac death (per 1 SD increase). The lower serum TBA and Lactobacillus level in ACS patients, especially in AMI, was independently linked to the risk of coronary lesions, all-cause death and cardiac death. In addition, according to our mediation model, serum TBA served as a partial intermediate in predicting coronary lesions and the risk of death by Lactobacillus, which is paramount to further exploring the mechanism of Lactobacillus and bile acids in ACS. Lower level of serum total bile acid (TBA) was highly associated with the severity of coronary lesions, myocardial damage, inflammation and gut Lactobacillus in acute coronary syndrome (ACS) patients, especially in acute myocardial infarction (AMI). Lower level of serum TBA was highly associated with mortality (including all-cause death and cardiac death) in patients with ACS, especially with AMI. Serum TBA had a partial mediating effect rather than regulating effect between gut Lactobacillus and coronary lesions and prognosis of ACS. [ABSTRACT FROM AUTHOR]

Patients with type 2 diabetes mellitus (T2DM) are susceptible to coronary artery disease (CAD), and coronary outcomes in these patients are heterogeneous. However, the impact of coronary plaque compositions on rapid plaque progression (RPP) in patients with T2DM has rarely been reported. This study aimed to investigate the association of coronary plaque compositions with rapid lesion volume progression in patients with T2DM. A total of 159 subjects (aged 62.51 ± 10.3 years, 68.6% were male) who underwent serial coronary computed tomography angiography (CCTA) with type 2 diabetic status were enrolled. Annual change of plaque volume (PV) (mm3/year) was defined as PV change divided by inter-scan period. RPP was defined as the progression of plaque burden (PV divided by vessel volume multiplied by 100) ≥0.59%/year. Plaque components were compared between RPP and no RPP groups. Then all patients were divided into 3 groups according to the baseline calcified plaque volume tertiles. The outcome was whether RPP occurred. The median inter-scan period was 2.09 (range 1.41–3.33) years. The overall incidence of RPP was 61.0%. The calcified plaque volume decreased significantly in the RPP group as compared to the no RPP group. The risk of RPP (odds ratio [OR] 0.39; 95% confidence interval [CI]: 0.17-0.88; p = 0.024) was reduced in tertiles III as compared to that in tertiles I even after adjustment for baseline variables (OR 0.21; 95% CI: 0.07–0.63; p = 0.005). Moreover, adding the calcified plaque volume significantly raised the predictive value for the RPP (0.370, p = 0.030, and 0.059, p = 0.025, NRI, and IDI respectively) as compared to traditional factors. The baseline calcified plaque volume is an independent protective factor for the rapid progression of coronary atherosclerosis in patients with T2DM. The calcified plaque volume of the coronary was significantly lower in T2DM subjects with RPP than in those without RPP. Higher levels of atherosclerotic calcification may have a protective value on plaque stabilization in patients with T2DM. Calcified plaque volume of the coronary should be considered when proposing risk stratification in T2DM patients. [ABSTRACT FROM AUTHOR]

This article discusses a case of a 28-year-old man who experienced unexpected coronary thrombosis (blood clot) after being infected with the delta variant of COVID-19. The man had no pre-existing health conditions or risk factors, and had previously contracted COVID-19 and received a vaccine. He presented with chest pain and further tests revealed the presence of a blood clot in one of his coronary arteries. Treatment was administered and the clot dissolved. The article highlights the importance of comprehensive coronary imaging in managing COVID-19 patients and emphasizes the thrombotic complications associated with the virus. [Extracted from the article]

Coronary Artery Disease (CAD) is a prevalent condition characterized by the presence of atherosclerotic plaques in the coronary arteries of the heart. The global burden of CAD has increased significantly over the years, resulting in millions of deaths annually and making it the leading health-care expenditure and cause of mortality in developed countries. The lack of cost-effective strategies for monitoring the prognosis of CAD warrants a pressing need for accurate and efficient markers to assess disease severity and progression for both reducing health-care costs and improving patient outcomes. To effectively monitor CAD, prognostic biomarkers and imaging techniques play a vital role in risk-stratified patients during acute treatment and over time. However, with over 1,000 potential markers of interest, it is crucial to identify the key markers with substantial utility in monitoring CAD progression and evaluating therapeutic interventions. This review focuses on identifying and highlighting the most relevant markers for monitoring CAD prognosis and disease severity. We searched for relevant literature using PubMed and Google Scholar. By utilizing the markers discussed, health-care providers can improve patient care, optimize treatment plans, and ultimately reduce health-care costs associated with CAD management. Coronary artery disease is a narrowing or blockage of coronary arteries due to the formation of plaque. The main risk factors are inflammation, aging, high cholesterol, shear stress, obesity, and smoking. Narrowing of the arteries results in decreased blood supply (nutrient and oxygen) to the tissue precipitating ischemia presented as angina or myocardial infarction. During ischemic events, there occurs a change in the expression of various molecular and cellular components and increased expressions of many of these factors have been used as biomarkers to diagnose the pathology. Myoglobin, fatty acid-binding proteins, and glycogen phosphorylase isoenzyme BB are early biomarkers, troponin-T and troponin-I are late biomarkers, while creatine kinase-myocardial band is a biomarker in the first 10–12 h for the diagnosis of AMI. However, there is a need for a panel of biomarkers that can help in the prediction, prognosis, and diagnosis of disease progression (atherosclerosis), pre-ischemic and ischemic events, and post-MI periods to design the treatment strategies in a specific and sensitive manner. There is a need for cost-effective sensitive biomarkers that can prevent progression, risk stratify, predict, diagnose, and prevent MI in a timely manner. In this comprehensive review, we discuss the key markers of substantial utility for monitoring coronary artery disease progression and the efficacy of therapeutic intervention among various markers of interest. [ABSTRACT FROM AUTHOR]

Myocardial bridging (MB) is a common congenital cardiovascular anomaly. There are reported associations of MB with different clinical presentations like effort angina, acute coronary syndromes (ACS) and sudden cardiac death. Acceleration of atherosclerosis in proximal vessel is reported in patients with MB, while bridged segments are reported to be free of atherosclerosis We assessed patients who underwent intravascular ultrasound (IVUS) guided percutaneous intervention (PCI) of left anterior descending (LAD) artery. Plaque characteristics derived from IVUS analysis were compared between those who displayed myocardial bridge versus those who did not harbour the anomaly. One hundred and forty-seven (147) patients underwent IVUS guided PCI. Incidence of MB was 44/147 (29.9%). Mean age of patients who had MB {+} was higher (62.1 ± 10.3 vs. 57.8 ± 11.2 (p =.03). 142/147 (96.6%) patients presented with ACS. ST elevation myocardial infarction (STEMI) was the most common presenting diagnosis (110/147 to 74.8%). There were no differences in qualitative plaque characteristics – attenuated plaque, calcification or calcium score between two groups. Plaque burden and length of the lesion in the proximal vessel were not different. Among patients with MB {+}, atheromatous extension to segments underlying the bridge was seen in 31/44 (70.5%) cases. In a series of patients who presented with advanced clinical atherosclerosis, plaque characteristics were not different in patients who harboured myocardial bridge vs. those who did not have the anomaly. Atheromatous involvement was seen extending into bridged segment contrary to previous reports. [ABSTRACT FROM AUTHOR]

An advancing atherosclerotic plaque is a risk factor for stroke. We conducted this study to assess the relationship between risk factors of stroke with changing in the thickness of carotid plaques thickness evident on sonography. We carried out a secondary analysis of data from a study on carotid bifurcation plaques. Data were collected in the sonography laboratories of two university hospitals. In total, 564 (240; 42.6% men) patients with atherosclerotic plaques in the carotid bifurcation and internal carotid artery with stenosis ≥ 30% evident on duplex sonography were included. We developed machine learning models using an extreme gradient boosting algorithm with Shapley additive explanation method to find important risk factors and their interactions. The outcome was a change in the carotid plaque thickness after 36 months, and the predictors were initial plaque thickness and the risk factors of stroke. Two regression models were developed for left and right carotid arteries. The R-squared values were 0.964 for the left, and 0.993 for the right model. Overall, the three top features were BMI, age, and initial plaque thickness for both left and right plaques. However, the risk factors of stroke showed stronger interaction in predicting plaque thickening of the left carotid more than the right carotid artery. The effect of each predictor on plaque thickness is complicated by interactions with other risk factors, particularly for the left carotid artery. The side of carotid artery involvement should be considered for stroke prevention. [ABSTRACT FROM AUTHOR]

Haemoglobin A1c (HbA1c) levels have been shown to be related to carotid artery plaques. However, studies on the relationship between HbA1c levels and carotid artery plaques in patients with coronary heart disease (CHD) are limited and inconsistent. Our objective was to examine the correlation between HbA1c levels and carotid artery plaques in patients with CHD. The study comprised 9275 Chinese adults with CHD from January 1, 2014, to September 30, 2020. HbA1c levels were assessed, and colour Doppler ultrasound was used to evaluate the carotid artery, including plaque presence, intima-media thickness, and plaque echo properties, to investigate the association between HbA1c and carotid plaque. A logistic regression model was used to assess the association between carotid artery plaques, carotid plaque echogenicity, and HbA1c. The HbA1c level of the plaque-present group was higher than that of the plaque-absent group [6.1 (5.6–7.2) vs. 5.8 (5.5–6.5), p < 0.001]. In multiple linear regression analysis, intima-media thickness was associated with HbA1c (p < 0.001). Logistic regression showed that a higher HbA1c level was associated with plaque incidence as well as hyperechoic and heterogeneous plaques (p < 0.001). These associations persist after adjusting for age, sex, blood pressure, lipid profiles, alcohol consumption, and tobacco exposure. HbA1c levels are notably associated with carotid artery plaque incidence, intima-media thickness, and plaque echogenicity in patients with CHD. These findings show that different levels of HbA1c may be an indicator for carotid artery plaques and thus, should be observed in patients with CHD. [ABSTRACT FROM AUTHOR]

Aim of the study: To present our rescue approach of carotid artery occlusion as well as to discuss other possible techniques that can be applied in similar situations.Materials and methods: Two cases from our institution with acute complications during carotid micro-endarterectomy (CEA).Results: Two cases from our institution with acute postoperative complications during CEA that were successfully addressed are presented with imaging and detailed description of the surgical techniques used.Conclusion: CEA are common surgical procedures pursued to achieve revascularization of carotid arteries when occluded partially or fully by an atherosclerotic plaque. As with any surgical procedure, associated complications exist in small percentage of the cases. These can include blood flow limitation due to an insufficient artery wall after atherosclerotic plaque extraction as well as distal kinking of the internal carotid artery. A direct end-to-end ACE-ACI bypass with occlusion of the proximal ACI and distal ACE stump preserves distal flow to the ACI, however the original arteriotomy of ACC must be completely sutured up to the arterial stumps. [ABSTRACT FROM AUTHOR]

Dysfunction in the macrophage lysosomal system including reduced acidity and diminished degradative capacity is a hallmark of atherosclerosis, leading to blunted clearance of excess cellular debris and lipids in plaques and contributing to lesion progression. Devising strategies to rescue this macrophage lysosomal dysfunction is a novel therapeutic measure. Nanoparticles have emerged as an effective platform to both target specific tissues and serve as drug delivery vehicles. In most cases, administered nanoparticles are taken up non-selectively by the mononuclear phagocyte system including monocytes/macrophages leading to the undesirable degradation of cargo in lysosomes. We took advantage of this default route to target macrophage lysosomes to rectify their acidity in disease states such as atherosclerosis. Herein, we develop and test two commonly used acidic nanoparticles, poly-lactide-co-glycolic acid (PLGA) and polylactic acid (PLA), both in vitro and in vivo. Our results in cultured macrophages indicate that the PLGA-based nanoparticles are the most effective at trafficking to and enhancing acidification of lysosomes. PLGA nanoparticles also provide functional benefits including enhanced lysosomal degradation, promotion of macroautophagy/autophagy and protein aggregate removal, and reduced apoptosis and inflammasome activation. We demonstrate the utility of this system in vivo, showing nanoparticle accumulation in, and lysosomal acidification of, macrophages in atherosclerotic plaques. Long-term administration of PLGA nanoparticles results in significant reductions in surrogates of plaque complexity with reduced apoptosis, necrotic core formation, and cytotoxic protein aggregates and increased fibrous cap formation. Taken together, our data support the use of acidic nanoparticles to rescue macrophage lysosomal dysfunction in the treatment of atherosclerosis. Abbreviations: BCA: brachiocephalic arteries; FACS: fluorescence activated cell sorting; FITC: fluorescein-5-isothiocyanatel; IL1B: interleukin 1 beta; LAMP: lysosomal associated membrane protein; LIPA/LAL: lipase A, lysosomal acid type; LSDs: lysosomal storage disorders; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MFI: mean fluorescence intensity; MPS: mononuclear phagocyte system; PEGHDE: polyethylene glycol hexadecyl ether; PLA: polylactic acid; PLGA: poly-lactide-co-glycolic acid; SQSTM1/p62: sequestosome 1 [ABSTRACT FROM AUTHOR]

The article discusses the potential of calycosin, a phytoestrogen extracted from Astragalus membranaceus, as a natural bioactive ingredient for preventing and treating atherosclerosis and cardiovascular disease. While the exact mechanism of action is still uncertain, recent studies have shown that calycosin has various favorable effects, including anti-inflammatory, anti-oxidative, and organ protective activities. The article highlights a study that found calycosin to have anti-atherogenic capability and the ability to suppress inflammatory reactions and oxidative stress. The study also identified IL-6 and MAPK-3 as pharmacological targets for calycosin. The findings suggest that calycosin may have lipid-lowering and anti-atherosclerotic effects, but further experimental and clinical validation is needed. [Extracted from the article]

Atherosclerotic plaques belong to the common vascular disease in the aged, which rupture will lead to acute thromboembolic diseases, the leading cause of fatal cardiovascular events. Accumulating evidence indicates that the lncRNAs-miRNAs-mRNA regulatory network plays a critical role in atherosclerosis. Based on RNA sequencing (GSE207252), we constructed expression profiles of lncRNAs, microRNAs, and mRNA in the carotid plaque of atherosclerosis patients and analyzed differentially expressed genes (DEGs). We identified three candidate lncRNAs using two algorithms (LASSO and SVM-RFE): lnc_GLRX3, lnc_FGF7-5, and DISC1FP1). LNCipedia, TargetScan, and miRDB databases were used to predict target miRNAs of lncRNAs and target genes of miRNAs. Gene ontology (GO) functional annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and Gene Set Enrichment Analysis (GSEA) analysis of DEGs was carried out using the R package clusterProfiler. A PPI network was constructed using the STRING website and visualized by Cytoscape. According to the "MCC" method of the plug-in cytoHubba in Cytoscape, ERCC4 was the top hub gene of the PPI network. We constructed a lncRNA_FGF7-5/lncRNA_GLRX3-miR-2681-5p-ERCC4 regulatory network for carotid plaque using lncRNA-miRNA and miRNA-mRNA pairs. Next, lncRNA_FGF7-5 and lncRNA_GLRX3 targeted miR-2681-5p directly to upregulate ERCC4 expression. Silencing of lncRNA_FGF7-5 and lncRNA_GLRX3 promoted apoptosis and TP53 expression in HUVECs treated with ox-LDL; however, these effects were reversed by ERCC4-overexpression. Taken together, these findings indicated that lncRNA_FGF7-5 and lncRNA_GLRX3 together reduced atherosclerosis-induced apoptosis of HUVECs via targeting miR-2681-5p to increase ERCC4 expression, thereby preventing the formation of carotid plaque and finally inhibiting atherosclerosis progression. [ABSTRACT FROM AUTHOR]

Our study aimed to illustrate the effect of the antihistaminic drug azelastine on aortic calcification in diabetic hyperlipidemic (DH) rats along with the underlying molecular mechanism. Twenty-four male albino Wistar rats were categorised into four groups. One group received normal rodent chow (normal group), while the other groups were rendered diabetic and hyperlipidemic; one received no drugs and served as a positive control while the other two groups received either azelastine (4 mg/kg) or 10-dehydrogingerdione (10 mg/kg) orally and daily for 8 weeks. Azelastine significantly reduced blood glucose, HbA1c and serum ALP, OCN, downregulated apo B, improved the lipid profile (LDL-c decrease and HDL-c increase), attenuated calcium deposition and aortic calcification as compared to control group. 10-DHGD showed comparatively lower effect. Anti-calcifying effect of azelastine might be related to upregulation of apo A (HDL-c) and downregulation of apo B mRNA expression indeed good modulator of aortic calcification. Many studies have indicated that high-density lipoprotein-cholesterol (HDL-c) is inversely correlated with atherosclerotic plaque progression and could reduce cardiovascular disease risk. An anti-calcifying effect of HDL-c has been reported and targeting this lipoprotein may therefore be a valuable approach to vascular calcification control. Azelastine is a selective H1 antagonist that was identified to increase mRNA expression of apolipoprotein A. This encouraged us to investigate the effect of azelastine on lipid profile and markers of aortic calcification in DH rats. Our findings showed that azelastine ameliorated aortic calcification and increased apoA expression along with a decline in apo B. This may represent the underlying mechanism while the histopathological findings offered a significant support to the collected biochemical data. [ABSTRACT FROM AUTHOR]

It has not been clarified whether the anti-atherosclerotic effect of lingonberry can be ascribed to its content of flavonoids or dietary fibre or both. The aim of this study was to evaluate the metabolic effects of whole lingonberries compared with isolated flavonoid and fibre fractions on atherosclerotic plaques, plasma lipid profiles, gut microbiota and microbiota-dependent metabolites in an Apoe–/– mouse model. Mice fed whole lingonberries showed the lowest amount of atherosclerotic plaques, while mice fed the fibre fraction had the highest formation of caecal butyric acid. Flavonoids, rather than dietary fibre, were suggested to be the components that favour proliferation of Akkermansia, as judged by the lowest abundance of this bacterium in mice fed the fibre fraction. All groups fed lingonberry diets had both, lower Firmicutes/Bacteroidetes ratios and creatinine concentrations, compared with the control. To conclude, different components in lingonberries are associated with different physiological effects in Apoe–/– mice. [ABSTRACT FROM AUTHOR]

Home blood pressure monitoring (HBPM) might be considered a valid alternative to ambulatory blood pressure monitoring (ABPM) for both the diagnosis and management of hypertension. Correct information on how to perform HBPM are crucial for its reliability. The aim of the present survey was to assess if hypertensive patients followed current recommendation on how to correctly perform HBPM measurements. The survey included 30 different items on how to perform the HBPM. It was developed by the 'Young Investigators' group of the Italian Society of Arterial Hypertension (SIIA) and it was administered during the office visit between May 2019 and December 2021. A total of 643 hypertensive patients participated in the study. Main results show that, despite the rate of informed patients was relatively high (71% of the whole population), unacceptable number of patients did not follow indications on how to perform a correct HBPM. Patients who were informed on how to measure home BP had a significantly higher rate of correct position during measurement (78 vs. 22%, p < 0.01), avoidance of talking and moving during measurement (68 vs. 32%, p < 0.0001), and correct number and time interval between two measurements (85 vs. 15%, p < 0.001). More accurate measurements of home BP were associated with less prevalence of carotid plaque. Correct performance for HBPM is low among patients treated in Italian hypertension centers. These findings shed light on the importance of correct HBPM measurements for the detection of accurate BP values for the proper management of hypertensive patients. [ABSTRACT FROM AUTHOR]

HDL is endowed with several metabolic, vascular, and immunoinflammatory protective functions. Among them, a key property is to promote reverse cholesterol transport from cells back to the liver. The aim of this study was to estimate the association of scavenger receptor class B type I (SR-BI)- and ATP binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux (the two major routes for cholesterol efflux to HDL) with the presence, extent, and severity of coronary artery disease (CAD), vascular wall remodelling processes, coronary plaque characteristics, and the incidence of myocardial infarction in the different subgroups of patients from the CAPIRE study. Patients (n = 525) from the CAPIRE study were divided into two groups: low-risk factors (RF), with 0–1 RF (n = 263), and multiple-RF, with ≥2 RFs; within each group, subjects were classified as no-CAD or CAD based on the segment involvement score (SIS) evaluated by coronary computed tomography angiography (SIS = 0 and SIS > 5, respectively). SR-BI- and ABCA1-mediated cholesterol efflux were measured using the plasma of all patients. SR-BI-mediated cholesterol efflux was significantly reduced in patients with CAD in both the low-RF and multiple-RF groups, whereas ABCA1-mediated cholesterol efflux was similar among all groups. In CAD patients, multivariable analysis showed that SR-BI-mediated cholesterol efflux <25th percentile predicted cardiovascular outcome (odds ratio 4.1; 95% CI: 1.3–13.7; p =.019), whereas ABCA-1-mediated cholesterol efflux and HDL-C levels significantly did not. Despite this finding, reduced SR-BI-mediated cholesterol efflux was not associated with changes in high-risk plaque features or changes in the prevalence of elevated total, non-calcified, and low-attenuation plaque volume. SR-BI-mediated cholesterol efflux capacity is lower in patients with diffuse coronary atherosclerosis. In addition, a lower SR-BI-mediated cholesterol efflux capacity is associated with the worst clinical outcomes in patients with CAD, independently of atherosclerotic plaque features. Increased cholesterol efflux capacity, an estimate of HDL function, is associated with a reduced CVD risk, regardless of HDL-C levels. HDL-C levels are significantly lower in patients with CAD. Lower SR-BI-mediated cholesterol efflux capacity is observed in patients with diffuse coronary atherosclerosis and is associated with the worst clinical outcomes in patients with CAD, independently of atherosclerotic plaque features. [ABSTRACT FROM AUTHOR]

At present, no early diagnostic markers for essential hypertension (EH)-induced subclinical target organs damage (such as carotid plaque) are available. This study aimed to identify the circular RNAs (circRNAs) in EH with carotid plaques, and assess their utility as biomarkers. First, circRNAs were identified through microarry analysis and database prediction. Second, a case-control study of EH patients with carotid plaque (n = 100) and healthy controls (n = 100) was performed to evaluate circRNAs expression in peripheral blood. Finally, receiver operating characteristic (ROC) curve was established to evaluate the diagnostic value. Five circRNAs (hsa_circ_0105130, hsa_circ_0109569, hsa_circ_0072659, hsa_circ_0079586 and hsa_circ_0064684) were identified as the candidate circRNAs. We found that circRNAs were increased in case group compared with controls (P <.05). The results of ROC shown that these five circRNAs, especially hsa_circ_0109569 (AUC = 0.741), all had the moderate predictive value. Our study revealed circulating circRNAs may act as promising noninvasive biomarkers for early detection and population screening of EH-induced subclinical target organ injury. [ABSTRACT FROM AUTHOR]

The risk of an acute coronary event stems from the amount and type of plaque present, as well as the fluid and structural dynamics in the coronary artery. If the plaque's structural stress exceeds the mechanical strength, the fibrous cap may rupture and lead to thrombosis. The patient is then likely to face a sudden myocardial infarction. An association between Coronary Heart Disease (CHD) and Sudden Cardiac Death (SCD) has been long recognised. For the first time, we are reporting a correlation between applied external pressure, such as Cardiopulmonary Resuscitation (CPR), coughing, sneezing, blowing one's nose, etc., and diseased coronary artery plaque via 3 D coronary artery models and two-way Fluid-Solid Interaction (FSI) models. Shear and von Mises stresses inside arteries and plaques have been shown to play a major role in plaque development, progression of disease, and the likelihood of plaque rupture. Our results show a drastic change in maximum shear (300%) and von Mises stresses (500%) with increasing external pressure. This change may indicate an onset of imminent plaque rupture. Furthermore, FSI modelling indicates a strong correlation between plaque thickness, location, and external pressure. With further clinical and simulation studies, this information could be helpful in understanding potential limit pressure in the CPR process for patients with CHD. [ABSTRACT FROM AUTHOR]

Vascular smooth muscle cells (VSMCs) contribute to plaque stability. VSMCs are also a major source of CTH (cystathionine gamma-lyase)-hydrogen sulfide (H2S), a protective gasotransmitter in atherosclerosis. However, the role of VSMC endogenous CTH-H2S in pathogenesis of plaque stability and the mechanism are unknown. In human carotid plaques, CTH expression in ACTA2+ cells was dramatically downregulated in lesion areas in comparison to non-lesion areas. Intraplaque CTH expression was positively correlated with collagen content, whereas there was a negative correlation with CD68+ and necrotic core area, resulting in a rigorous correlation with vulnerability index (r = −0.9033). Deletion of Cth in VSMCs exacerbated plaque vulnerability, and were associated with VSMC autophagy decline, all of which were rescued by H2S donor. In ox-LDL treated VSMCs, cth deletion reduced collagen and heightened apoptosis association with autophagy reduction, and vice versa. For the mechanism, CTH-H2S mediated VSMC autophagosome formation, autolysosome formation and lysosome function, in part by activation of TFEB, a master regulator for autophagy. Interference with TFEB blocked CTH-H2S effects on VSMCs collagen and apoptosis. Next, we demonstrated that CTH-H2S sulfhydrated TFEB at Cys212 site, facilitating its nuclear translocation, and then promoting transcription of its target genes such as ATG9A, LAPTM5 or LDLRAP1. Conclusively, CTH-H2S increases VSMC autophagy by sulfhydration and activation of TFEB, promotes collagen secretion and inhibits apoptosis, thereby attenuating atherogenesis and plaque vulnerability. CTH-H2S may act as a warning biomarker for vulnerable plaque. Abbreviations ATG9A: autophagy related 9A; CTH: cystathionine gamma-lyase; CQ: chloroquine; HASMCs: human aortic smooth muscle cells; H2S: hydrogen sulfide; LAMP1: lysosomal associated membrane protein 1; LAPTM5: lysosomal protein transmembrane 5; NaHS: sodium hydrosulfide hydrate; ox-LDL: oxidized-low density lipoprotein; PPG: DL- propagylglycine; TFEB: transcription factor EB; 3-MA: 3-methyladenine; VSMCs: vascular smooth muscle cells. [ABSTRACT FROM AUTHOR]

Proactive management of plaque psoriasis with twice-weekly topical calcipotriol/betamethasone dipropionate (Cal/BD) foam has a demonstrated clinical benefit in preventing disease relapse compared to reactive management, where Cal/BD foam is only given as rescue therapy once-daily for four weeks after relapse. The impact of proactive management with Cal/BD foam on a wider range of clinical responses is not yet known, nor is its potential cost-effectiveness in the healthcare system of Finland. This study involved a post-hoc analysis exploring the clinical and patient-reported benefits of proactive versus reactive management with Cal/BD foam observed in the PSO-LONG trial (NCT02899962). A range of response criteria based on modified psoriasis area and severity index (mPASI) and dermatology life quality index (DLQI) were analyzed, and the cost-effectiveness of proactive versus reactive management was estimated in a Finnish healthcare setting. The analysis found a consistent clinical benefit of proactive management compared to reactive management on all response criteria, and a markedly lower cost-per-responder for the response criteria of mPASI 75, mPASI ≤ 2 and DLQ1 ≤ 1. The analysis was robust to sensitivity analyses on key inputs and demonstrates the cost and clinical benefits of proactive over reactive management of plaque psoriasis with Cal/BD foam in the Finnish healthcare setting. [ABSTRACT FROM AUTHOR]

This study is dealt with the two-phase binding (specific and nonspecific) of drug eluted from a half- embedded drug-eluting stent in presence of atherosclerotic plaque. The specific binding due to the interaction of drug molecules with specific receptors and nonspecific binding caused by the trapping of drug in the extra-cellular matrix have been paid due attention. An idealised wall consisting of a plaque and a healthy tissue region has been considered. Moreover, a Dirichlet release condition is imposed on the strut surface. In this investigation, a two-dimensional model governing drug transport and its two-phase binding in cylindrical polar coordinate system has been solved numerically by a finite-difference method. Our simulation predicts that plaque behaves like a physical barrier in two types of the binding process and there is an inverse relationship between bound drug concentration and plaque thickness. Simulations show that a single peak profile of drug is noted when the struts are situated one-strut radius apart and as the inter-strut distance increases, the peak concentration falls and distinct peak profiles over each strut are visualised. The model also reveals that in the region downstream of a strut, the concentration of both bound drug forms in the plaque and healthy regions increases, and eventually, the saturation length of binding sites increases. Predicted results show for smaller Damköhler number, the rapid saturation of binding sites takes place and the stent having thinner strut may perform well in terms of effectiveness as well as efficacy in the stent-based delivery. [ABSTRACT FROM AUTHOR]

The pathophysiology of atherosclerosis and its acute complications, such as the Acute Coronary Syndromes (ACS), is continuously under investigation. Immunity and inflammation seem to play a pivotal role in promoting formation and grow of atherosclerotic plaques. At the same time, plaque rupture followed by both platelets' activation and coagulation cascade induction lead to intracoronary thrombus formation. Although these phenomena might be considered responsible of about 90% of ACS, in up to 5–10% of acute syndromes, a non-obstructive coronary artery disease (MINOCA) might be documented. This paper gives an overview on atherothrombosis and immuno-inflammation processes involved in ACS pathophysiology, also emphasizing the pathological mechanisms potentially involved in MINOCA. The relationship between immuno-inflammation and atherothrombosis is continuously updated by recent findings. At the same time, pathophysiology of MINOCA still remains a partially unexplored field, stimulating the research of potential links between these two aspects of ACS pathophysiology. Pathophysiology of ACS has been extensively investigated; however, several gray areas still remain. MINOCA represents one of these areas. At the same time, many aspects of immune-inflammation processes are still unknown. Thus, research should be continued to shed a brighter light on both these sides of "ACS" moon. [ABSTRACT FROM AUTHOR]

Traditionally atherosclerosis was thought to be progressive and medical treatment solely focused on delaying the progression of atherosclerosis rather than treating the disease itself. Multiple recent studies, however, have demonstrated a significant decrease in cardiovascular mortality with the use of additional anti-atherosclerotic therapies beyond statins. Consistent with these observations, mechanistic studies indicate that these additional anti-atherosclerotic therapies have a positive effect on both halting and reversing the course of atherosclerosis. We examine the progression of atherosclerosis and the efficacy of various anti-atherosclerotic treatment classes in this review utilizing multimodality imaging techniques. Searches were conducted in electronic databases: PubMed and EMBASE for all peer reviewed publications that examined coronary plaque progression, regression and stabilization using different imaging modalities and antiatherosclerosis therapies. All relevant published articles on this topic were identified and their reference lists were screened for relevance. Though lipoprotein levels have traditionally been the target for antiatherosclerosis medication, several newer strategies have emerged creating novel targets in the treatment of coronary atherosclerosis. Using a combination of antiatherosclerosis therapies in conjunction with noninvasive imaging modalities like CCTA to directly visualize the plaque, is currently the focus of the future, with the aim of preventing and reversing atherosclerosis. [ABSTRACT FROM AUTHOR]

In this manuscript, a novel method of rational-dilation wavelet transform (RDWT) is proposed for carotid plaque characterisation and classification in Ultrasound images. RDWT is mainly utilised for image acquisition, pre-processing, feature extraction and ensemble classification in automated plaque classification. Here, the transition bands are constructed from the transition function. The statistical features, viz mean, standard deviation, skewness, Renyi entropy, energy are extracted from the sub-bands of RDWT. The Salp Swarm Algorithm (SSA) is mainly used for selecting the optimum features. In this for selecting optimum features using SSA algorithm two conditions are satisfied such as, in the first approach, mean, standard deviation, skewness are selected and then utilised for converting the continual version of salp swarm algorithm to binary. Subsequently, the crossover operator is utilised to select the Renyi entropy, energy features including transfer functions for replacing the average operator and enhancing the characteristics of research method. Plaque Classification uses K Nearest Neighbour (KNN), Probabilistic Neural Network (PNN) and Support Vector Machine (SVM) classifiers. Experimental outcomes show the efficiency of the proposed method depending on accuracy, specificity and sensitivity. The proposed method attains accuracy of 93%, sensitivity of 90% and specificity of 94% when likened to the existing techniques, such as KNN, PNN and SVM. [ABSTRACT FROM AUTHOR]

Moderate-to-severe plaque psoriasis can be treated very successfully with systemic therapies. Often the therapeutics must be injected subcutaneously. This prospective observational study aimed to compare the correct preparation and performance of subcutaneous injections in trained and untrained patients with plaque psoriasis. We asked 110 patients (29.1% women, 70.9% men, injection system: 75.5% prefilled syringe, 24.5% autoinjector) to what extent they were trained for self-injection. While participants injected a sham injection with their current system, we evaluated the preparation, execution, and follow-up using a newly developed scoring system. 87.3% (n = 96) of the participants declared that they had been trained for self-injection. No statistically significant difference was observed between the trained and untrained participants in performing the injection correctly (p =.458). The most common mistakes were the wrong preparation and follow-up of the injection. A bifactorial rank-variance analysis showed a negative influence of the factor injection system (prefilled syringe) on the total score (p =.005). We can indicate that patients with plaque psoriasis are well prepared for subcutaneous self-injection. Self-injection of systemic therapies is easy to perform, especially with patient-friendly systems, and does not require specialized training. [ABSTRACT FROM AUTHOR]

The use of external fields such as magnet and ultrasound to enhance the targeted drug delivery (TDD) by nano-microcarriers could be a potential method. In this research, the drug delivery of magnetic nanoparticles (NPs) coated nanoliposomes and microbubbles (MBs) to the atherosclerosis plaque was investigated under magnetic and ultrasound fields in terms of their adhesion to the plaque through ligand–receptor binding. The Halbach arrangement enhanced the surface density of nanoliposomes and MBs adhered to the plaque by ∼ 121 \% and ∼ 94 \% , respectively. A focused transducer at the power of 60 W led to better drug delivery performance and caused ∼ 67 \% and ∼ 58 \% enhancement in the surface density of nanoliposomes and MBs adhered to the plaque, respectively. Better drug delivery efficiency was achieved upon using a magnetic field as compared with the ultrasound field. The simultaneous employment of magnetic and ultrasound fields can increase the delivery of nanoliposomes and MBs by ∼ 148 \% and ∼ 121 \% , respectively. The results of this study can broaden our insight on the effects of a magnet (its size, location, and arrangement) and the type of ultrasound transducer on TDD to the carotid artery disease using nanoliposomes and MBs. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a systemic disease associated with inflammatory cell infiltration and activation of immune-related pathways. In our study, we aimed to uncover immune-related changes and explore novel immunological features in the development of carotid atherosclerotic plaques. First, we applied integrated bioinformatics methods, including CIBERSORT and gene set enrichment analysis (GSEA). The gene expression matrices GSE28829, GSE41571, and GSE43292 were obtained from the Gene Expression Omnibus (GEO) dataset. After a series of data pre-processing steps, the resulting combined expression matrices were analysed using the CIBERSORT, GSEA, and Cluster Profiler packages. After the comparison and analysis between the carotid atherosclerotic plaques in the early and advanced stages, we discovered that there is a higher percentage of activated memory CD4 T cells and a lower percentage of resting memory CD4 cells in advanced-stage plaques. Moreover, activation of memory CD4 T cells can promote the development of carotid atherosclerotic plaques. Additionally, FOXP3+ Treg cell maturation can also participate in the progression of carotid plaques. [ABSTRACT FROM AUTHOR]

Background: Gadolinium enhancement on high resolution magnetic resonance imaging (HR-MRI) has been considered a sign of instability and inflammation of intracranial atherosclerotic plaques. Our research objective was to explore the relationship between the extent of plaque enhancement (PE), the degree of intracranial artery stenosis, and acute ischemic stroke events. Methods: HR-MRI was performed in 91 patients with intracranial vascular stenosis to determine the existence and intensity of PE. Results: Among 91 patients enrolled in the trial, there were 43 patients in the acute/subacute group (≤1 month from ischemic stroke event), 15 patients in the chronic group (>1 month from ischemic stroke event), and 33 patients in the non-culprit plaques group (no ischemic stroke event). A total of 105 intracranial atherosclerotic plaques were detected in 91 patients. 14 (13.3%) were mild-stenosis plaques, 22 (21.0%) were moderate-stenosis plaques, and 69 (65.7%) were severe-stenosis plaques. There were 12 (11.4%), 18 (17.1%), and 75 (71.4%) plaques in the non-enhanced plaque group, the mild-enhancement group, and the significant-enhancement group, respectively. The degree of PE among the acute/subacute group, the chronic group, and the non-culprit plaque group had a significant difference (P = 0.005). Enhanced plaques were more often observed in culprit plaques (acute/subacute group and chronic group) than non-culprit plaques (96.7% vs 77.3%). Non-enhanced plaques were more often observed in non-culprit plaques than culprit plaques (acute/subacute group and chronic group) (22.7% vs 3.3%). And 36.6% of the enhanced plaques were non-culprit plaques. After performing univariate and multivariate logistic regression analysis, the results showed that strong plaque enhancement (P = 0.025, odds ratio [OR] 3.700, 95% confidence interval [95% CI] 1.182–11.583) and severe stenosis (P = 0.008, OR 4.393, 95%CI 1.481–13.030) were significantly associated with acute ischemic events. Conclusion: Enhanced plaques were more often observed in culprit plaques, and non-enhanced plaques were more often observed in non-culprit plaques. Moreover, significant plaque enhancement and severe ICAS were closely associated with acute ischemic events. [ABSTRACT FROM AUTHOR]

Atherosclerosis is one of the leading causes of mortality and morbidity worldwide. Chemokines and their receptors are implicated in the pathogenesis of atherosclerosis. CXCL12 is a member of the chemokine family exerting a myriad role in atherosclerosis through its classical CXCR4 and atypical ACKR3 (CXCR7) receptors. The modulatory and regulatory functional spectrum of CXCL12/CXCR4/ACKR3 axis in atherosclerosis spans from proatherogenic, prothrombotic and proinflammatory to atheroprotective, plaque stabilizer and dyslipidemia rectifier. This diverse continuum is executed in a wide range of biological units including endothelial cells (ECs), progenitor cells, macrophages, monocytes, platelets, lymphocytes, neutrophils and vascular smooth muscle cells (VSMCs) through complex heterogeneous and homogenous coupling of CXCR4 and ACKR3 receptors, employing different downstream signalling pathways, which often cross-talk among themselves and with other signalling interactomes. Hence, a better understanding of this structural and functional heterogeneity and complex phenomenon involving CXCL12/CXCR4/ACKR3 axis in atherosclerosis would not only help in formulation of novel therapeutics, but also in elucidation of the CXCL12 ligand and its receptors, as possible diagnostic and prognostic biomarkers. The role of CXCL12 per se is proatherogenic in atherosclerosis development and progression. The CXCL12 receptors, CXCR4 and ACKR3 perform both proatherogenic and athero-protective functions in various cell types Due to functional heterogeneity and cross talk of CXCR4 and ACKR3 at receptor level and downstream pathways, regional boosting with specific temporal and spatial modulators of CXCL12, CXCR4 and ACKR3 need to be explored. [ABSTRACT FROM AUTHOR]

There is increasing concern regarding cardiovascular risk in non-alcoholic fatty liver disease (NAFLD) patients with liver fibrosis. This study aims: (1) to assess the association between NAFLD and liver fibrosis status and the development of carotid plaque (CP), and (2) to identify CP risk factors among general population with different baseline NAFLD and liver fibrosis status. This retrospective cohort study included 14,288 adult participants who went for regular health check-ups between 2014 and 2019, in one hospital in Zhejiang, China. NAFLD was diagnosed by abdominal ultrasound and the NAFLD fibrosis score (NFS) was calculated to reflect the extent of liver fibrosis. Cox proportional hazards analyses were applied to assess the risk of CP development across groups with different baseline NAFLD and NFS status. NAFLD participants with high NFS had higher risk of CP compared to non-NAFLD participants (adjusted hazard ratio 1.68, 95% confidence interval [CI] 1.43–1.96, p <.001). Progression from NAFLD free and NAFLD with low NFS to NAFLD with high NFS are associated with 1.56-fold (95% CI 1.21–2.01, p =.001) and 1.43-fold (95% CI 1.11-1.84, p =.006) increased risk of CP, respectively. Risk factors associated with CP vary based on baseline NAFLD and NFS status. Among NAFLD participants with high NFS, hypertension is the only significant risk factor after adjustment for other potential influencing factors. NAFLD and liver fibrosis status can be an independent predictor for CP development regardless of metabolic abnormalities. Hypertension is a major risk factor for CP development among NAFLD patients with high NFS. Non-alcoholic fatty liver disease (NAFLD) and liver fibrosis status can be an independent predictor for development of carotid plaque. Progression from NAFLD free and NAFLD with low NAFLD fibrosis score (NFS) to NAFLD with high NFS are associated with increased risk of carotid plaque. Risk factors associated with carotid plaque vary based on baseline NAFLD and NFS status, and hypertension plays the most important role among patients with NAFLD and high NFS. [ABSTRACT FROM AUTHOR]

Background and aim: Since the relation between Helicobacter pylori (H. pylori) and atherosclerosis has been evidenced, we aimed to analyze whether there is a relationship between the patient's H. pylori infection and age, gender, BMI, blood lipids, and carotid plaque formation. Methods: 810 patients from January 2016 to December 2019 were enrolled in this study, and divided the subjects into H. pylori (+) group and H. pylori (-) group based on the results of UBT. To analyze whether H. pylori infection is related to gender, age, BMI, blood lipids, and neck vascular plaque formation. Results: The single-factor analysis showed that the BMI ≥ 25kg/m2, triglycerides >1.7 mmol/l, the formation of cervical plaques were significantly higher in patients infected with H. pylori in compared to normal cases. Also, multi-variant logistic regression analysis showed that H. pylori infection affects the BMI ≥ 25kg/m2 and triglycerides >1.7 mmol/l to induce vascular plaque. Also, we showed that patients with H. pylori infection are 1.424 times higher than the non-infected group to have triglycerides more elevated than 1.7mmol/l. Conclusion: In this study, we conclude that H. pylori infection is an independent risk factor for higher BMI (>25), triglyceride (>1.7 mmol/l), and neck vascular plaque formation. The multi-variant analysis showed that patients with H. pylori infection are prone to have higher BMI, triglycerides, and neck vascular plaque formation over 1.4-times higher in non-infected individuals. H. pylori infection is an independent risk factor for higher BMI, triglyceride, and neck vascular plaque formation. H. pylori can accelerate vascular plaque formation through increasing BMI and triglyceride. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a condition in human circulatory, where the arteries become narrowed and hardened due to accumulation of plaque around artery wall. The growth of the disease is slow and asymptomatic. Currently, imaging methods are applied for predicting the disease progression; however, they are deficient in the required resolution and sensitivity for detection. In this work, clinical observations and habits of individuals are considered for assorting the pathologic community. Intelligent machine learning technique, decision tree forest is used for assorting the individuals. A case study was made in this work regarding the atherosclerosis disease progression and crucial features were extracted. Optimised missing value imputation strategy, iterative principal component analysis for STULONG data-set and efficient feature subset selection method, hybrid fast correlation-based filter (FCBF) have been employed for extracting the relevant features and ignoring the redundant features. Further proceeding with the methodology, our work has outperformed with extreme overall accuracy of about 99.47% compared with other state-of-the-art machine learning techniques. [ABSTRACT FROM PUBLISHER]

Cardiovascular diseases (CVDs) remain leading causes of death worldwide. While platelet-mediated thrombus formation following the rupture of an atherosclerotic plaque is one of the key pathophysiologic events in CVDs, the role of platelets in previous or more advanced stages of atherosclerosis is less known. Interestingly, the presence of platelets has been observed at the core of the atherosclerotic plaque. In order to study the conditions necessary for platelets to migrate toward an atherosclerotic lesion, we designed an in vitro co-culture model. Platelets were co-cultured with monocytes in Transwell inserts covered with a confluent endothelium and the number of migrating platelets and/or monocytes was determined under different conditions. Platelets were also exposed to media conditioned obtained from co-cultures prior to migration assays. Here we show that coculturing platelets and monocytes increased platelet transmigration, with a considerable number of transmigrated platelets found not associated to monocytes. Interestingly, conditioned media from platelet-monocyte co-cultures also increased platelet transmigration and aggregation, suggesting the existence of soluble factors secreted by monocytes that enhance the migratory and pro-aggregating capabilities of platelets. We conclude that platelets have the machinery to migrate through an activated endothelium, a response that requires the interaction with secreted factors produce in the context of the interaction with monocytes under atherogenic conditions. [ABSTRACT FROM AUTHOR]

To characterize atherogenesis functionally, we studied the functional heterogeneity of endotheliocytes in carotid vessels with atherosclerotic plaques and identified several distinct cell clusters. We measured the Ki-67 labeling index (Ki-67 LI), percentage of Bcl-2 cells (CP) and expression of CCL5, IL 6 and VCAM1 in each cell cluster. We also investigated how these indicators change when the plaque becomes unstable and how they affect the risk of adverse cerebrovascular events in patients. We evaluated the inter-cluster gradient of marker activity and its relation to patient prognosis. We identified five endothelial clusters: the under plaque cluster (UPC), peripheral cluster (PC), marginal cluster (MC), transient cluster (TC) and outside plaque cluster (OC). The UPC exhibited the greatest proliferative, proinflammatory and adhesive activity, but low anti-apoptotic activity. The PC exhibited the second greatest proliferative, adhesive and proinflammatory activity. Progression of atherosclerosis and transition of a stable atherosclerotic plaque to an unstable one was accompanied by increased expression of nearly all markers. The proliferative activity in the UPC, PC and OC, and the pro-inflammatory activity in UPC and anti-apoptotic activity in the PC, were correlated with prognosis. Also, two gradients of proliferative activity and a gradient of pro-inflammatory activity were associated with risk of adverse events. [ABSTRACT FROM AUTHOR]