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

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

Amyloid plaques composed of fibrils of misfolded Aβ peptides are pathological hallmarks of Alzheimer\'s disease (AD). Aβ fibrils are polymorphic in their tertiary and quaternary molecular structures. This structural polymorphism may carry different pathologic potencies and can putatively contribute to clinical phenotypes of AD. Therefore, mapping of structural polymorphism of Aβ fibrils and structural evolution over time is valuable to understanding disease mechanisms. Here, we investigated how Aβ fibril structures in situ differ in Aβ plaque of different mouse models expressing familial mutations in the AβPP gene. We imaged frozen brains with a combination of conformation-sensitive luminescent conjugated oligothiophene (LCO) ligands and Aβ-specific antibodies. LCO fluorescence mapping revealed that mouse models APP23, APPPS1, and AppNL-F have different fibril structures within Aβ-amyloid plaques depending on the AβPP-processing genotype. Co-staining with Aβ-specific antibodies showed that individual plaques from APP23 mice expressing AβPP Swedish mutation have two distinct fibril polymorph regions of core and corona. The plaque core is predominantly composed of compact Aβ40 fibrils, and the corona region is dominated by diffusely packed Aβ40 fibrils. Conversely, the AβPP knock-in mouse AppNL-F, expressing the AβPP Iberian mutation along with Swedish mutation has tiny, cored plaques consisting mainly of compact Aβ42 fibrils, vastly different from APP23 even at elevated age up to 21 months. Age-dependent polymorph rearrangement of plaque cores observed for APP23 and APPPS1 mice >12 months, appears strongly promoted by Aβ40 and was hence minuscule in AppNL-F. These structural studies of amyloid plaques in situ can map disease-relevant fibril polymorph distributions to guide the design of diagnostic and therapeutic molecules.

OBJECTIVE: The relationship between high-risk coronary plaque characteristics regardless of the severity of lesion stenosis and myocardial ischemia remains unsettled. High-intensity plaques (HIPs) on non-contrast T1-weighted magnetic resonance imaging (T1WI) have been characterized as high-risk coronary plaques. We sought to elucidate whether the presence of coronary HIPs on T1WI influences fractional flow reserve (FFR) in the distal segment of the vessel.
METHODS: We retrospectively analyzed 281 vessels in 231 patients with chronic coronary syndrome who underwent invasive FFR measurement and coronary T1WI using a multicenter registry. The plaque-to-myocardial signal intensity ratio (PMR) of the most stenotic lesion was evaluated; a coronary plaque with PMR ≥1.4 was defined as a HIP.
RESULTS: The median PMR of coronary plaques on T1WI in vessels with FFR ≤0.80 was significantly higher than that of plaques with FFR >0.80 (1.17 [interquartile range (IQR): 0.99-1.44] vs. 0.97 [IQR: 0.85-1.09]; p < 0.001). Multivariable analysis showed that an increase in PMR of the most stenotic segment was associated with lower FFR (beta-coefficient, -0.050; p < 0.001). The presence of coronary HIPs was an independent predictor of FFR ≤0.80 (odds ratio (OR), 6.18; 95% confidence interval (CI), 1.93-19.77; p = 0.002). Even after adjusting for plaque composition characteristics based on computed tomography angiography, the presence of coronary HIPs was an independent predictor of FFR ≤0.80 (OR, 4.48; 95% CI, 1.19-16.80; p = 0.026).
CONCLUSIONS: Coronary plaques with high PMR are associated with low FFR in the corresponding vessel, indicating that plaque morphology might influence myocardial ischemia severity.

UNASSIGNED: To analyze the relationship among distribution location, characteristics, and vulnerability of carotid plaque using CTA and provide more information on the risk factors of carotid atherosclerotic plaque.
UNASSIGNED: We retrospectively analyzed the CTA images of the head and neck of 93 patients with carotid atherosclerosis. Atherosclerosis was developed in 148 carotid arteries. The plaques were divided into a high-risk plaque group and a low-risk plaque group according to whether the plaques had high-risk characteristics. The maximum cross-sectional area of carotid artery bifurcation plaque on the axial image was selected, and the cross-sectional lumen was equally divided into four 90-degree sectors, ventral side wall, dorsal side wall, inner side wall, and outer side wall. The differences in the characteristics and distribution locations of the plaques in the two groups were analyzed. The characteristic parameters of the cross-sectional plaques at the bifurcation of the carotid artery. The logistic regression analysis was used to further analyze the risk factors associated with plaque vulnerability.
UNASSIGNED: Among 148 carotid arteries,80 were classified as high-risk and 68 as low-risk groups. There were significant differences between the two groups concerning the thickness, length, maximum cross-sectional area, burden, and cross-sectional distribution of the plaques (P < 0.05). The plaque distribution on the dorsal side wall of the carotid bifurcation was higher in the high-risk group than that in the low-risk group (P < 0.05), dorsal side wall plaque-independent risk factors for the development of vulnerability of plaques in transient ischemic attack (TIA) patients (95% CI:1.522~6.991, P<0.05).
UNASSIGNED: High-risk plaques tend to occur on the dorsal side wall of the carotid bifurcation, whereas low-risk plaques tend to occur on the outer side wall of the carotid bifurcation.

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Bacteriophages, or phages, are viruses that infect bacteria shaping microbial communities and ecosystems. They have gained attention as potential agents against antibiotic resistance. In phage therapy, lytic phages are preferred for their bacteria killing ability, while temperate phages, which can transfer antibiotic resistance or toxin genes, are avoided. Selection relies on plaque morphology and genome sequencing. This review outlines annotating genomes, identifying critical genomic features, and assigning functional labels to protein-coding sequences. These annotations prevent the transfer of unwanted genes, such as antimicrobial resistance or toxin genes, during phage therapy. Additionally, it covers International Committee on Taxonomy of Viruses (ICTV)-an established phage nomenclature system for simplified classification and communication. Accurate phage genome annotation and nomenclature provide insights into phage-host interactions, replication strategies, and evolution, accelerating our understanding of the diversity and evolution of phages and facilitating the development of phage-based therapies.

OBJECTIVE: To investigate the differences in serum iron index and iron metabolizing protein expression in plaques in patients with different degrees of carotid artery stenosis and the relationship with plaque traits.
METHODS: A total of 100 patients eligible for carotid endarterectomy (CEA) from August 2021 to February 2022 were included. Patients completed a computed tomography (CTA) scan for patient grouping and a magnetic resonance imaging (MRI) for precise quantification of carotid plaque traits within 1 week prior to surgery. Clinical indicators associated with the progression of carotid stenosis to occlusion were analyzed using ordered logistic regression. Twenty carotid plaques were analyzed immunohistochemically to investigate the relationship between plaque traits and the iron metabolism indexes.
RESULTS: No significant correlation between high serum ferritin (SF), unsaturated iron binding capacity (UIBC) and progression of carotid stenosis (OR 1.100, 95% CI 0.004-0.165, p = 0.039; OR 1.050, 95% CI 0.005-0.094, p = 0.031). SF and serum transferrin receptor (sTfR) were correlated with normalized wall index (NWI) (R = 0.470, p = 0.036; R = 0.449, p = 0.046), and the results of multiple linear regression suggested that SF and sTfR remained associated with NWI (R = 0.630, R2 = 0.397, Adjusted R2 = 0.326, p = 0.014). In plaques, H-type ferritin (H-FT) was correlated with NWI and lipid-rich necrotic core (LRNC) volume (R = 0.502, p = 0.028; R = 0.468, p = 0.043). Transferrin receptor 1 (TfR1) was correlated with LRNC volume and intraplaque hemorrhage (IPH) volume (R = 0.538, p = 0.017; R = 0.707, p = 0.001).
CONCLUSIONS: There were statistical differences in the expression of iron metabolism proteins in carotid plaques with different degrees of stenosis. Serum iron metabolism index (SF and sTfR) and expression of iron metabolizing proteins (H-FT and TfR1) in plaques were positively correlated with carotid plaque vulnerability index (NWI, LRNC volume).

Inhibition of Renin-Angiotensin-Aldosterone-System (RAAS) has been hypothesized to improve endothelial function and reduce plaque inflammation, however, their impact on the progression of coronary atherosclerosis is unclear. We aim to study the effects of RAAS inhibitor on plaque progression and composition assessed by serial coronary CT angiography (CCTA).
We performed a prospective, multinational study consisting of a registry of patients without history of CAD, who underwent serial CCTAs. Patients using RAAS inhibitors were propensity matched to RAAS inhibitor naïve patients based on clinical and CCTA characteristics at baseline. Atherosclerotic plaques in CCTAs were quantitatively analyzed for percent atheroma volume (PAV) according to plaque composition. Interactions between RAAS inhibitor use and baseline PAV on plaque progression were assessed in the unmatched cohort using a multivariate linear regression model.
Of 1248 patients from the registry, 299 RAAS inhibitor taking patients were matched to 299 RAAS inhibitor naïve patients. Over a mean interval of 3.9 years, there was no significant difference in annual progression of total PAV between RAAS inhibitor naïve vs taking patients (0.75 vs 0.79%/year, p = 0.66). With interaction testing in the unmatched cohort, however, RAAS inhibitor use was significantly associated with lower non-calcified plaque progression (Beta coefficient -0.100, adjusted p = 0.038) with higher levels of baseline PAV.
The use of RAAS inhibitors over a period of nearly 4 years did not significantly impact on total atherosclerotic plaque progression or various plaque components. However, interaction testing to assess the differential effect of RAAS inhibition based on baseline PAV suggested a significant decrease in progression of non-calcified plaque in patients with a higher burden of baseline atherosclerosis, which should be considered hypothesis generating.

Drug-coated balloon (DCB) became a potential treatment option for patients with acute coronary syndrome (ACS); however, factors associated with target lesion failure (TLF) remain uncertain.
This retrospective, multicentre, observational study included consecutive ACS patients who underwent optical coherence tomography (OCT)-guided DCB treatment. Patients were divided into two groups according to the occurrence of TLF, a composite of cardiac death, target vessel-related myocardial infarction, and ischemia-driven target lesion revascularisation.
We enrolled 127 patients in this study. During the median follow-up period of 562 (IQR: 342-1164) days, 24 patients (18.9%) experienced TLF, and 103 patients (81.1%) did not. The cumulative 3-year incidence of TLF was 22.0%. The cumulative 3-year incidence of TLF was the lowest in patients with plaque erosion (PE) (7.5%), followed by those with rupture (PR) (26.1%) and calcified nodule (CN) (43.5%). Multivariable Cox regression analysis revealed that plaque morphology was independently associated with TLF on pre-PCI (percutaneous coronary intervention) OCT, and residual thrombus burden (TB) was positively associated with TLF on post-PCI OCT. Further stratification by post-PCI TB revealed a comparable incidence of TLF in patients with PR (4.2%) to that of PE if the culprit lesion had a smaller post-PCI TB than the cut-off value (8.4%). TLF incidence was high in patients with CN, regardless of TB size on post-PCI OCT.
Plaque morphology was strongly associated with TLF for ACS patients after DCB treatment. Residual TB post-PCI might be a key determinant for TLF, especially in patients with PR.