Plaque Location Research Articles

Artificial intelligence applied to coronary artery calcium scans (AI-CAC) significantly improves cardiovascular events prediction

Coronary artery calcium (CAC) scans contain valuable information beyond the Agatston Score which is currently reported for predicting coronary heart disease (CHD) only. We examined whether new artificial intelligence (AI) applied to CAC scans can predict non-CHD events, including heart failure, atrial fibrillation, and stroke. We applied AI-enabled automated cardiac chambers volumetry and calcified plaque characterization to CAC scans (AI-CAC) of 5830 asymptomatic individuals (52.2% women, age 61.7 ± 10.2 years) in the multi-ethnic study of atherosclerosis during 15 years of follow-up, 1773 CVD events accrued. The AUC at 1-, 5-, 10-, and 15-year follow-up for AI-CAC vs. Agatston score was (0.784 vs. 0.701), (0.771 vs. 0.709), (0.789 vs. 0.712) and (0.816 vs. 0.729) (p < 0.0001 for all), respectively. AI-CAC plaque characteristics, including number, location, density, plus number of vessels, significantly improved CHD prediction in the CAC 1–100 cohort vs. Agatston Score. AI-CAC significantly improved the Agatston score for predicting all CVD events.

Coronary artery plaque characteristics in smokers assessed by intracoronary multi-modality imaging: a NIRS-IVUS guided PROSPECT II substudy

Abstract Background Smoking is a risk factor for coronary artery disease and myocardial infarction. Purpose Among patients with myocardial infarction, we hypothesized smokers would have increased prevalence of nonculprit high-risk plaque characteristics as assessed by intracoronary multimodality imaged when compared to nonsmokers. Method This is a prespecified post-hoc analysis of the PROSPECT II (Providing Regional Observations to Study Predictors of Events in the Coronary Tree). Altogether 898 patients with acute myocardial infarction with or without ST-segment elevation who after successful percutaneous coronary intervention had near-infrared spectroscopy and intravascular ultrasound imaging performed. Data on lesion location, plaque burden, and lipid content were collected. Current, former, and nonsmokers were examined regarding the presence of high-risk plaques in both culprit and nonculprit lesions as well as plaque location. High-risk plaque characteristics were defined as a maximum plaque burden (maxPB) of ≥70% and a maximum 4 mm lipid core burden index (maxLCBI4mm) of ≥324.7. Results Out of 886 patients with known smoking history, 32% were smokers, 32% former, and 37% nonsmokers. Smokers were younger (median age: smokers 59.0; former 65.5; nonsmokers 64.0 years, p&amp;lt;0.001) with fewer co-morbidities and presented more often with STEMI (% presenting with STEMI: smokers 22.2%; former 18.9%; nonsmokers 19.4%, p=0.006). LDL was similar but CRP was higher in smokers (median µg/mL: smokers 4.0; former 3.1; nonsmokers 2.9, p=0.004). In multivariate models of nonculprit lesion morphology smoking history was not associated with maxPB or maxLCBI4mm but was associated with presence of calcified nodules (OR: 2.88 (95% CI 1.46–5.69) p=0.002 [smokers vs nonsmokers]). Calcified nodules were also associated with number of years smoked (OR: 1.02 (95% CI 1.01–1.03) p=0.004). Smoking was not associated with presence of ≥1 lesions with MaxLCBI4mm, ≥ 324.7, maxPB &amp;gt;=70% or the combination of both. Smoking was not associated with presence of plaque rupture or thrombus. Right coronary artery culprit lesions were more common in smokers and former smokers (smokers 29.9%; former 30.9%; nonsmokers 21.6%; OR: 1.12 (95% CI 1.04–1.21) p&amp;lt;0.001 [smokers vs nonsmokers]). Conclusion In this prospective intracoronary multimodality imaging study of patients with recent acute myocardial infarction, smoking was not associated with a higher rate of high-risk nonculprit plaques based on lipid content by NIRS or PB by IVUS when compared to former or nonsmokers. However, smoking was associated with higher presence of IVUS-detected calcified nodules, higher CRP-levels, and the right coronary artery as it angiographically was a more common site for culprit lesions. These results indicate that the elevated risk in smokers is unrelated to vulnerable plaque morphology defined by high PB and lipid content, and instead possibly related to inflammation, calcification, or hemodynamic changes.Table 1

Location-specific prognostic significance of plaque burden, stenosis, and plaque morphology in coronary artery disease

Abstract Background The prognostic significance of coronary plaque localization, percentage atheroma volume (PAV), stenosis, and plaque morphology has been underexplored. Purpose To investigate the prognostic significance of plaque localization beyond plaque burden, presence of stenosis and plaque morphology. Methods Patients with no cardiac history who underwent coronary CTA were included. PAV, maximum diameter stenosis, and plaque morphology were assessed and classified into proximal, mid, or distal segments of the coronary tree. Major adverse cardiac events (MACE) were defined as death or non-fatal myocardial infarction. Results Among 2819 patients 267 events (9.5%) occurred during a median follow-up of 6.9 years. PAV of the proximal segments was strongly correlated to PAV localized at of the mid (R= 0.76) and distal segments (R = 0.74, p &amp;lt; 0.01 for both). When adjusted for traditional risk factors and presence of plaque on other locations, only proximal PAV was independently associated with MACE (3rd quartile HR 2.08, 95% 1.17–3.71, p=0.01 and 4th quartile HR 2.29, 95% CI 1.21–4.34, p=0.01). Similar results were seen for presence of stenosis. Proximal, mid, and distal PAV as a solitary metric (unadjusted) had similar predictive value for MACE with an AUC of 0.73 (95% CI 0.69-0.76) for proximal PAV and 0.72 (95% CI 0.68-0.76) for both mid and distal localized plaque). Similar results were obtained using diameter stenosis instead of PAV. The presence of low-attenuation plaque (LAP) in the proximal segments had additional prognostic value. Calcified or noncalcified PAV did not provide additional value beyond total location-specific PAV and presence of low-attenuation plaque. Conclusions Proximal located PAV is an independent predictor of death and non-fatal MI, while there was no incremental prognostic value of plaque localized at the mid or distal coronary segments. The presence of LAP in the proximal segments provided additional prognostic value for prediction of MACE.

Plaque characteristics and long-term outcome of non-culprit plaque rupture in AMI patients

Abstract Background Non-culprit plaque rupture (PR) had widespread nature in patients with acute coronary syndrome, indicating generalized acute destabilization. However, morphological features and long-term outcomes of non-culprit PR in acute myocardial infarction (AMI) patients have not been systemically investigated. Objectives We aimed to investigate the pancoronary picture (plaque characteristics and location) and long-term outcomes of non-culprit PR in AMI patients. Methods From January 2017 to May 2019, 3757 non-culprit plaques were analyzed in 883 AMI patients treated by 3-vessel optical coherence tomography. Patients and lesions were divided into two groups based on the presence or absence of non-culprit PR. All patients enrolled were followed for up to four years. Results Non-culprit PR was found in 178 patients (20.2%) and 200 lesions (5.3%). Patients with non-culprit PR had a more non-culprit lesions (NCLs) (p &amp;lt; 0.001), diseased arteries (p &amp;lt; 0.001) and multi-vessel disease (p &amp;lt; 0.001) compared with patients without non-culprit PR, both in angiography and OCT analyses. In vulnerable plaque feature, non-culprit PR group had higher incidence of thin-cap fibroatheroma (TCFA) (p &amp;lt; 0.001; p &amp;lt; 0.001), minimal lumen area (MLA) &amp;lt; 3.5mm² (p = 0.004; p = 0.012), CLIMA-defined high-risk plaque (p &amp;lt; 0.001; p &amp;lt; 0.001), thrombus (p &amp;lt; 0.001; p &amp;lt; 0.001), lipid rich plaque (p &amp;lt; 0.001; p &amp;lt; 0.001), calcification (p &amp;lt; 0.001; p &amp;lt; 0.001), macrophage (p &amp;lt; 0.001; p &amp;lt; 0.001), microchannel (p &amp;lt; 0.001; p &amp;lt; 0.001), cholesterol crystals (p &amp;lt; 0.001; p &amp;lt; 0.001), and layered tissue (p &amp;lt; 0.001; p &amp;lt; 0.001) compared with the other group, in patient and lesion level. In addition, non-culprit PR was highly populated at "hot spots" in the right coronary artery (56.5% vs. 40.2%; p &amp;lt; 0.001), and the originally treated culprit artery (33.5% vs. 25.2%; p = 0.008), and tended to cluster proximal to the coronary ostium [26.1 (15.5-38.0) vs. 29.4 (15.8-44.5); p = 0.009]. Multivariate analysis identified the NCL in the initially treated culprit artery (odds ratio [OR]: 1.874, 95% confidence interval [CI]: 1.230–2.857, p = 0.003), distance from coronary ostium to MLA site (OR: 0.987, 95% CI: 0.978–0.997, p = 0.008), mean lipid arc (OR: 1.006, 95% CI: 1.003–1.010, p = 0.001), TCFA (OR: 15.870, 95% CI: 10.259–24.551, p &amp;lt; 0.001), thrombus (OR: 4.333, 95% CI: 2.346–8.003, p &amp;lt; 0.001), and microchannel (OR: 1.679, 95% CI: 1.136–2.482, p = 0.009) were independent predictors of non-culprit PR. Non-culprit PR showed higher 4-year rates of NCL-related major adverse cardiac events in the patient (14.0% vs. 5.1%; p = 0.001) and lesion (6.5% vs. 0.9%; p &amp;lt; 0.001) levels. Conclusions NCLs with non-culprit PR had a unique pancoronary picture (pancoronary vulnerability and "hot spots") and worse long-term outcomes in AMI patients.

Research on carotid artery plaque anomaly detection algorithm based on ultrasound images

Carotid artery plaque is a key factor in stroke and other cardiovascular diseases. Accurate detection and localization of carotid artery plaque are essential for early prevention and treatment of diseases. However, current carotid artery ultrasound image anomaly detection algorithms face several challenges, such as scarcity of anomaly data in carotid arteries and traditional convolutional neural networks (CNNs) overlooking long-distance dependencies in image processing. To address these issues, we propose an anomaly detection algorithm for carotid artery plaques based on ultrasound images. The algorithm innovatively introduces an anomaly sample pair generation method to increase dataset diversity. Moreover, it employs an improved adaptive recursive gating pyramid pooling module to extract image features. This module significantly enhances the model’s capacity for high-order spatial interactions and adaptive feature fusion, thereby greatly improving the neural network’s feature extraction ability. The algorithm uses a Sigmoid layer to map each pixel’s feature vector to a probability distribution between 0 and 1, and anomalies are detected through probability threshold binarization. Experimental results show that our algorithm’s AUROC index reached 90.7% on a carotid artery dataset, improving by 2.1% compared to the FPI method. This research is expected to provide robust support for the early prevention and treatment of cardiovascular diseases.

Location-Specific Prognostic Significance of Plaque Burden, Stenosis, and Plaque Morphology in Coronary Artery Disease.

To investigate the location-specific prognostic significance of plaque burden, diameter stenosis and plaque morphology. Patients without a documented cardiac history who underwent coronary computed tomography angiography (CCTA) for suspected coronary artery disease were included. Percentage atheroma volume (PAV), maximum diameter stenosis, and plaque morphology were assessed and classified into proximal, mid, or distal segments of the coronary tree. Major adverse cardiac events (MACE) were defined as death or non-fatal myocardial infarction. Among 2819 patients 267 events (9.5%) occurred during a median follow-up of 6.9 years. When adjusted for traditional risk factors and presence of PAV on other locations, only proximal PAV was independently associated with MACE. However, PAV of the proximal segments was strongly correlated to PAV localized at the mid (R= 0.76) and distal segments (R=0.74, p<0.01 for both). When only adjusted for cardiovascular risk factors, the area under the curve (AUC) to predict MACE for proximal PAV was 0.73 (95%CI 0.69-0.76), which was similar compared to mid PAV (AUC 0.72, 95%CI 0.68-0.76) and distal PAV (AUC 0.72, 95%CI 0.68-0.76). Similar results were obtained using diameter stenosis instead of PAV. The presence of proximal low-attenuation plaque had borderline additional prognostic value. Proximal PAV was the strongest predictor of MACE when adjusted for cardiovascular risk factors and plaque at other locations. However, when presence of plaque was only adjusted for cardiovascular risk factors, proximal, mid, and distal plaque localization showed a similar predictive ability for MACE.

Numerical simulation of non-Newtonian blood flow in a human arterial bifurcation model

Hemodynamic factors play a role in atherogenesis and the localization of atherosclerotic plaques. The human aorta and coronary arteries are susceptible to arterial disease, and there have been many studies of flows in models of these vessels. Atherosclerosis is a systemic disease occurring in specific sections of the cardiovascular tree such as the carotid and the coronary arteries. This paper aims to simulate the human arterial bifurcation and investigates some hemodynamic parameters as blood propagates from the aortic artery toward the carotid artery. We analyze the velocity, static pressure, shear stress. The simulation results showed disturbed flow patterns, such as flow separation and stagnation, as well as abnormal hemodynamic parameters (HPs) distributions including the low and high wall shear stress (WSS) and oscillation of wall shear stress. Based on our simulating characteristic results, the CFD tools can not only monitor the hemodynamic parameters obviously, but also help to analyze the diagnostic for the treatment of vascular diseases. CFD can be an effective technology for the examination and treatment of patients with failure of blood supply of the head and brain.

Prognostic value of angiographic based quantitative flow ratio and anatomic features in intracranial atherosclerotic stenosis

BackgroundPatients with intracranial atherosclerotic stenosis (ICAS) are prone to stroke recurrence despite aggressive medical treatment. Further assessment of the anatomy and physiology of ICAS is urgently needed to facilitate individualized...

Relationship between carotid atherosclerosis and localization of ischemic stroke

Background. Carotid atherosclerosis is the main factor in the development of ischemic stroke. Determining the location and structure of atherosclerotic plaques and the degree of stenosis of the internal carotid artery can help to predict the development of cerebral hemodynamic disorders using a comprehensive ultrasound examination of the carotid arteries. Purpose. To assess the relationship between the nature of atherosclerosis of the carotid arteries and the location of ischemic stroke by means of echography. Materials and methods. In 127 patients (age 37–74 years, average 56±7 years) with ischemic stroke (IS), atherosclerotic plaques in the carotid arteries were visualized, their predominant localization, internal structure and degree of stenosis were determined in two-dimensional and color Doppler modes. Result. Carotid stenosis of &gt;60% was recorded in 23 (18.1±3.4%) patients with rightsided IS and in 38 (30.0±4.1%) patients with left-sided IS (LSIS) (p=0.04). With carotid stenosis more than 60%, the Vica/Vcca index in patients with RSIS was 3.07±0.34, and in patients with LSIS – 3.21±0.45, which was significantly (p=0,01) higher than in stenosis &lt;60%.

AI-enabled Cardiac Chambers Volumetry and Calcified Plaque Characterization in Coronary Artery Calcium (CAC) Scans (AI-CAC) Significantly Improves on Agatston CAC Score for Predicting All Cardiovascular Events: The Multi-Ethnic Study of Atherosclerosis.

Coronary artery calcium (CAC) scans contain valuable information beyond the Agatston Score which is currently reported for predicting coronary heart disease (CHD) only. We examined whether new artificial intelligence (AI) algorithms applied to CAC scans may provide significant improvement in prediction of all cardiovascular disease (CVD) events in addition to CHD, including heart failure, atrial fibrillation, stroke, resuscitated cardiac arrest, and all CVD-related deaths. We applied AI-enabled automated cardiac chambers volumetry and automated calcified plaque characterization to CAC scans (AI-CAC) of 5830 individuals (52.2% women, age 61.7±10.2 years) without known CVD that were previously obtained for CAC scoring at the baseline examination of the Multi-Ethnic Study of Atherosclerosis (MESA). We used 15-year outcomes data and assessed discrimination using the time-dependent area under the curve (AUC) for AI-CAC versus the Agatston Score. During 15 years of follow-up, 1773 CVD events accrued. The AUC at 1-, 5-, 10-, and 15-year follow up for AI-CAC vs Agatston Score was (0.784 vs 0.701), (0.771 vs. 0.709), (0.789 vs.0.712) and (0.816 vs. 0.729) (p<0.0001 for all), respectively. The category-free Net Reclassification Index of AI-CAC vs. Agatston Score at 1-, 5-, 10-, and 15-year follow up was 0.31, 0.24, 0.29 and 0.29 (p<.0001 for all), respectively. AI-CAC plaque characteristics including number, location, and density of plaque plus number of vessels significantly improved NRI for CAC 1-100 cohort vs. Agatston Score (0.342). In this multi-ethnic longitudinal population study, AI-CAC significantly and consistently improved the prediction of all CVD events over 15 years compared with the Agatston score.

Predicting vulnerable carotid plaques by detecting wall shear stress based on ultrasonic vector flow imaging

ObjectiveCarotid plaque vulnerability is a significant factor in the risk of cardiocerebrovascular events, with intraplaque neovascularization (IPN) being a crucial characteristic of plaque vulnerability. This study investigates the value of ultrasound vector flow imaging (V-flow) for measuring carotid plaque wall shear stress (WSS) in predicting the extent of IPN. MethodsWe enrolled 140 patients into three groups: 53 in the plaque group (72 plaques), 23 in the stenosis group (27 plaques), and 64 in the control group. V-flow was used to measure WSS parameters, including the average WSS (WSS mean) and the maximum WSS (WSS max), across three plaque locations: mid-upstream, maximum thickness, and mid-downstream. Contrast-enhanced ultrasound examination was used in 76 patients to analyze IPN and its correlation with WSS parameters. ResultsWSS max in the stenosis group was significantly higher than that in the control and plaque groups at the maximum thickness part (P < .05) and WSS mean in the stenosis group was significantly lower than that in the control group at the mid-upstream and mid-downstream segments (P < .05). WSS mean in the plaque group was significantly lower than that of the control group at all three locations (P < .05). Contrast-enhanced ultrasound examination revealed that plaques with neovascularization enhancement exhibited significantly higher WSS values (P < .05), with a positive correlation between WSS parameters and IPN enhancement grades, particularly WSS max at the thickest part (r = 0.508). Receiver operating characteristic curve analysis of WSS parameters for evaluating IPN showed that the efficacy of WSS max in evaluating IPN was better than that of WSS mean (P < .05), with an area under the curve of 0.7762 and 0.6973 (95% confidence intervals, 0.725-0.822 and 0.642-0.749, respectively). The cut-offs were 4.57 Pa and 1.12 Pa, sensitivities were 74.03% and 63.64%, and specificities were 75.00% and 68.18%. ConclusionsV-flow effectively measures WSS in carotid plaques. WSS max provides a promising metric for assessing IPN, offering potential insights into plaque characteristics and showing some potential in predicting plaque vulnerability.

Au/FeNiPO4‐Based Multiple Spectra Optoacoustic Tomography/CT Dual‐Mode Nanoprobe for Systemic Screening of Atherosclerotic Vulnerable Plaque

AbstractCurrent diagnostic technique in direct identification of multi‐site plaques and simultaneous assessment of plaque vulnerability remains a challenge, which is crucial for indicating the risk of atherosclerotic cardiovascular diseases (ASCVD). Herein, an osteopontin (OPN)‐specific nanoprobe (OPN Ab‐Au/FeNiPO4@ICG) with both multiple spectra optoacoustic tomography (MSOT) and computed tomography (CT) imaging, is constructed successfully realizing systemic screening of vulnerable plaque. OPN Ab‐Au/FeNiPO4@ICG nanoprobe specifically targeted OPN‐overexpressed foam cells and recognized the vulnerable plaque at the molecular level. In AS mice, CT imaging exhibits that OPN Ab‐Au/FeNiPO4@ICG nanoprobe effectively avoid interference from calcification and accurately visualized AS plaque. MSOT functional imaging results reveals that after the injection of OPN Ab‐Au/FeNiPO4@ICG nanoprobe, the carotid plaque exhibited a much higher MSOT signal than the aortic arch plaque (P = 0.0291). Further pathological analysis displays that the carotid plaque possessed a much higher vulnerability score (P = 0.0247), in agreement with the MSOT signals. More importantly, the linear regression analysis confirms the high correlation between the MSOT signals and plaque vulnerability with R = 0.7095 (P = 0.0216), demonstrating the potential of the proposed nanoprobe in systematic evaluation of plaque vulnerability. This work employs the dual‐model nanoprobe strategy for both plaque localization and vulnerability assessment, greatly advancing the accurate diagnosis of ASCVD.

Significance of atherosclerotic plaque location in recanalizing non-acute long-segment occlusion of the internal carotid artery

To investigate the significance of atherosclerotic plaque location in hybrid surgery comprising both endovascular recanalization approaches and carotid endarterectomy for symptomatic atherosclerotic non-acute long-segment occlusion of the internal carotid artery (ICA), 162 patients were enrolled, including 120 (74.1%) patients in the proximal plaque group and 42 (25.9%) in the distal plaque group. Surgical recanalization was performed in all patients, with successful recanalization in 119 (99.2%) patients in the proximal and 39 (92.9%) in the distal plaque group. The total successful recanalization rate was 97.5% (158/162) with a failure rate of 2.5% (4/162). Periprocedural complications occurred in 5 (4.2% or 5/120) patients in the proximal plaque group, including neck infection in two (1.7%), recurrent nerve injury in 1 (0.8%), and laryngeal edema in 2 (1.7%), and 2 (4.8%) in the distal plaque group, including femoral puncture infection in 2 (4.8%). No severe complications occurred in either group. Univariate analysis showed plaque location was a significant (P = 0.018) risk factor for successful recanalization, and multivariate analysis indicated that the plaque location remained a significant independent risk factor for recanalization success (P = 0.017). In follow-up 6–48 months after the recanalization surgery, reocclusion occurred in two (2.8%) patients in the proximal plaque group and 4 (13.3%) in the distal plaque group. In conclusion, although hybrid surgery achieves similar outcomes in patients with ICA occlusion caused by either proximal or distal atherosclerotic plaques, plaque location may be a significant risk factor for successful recanalization of symptomatic non-acute long-segment ICA occlusion.

Peripheral HMGB1 is linked to O3 pathology of disease-associated astrocytes and amyloid.

Ozone (O3) is an air pollutant associated with Alzheimer's disease (AD) risk. The lung-brain axis is implicated in O3-associated glial and amyloid pathobiology; however, the role of disease-associated astrocytes (DAAs) in this process remains unknown. The O3-induced astrocyte phenotype was characterized in 5xFAD mice by spatial transcriptomics and proteomics. Hmgb1fl/fl LysM-Cre+ mice were used to assess the role of peripheral myeloid cell high mobility group box 1 (HMGB1). O3 increased astrocyte and plaque numbers, impeded the astrocyte proteomic response to plaque deposition, augmented the DAA transcriptional fingerprint, increased astrocyte-microglia contact, and reduced bronchoalveolar lavage immune cell HMGB1 expression in 5xFAD mice. O3-exposed Hmgb1fl/fl LysM-Cre+ mice exhibited dysregulated DAA mRNA markers. Astrocytes and peripheral myeloid cells are critical lung-brain axis interactors. HMGB1 loss in peripheral myeloid cells regulates the O3-induced DAA phenotype. These findings demonstrate a mechanism and potential intervention target for air pollution-induced AD pathobiology. Astrocytes are part of the lung-brain axis, regulating how air pollution affects plaque pathology. Ozone (O3) astrocyte effects are associated with increased plaques and modified by plaque localization. O3 uniquely disrupts the astrocyte transcriptomic and proteomic disease-associated astrocyte (DAA) phenotype in plaque associated astrocytes (PAA). O3 changes the PAA cell contact with microglia and cell-cell communication gene expression. Peripheral myeloid cell high mobility group box 1 regulates O3-induced transcriptomic changes in the DAA phenotype.

Prevalence of primary headaches in multiple sclerosis patients

BackgroundMultiple sclerosis (MS) is the most common immune-mediated inflammatory disease of the central nervous system. It is characterized by symptoms such as visual disturbances, paresis with spasticity, paresthesia, numbness, and fatigue. However, several studies have shown a high prevalence of headaches in individuals with MS. Migraine and tension-type headaches are the most frequent types of headaches experienced by those with MS. Additionally, the role of MS disease-modifying agents must be considered. These agents have different modes of action and side effect profiles, and their use may sometimes trigger headaches in patients with MS. ObjectivesThis study aimed to explore the prevalence and clinical characteristics of primary headaches in MS patients. The relationship between headache and clinical features of MS (Course of MS, duration, EDSS, brain imaging and DMD) are also investigated. Subjects and MethodsTwo hundred and eighty-one MS patients diagnosed according to according to the 2017 revisions to the McDonald Criteria were included in the study. Data was collected from the MS unit medical records and from the interview with the patients. Patients with reported headaches are asked to recall their headache characteristics and patterns using an interviewer administered Arabic language-structured validated questionnaire. ResultsThe median age of patients was 33 years old, with a range of 22–55. Tension-type headache (TTH) was more common in males, patients with more severe disability (EDSS ≥ 3), and those with SPMS and PPMS phenotypes. Additionally, patients on rituximab or cyclophosphamide therapy were more likely to have TTH. On the other hand, females, patients with milder disability (EDSS < 3), and those with RRMS phenotype were more likely to have migraine. This was also true for patients with MRI lesions involving the periaqueductal gray, and those receiving INF or fingolimod (P < 0.05). Periaqueductal gray matter lesions were found in the MRI of 48 patients (40 %) who experienced headaches on more than 10 days per month. Sensorimotor lesions in the brain were found in 55 patients (53.4 %) with severe headaches (p-value < 0.001). Interferons were associated with an increased risk of worsening preexisting headaches and the appearance of de novo headaches related to its intake (odds ratio: 2.84, 3.72; relative risk: 1.63, 2.04; p-value = 0.03, < 0.001, respectively). On the other hand, rituximab was associated with a decreased risk of worsening preexisting headaches and the appearance of de novo headaches related to its intake (odds ratio: 0.04, 0.09; relative risk: 0.11, 0.18; p-value = < 0.001, < 0.001, respectively). ConclusionPrimary headaches are a common occurrence in patients with MS. Migraines and tension-type headaches (TTH) are among the most prevalent types. It has been observed that interferon can exacerbate preexisting headaches and even cause new ones. Additionally, the location of MS plaques may play a role in the frequency and severity of headaches.

Lessons from autopsy: Topographical variability of atherosclerosis plaques.

Atherosclerosis is a complex disease characterized by the accumulation of plaques in arterial walls. Understanding its pathogenesis remains incomplete, with factors like inflammation, oxidative stress, and hypertension playing critical roles. The disease exhibits preferential localization of plaques, with variability observed even within the same individual. Genetic, environmental, and lifestyle factors contribute to its heterogeneity. Histological plaque phenotypes vary widely, prompting classification schemes focusing on systemic and local factors deteriorating fibrous caps. Recent research highlights differences in plaque histology among arterial systems, suggesting unique pathophysiological mechanisms. This study reports on multiple atherosclerotic plaques detected at autopsy in various vascular sites of a single subject, emphasizing their histological diversity and underscoring the systemic nature of atherosclerosis.

Aiming at early-stage vulnerable plaques: A nanoplatform with dual-mode imaging and lipid-inflammation integrated regulation for atherosclerotic theranostics

The vulnerable plaques in atherosclerosis can cause severe outcome with great danger of acute cardiovascular events. Thus, timely diagnosis and treatment of vulnerable plaques in early stage can effectively benefit the clinical management of atherosclerosis. In this work, a targeting theranostic strategy on early-stage vulnerable plaques in atherosclerosis is realized by a LAID nanoplatform with X-CT and fluorescent dual-mode imaging and lipid-inflammation integrated regulation abilities. The iodinated contrast agents (ICA), phenylboronic acid modified astaxanthin and oxidized-dextran (oxDEX) jointly construct the nanoparticles loaded with the lipid-specific probe LFP. LAID indicates an active targeting to plaques along with the dual-responsive disassembly in oxidative stress and acidic microenvironment of atherosclerosis. The X-CT signals of ICA execute the location of early-stage plaques, while the LFP combines with lipid cores and realizes the recognition of vulnerable plaques. Meanwhile, the treatment based on astaxanthin is performed for restraining the progression of plaques. Transcriptome sequencing suggests that LAID can inhibit the lipid uptake and block NF-κB pathway, which synergistically demonstrates a lipid-inflammation integrated regulation to suppression the plaques growing. The in vivo investigations suggest that LAID delivers a favorable theranostics to the early-stage vulnerable plaques, which provides an impressive prospect for reducing the adverse prognosis of atherosclerosis.

(097) 3 Year Follow Up After Modified Grid Incision and Sealing with Collagen Fleece for Treatment of Peyronie’s Disease

Abstract Introduction Previously, we introduced a less invasive modified technique by multiple grid incisions of Peyronie’s plaque. Objective To assess the efficacy of technique in 32 patients with 3 year follow-up. Methods From 2018, 32 patients with stable Peyronie’s disease were included with 3 major steps of surgery; 1) dissection of neurovascular bundle/urethra according to plaque location, 2) multiple deep grid incisions of plaque for complete correction of curvature/deformity, 3) sealing with TachoSil®. Prospectively, the stretched penile length (SPL), totally straightness, penile sono, erectile function at preoperative, and 6, 12, 24, 36 months postoperatively under approval of Institutional Review Board. Results Mean age was 59.2 years (46–72). Mean curvature was 53.5 (40–80) degree, 8 with hinge and 7 with hourglass deformity. IPP was inserted in 4 and 1 at postoperative 30 months for poor erectile function. Mean follow-up was 35.4 months (12–57). Daily massage softened the hard thickening of penis gradually from 3 months until 3 year. On follow-up sonography, subcutaneous thickening gradually decreased to near normal at 1–3 year and tunical breakage by grid incision reunited at postoperative 10–12 months. 2 patients immediately recurred dorsal curvature but most patients achieved totally straightness. Most patients gained preoperative length after 1.6 year. 96% of patients satisfied in GAQ at 2 year. Minor skin problem was occurred in two of IPP. Subcutaneous bulging hematoma was occurred in 3 patients but subsided in two within 3 months. One patients need revision surgery. In postoperative erectile function of 23 patients without IPP, spontaneous hard erection was recovered in 5 and the rest are satisfied with PED5 inhibitors. Conclusions Our prospective progress reports with technical modification of various plaque incisions shows that one can achieve a sufficient surgical effect without making defect of tunica albuginea but need long term follow up for 3 years at best. Disclosure No.

Carotid atherosclerotic plaque predicts progression of intracranial artery atherosclerosis: A MR imaging-based community cohort study

PurposeIntracranial artery atherosclerosis (ICAS) progression is associated with stroke. However, the association of carotid plaque with ICAS progression among stroke-free participants is still unclear. This study aimed to evaluate the association between carotid plaque and ICAS progression in stroke-free participants. MethodStroke-free participants were recruited from a community-based cohort study. All participants underwent questionnaire interviews, blood tests, and high-resolution vessel wall magnetic resonance (MR) imaging at baseline and follow-up for around three years. The atherosclerotic plaque was defined as eccentric wall thickening on MR imaging. The presence, location, total number, and burden (maximum wall thickness, length, and stenosis) of carotid and intracranial plaque were evaluated. ICAS progression was defined as the number increased or plaque burden (maximum wall thickness, length, or stenosis increase) increased by ≥ 20 %. The association between carotid plaque and ICAS progression was evaluated using multivariable logistic regression. ResultsOf the 312 participants (mean age at baseline: 59.85 ± 13.04 years; 136 males) who completed baseline and follow-up studies with a mean time interval of 3.15 ± 0.59 years, 85 (27.24 %) had progression of ICAS during follow-up. At least one carotid plaque was detected at baseline in 167 (53.53 %) participants. In the multivariable logistic analysis, carotid plaque was a significant predictor for the progression of ICAS (odds ratio, 2.04; 95 % confidence interval, 1.06–3.92; P = 0.032). ConclusionsCarotid plaque is associated with intracranial artery atherosclerosis progression in stroke-free population. Our findings suggest that carotid plaque may be an effective predictor for intracranial artery atherosclerosis progression.

Dataset for Automatic Region-based Coronary Artery Disease Diagnostics Using X-Ray Angiography Images

X-ray coronary angiography is the most common tool for the diagnosis and treatment of coronary artery disease. It involves the injection of contrast agents into coronary vessels using a catheter to highlight the coronary vessel structure. Typically, multiple 2D X-ray projections are recorded from different angles to improve visualization. Recent advances in the development of deep-learning-based tools promise significant improvement in diagnosing and treating coronary artery disease. However, the limited public availability of annotated X-ray coronary angiography image datasets presents a challenge for objective assessment and comparison of existing tools and the development of novel methods. To address this challenge, we introduce a novel ARCADE dataset with 2 objectives: coronary vessel classification and stenosis detection. Each objective contains 1500 expert-labeled X-ray coronary angiography images representing: i) coronary artery segments; and ii) the locations of stenotic plaques. These datasets will serve as a benchmark for developing new methods and assessing existing approaches for the automated diagnosis and risk assessment of coronary artery disease.