Welcome to the WSC 2022 Interactive Program
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*Please note that all sessions in halls Summit 1, Summit 2 & Hall 406 will be live streamed in addition to the onsite presentation
ASK THE SPEAKER
Sessions in Halls 406, Summit 1 and Summit 2 have a Q&A component, through the congress App called “Ask the Speaker”
PLAQUE RUPTURE IN CAROTID ATHEROSCLEROSIS IS ASSOCIATED WITH INCREASED PLAQUE STRUCTURAL STRESS
Abstract
Background and Aims
OBJECTIVES： This study aimed to identify the determinants of plaque structural stress (PSS) and the relationship between PSS and plaques with rupture.
BACKGROUND: Plaque rupture is the most common cause of cardiovascular and cerebrovascular diseases. The mechanism causing plaque rupture is not clear, and there is no reliable method to assess the risk of plaque rupture. PSS quantifies the complex morphological characteristic of the plaques. Plaque rupture occurs when PSS exceeds its mechanical strength.
Methods
METHODS： We analyzed plaque structure and composition in 47 slices of histology from 8 patients. Comparing the geometric variables and PSS In the plaque rupture group and non-ruptured plaque group. And assessing the correlation between the plaque geometric characteristics and PSS. Maximum principal PSS were calculated by finite element and can be used to predict the plaque rupture.
Results
RESULTS： The ruptured plaque showed higher PSS (median,133.4Kpa vs 87.7Kpa) compared to non- ruptured plaque. PSS increased with increasing vessel wall area（r=0.39，p=0.006），plaque burden （r=0.45，p=0.001), necrotic core area,（r=0.67，p<0.001），and the curvature of the necrotic core（r=0.49，p=<0.001）. But reduced when the percent of lumen area increases （r=0.67，p<0.001).
Conclusions
CONCLUSIONS: PSS is determined by plaque composition, plaque architecture, and lumen geometry. The PSS was significantly higher in the ruptured plaques than in the non-ruptured plaques. Incorporating PSS into plaque assessment may improve the identification of rupture-prone plaques
HIGH PREVALENCE OF ABDOMINAL AORTIC ANEURYSM IN MEN OVER 59 YEARS OF AGE WITH STROKE OR TIA : THE USEFULNESS OF SCREENING AORTIC ULTRASONOGRAPHY
Abstract
Background and Aims
The prevalence of abdominal aortic aneurysm (AAA) has increased during recent decades. Etiology of AAA is degeneration and inflammation of the aortic wall, with a strong association with atherosclerosis. AAA-related death is an important cause of preventable death. Screening aortic ultrasonography is cost-effective and reported that reducing risk of AAA-related death by 50%. The aim of the research was to study current rate of AAA in patient over 59 years of age presenting with stroke or TIA and associated factors.
Methods
We enrolled consecutive patients over 59 years of age who presented with cerebral infarction or TIA, visited Seoul Saint Mary’s hospital from November 2020 to October 2021. Medical records, laboratory results and screening abdominal aortic ultrasonography were retrospectively reviewed.
Results
Total 355 patients were enrolled in this study. 192 patients (54.1%) were men and 163 patients (45.9%) were women. The mean age was 75.4±8.7 years. Overall, AAA was present in 16 patients (4.7%) and the AAA was present in 11 patients (5.7%) among men. Among men with AAA, the comorbiditis included hypertension (64%), diabetes (36%), dyslipidemia (27%) and smoking (55%). There was no correlation between the presence of an AAA and risk factors.
Conclusions
As a preliminary study, men over the age of 59 who present with a stroke or transient ischemic attack (TIA) have been found to still have a higher rate of AAA. Integrating aortic ultrasonography into the neurological examination of these patients could create an effective screening program and prevent AAA-related death.
PREDICTION OF MECHANOSENSITIVE GENES IN VASCULAR ENDOTHELIAL CELLS UNDER HIGH WALL SHEAR STRESS
Abstract
Background and Aims
The vulnerability in atherosclerotic plaques is a major cause of ischemic stroke. High wall shear stress(WSS) accelerates plaque erosion and rupture by direct mechanical stimulation at the luminal surface, but distinct pathophysiologic mechanisms remain largely unknown. We speculate that modulation of mechanosensitive genes underlies driving plaque destabilization. We combine microarray data with bioinformatics to find mechanosensitive genes in vascular endothelial cells and further explore the dynamics-associated mechanisms of disease severity progression.
Methods
Data for the GEO datasets were retrieved from the GEO website. We identified differentially expressed genes(DEGs), and the potential functions and signaling pathways were then performed via enrichment analysis and protein-protein interaction(PPI) network. Hub genes were screened and validated. A TF-miRNA-target gene interaction was predicted based on NetworkAnalyst.
Results
260 DEGs were detected between high and normal WSS. 10 hub genes and 4 cluster modules were filtered out. The enrichment analysis had identified critical biological functions and pathways involved in responses to unfolded protein, topologically incorrect protein, and protein processing in the endoplasmic reticulum. 3 hub genes, ATF3, HSPA6, and DUSP1 were validated. DUSP1 tended to be expressed at higher levels in the senescent cell relative to that in the young cell. A TF–miRNA–mechanosensitive gene co-association network was conducted.
Conclusions
The study identified and validated three potential mechanosensitive genes and one senescence-associated gene in human blood vessels, which might emerge as potential targets for the prediction and prevention of ischemic stroke. Furthermore, a TF–miRNA–mechanosensitive gene co-regulatory network uncovered a fundamental mechanism for protesting against disease progression.