This site uses cookies to improve your experience. To help us insure we adhere to various privacy regulations, please select your country/region of residence. If you do not select a country, we will assume you are from the United States. Select your Cookie Settings or view our Privacy Policy and Terms of Use.
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Used for the proper function of the website
Used for monitoring website traffic and interactions
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Strictly Necessary: Used for the proper function of the website
Performance/Analytics: Used for monitoring website traffic and interactions
While advances in treatment have reduced mortality in some regions, the atherosclerosis prevention remains challenging. This shift results from an epidemiologic transition: as infectious diseases decline, chronic conditions like atherosclerosis dominate.
Atherosclerosis, the leading cause of death worldwide, is a chronic inflammatory disease leading to the accumulation of lipid-rich plaques in the intima of large and medium-sized arteries. Accumulating evidence indicates the important regulatory role of the adaptive immune system in atherosclerosis during all stages of the disease.
Atherosclerosis, or the buildup of plaque in the arteries, develops when low-density lipoprotein cholesterol (LDL-C) enters the blood vessel walls through dysfunctional endothelial cells (EC), leading to the formation of plaques.
Researchers show that genetic traits influence the cellular composition of atherosclerotic plaques, which over time will affect the risk of such lesions to cause a stroke or heart attack. The new knowledge can be used to improve the risk assessment and treatment of patients with atherosclerosis in the future.
MILLER, PHD, LED THE DEVELOPMENT OF A NEW "ATHEROSCLEROSIS ATLAS" THAT DETAILS, AT THE LEVEL OF INDIVIDUAL CELLS, CRITICAL PROCESSES RESPONSIBLE FOR FORMING THE HARMFUL PLAQUE BUILDUP THAT CAUSES HEART ATTACKS, STROKES AND CORONARY ARTERY DISEASE. Over time, fatty plaques build up inside the arteries, where they can slow blood flow.
University of Virginia School of Medicine researchers have created an "atlas of atherosclerosis" that reveals, at the level of individual cells, critical processes responsible for forming the harmful plaque buildup that causes heart attacks, strokes, and coronary artery disease.
Researchers at Case Western Reserve University have identified a new target to treat atherosclerosis, a condition where plaque clogs arteries and causes major cardiac issues, including stroke and heart attack.
In a new study published in the European Heart Journal, researchers at Karolinska Institutet show that genetic traits influence the cellular composition of atherosclerotic plaques, which over time will affect the risk of such lesions for causing a stroke or heart attack.
In this 6-month randomized controlled study, twice-weekly HIIT reduced coronary plaque volume, increased aerobic fitness, and improved body composition in adults with stable heart disease, suggesting benefits for cardiovascular disease progression. Does this greater plaque presence put athletes at a greater risk of CVD events?
IntroductionCardiovascular disease (CVD) caused by atherosclerosis (AS) remains the leading cause of mortality in developed countries. Targeting this cell-cell interaction may offer new therapeutic avenues for managing atherosclerosis. These macrophages were associated with lipid transport, storage, and cell migration pathways.
Aging is known to be a risk factor for the biological changes that create the dangerous buildup of plaque in arteries called atherosclerosis, and aging also induces a buildup of memory CD8 T cells, a type of immune cell, in mice and humans.
Nature Reviews Cardiology, Published online: 02 January 2025; doi:10.1038/s41569-024-01110-1 In this Review, Dey and colleagues explore the pathobiology of coronary atherosclerotic plaques and perivascular adipose tissue, describe their phenotyping with computed tomography coronary angiography, and discuss potential future applications in clinical (..)
Atherosclerosis, a disease characterized by the accumulation of lipids and inflammatory cells in the arterial wall, is a significant cause of cardiovascular events.
Researchers have identified a new target to treat atherosclerosis, a condition where plaque clogs arteries and causes major cardiac issues, including stroke and heart attack.
Nature Reviews Cardiology, Published online: 02 January 2024; doi:10.1038/s41569-023-00957-0 Macrophages in atherosclerotic plaques can undergo apoptosis and several forms of regulated necrosis, including necroptosis, pyroptosis and ferroptosis.
The findings support that metals in the body are associated with the progression of plaque buildup in the arteries and potentially provide a new strategy for managing and preventing atherosclerosis.
Introduction The progression of coronary atherosclerosis is an active and regulated process. The Wnt signaling pathway is thought to play an active role in the pathogenesis of several cardiovascular diseases; however, a better understanding of this system in atherosclerosis is yet to be unraveled.
People with type 2 diabetes have a higher risk of suffering a stroke, a heart attack and premature death due to atherosclerosis, but it has been unclear what the underlying mechanisms are.
Notably, Apoe–/– mice expressing LL37 developed larger atheroma plaques than did control mice, and a positive correlation between plasma LL37 and oxidized phospholipid on apolipoprotein B (OxPL-apoB) levels was observed in individuals with cardiovascular disease.
Background Carotid artery atherosclerosis is a major cause of ischemic stroke, and ischemic stroke is the leading cause of morbidity and mortality worldwide. Unfortunately, the reason for the build-up of atherosclerosisplaque is unknown. However, such studies are rare and limited to animal experiments.
Common examples of vascular disease are aneurysms (a dangerous bulge in an artery wall), atherosclerosis (plaque buildup in the… Source Vascular disease affects the body’s vast network of blood vessels, veins and arteries.
Biomechanical forces, including vascular shear stress, cyclic stretching, and extracellular matrix stiffness, which influence mechanosensitive channels in the plasma membrane, determine cell function in atherosclerosis.
Although the entire vascular bed is constantly exposed to the same risk factors, atherosclerosis manifests a distinct intra-individual pattern in localization and progression within the arterial vascular bed.
Researchers have discovered that the smooth muscle cells that line the arteries of people with atherosclerosis can change into new cell types and develop traits similar to cancer that worsen the disease.
Heart disease is the presence of plaque or atherosclerosis in the coronary arteries. Over a long enough time horizon, pretty much everyone will develop a significant amount of plaque and have a heart attack. We have very strong evidence to support the idea that the more plaque you have, the greater your risk of a heart attack 1.
Thus, it has recently become generally accepted that most plaque ruptures resulting in myocardial infarction occur in plaques that narrow the lumen diameter by 40% of the arterial cross section may be involved by plaque. The pathologist may see a plaque that constitutes, for example, 50% of the cross-sectional area.
Background Inflammation is pivotal to the progression of atherosclerosis. Cholesterol crystals (CCs) that grow and enlarge within the plaque core can cause plaque rupture and trigger inflammation as they deposit into the atherosclerotic bed. Method Different dosages of colchicine mixed with cholesterol (0.05–5 mg/ml/g
The early detection of plaques by circulating biomarkers is highly clinically relevant to prevent the occurrence of major complications such as stroke or heart attacks. miRNA expression profiles of serum-derived EVs were obtained by small RNA sequencing and in plaque material simultaneously acquired from patients.
Doctor, do you have any investigation to know how much the total plaque burden is in my coronary artery? I recently read in Forbes Sunday health supplement, It says ,it is better to know the thickness of the cap covering the plaque. So, you want me to teach you the molecular biology of Atherosclerosis ,right ? Korean Circ J.
This registry will aim to provide world-wide physicians the most accurate information on coronary plaque to improve cardiovascular risk prediction and support the selection of patient-specific treatment,” said Dr. De Cecco. The ultimate goal is to positively impact cardiovascular health globally with a reduction in cardiovascular events."
The sections were also used for immunohistochemistry with cell marker antibodies (to measure % plaque smooth muscle cells (SMC), macrophages (MF), and endothelial cells (EC)). to D: 30.7%), elevation in plaque MF (A: 16.7% to D: 22.5%), increase in plaque cell apoptosis (A: 5.2% to D:17.9%) and plaque EC (A:3.21% to D:1.48%).
Ipsilateral and contralateral carotid artery plaque features were compared, then the carotid artery plaque characteristics on the infarct side were correlated with the infarct pattern.Results:the mean age of subjects included was 68 years old, 79.6% of them were male. 0.15), larger wall area (0.50±0.19 0.23), all p values<0.05.
The EAS 2024 Congress (May 26-29, 2024) has concluded, providing critical insights into atherosclerosis and related vascular disease. Giovanna Liuzzo (Italy) revealed that advancements in noninvasive imaging recently allow for direct visualization of coronary atherosclerotic plaques. Here are some notable highlights: Prof.
15, 2024 – Elucid has announced that four of the seven Medicare Administrative Contractors (MACs) will extend coverage for AI-enabled quantitative coronary plaque analysis, including its FDA-cleared PlaqueIQ image analysis software, beginning Nov. tim.hodson Tue, 10/15/2024 - 12:12 Oct.
The reason: They were accumulating plaque in their coronary arteries much earlier than their peers. You can’t have a heart attack if you don’t have plaque in your coronary arteries. And plaque in your coronary arteries is the result of exposure to risk factors over time. The answer: Risk Factors. The answer.
When we say heart disease, what we really mean is plaque in the artery wall. This Is Known As Atherosclerosis. The fundamental cause of atherosclerosis is when a cholesterol particle crosses into the artery wall from the bloodstream, gets stuck, and sets off an inflammatory process 1. No atherosclerosis. No heart attacks.
Atherosclerosis is a chronic inflammatory disease characterized by endothelial dysfunction and plaque formation. Under pro-inflammatory conditions, endothelial cells can undergo endothelial-to-mesenchymal transition (EndMT), contributing to atherosclerosis development.
You cannot eliminate the plaque entirely, but multiple clinical trials have shown plaque regression using high-intensity cholesterol-lowering treatments, which I have discussed previously. All of these parameters are important and need to be considered when evaluating plaque regression. REVERSAL Investigators.
Objective Assessing the impact of lumbar disc herniation (LDH) on the plaque burden of coronary atherosclerosis is our objective. Gensini scores were calculated to assess the plaque burden of coronary. The association between lumbar disc lesions grading and coronary plaque burden was analysed by Spearman's correlation test.
In recent years, the role of macrophages as the primary cell type contributing to foam cell formation and atheroma plaque development has been widely acknowledged. Recent studies have further supported the notion that SMCs constitute the majority of foam cells in advanced atherosclerotic plaques.
people from the general population), coronary artery calcium scores (CACS) are higher, indicating more calcification and the presence of atherosclerotic plaques. Calcified plaques are known to be more stable and less prone to rupture and lead to a heart attack. When comparing athletes to control groups (i.e., hours per week).
We organize all of the trending information in your field so you don't have to. Join thousands of users and stay up to date on the latest articles your peers are reading.
You know about us, now we want to get to know you!
Let's personalize your content
Let's get even more personalized
We recognize your account from another site in our network, please click 'Send Email' below to continue with verifying your account and setting a password.
Let's personalize your content