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Excess cholesterol is known to form artery-clogging plaques that can lead to stroke, arterial disease, heart attack, and more, making it the focus of many heart health campaigns. But what if there's more to the picture than just cholesterol?
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.
10th December 2023 A very important study – please watch Very high low density lipoprotein levels with no impact on plaque progression I interrupt my series on what is wrong with the health service to bring you breaking news. The one major difference being that one group had high LDL cholesterol, and the other had “normal” LDL cholesterol.
Nature Reviews Cardiology, Published online: 04 January 2024; doi:10.1038/s41569-023-00979-8 In this Review, Sarraju and Nissen summarize the clinical trial evidence for coronary atherosclerotic plaque stabilization and regression with plasma LDL-cholesterol-lowering therapy and other treatments.
More than 70% of American Indian young adults aged 20-39 and 50% of American Indian teens have cholesterol levels or elevated fat in the blood that put them at risk for cardiovascular disease, a new study suggests.
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?
BACKGROUND:Recently, it was reported that noncalcified plaque (NCP) volume was an independent predictor for cardiac events. Plaque volume was measured by computed tomography angiography, plaque vulnerability by optical coherence tomography, and the level of coronary inflammation by PCAT attenuation. versus 75.9%;P<0.001),
After the introduction of statins in 1987 and the publication of the landmark Scandinavian Simvastatin Survival Trial in 1996, extraordinarily robust evidence has accumulated demonstrating that lowering levels of low-density lipoprotein cholesterol (LDL-C) is associated with a major reduction in cardiovascular morbidity and mortality.
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 Method Different dosages of colchicine mixed with cholesterol (0.05–5 mg/ml/g
BackgroundPlaque progression (PP) is critical between subclinical atherosclerosis and plaque rupture. Small dense lowdensity lipoprotein cholesterol (sdLDLC) is considered as the most atherogenic lipoprotein. Journal of the American Heart Association, Ahead of Print.
This interaction led to increased cytosolic cholesterol in macrophages and changes in expression of lipid metabolism genes consistent with increased cholesterol uptake. This function of LDL uptake is unique to cathelicidins from humans and some primates and was not observed with cathelicidins from mice or rabbits.
The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, in collaboration with researchers across multiple institutions, has published a new study that challenges the long-held belief that high cholesterol correlates and even directly causes coronary artery disease, or plaque buildup in the arteries in metabolically healthy (..)
Controlling Cholesterol What is cholesterol? Cholesterol is a type of fat. Your body uses cholesterol to make hormones and to build and maintain nerve cells. However, when your body has too much cholesterol, deposits of fat in the blood called plaque form inside blood vessel walls.
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.
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. to decode the histological, biochemical, pathological secrets within the atherosclerotic plaques.
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.
The complex development of atherosclerosis manifests as intimal plaque which occurs in the presence or absence of traditional risk factors. For cardiovascular disease, only low-density lipoprotein cholesterol and blood pressure are approved as surrogates for cardiovascular disease.
We used carotid ultrasounds to detect plaque at baseline and follow‐up in 2006 to 2009 (median follow‐up=5.5 had low‐density lipoprotein cholesterol ≥160 mg/dL, which is higher than the recommended threshold for lifestyle or medical interventions in young adults of 20 to 39 years old. Lipids were measured after a 12‐hour fast.
In a major study, researchers have discovered a link between the levels of certain bacteria living in the gut and coronary atherosclerotic plaques. Such atherosclerotic plaques, which are formed by the build-up of fatty and cholesterol deposits, constitute a major cause of heart attacks.
Michael Blaha, MD, discusses the efficacy and safety of novel targeted therapies for lowering LDL cholesterol and emphasizes the importance of long-term data in building patient confidence in this new treatment option.
The abnormal low-density protein cholesterol (LDL-C) level in the development of atherosclerosis is often comorbid in individuals with type 2 diabetes mellitus(T2DM). This study aimed to investigate the aggrav.
A research team based at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) in Madrid and Aarhus University in Denmark has identified an important mechanism that can result in the regression, or shrinkage, of atherosclerotic plaques.
Vascular plaque. It starts with inflammation. Perhaps your blood pressure has been a little too high for a little too long, putting strain on your blood vessels.
We all want to be heart-healthy and ensuring our cholesterol levels are in the normal range is one of the most critical steps. High cholesterol can increase your risk of severe conditions like heart disease and heart attacks. Continue reading to learn four heart-healthy habits that can improve your cholesterol.
This is because the test is widely available, fast, highly reproducible, low radiation, directly reflective of total coronary plaque burden, and highly predictive of future atherosclerotic cardiovascular disease (ASCVD) events.
It is well known that high levels of low-density lipoprotein (LDL) cholesterol, known as the “bad” cholesterol, heighten cardiovascular risk. In addition, he said, the reduction in levels of apoB is of interest because this protein is found on all of the lipid particles that contribute to cholesterol buildup in the arteries. “If
Labelling of cholesterol as Good and bad , are immature scientific conclusions. Can any one believe this as truth, that there is little correlation between circulating blood lipids with arterial plaque lipids ? Remember , there is no intravascular war going on between good and bad cholesterol. Final message.
BACKGROUND:Small dense low-density lipoprotein cholesterol (sdLDL-C) particles are more atherogenic than large and intermediate low-density lipoprotein cholesterol (LDL-C) subfractions. Incident carotid plaques and their vulnerability were detected by carotid ultrasound at follow-up (2021). Stroke, Ahead of Print.
Introduction:Serum remnant lipoprotein particle cholesterol (RLP-C), which includes very-low density lipoproteins (VLDL) and its lipolytic products, contributes to atherosclerotic plaque formation. Novel methods for estimating RLP-C and VLDL-cholesterol (VLDL-C) from a serum fasting lipid profile (FLP) have been proposed (Figure).1,2,3We
BackgroundIntracranial atherosclerotic stenosis is a leading cause of ischemic stroke and recurrent events due to plaque instability. Highresolution magnetic resonance imaging identifies plaque enhancement as a key marker of instability. After therapy, stenosis decreased from 75.9% (interquartile range, 69.5%84.8%) P<0.001).
However, the underlying pathology in different age groups of patients with diabetes has not been studied.Methods and ResultsThe aim of this study was to investigate the plaque characteristics and underlying pathology of acute coronary syndrome in different age groups of patients with or without diabetes in a large cohort. versus 64.8%,P=0.016),
Methods In this study, real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting were used to quantify the expression of Wnt3a, Wnt5a, and Wnt5b in the human coronary plaque, and immunohistochemistry was used to identify sites of local expression.
Carotid ultrasound results were divided into two groups based on the presence or absence of plaque. Carotid plaque was observed in 1140 (43.5%) subjects and CACS>0 in 1172 (44.7%) subjects. Carotid plaque was observed in 1140 (43.5%) subjects and CACS>0 in 1172 (44.7%) subjects. 1692 (64.6%) were male.
PAD is a serious condition affecting circulation and blood vessels, causing them to narrow from plaque buildup in the arteries and blocking blood flow to the extremities, typically the legs and feet. It is triggered by atherosclerosis, which occurs when fatty deposits or cholesterol accumulates… Source
Only when you have a clear idea of those three factors can you decide whether or not to take a medication to lower your LDL cholesterol. I use statins in the question posed above because that is what most people think and, in fact, what they will start with when looking to lower their LDL cholesterol with a medication. Not zero risk.
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.
Introduction Studies in cholesterol-fed rabbits showed that anti-proliferative chemotherapeutic agents such as paclitaxel associated with solid lipid nanoparticles (LDE) have marked anti-atherosclerotic effects. Regarding plaque progression analysis, variation in plaque parameter values was wide, and no difference between groups was observed.
The primary outcome was the prevalence of carotid artery plaques assessed by ultrasound. Secondary outcomes included changes in NMR-derived lipoprotein subclasses and their mediation effects on carotid plaque. Fish oil supplementation was significantly associated with reduced prevalence of carotid plaques (P=0.023).
Plaque regression can be demonstrated by ultrasound evaluation of the carotids which are easily accessible. High density lipoprotein cholesterol in the blood increases with regular exercise. HDL is involved in reverse cholesterol transport from the blood vessels to the liver.
Virchow described the inflammatory features of atheromatous plaque in 1858,1 and 55 years later, Anitschkow and Chalatow first showed the presence of lipid-laden macrophages (foam cells) in atheroma in a cholesterol-fed rabbit model.2,3. The role of inflammation in atherothrombosis has been recognized since the mid-19th century.
Atherosclerosis, also called " hardening of the arteries, " occurs when fat, cholesterol and other substances are deposited in the walls of the arteries. These deposits are called plaques. Over time, these plaques can narrow or completely block arteries and cause problems throughout the body. Atherosclerosis is a common disease.
Cholesterol levels go up when thyroid function comes down. This in turn can enhance the chance of plaque build-up in the blood vessels of the heart (coronary arteries). If these clots migrate to the blood vessels of the brain, a stroke may result. Reduced function of the thyroid gland is also associated with heart disease.
Understanding Peripheral Artery Disease Peripheral artery disease or PAD is a condition in which plaque builds up in the arteries that lead to the legs and feet. A diet rich in fruits, vegetables, whole grains and lean proteins can help control blood pressure, cholesterol levels and weight.
M-MDSCs phenotype switch, atherosclerotic lesion development and plaque phenotype was studiedin vivo.Results:We observed CCR5 elevation on Monocytic-MDSCs in the early phase of atherosclerosis. Additionally, DAPTA reduced the migratory potential, reduced cholesterol uptake and improved the functionality (suppression of T cell) of M-MDSCs.
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