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IntroductionDecreased stability of coronary atherosclerotic plaques correlates with a heightened risk of acute coronary syndrome (ACS). Thus, early diagnosis and treatment of unstable plaques are imperative in averting adverse cardiovascular events.
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 (..)
The registry will collect multi-site, real-world information on how the Plaque Analysis product provides enhanced patient insights, empowering physicians and helping to inform their medical management decisions for patients with suspected coronary artery disease (CAD). 2 “Data from the DECODE study shows the value of using Plaque Analysis.
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.
Their findings could lead to new therapies for people with endothelial dysfunction, a type of disorder that contributes to coronary artery disease that may occlude with plaque and lack ability to carry sufficient blood into the heart tissue causing a heart attack.
This substudy of a randomized clinical trial investigates the effects of pitavastatin on noncalcified coronary artery plaque using coronary computed tomography angiography and on inflammatory biomarkers as potential mechanisms for major adverse cardiovascular event prevention.
BackgroundComplex aortic plaque (CAP) is a potential embolic source in patients with cryptogenic stroke (CS). From 2293 studies, 45 were reviewed for CAP imaging biomarker criteria in patients with acute CS (N=37 TEE; N=9 CTA; N=6 magnetic resonance imaging). The most common CAP imaging biomarker was ≥4 mm plaque thickness.
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.
The complex development of atherosclerosis manifests as intimal plaque which occurs in the presence or absence of traditional risk factors. Atherosclerotic coronary artery disease (CAD) is the causal pathological process driving most major adverse cardiovascular events (MACE) worldwide.
Advancements in magnetic resonance angiography (MRA) with vessel wall imaging (VWI) have enabled the identification of vulnerable plaques, aiding in risk stratification for neurovascular events. Eleven plaques were vulnerable in preoperative MRI with VWI. There were 73.3% male patients. of patients had symptomatic disease.
I am excited about the potential of the FAI-Score biomarker, which has promising prognostic value beyond existing CT-based methods such as plaque, calcium scoring, and CAD-RADS based interpretation." Details of the study, included in a written statement issued by Caristo Diagnostics, follow.
This clearance comes in advance of disease-modifying therapies on the horizon expected to help clinicians use this biomarker to guide patients to improved cardiovascular health, saidBrad Moore, president and CEO at Roche Diagnostics North America. The development of the Tina-quant Lipoprotein (a) Gen.2
We investigated whether treatment with LDE-paclitaxel changes plaque progression by coronary CT angiography and is safe in patients with chronic coronary artery disease. Analysis of inflammatory biomarkers and coronary CTA was also performed at baseline and 4 weeks after treatment.
Introduction/Background:According to the American Heart Association, the accumulation of plaque in the walls of arteries is identified as the primary cause of atherosclerotic cardiovascular disease (ASCVD). Circulation, Volume 150, Issue Suppl_1 , Page A4146638-A4146638, November 12, 2024.
Detailed analysis of the excised carotid plaques were carried out with pyrolysis-gas chromatography-mass spectrometry, stable isotope analysis, and electron microscopy. Inflammatory biomarkers were also estimated. Comparison was with those who had no evidence of these plastics in the plaques.
Nevertheless, the relationship between CAC and the susceptibility of a plaque to provoke a thrombotic event remains incompletely understood. This review summarizes the current understanding and literature on CAC.
Atherosclerotic cardiovascular disease (ASCVD), caused by plaque buildup in arterial walls, is one of the leading causes of disability and death worldwide.1,2 7 Research has shown inflammation plays a significant role in the development of atherosclerosis and ASCVD,8-10 and even the formation of plaque.11 4 In the U.S. N Engl J Med.
The expression of GPBAR1 in the human endothelium correlated with the expression of inflammatory biomarkers. Mice lackingFxrandGpbar1−/−/Fxr−/−display hypotension and aortic inflammation, along with altered intestinal permeability that deteriorates with age, and severe dysbiosis, along with dysregulated bile acid synthesis.
Most of the evidence on the harms of extreme exercise is related to a biomarker of cardiovascular disease known as coronary artery calcification or CAC. Numerous reports in the last decade have found that lifetime endurance athletes have higher levels of coronary artery calcification and plaque compared to age-matched non-athletes.
18F-flourodeoxyglucose resting amygdalar uptake, an imaging biomarker of stress-related neural activity, coronary inflammation (fat attenuation index), and high-risk plaque characteristics were assessed by coronary computed tomography angiography. P=0.004), while men had a higher frequency of high-risk plaques (53.7%
Cross-sectional studies reveal that endurance athletes, particularly middle-aged and older men, often exhibit higher coronary artery calcium scores (CACS) and plaque prevalence compared to less-active individuals. Notably, athletes engaging in very vigorous-intensity exercise are more likely to develop calcified plaques.
He emphasized the evolving landscape of biomarker utility in enhancing the accuracy of HF prediction and the need for targeted interventions based on these biomarkers. He emphasized the evolving landscape of biomarker utility in enhancing the accuracy of HF prediction and the need for targeted interventions based on these biomarkers.
Further external validation of single gene differential analysis and nomogram identified SGCE, PCDH7, RAB23, and RIMKLB as hub genes; SGCE and PCDH7 were also used as biomarkers to characterize CAS plaque stability.
In these patients there is no plaque triggered ACS. How can biomarkers help us grade these ACSs? One big chunk of ACS-UA is secondary UA where there is increased demand as in stable angina with tachycardia*. For example, in a febrile patient who has associated HT, anemia, etc., It is next to foolishness to rush them to cath lab.
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