Background: Relationships between plaque morphology on optical coherence tomography (OCT) and biomarker levels in the patients with acute coronary syndrome (ACS) have not been fully investigated.
Methods: ACS patients (n=128) were prospectively enrolled and their plasma levels of soluble lectin-like oxidized LDL receptor-1 (sLOX-1), high-sensitivity C-reactive protein (hs-CRP), and high-sensitivity troponin T (hs-TnT) were measured. Another set of 20 patients with stable angina pectoris (SAP) without plaque rupture or erosion served as controls. Among 128 ACS patients, 75 patients underwent OCT procedure to evaluate culprit plaque morphology, and were categorized into two groups; ACS with plaque rupture (ruptured ACS; R-ACS, n=54) and ACS without plaque rupture (non-ruptured ACS; N-ACS, n=21).
Results: Levels of sLOX-1 (p<0.001), hs-CRP (p=0.048) and hs-TnT (p<0.001) were significantly higher in R-ACS than SAP. Levels of sLOX-1 were also significantly higher in R-ACS than in N-ACS (p<0.001); whereas levels of hs-CRP (p=0.675), as well as those of hs-TnT (p=0.055), were comparable between R-ACS and N-ACS. Comparison of receiver operating characteristic (ROC) curves among sLOX-1, hs-CRP and hs-TnT to differentiate R-ACS from N-ACS revealed that the area under the curve (AUC) values of sLOX-1, hs-CRP and hs-TnT were 0.782, 0.531 and 0.643, respectively. ROC curves, generated for these biomarkers, to differentiate ACS with thin-cap fibroatheroma (TCFA) from those without demonstrated that the AUC values of sLOX-1, hs-CRP and hs-TnT were 0.718, 0.506 and 0.524, respectively.
Conclusion: sLOX-1, but not hs-CRP or hs-TnT, can differentiate ACS with plaque rupture from those without, and ACS with TCFA from those without.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.ijcard.2013.04.110 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Newcastle, Callaghan, NSW, Australia.
Background: UK Biobank data show mutations related to the iron disorder hemochromatosis can approximately double the risk of dementia, in particular clinically diagnosed vascular dementia. Insights into the etiology of this dementia may be provided by cerebrovasculopathy in our new "Aβ+Iron" mouse model, which combines hemochromatosis-related mutations and amyloidosis, with increases in soluble Aβ species and plaques. This was created by crossing an established APP/PS1 model of β-amyloidosis with our reported HfexTfr2 model of hemochromatosis-related mutations exhibiting brain iron dyshomeostasis (Heidari Mol.
View Article and Find Full Text PDFVarying pixel resolution significantly improves deep learning-based carotid plaque histology segmentation.
Sci Rep
January 2025
Medical Physics, University of Wisconsin School of Medicine and Public Health (UW-SMPH), Madison, USA.
Carotid plaques-the buildup of cholesterol, calcium, cellular debris, and fibrous tissues in carotid arteries-can rupture, release microemboli into the cerebral vasculature and cause strokes. The likelihood of a plaque rupturing is thought to be associated with its composition (i.e.
View Article and Find Full Text PDFResearch Progress of Regulatory Cell Death in Coronary Microembolization.
Int J Med Sci
January 2025
Department of Cardiology, Jiangbin Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, Guangxi, People's Republic of China.
Coronary microembolization (CME) is defined as atherosclerotic plaque erosion, spontaneous rupture, or rupture of the plaque while undergoing interventional therapy resulting in the formation of tiny emboli that obstruct the coronary microcirculatory system. For percutaneous coronary intervention, CME is a major complication, with a periprocedural incidence of up to 25%. Recent studies have demonstrated that regulatory cell death (RCD) exerts a profound influence on CME through its modulation of inflammatory responses, oxidative stress, cell death, and angiogenesis.
View Article and Find Full Text PDFMelatonin stabilizes atherosclerotic plaques: an association that should be clinically exploited.
Front Med (Lausanne)
December 2024
CENECON, Faculty of Medical Sciences, Universidad de Buenos Aires, and Pontificia Universidad Catolica Argentina, Buenos Aires, Argentina.
Atherosclerosis is the underlying factor in the premature death of millions of humans annually. The cause of death is often a result of the rupture of an atherosclerotic plaque followed by the discharge of the associated molecular debris into the vessel lumen which occludes the artery leading to ischemia of downstream tissue and to morbidity or mortality of the individual. This is most serious when it occurs in the heart (heart attack) or brain (stroke).
View Article and Find Full Text PDFObjective: Aim: To summarise what is known about the inflammatory nature of atherosclerosis to date.
Patients And Methods: Materials and Methods: We conducted the search using Google Scholar and Medline and selected state-of-the-art articles that were consistent with the aim of study.
Conclusion: Conclusions: To date, there is sufficient evidence that atherosclerosis is driven by the inflammatory process.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!