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1.
PLoS One ; 19(5): e0304137, 2024.
Article in English | MEDLINE | ID: mdl-38805487

ABSTRACT

This study aims to evaluate the role of the peri-coronary Fat Attenuation Index (FAI) and High-Risk Plaque Characteristics (HRPC) in the assessment of coronary heart disease risk. By conducting coronary CT angiography and coronary angiography on 217 patients with newly developed chest pain (excluding acute myocardial infarction), their degree of vascular stenosis, FAI, and the presence and quantity of HRPC were assessed. The study results demonstrate a correlation between FAI and HRPC, and the combined use of FAI and HRPC can more accurately predict the risk of major adverse cardiovascular events (MACE). Additionally, the study found that patients with high FAI were more prone to exhibit high-risk plaque characteristics, severe stenosis, and multiple vessel disease. After adjustment, the combination of FAI and HRPC improved the ability to identify and reclassify MACE. Furthermore, the study identified high FAI as an independent predictor of MACE in patients undergoing revascularization, while HRPC served as an independent predictor of MACE in patients not undergoing revascularization. These findings suggest the potential clinical value of FAI and HRPC in the assessment of coronary heart disease risk, particularly in patients with newly developed chest pain excluding acute myocardial infarction.


Subject(s)
Chest Pain , Computed Tomography Angiography , Coronary Angiography , Plaque, Atherosclerotic , Humans , Male , Female , Middle Aged , Computed Tomography Angiography/methods , Chest Pain/diagnostic imaging , Plaque, Atherosclerotic/diagnostic imaging , Plaque, Atherosclerotic/complications , Coronary Angiography/methods , Aged , Myocardial Infarction/diagnostic imaging , Myocardial Infarction/complications , Risk Assessment , Adipose Tissue/diagnostic imaging , Adipose Tissue/pathology , Coronary Artery Disease/diagnostic imaging , Coronary Artery Disease/complications , Risk Factors , Coronary Vessels/diagnostic imaging , Coronary Vessels/pathology
3.
BMC Endocr Disord ; 21(1): 43, 2021 Mar 05.
Article in English | MEDLINE | ID: mdl-33673843

ABSTRACT

BACKGROUND: Subclinical hypothyroidism (SCH) is reportedly associated with an increased risk of adverse events in patients undergoing percutaneous coronary intervention (PCI). The prognostic significance of SCH in the elderly was poorly defined. The purpose of this study was to evaluate the association between SCH and long-term outcomes in older patients undergoing PCI. METHODS: Three thousand one hundred sixty-eight patients aged 65 years or older who underwent PCI from January 2012 to October 2014 were included. Patients were divided into SCH group (n = 320) and euthyroidism (ET) group (n = 2848) based on thyroid function test. Cox proportional hazard regression analyses were used to estimate the relative risks (RRs) of all-cause death and cardiac death for patients with SCH during a 4-year follow-up period. RESULTS: There were 227 deaths during the follow-up period including 124 deaths caused by cardiac events. There was no significant difference in mortality rate between the SCH group and the ET group (p > 0.05). After adjustment for covariates, compared with patients with ET, the RRs of death from all-cause and cardiac in patients with SCH were 1.261 (95%CI: 0.802-1.982, p = 0.315) and 1.231 (95%CI: 0.650-2.334, p = 0.524), respectively. When SCH was stratified by age, gender, and degree of thyroid-stimulating hormone elevation, no significant associations were also found in any stratum. CONCLUSION: Our investigation revealed that SCH was negatively associated with the outcome of PCI in older patients.


Subject(s)
Coronary Artery Disease , Hypothyroidism/diagnosis , Percutaneous Coronary Intervention/mortality , Aged , Aged, 80 and over , Asymptomatic Diseases , Cause of Death , China/epidemiology , Coronary Artery Disease/complications , Coronary Artery Disease/diagnosis , Coronary Artery Disease/mortality , Coronary Artery Disease/surgery , Female , Follow-Up Studies , Humans , Hypothyroidism/complications , Hypothyroidism/mortality , Male , Mortality , Percutaneous Coronary Intervention/adverse effects , Percutaneous Coronary Intervention/statistics & numerical data , Postoperative Complications/diagnosis , Postoperative Complications/etiology , Postoperative Complications/mortality , Prognosis , Retrospective Studies , Risk Factors , Treatment Outcome
4.
Gen Physiol Biophys ; 39(5): 437-448, 2020 Sep.
Article in English | MEDLINE | ID: mdl-33084597

ABSTRACT

Macrophages conversion to foam cells strongly promoted atherosclerosis progression by plaque formation and plaque rupture. Macrophages swallow oxidized-low density lipoprotein (ox-LDL) to promote foam cell formation. Protease-activated receptor 2 (PAR2) has been reported to take part in atherosclerotic development. However, the effects of PAR2 in macrophages were rarely investigated. In this study, human monocyte, THP-1 was induced to macrophages by using phorbol 12-myristate 13-acetate (PMA). Subsequently, an in vitro model was arranged by using ox-LDL to treat the macrophages. The data showed that inhibition of PAR2 reduced ox-LDL-induced foam cell formation, inflammation, and apoptosis. Additionally, ox-LDL increased PAR2 and inhibited Dickkopf-related protein 1 (DKK1) expression, which is a Wnt signaling inhibitor. PAR2 knocked-down decreased DKK1 and enhanced expression of Wnt3a, ß-catenin. Meanwhile, DKK1 overexpression reversed the effects of PAR2 on foam cell formation, inflammation, and apoptosis. In summary, PAR2 is essential for the formation of foam cells, inflammation, and apoptosis in macrophages which plays a critical role during atherosclerosis. PAR2 plays roles in macrophages treated with ox-LDL via DKK1/Wnt/ß-catenin signaling.


Subject(s)
Apoptosis , Inflammation , Lipoproteins, LDL/metabolism , Receptor, PAR-2 , Wnt Signaling Pathway , Gene Silencing , Humans , Intercellular Signaling Peptides and Proteins/metabolism , Macrophages/drug effects , Macrophages/metabolism , Receptor, PAR-2/genetics , THP-1 Cells , Wnt3A Protein/metabolism , beta Catenin/metabolism
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