Inflammatory comments in coronary artery disease: when to suspect polyarteritis nodosa or other primary systemic vasculitis

2021 ◽  
Author(s):  
Youheng Xie ◽  
Michael A. Seidman
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Polyarteritis Nodosa ◽  
Systemic Vasculitis ◽  
Primary Systemic Vasculitis ◽  
Artery Disease

scholarly journals Association of PECAM-1 Gene Polymorphisms with Kawasaki Disease in Chinese Children

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Zhuoying Li ◽  
Dong Han ◽  
Jie Jiang ◽  
Jia Chen ◽  
Lang Tian ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Kawasaki Disease ◽  
Gene Polymorphisms ◽  
Cell Adhesion Molecule ◽  
Systemic Vasculitis ◽  
Healthy Children ◽  
Coronary Artery Lesions ◽  
Artery Disease ◽  
The Relationship

Kawasaki disease (KD) is an acute systemic vasculitis complicated by development of coronary artery lesions. PECAM-1 is a kind of cell adhesion molecule, which plays an important role in coronary artery disease. The relationship between PECAM-1 gene polymorphisms and their susceptibility to Kawasaki diseases (KD) is still unclear. In our study, we examined the PECAM-1 gene polymorphisms in 44 KD patients and 59 healthy children and revealed the correlation of PECAM-1 gene polymorphisms in KD children with and without coronary artery lesions (CAL).

scholarly journals OP0311 THE ROLE OF COMORBID PATHOLOGY IN THE PROGRESSIVE COURSE OF ANCA-ASSOCIATED SYSTEMIC VASCULITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 191.3-191
Author(s):  
A. Chudinov ◽  
I. Belyaeva ◽  
V. Mazurov ◽  
O. Inamova
Keyword(s):  
Diabetes Mellitus ◽  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Granulomatosis With Polyangiitis ◽  
Systemic Vasculitis ◽  
Comorbid Conditions ◽  
Artery Disease ◽  
Progressive Course

Background:ANCA-associated systemic vasculitis (AAV) is characterized by a high incidence of complications and high damage index. Comorbid pathology at the onset can significantly worsen the prognosis AAV. The most significant comorbid conditions in patients with AAV are coronary artery disease, hypertension and dyslipidemia.Objectives:The aim of this study was to determine the role of comorbid pathology in the progressive course in patients with AAV.Methods:Patients with granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA) and eosinophilic granulomatosis with polyangiitis (EGPA) were observed during the first 3 years of the disease and included in this study between 2010 and 2018. At the onset of AAV 75% of patients had significant comorbidities (coronary artery disease, hypertension, dyslipidemia, chronic obstructive pulmonary disease, peptic ulcer, diabetes mellitus, autoimmune thyroiditis and others).Results:In total 209 (165 [79%] female and mean age 51.8 ± 13.2 years) AAV patients (94 GPA; 46 MPA; and 69 EGPA) were included in the analysis. Formation of chronic kidney disease was significantly more frequent in the group of AAV patients with hypertension at the onset, than in patients without hypertension (respectively 37% and 23.6%, p=0.041). Development of thromboembolic complications was significantly more frequent in the group of AAV patients with coronary artery disease at the onset of AAV, than in patients without coronary artery disease (respectively 34% and 14.8%, p=0.034). Dyslipidemia also was risk factor for cardiovascular complications (OR – 3.81, 95% CI (2.43; 8.2) p=0.009). Presence of diabetes mellitus in the AAV onset was risk factor for infectious complications (OR – 1.77, 95% CI (1.14; 3.45) p=0.038).Conclusion:Our study has shown that comorbid pathology increase risk of serious complications and can significantly worsen the prognosis AAV. Prevention of development of comorbid conditions and control of lipid levels, hypertension levels are necessary to prevent the formation of irreversible organ damage.Disclosure of Interests:None declared.

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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