Enzymatic antioxidant system in vascular inflammation and coronary artery disease

The aim: To study the effectiveness of using medicine meldonium in standard therapy to the correction of prooxidant-antioxidant and kallikrein-kinin disorders in patients with chronic pancreatitis andstable coronary artery disease. Materials and methods: The study included 90 patients with chronic pancreatitis andstable coronary artery disease.They were divided into two groups: I group (45 patients) received standard treatment; II group (45 patients) along with basic therapy received medication meldonium (Vazonat) for 2 capsules (500 mg) once daily for two months. Indicators prooxidant-antioxidant system in blood plasma was determined by biochemical method, indicators of kallikrein-kinin system– by chromatographic method. Results: The better status of the prooxidant-antioxidant system and kallikrein-kinin system was observed in patients who received in addition to standard protocol treatment with meldonium. Conclusions: Adding to the complex therapy of patients with chronic pancreatitis and stable coronary artery disease of the medicine meldonium helps to improve the prooxidation-antioxidant status and disorders in the kallikrein-kinin system more significantly compared with standard basic therapy.

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Abstract 021: ARHGEF26 is a Novel Genetic Risk Factor for Vascular Inflammation and Coronary Artery Disease

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.38.suppl_1.021 ◽

2018 ◽

Vol 38 (Suppl_1) ◽

Author(s):

Qiuyu M Zhu ◽

Derek Klarin ◽

Connor A Emdin ◽

Mark Chaffin ◽

Steven Horner ◽

...

Keyword(s):

Coronary Artery Disease ◽

Risk Factor ◽

Coronary Artery ◽

Genetic Risk ◽

Vascular Inflammation ◽

Genetic Risk Factor ◽

Artery Disease

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Association of Interaction Between Smoking and CYP 2C19*3 Polymorphism With Coronary Artery Disease in a Uighur Population

Clinical and Applied Thrombosis/Hemostasis ◽

10.1177/1076029610364522 ◽

2010 ◽

Vol 16 (5) ◽

pp. 579-583 ◽

Cited By ~ 19

Author(s):

Yi-Ning Yang ◽

Xin-Lei Wang ◽

Yi-Tong Ma ◽

Xiang Xie ◽

Zhen-Yan Fu ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Vascular Inflammation ◽

Multiple Logistic Regression Analysis ◽

Rflp Analysis ◽

Biologically Active ◽

Pcr Rflp ◽

Cyp2c19 Gene ◽

Independent Risk Factors ◽

Artery Disease

Objectives: Cytochrome P450 (CYP) 2C19 is expressed in vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which are potent endogenous vasodilators and inhibitors of vascular inflammation. The purpose of this study is to explore the relationship between the interaction of CYP2C19*3 polymorphism and smoking and coronary artery disease (CAD) in a Uighur population. Methods: In a Chinese Uighur case-control study of patients with CAD (n = 336) and healthy controls (n = 370), we investigated the roles of polymorphism in the CYP2C19 gene by the use of polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) analysis. Results: The CYP2C19*3 AG + AA genotype was significantly more prevalent in patients with CAD (6.25.0% vs 2.96%; P = .03). Multiple logistic regression analysis showed 4 independent risk factors: the interaction of CYP2C19*3 and smoking (OR 7.22, 95% confidence interval [CI] 2.32-10.23; P = .009), smoking (OR 3.23, 95% CI 1.72-5.44; P = .003), blood sugar (OR 2.12, 95% CI 1.03-4.21; P < .01), and hypertension (OR 1.74, 95% CI 0.98-2.34; P = .013). Conclusions: The CYP2C19*3 polymorphism and CAD were synergistically and significantly associated in Chinese Uighur patients.

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Vascular Inflammation and Angiographic Severity of Coronary Artery Disease in Young Asian Indians

Journal of Cardiovascular Disease Research ◽

10.5530/jcdr.2014.1.3 ◽

2014 ◽

Vol 5 (1) ◽

pp. 15-21

Author(s):

Imran Ahmed ◽

Achyut Sarkar ◽

Arindam Pande ◽

Naveen Chandra GS ◽

Shailesh Patil ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Asian Indians ◽

Vascular Inflammation ◽

Artery Disease

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Functional investigation of the coronary artery disease gene SVEP1

Basic Research in Cardiology ◽

10.1007/s00395-020-00828-6 ◽

2020 ◽

Vol 115 (6) ◽

Author(s):

Michael J. Winkler ◽

Philipp Müller ◽

Amin M. Sharifi ◽

Jana Wobst ◽

Hanna Winter ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Vascular Inflammation ◽

Missense Variant ◽

Leukocyte Recruitment ◽

Wild Type ◽

Cellular Source ◽

Elevated Expression ◽

Artery Disease

AbstractA missense variant of the sushi, von Willebrand factor type A, EGF and pentraxin domain containing protein 1 (SVEP1) is genome-wide significantly associated with coronary artery disease. The mechanisms how SVEP1 impacts atherosclerosis are not known. We found endothelial cells (EC) and vascular smooth muscle cells to represent the major cellular source of SVEP1 in plaques. Plaques were larger in atherosclerosis-prone Svep1 haploinsufficient (ApoE−/−Svep1+/−) compared to Svep1 wild-type mice (ApoE−/−Svep1+/+) and ApoE−/−Svep1+/− mice displayed elevated plaque neutrophil, Ly6Chigh monocyte, and macrophage numbers. We assessed how leukocytes accumulated more inside plaques in ApoE−/−Svep1+/− mice and found enhanced leukocyte recruitment from blood into plaques. In vitro, we examined how SVEP1 deficiency promotes leukocyte recruitment and found elevated expression of the leukocyte attractant chemokine (C-X-C motif) ligand 1 (CXCL1) in EC after incubation with missense compared to wild-type SVEP1. Increasing wild-type SVEP1 levels silenced endothelial CXCL1 release. In line, plasma Cxcl1 levels were elevated in ApoE−/−Svep1+/− mice. Our studies reveal an atheroprotective role of SVEP1. Deficiency of wild-type Svep1 increased endothelial CXCL1 expression leading to enhanced recruitment of proinflammatory leukocytes from blood to plaque. Consequently, elevated vascular inflammation resulted in enhanced plaque progression in Svep1 deficiency.

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