The relationship among angiotensinogen genes polymorphisms and hs‐CRP and coronary artery disease

Abstract

ObjectiveTo assess the association of gene polymorphisms of angiotensinogen (AGT), the key factor in rennin‐angiotensin‐aldosterone system (RAAS), with high‐sensitivity C‐reactive protein (hs‐CRP) and coronary artery disease (CAD).MethodsThe current study recruited the patients who were hospitalized and assessed by coronary angiography for suspected CAD. The patients with documented CAD served as CAD group (n = 492) while the patients without documented CAD (n = 87) served as control group. We compared laboratory data and CAD risk factors between the two groups. Furthermore, we analyzed the association of AGT M235T, G217A, G152A, G‐6A, A‐20C genotypes with coronary artery stenosis and in‐stent restenosis.ResultsThere were significantly differences between two patient groups in sex, smoking history, diabetes mellitus, carotid atherosclerosis, lower limb arteriosclerosis, hs‐CRP, blood glucose, and the level of high‐density lipoprotein (HDL; P < 0.05). In CAD group, hs‐CRP levels increased with increasing number of coronary artery branches (1, 2, or ≥3; P < 0.01), and Gensini integral was positively correlated with hs‐CRP levels (r = 0.361, P < 0.01). Frequencies of genotype and allele distribution in individual angiotensinogen loci (M235T, G217A, G152A, G‐6A, A‐20C) did not differ in two patient groups. Following stratification of patients according to hs‐CRP levels (<1 mg/L, 1‐3 mg/L, and >3 mg/L), the distribution frequency of allele M235T was statistically different among the groups (P < 0.05).ConclusionIn CAD patients, M235T among several AGT gene polymorphisms is associated with elevated hs‐CRP levels with AGT C allele as the significant factor for patients with hs‐CRP level of more than 1 mg/L.

Association Between M235T-AGT and I/D-ACE Polymorphisms and Carotid Atheromatosis in Hypertensive Patients: A Cross-Sectional Study

“…The study carried out by Min et al (2019) has confirmed the association of CA with metabolic syndrome and HS (39). Also, the study performed by Targher et al (2006) has confirmed that CA reflects generalized ATS and ischemic vascular disease and is influenced by age, sex, the geographical area, smoking, EHT, type 2 DM, high LDL-C (49).…”

“…Hazzani et al (2014) have demonstrated that the TT235 genotype increases susceptibility to coronary disease in the Egyptian population, independently of other risk factors such as smoking, DM, lipid profile (38). Min et al (2019) have mentioned that a Chinese population carrying the M235T-AGT genetic variant was susceptible to MI (39). Jeng et al (1999), in a study on a population of Chinese origin, have shown that in patients with EHT, the TT235 genotype might be considered a risk factor for the development of LVH, but not CA (40).…”

“…Chapman et al (2001), in a study conducted in a population of Chinese origin, determined the risk of developing CA and found an increase in cIMT in the case of patients carrying the M235T-AGT genetic variant (42). (39,43). The study conducted by Kretowski et al (2007) has demonstrated that type 1 DM associated with TT235 genotype could lead to CA progression (44).…”

Gene polymorphism associated with angiotensinogen (M235T), endothelial lipase (584C/T) and susceptibility to coronary artery disease: a meta-analysis

“…According to the inclusion and exclusion criteria, 29 articles were collected in this meta-analysis, including 16 studies on the relationship between AGT M235T polymorphism and CAD susceptibility [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31], and 13 studies on EL 584C/T polymorphism and CAD susceptibility [32][33][34][35][36][37][38][39][40][41][42][43]. The specific literature screening process was displayed in Figure 1.…”

Spontaneous Coronary Artery Dissection Secondary to Rheumatological Diseases: A Comprehensive Review

“…Inflammatory markers, such as high-sensitivity C-reactive protein (hsCRP), have been found to be elevated in such cases [21]. Elevated hsCRP levels play a direct regulatory role in the process of atherosclerosis with the levels correlating with the severity of anatomical lesions and predicting adverse outcomes [22]. In our review of these cases of SCAD associated with rheumatological pathology, these inflammatory markers were not investigated.…”