Coronary plaque tissue characterization in patients with premature coronary artery disease

Xie, Jianchang; Qi, Jie; Mao, Hengyi; Wang, Ningfu; Ye, Xianhua; Zhou, Liang; Tong, Guoxiang; Yang, Jing; Pān, Hào; Huang, Jinyu

doi:10.1007/s10554-020-01794-9

Cited by 12 publications

(15 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, our study suggests that negatively remodeled plaques may be associated with increased risk of MACE. It can be explained by different plaque subtypes described by several former IVUS studies [ 22 , 23 ]. According to investigators, atherosclerotic plaque capability to remodel diminishes with time due to CAD progress.…”

Section: Discussionmentioning

confidence: 99%

Coronary CT Value in Quantitative Assessment of Intermediate Stenosis

et al. 2022

View full text Add to dashboard Cite

Background and Objectives: Cardiac computed tomography angiography (CCTA) is an excellent non-invasive imaging tool to evaluate coronary arteries and exclude coronary artery disease (CAD). Managing intermediate coronary artery stenosis with negative or inconclusive functional tests is still a challenge. A regular stenosis evaluation together with high-risk plaque features, using semi-automated programs, are becoming promising tools. This case–control study was designed to evaluate the intermediate lesion features’ impact on CAD outcomes, using a semi-automated CCTA atherosclerotic plaque analysis program. Materials and Methods: We performed a single-center, prospective cohort study. A total of 133 patients with low to intermediate risk of CAD, older than 18 years with no previous history of CAD and good quality CCTA images were included in the study, and 194 intermediate stenosis (CAD-RADS 3) were analyzed. For more detailed morphological analysis, we used semi-automated CCTA-dedicated software. Enrolled patients were prospectively followed-up for 2 years. Results: Agatston score was significantly higher in the major adverse cardiovascular events (MACE) group (p = 0.025). Obstruction site analysis showed a significantly lower coronary artery remodeling index (RI) among patients with MACE (p = 0.037); nonetheless RI was negative in both groups. Plaque consistency analysis showed significantly bigger necrotic core area in the MACE group (p = 0.049). In addition, unadjusted multivariate analysis confirmed Agatston score and RI as significant MACE predictors. Conclusions: The Agatston score showes the total area of calcium deposits and higher values are linked to MACE. Higher plaque content of necrotic component is also associated with MACE. Additionally, negatively remodeled plaques are linked to MACE and could be a sign of advanced CAD. The Agatston score and RI are significant in risk stratification for the development of MACE.

show abstract

Section: Discussionmentioning

confidence: 99%

Coronary CT Value in Quantitative Assessment of Intermediate Stenosis

et al. 2022

View full text Add to dashboard Cite

show abstract

“…It is well documented that high cholesterol levels and dyslipidemia/hyperlipidemia, are related to carotid artery disease and CAD [16,17,23]. Reduction in total cholesterol level may be beneficial for CAD, Table 3.…”

Section: Discussionmentioning

confidence: 99%

“…Homocysteine as a novel biomarker, in association with traditional biomarkers, such as creatinine, blood sugar and lipid levels, is associated with acute myocardial infarction and coronary artery stenosis [14,15]. Serum homocysteine along with cholesterol levels is associated with higher risk as well as greater progression of CAD [16,17]. The SNPs in MTHFR gene, C677T polymorphism (rs1801133) and A1298C polymorphism (rs1801131) are independent risk factors for CAD, and these SNPs, furthermore are associated with hyperhomocystenemia, hypercholesterolemia, higher creatinine levels and higher risk of CAD [2,9,18,19].…”

Section: Introductionmentioning

confidence: 99%

The Correlation of MTHFR SNPs, Homocysteine, and Conventional Risk Predictors with Coronary Artery Disease

Rizwan¹,

Khan²,

Baqai³

et al. 2021

Russ J Genet

View full text Add to dashboard Cite

Arterial thromboembolic disease affects coronary vasculature and has an exhaustive list of etiologies. The aim of the present study was to investigate the effects of genetic variants in homocysteine pathway genes, homocysteine levels, and other modifiable and non-modifiable conventionally allotted risk factors for coronary artery disease. Study was retrospective case control study, comprised 404 participants (controls, n = 179, ischemic heart disease (IHD) patients, n = 89, and myocardial infarction (MI) cases, n = 136, respectively). Single nucleotide polymorphisms (SNPs); rs1801133, rs1801131 in methylenetetrahydrofolate reductase 'MTHFR' gene, rs1805087 in methyl tetrahydrofolate homocysteine methyltransferase 'MTR' gene, and rs662 in paroxanse1 'PON1' gene, rs4646994, angiotensin converting enzyme 'ACE' insertion/deletion (I/D) polymorphism were resolved employing conventional, and by tetra primer allele refractory mutation system polymerase chain reaction (PCR). ANOVA association testing revealed that homocysteine, cholesterol, creatinine, triglyceride levels, age, family history of CAD, and polymorphisms in MTHFR and PON1 related to coronary artery disease. The post HOC analysis also maintained significance differences in the control, ischemic heart disease and case groups respectively. The regression analysis failed to maintain statistical significance for creatinine, triglycerides, age, and rs662 PON1 polymorphism, whereby, serum homocysteine, cholesterol, family history, and rs1801133/rs1801131 MTHFR SNPs maintained statistical significance. The results from the present study provide hint into interlaced nature of traditional and novel risk factors in the causation of arterial disease and an insight into their shared detrimental effects in affecting the coronary vasculature.

show abstract

“…The expression of ABCA1 mRNA need to be further investigated. Third, as the definition of pCAD is not uniformly established, and consider the actual situation of our centre and various literature studies [4][5][6][7], we used the common age cut-off value (before age 55 in men and 65 in women) in China, especially for women, due to the large age range, our findings may be more applicable to the relatively young patients with CAD.…”

Section: Study Limitationsmentioning

confidence: 99%

“…However, the definition of pCAD was not uniformly established, the age cut-off can vary from 45 to 65 years among studies due to the variation in risk factors affecting different populations and ethnicities [3][4][5][6]. Chinese Studies on pCAD commonly used the definition of onset age < 55 years for males and < 65 years for females [7].…”

Section: Introductionmentioning

confidence: 99%

Effect of ABCA1 promoter methylation on premature coronary artery disease and its relationship with inflammation

Liu

Wang

et al. 2021

BMC Cardiovasc Disord

View full text Add to dashboard Cite

Background ATP-binding cassette transporter A1 (ABCA1) plays a major role in high-density lipoprotein (HDL) metabolism and reverse cholesterol transport (RCT) and exerts anti-inflammatory effects. Increased ABCA1 promoter methylation level may result in the progression of coronary artery disease. Thus, the present study investigated the association between promoter methylation status of ABCA1 and inflammation in the development of premature coronary artery disease (pCAD). Methods PCAD patients and healthy individuals (n = 90 each) were recruited from the Characteristic Medical Center of the Chinese People's Armed Police Force from June to December 2019. Using pyrosequencing, the levels of ABCA1 promoter methylation in their blood samples were evaluated. Serum concentrations of lipids, interleukin 1β (IL-1β), C-reactive protein (CRP), and circulating free DNA/Neutrophil extracellular traps (cfDNA/NETs) were also routinely measured and compared between the two groups. P values < 0.05 were considered statistically significant. Results The mean ABCA1 promoter methylation levels were significantly higher in the pCAD group than in the control group (44.24% ± 3.66 vs. 36.05% ± 2.99, P < 0.001). Based on binary logistic regression analysis, ABCA1 promoter methylation level was identified as an independent risk factor for pCAD development (odds ratio = 2.878, 95% confidence interval: 1.802–4.594, P < 0.001). Furthermore, ABCA1 promoter methylation levels were negatively correlated with HDL levels (r = − 0.488, P < 0.001) and positively correlated with the levels of CRP, cfDNA/NETs, and IL-1β (r = 0.389, 0.404, 0.385, respectively; P < 0.001). Multiple regression analysis showed that the serum levels of CRP, IL-1β, and cfDNA/NETs independently affect ABCA1 promoter methylation. Conclusions Our findings indicate that high methylation levels at the ABCA1 promoter are associated with low HDL cholesterol levels and an increased risk of pCAD. Inflammatory factors and NETs may be involved in the progression of pCAD by affecting ABCA1 promoter methylation levels.

show abstract

Coronary plaque tissue characterization in patients with premature coronary artery disease

Cited by 12 publications

References 41 publications

Coronary CT Value in Quantitative Assessment of Intermediate Stenosis

Coronary CT Value in Quantitative Assessment of Intermediate Stenosis

The Correlation of MTHFR SNPs, Homocysteine, and Conventional Risk Predictors with Coronary Artery Disease

Effect of ABCA1 promoter methylation on premature coronary artery disease and its relationship with inflammation

Contact Info

Product

Resources

About