The effects of CES1A2 A(−816)C and CYP2C19 loss-of-function polymorphisms on clopidogrel response variability among Chinese patients with coronary heart disease

2014 ◽  
Vol 24 (4) ◽  
pp. 204-210 ◽  
Author(s):  
Cheng Xie ◽  
Xiaoliang Ding ◽  
Jie Gao ◽  
Haipeng Wang ◽  
Yongfu Hang ◽  
...  
2021 ◽  
Vol 8 ◽  
Author(s):  
Yi Sun ◽  
Shuna Huang ◽  
Chunyu Wan ◽  
Qishuang Ruan ◽  
Xiaoxu Xie ◽  
...  

Background: This study investigated the association between long non-coding RNAs (lncRNAs) and coronary heart disease (CHD) and further elucidated the potential biological roles of lncRNAs in CHD pathogenesis.Methods: A case-control study (590 patients and 590 controls) was conducted from February 2017 and March 2019 in Fuzhou, China. Environmental factors were investigated using questionnaires and physical examinations. Five representative lncRNAs were screened using lncRNA microarray (peripheral blood in 5 cases and 5 controls) and further verified by quantitative real-time polymerase chain reaction (peripheral blood leukocyte in 100 cases and 100 controls). Oxidized low-density lipoprotein (oxLDL) was used to induce a human coronary artery endothelial cell (HCAECs) injury model, and loss of function was used to elucidate the role of lncRNA ENST00000609755.1 (lnc-MICALL2-2) in oxLDL-induced HCAECs injury.Results: A total of 320 lncRNAs were found dysregulated in CHD patients (fold change> 2, p < 0.05). The results of a discovery microarray, population verification and HCAEC experiments suggested the lnc-MICALL2-2 is upregulated in CHD subjects and in an oxLDL-induced HCAECs injury model. Conversely, lnc-MICALL2-2 inhibition in vitro attenuated the effects of oxLDL on HCAECs morphology, proliferation, and apoptosis.Conclusion: Elevated expression of lnc-MICALL2-2 is an independent risk factor for CHD, and knockdown subsequently confers protection against early pathological processes of oxLDL-induced CHD.


2017 ◽  
Author(s):  
Abhiram S. Rao ◽  
Daniel Lindholm ◽  
Manuel A. Rivas ◽  
Joshua W. Knowles ◽  
Stephen B. Montgomery ◽  
...  

AbstractPCSK9 inhibitors are a potent new therapy for hypercholesterolemia and have been shown to decrease risk of coronary heart disease. Although short-term clinical trial results have not demonstrated major adverse effects, long-term data will not be available for some time. Genetic studies in large well-phenotyped biobanks offer a unique opportunity to predict drug effects and provide context for the evaluation of future clinical trial outcomes. We tested association of the PCSK9 loss-of-function variant rsll591147 (R46L) in a hypothesis-driven 11 phenotype set and a hypothesis-generating 278 phenotype set in 337,536 individuals of British ancestry in the United Kingdom Biobank (UKB), with independent discovery (n = 225K) and replication (n = 112K). In addition to the known association with lipid levels (OR 0.63) and coronary heart disease (OR 0.73), the T allele of rs11591147 showed a protective effect on ischemic stroke (OR 0.61, p = 0.002) but not hemorrhagic stroke in the hypothesis-driven screen. We did not observe an association with type 2 diabetes, cataracts, heart failure, atrial fibrillation, and cognitive dysfunction. In the phenome-wide screen, the variant was associated with a reduction in metabolic disorders, ischemic heart disease, coronary artery bypass graft operations, percutaneous coronary interventions and history of angina. A single variant analysis of UKB data using TreeWAS, a Bayesian analysis framework to study genetic associations leveraging phenotype correlations, also showed evidence of association with cerebral infarction and vascular occlusion. This result represents the first genetic evidence in a large cohort for the protective effect of PCSK9 inhibition on ischemic stroke, and corroborates exploratory evidence from clinical trials. PCSK9 inhibition was not associated with variables other than those related to low density lipoprotein cholesterol and atherosclerosis, suggesting that other effects are either small or absent.


2021 ◽  
Author(s):  
Ling Liu ◽  
Qiu-Zhen Lin ◽  
Xue-Yan Zang ◽  
Yan Fu ◽  
Xingyu Wen ◽  
...  

Abstract High-sensitivity C-reactive protein (hs-CRP) is a key inflammatory factor in atherosclerotic cardiovascular diseases. In Chinese patients with coronary heart disease (CHD), the changes in hs-CRP levels after a daily meal and the effect of statins on those were never explored. A total of 300 inpatients with CHD were included. Hs-CRP levels were measured in fasting and non-fasting state at 2 hour (h) and 4h after a daily breakfast. Group with fasting hs-CRP ≤ 3mg/L had significantly higher percentage of patients with statins using ≥ 1 month (m) than that with fasting hs-CRP > 3mg/L (51.4% vs. 23.9%, P < 0.05). Hs-CRP levels were significantly higher in non-fasting state (P < 0.05). Interestingly, the hs-CRP didn’t elevate significantly in inpatients with statins using ≥ 1m in hs-CRP > 3mg/L group, but it elevated significantly after meal in inpatients without and with statins using < 1m (P < 0.05). About 32% of patients with non-fasting hs-CRP > 3mg/L came from those with fasting hs-CRP ≤ 3mg/L. In conclusion, hs-CRP levels increased significantly in CHD patients after a daily meal. When fasting hs-CRP > 3mg/L but not ≤ 3mg/L, statins work partly in reducing hs-CRP elevation in non-fasting state.


2020 ◽  
Author(s):  
Li-Ling Guo ◽  
Yan-qiao Chen ◽  
Qiu-zhen Lin ◽  
Feng Tian ◽  
Qun-Yan Xiang ◽  
...  

Abstract Background: Although the detection of non-fasting blood lipids has been recommended in patients with coronary heart disease (CHD), the non-fasting cut-off points corresponding to the fasting goals of LDL-C < 1.8 mmol/Land non-HDL-C < 2.6 mmol/L, respectively, have not been explored. Methods: This study enrolled 397 inpatients with CHD. One hundred and ninety-seven patients took statins for < 1 month (m) or did not take any statin before admission (i.e. CHD1 group), while 204 patients took statins for ≥ 1 m before admission (i.e. CHD2 group). Blood lipid levels were measured at 0 h, 2 h, and 4 h after a daily breakfast. Results: Non-fasting low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C) levels significantly decreased after a daily meal ( P < 0.05). Both fasting and non-fasting LDL-C or non-HDL-C levels were significantly lower in the CHD2 group. The percent attainment of LDL-C < 1.8 mmol/L at 2 h or 4 h after a daily breakfast was significantly higher than that of its fasting point ( P < 0.05), whereas that of non-HDL-C < 2.6 mmol/L was significantly higher only at 4 h ( P < 0.05). Analysis of c-statistic showed that non-fasting cut-off points for LDL-C and non-HDL-C were 1.5 mmol/L and 2.4 mmol/L, corresponding to their fasting goal levels of 1.8 mmol/L and 2.6 mmol/L, respectively. When postprandial LDL-C and non-HDL-C goal attainments were re-evaluated by non-fasting cut-off points, there were no significant differences in percent attainment between fasting and non-fasting states. Conclusions: Determination ofnon-fasting cut-off points is important to evaluate the efficacy of cholesterol-lowering therapy if blood lipids are detected after a daily meal.


2021 ◽  
Vol 8 ◽  
Author(s):  
Li-Yuan Zhu ◽  
Xing-Yu Wen ◽  
Qun-Yan Xiang ◽  
Li-Ling Guo ◽  
Jin Xu ◽  
...  

Background: Xuezhikang, an extract of red yeast rice, effectively lowers fasting blood lipid levels. However, the influence of Xuezhikang on the non-fasting levels of low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C) has not been explored in Chinese patients with coronary heart disease (CHD).Methods: Fifty CHD patients were enrolled and randomly divided into two groups (n = 25 each) to receive 1,200 mg/d of Xuezhikang or a placebo for 6 weeks as routine therapy. Blood lipids were repeatedly measured before and after 6 weeks of treatment at 0, 2, 4, and 6 h after a standard breakfast containing 800 kcal and 50 g of fat.Results: The serum LDL-C levels significantly decreased, from a fasting level of 3.88 mmol/L to non-fasting levels of 2.99, 2.83, and 3.23 mmol/L at 2, 4, and 6 h, respectively, after breakfast (P &lt; 0.05). The serum non-HDL-C level mildly increased from a fasting level of 4.29 mmol/L to non-fasting levels of 4.32, 4.38, and 4.34 mmol/L at 2, 4, and 6 h post-prandially, respectively, and the difference reached statistical significance only at 4 and 6 h after breakfast (P &lt; 0.05). After 6 weeks of Xuezhikang treatment, the patients had significantly lower fasting and non-fasting serum levels of LDL-C and non-HDL-C (P &lt; 0.05) than at pretreatment. The LDL-C levels were reduced by 27.8, 28.1, 26.2, and 25.3% at 0, 2, 4, and 6 h, respectively, and the non-HDL-C levels were reduced by 27.6, 28.7, 29.0, and 28.0% at 0, 2, 4, and 6 h, respectively, after breakfast. No significant difference was found in the percent reductions in the LDL-C and non-HDL-C levels among the four different time-points.Conclusions: Six weeks of Xuezhikang treatment significantly decreased LDL-C and non-HDL-C levels, with similar percent reductions in fasting and non-fasting states in CHD patients, indicating that the percent change in non-fasting LDL-C or non-HDL-C could replace that in the fasting state for evaluation the efficacy of cholesterol control in CHD patients who are unwilling or unable to fast.


Cardiology ◽  
2019 ◽  
Vol 144 (3-4) ◽  
pp. 90-96
Author(s):  
Ping Wang ◽  
Hua Qiang ◽  
Yan Song ◽  
Ying Dang ◽  
Hui Luan ◽  
...  

Introduction: Obesity is one of the important risk factors of coronary heart disease (CHD). Nonalcoholic fatty liver disease (NAFLD) is always accompanied by obesity. Therefore, this study was designed to elucidate the relationship between NAFLD and CHD in obese and nonobese populations. Methods: We conducted a cross-sectional study of 454 Chinese patients diagnosed with CHD. Patients were grouped into non-NAFLD + nonobese, non-NAFLD + obese, NAFLD + nonobese, and NAFLD + obese based on the presence or absence of both NAFLD and obesity. Results: The mean Gensini score was significantly higher in patients with fatty liver compared to those without. Logistic regression analysis found that fatty liver, uric acid, and blood glucose levels were risk factors for a high Gensini score. Conclusions: Irrespective of the presence of obesity, NAFLD is a risk factor for CHD, and the clinical effect of nonobese fatty liver (especially in women) should be carefully considered.


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