Elevated LDL-C/HDL-C ratio has been shown to be a marker of lipid metabolism as well as a good predictor of coronary artery disease (CAD). Thus, the aim of this study was to investigate whether the LDL-C/HDL-C ratio is useful for detecting cardiovascular disease (CVD) risk factors in general healthy Uygur adults in Xinjiang. A total of 4047 Uygur subjects aged ≥35 years were selected from the Cardiovascular Risk Survey (CRS) study which was carried out from October 2007 to March 2010. Anthropometric data, blood pressure, lipid profile and fasting glucose were measured in all participants. The prevalence, sensitivity, specificity and distance on the receiver operating characteristic (ROC) curve of each LDL-C/HDL-C ratio were calculated. The prevalence of high LDL-C and low HDL-C cholesterol was high and positively correlated with higher LDL-C/HDL-C ratio in the Uygur population. In both men and women, we detected a slight apparent trend of high prevalence of hypertension and hypercholesterolemia with higher LDL-C/HDL-C ratio. Our study also demonstrated that the discriminatory power of the LDL-C/HDL-C ratio for CVD risk factors was slightly stronger in men than in women. Analysis of the shortest distance in the ROC curves for hypertension, dyslipidemia, diabetes, or ≥two of these risk factors suggested a LDL-C/HDL-C ratio cutoff of 2.5 for both men and women. The results of this study showed that a LDL-C/HDL-C ratio cut-off of 2.5 might be used as the predictive marker to detect CVD risk factors among Uygur adults in Xinjiang.

Prevalence of cardiovascular disease (CVD) risk factors have been scarcely studied in Xinjiang, a multi-ethnic region. Multi-ethnic, cross-sectional cardiovascular risk survey study in Xinjiang, including individuals of Uygur (n = 4695), Han (n = 3717) and Kazakh (n = 3196) ethnicities, aged 35-74 years. Analyses involved 11,608 participants with complete data enrolled between October 2007 and March 2010. There were differences in age-standardized prevalence of CVD risk factors between the three groups (all P < 0.001). Hypertension, obesity and smoking rates were higher among Kazakh (54.6%, 24.5%, and 35.8%, respectively). Dyslipidemia prevalence was higher among Uygur (54.3%), and diabetes prevalence was higher among Hans (7.1%). Age-standardized prevalence of adverse CVD risk profiles was different across different ethnicities. Compared with the Han participants, the Uygur and Kazakh had more CVD risk factors (P < 0.001). Compared with the Han participants, the adjusted odds ratios of 1, 2, and ≥3 risk factors profiles for Kazakh and Uygur participants were higher (all P < 0.001). The present study showed the pervasive burden of CVD risk factors in all participant groups in the Xinjiang region. Three major ethnic groups living in Xinjiang had striking differences in the prevalence of major CVD risk factors and adverse risk profiles. Ethnic-specific strategies should be developed to prevent CVD in different ethnic groups, as well as to develop strategies to prevent future development of adverse CVD risk factors at a younger age.

The association between mean platelet volume (MPV) and coronary plaque vulnerability in patients with non-ST-elevation ACS (NSTE-ACS) has not been investigated. We performed a retrospective study to evaluate the association between MPV and plaque vulnerability using optical coherence tomography (OCT). Consecutive NSTE-ACS patients who underwent pre-intervention OCT examination in our center were included in this study. Features of coronary plaques in the culprit arteries were classified as rupture, nonrupture with thin-cap fibroatheroma (TCFA), and nonrupture and non-TCFA. ROC analyses were used to determine the predictive efficacy of MPV for plaque rupture, and multivariate logistic regression analysis was performed to evaluate the potential independent predictors of plaque vulnerability. Overall, 94 patients were included in this study. We identified 17 patients with plaque rupture, 10 with nonrupture with TCFA, and 67 with nonrupture and non-TCFA. ROC analyses showed that MPV ≥ 10.5 fL was predictive of plaque rupture in NSTE-ACS patients. Univariate analyses indicated that patients with higher MPV (≥ 10.5 fL) had higher body mass index and poorer lipid profiles compared to those with lower MPV. Moreover, those with higher MPV had higher incidences of plaque rupture and thrombosis (both P < 0.05). Results of multivariate analyses showed that diabetes and higher platelet distribution width (PDW) were independent risk factors of TCFA (P = 0.032 and 0.046, respectively), while diabetes, higher BMI, higher PDW, and higher MPV were independent determinants of plaque rupture in our cohorts (P all < 0.05). Higher MPV is independently associated with higher risk of plaque rupture as evidenced by OCT in our cohort of NSTE-ACS patients.

Lately, there is accumulating evidence that the Wnt/Frizzled pathway is reactivated after myocardial infarction, the inhibition of the pathway is beneficial since it reduce of myocardial apoptosis and prevents heart failure. FrzA/Sfrp-1, a secreted frizzled-related protein and antagonist for the wnt/frizzled pathway. We assessed the hypothesis that FrzA protects cardiomyocytes from H2O2-Induced Oxidative damage through the inhibition of Wnt/Frizzled pathway activity. We used a recombinant AAV9 vector to deliver FrzA gene into neonatal rat ventricle myocytes and developed an oxidative stress model using H2O2. The cell vitality was measured by MTT colorimetric assay. Western blot and RT-PCR were used to evaluate the expressions of Dvl-1, β-catenin, c-Myc, Bax and Bcl-2. Flow cytometry analysis of cardiomyocytes apoptosis. We confirmed that Wnt/frizzled pathway is involved in H2O2-induced apoptosis in cardiomyocytes. Compared with controls, H2O2 induced the upregulation of Dvl-1, β-catenin, and c-Myc. FrzA suppressed the expression of Dvl-1, β-catenin, c-Myc and the activity of the Wnt/frizzled pathway. Furthermore, FrzA over-expression decreased the apoptotic rate, and the Bax/Bcl-2 ratio in cardiomyocytes treated with H2O2. FrzA, through the inhibition of Wnt/Frizzled pathway activity reduced H2O2-induced cardiomyocytes apoptosis and could be a potential therapeutic target for prevention of cardiac oxidative damage.

CYP17A1 gene encodes P450c17 proteins, which is a key enzyme that catalyzes the formation of sex hormones. Many clinical studies showed that sex hormones levels play an important role in the pathogenesis of coronary artery disease (CAD). However, the relationship between CYP17A1 genetic polymorphisms and CAD remains unclear. The aim of this study was to investigate the association of CYP17A1 genetic polymorphisms with CAD in a Han population of China. A total of 997 people include 490 patients and 507 controls were selected for the present study. Five single-nucleotide polymorphisms (SNPs) (rs4919686, rs1004467, rs4919687, rs10786712, and rs2486758) were genotyped by using the real-time PCR (TaqMan) method. For men, the rs10786712 was found to be associated with CAD in a recessive model (P = 0.016), after adjustment of the major confounding factors, the significant difference was retained (OR = 1.644, 95% confidence interval [CI]: 1.087-2.488, P = 0.019). For women, the rs1004467 was also found to be associated with CAD in a dominant model (P = 0.038), the difference remained statistically significant after multivariate adjustment (OR = 1.623, 95% CI: 1.023-2.576, P = 0.040). The distribution of rs4919687 genotypes showed a significant difference between CAD and control participants in a recessive model (P = 0.019), the significant difference was retained after adjustment for covariates (OR = 0.417, 95% CI: 0.188-0.926, P = 0.032). Rs1004467, rs4919687, rs10786712 of CYP17A1 gene are associated with CAD in Han population of China. The TT genotype of rs10786712 could be a protective genetic marker of CAD in men. The CC genotype of rs1004467 and the AA genotype of rs4919687 could be risk genetic markers of CAD in women. However, large sample size study including other SNPs of CYP17A1 should be performed in future studies.

Background: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) participates in the occurrence and development of cardiovascular and cerebrovascular diseases such as stroke and coronary heart disease by regulating inflammatory reactions, programmed cell death, and other pathological processes. Previous studies revealed that theMALAT1gene polymorphism was associated with cardiac and cerebrovascular diseases. However, the prognostic role of theMALAT1polymorphism in major adverse cardiac and cerebrovascular events (MACCEs) remains unknown. Therefore, this study intends to explore the association between theMALAT1rs3200401 polymorphism and MACCEs.Method: We enrolled 617 myocardial infarction (MI) patients and 1125 control participants who attended the First Affiliated Hospital of Xinjiang Medical University from January 2010 to 2018. SNPscan™ typing assays were used to detect theMALAT1rs3200401 genotype. During the follow-up, MACCEs were recorded. Kaplan–Meier curves and univariate and multivariate Cox survival analyses were used to explore the correlation betweenMALAT1gene polymorphisms and the occurrence of MACCEs.Results: Among the total participants and MI patients, the frequencies of the T allele (total Participants 19.5% vs. 15.3%,P = 0.047, MI patients 20.7% vs. 14.1%,P = 0.014) and CT + TT genotypes (total Participants 37.4% vs. 28.1%,P = 0.013, MI patients 39.5% vs. 25.8%,P = 0.003) were significantly higher in subjects with MACCEs than in subjects without MACCEs. However, in control participants, the frequencies of the T allele (16.6% vs. 16.0%,P = 0.860) and CT + TT genotypes (31.4% vs. 29.3%,P = 0.760) were not higher in subjects with MACCEs than in subjects without MACCEs. In addition, among the total participants and MI patients, the Kaplan–Meier curve analysis indicated that the subjects with rs3200401 CT + TT genotypes had a higher incidence of MACCEs than CC genotype carriers (P = 0.015,P = 0.001). Nevertheless, similar results were not observed in the control participants (P = 0.790). Multivariate Cox regression indicated that compared with patients with the CC genotype, patients with CT + TT genotypes had a 1.554-fold increase in MACCE risk (hazard ratio: 1.554, 95% confidence interval: 1.060–2.277,P = 0.024).Conclusions: TheMALAT1rs3200401 CT + TT genotypes could be a risk factor for MACCEs in MI patients, suggesting that theMALAT1gene may become a biomarker for poor prognosis in MI patients.