Uric acid and evaluate the coronary vascular stenosis gensini score correlation research and in gender differences.

BACKGROUND AND AIMS: Recent studies have shown that the negative effect of uric acid (UA) on coronary arteries determines the severity of atherosclerotic disease. This study aims to explore the relationship between serum UA level and Gensini score, which reflects the severity of coronary artery disease. METHODS: A total of 860 patients with suspected coronary heart disease who were admitted to hospital due to angina pectoris or myocardial ischemia related symptoms and received coronary angiography were selected. Based on the findings of the angiography, they were categorized into two groups: the coronary heart disease (CHD) group (n = 625) and the control group (n = 235). The uric acid levels and other clinical data were compared between these groups. Additionally, the prevalence of coronary heart disease and Gensini score were compared between the groups, considering gender-specific quartiles of uric acid levels. The clinical baseline data were analyzed using appropriate statistical methods, and multivariate logistic regression analysis was conducted to identify independent risk factors for coronary heart disease. RESULTS: Of 860 patients (mean age, 63.97 ± 11.87 years), 528 were men (mean age, 62.06 ± 11.5 years) and 332 were women (mean age, 66.99 ± 10.11 years). The proportion of smoking, diabetes, hypertension, and hyperlipidemia in the coronary heart disease group was higher than that in the control group (P < 0.05). HbA1C, Gensini score, BMI, TG and hsCRP in the coronary heart disease group were higher than those in the control group (P < 0.05), and HDL-C was lower than that in the control group (P < 0.05). There were no significant differences in age, heart rate, Cr, TC and LDL-C between the two groups (P > 0.05).Multivariate logistic regression analysis showed that age, hypertension, hsCRP and SUA levels increased the risk of coronary heart disease, and the difference was statistically significant(OR = 1.034,95%CI 1.016-1.052, P = 0.001; OR = 1.469,95%CI 1.007-2.142, P = 0.046;OR = 1.064,95%CI 1.026-1.105, P = 0.001; OR = 1.011,95%CI 1.008-1.014, P < 0.001). CONCLUSION: Serum uric acid is positively correlated with Gensini score in patients with coronary heart disease, which is an independent factor for evaluating the degree of coronary artery stenosis and has a predictive effect.

Diagnostic performance of resting full-cycle ratio in identifying coronary lesions causing myocardial ischaemia: a meta-analysis.

BACKGROUND: The resting full-cycle ratio (RFR), a new non-congestive resting index, is commonly used for physiological evaluations of coronary arteries. AIMS: This study aims to evaluate the accuracy of RFR in detecting coronary artery stenosis with hemodynamic significance using fractional flow reserve (FFR) as the reference standard. METHODS: Using 'RFR, resting full-cycle ratio' as the search term, we searched PubMed, Embase, Cochrane Library, and Web of Science databases, screening the literature according to the inclusion and exclusion criteria. By applying FFR ≤ 0.80 and RFR ≤ 0.89 as the diagnostic criteria for ischaemia, we analysed the synthetic sensitivity, specificity, and corresponding 95% confidence intervals, then synthesised the summary receiver operating characteristic curve (SROC). RESULTS: Three studies were included in this meta-analysis, comprising 1,084 patients with 1,312 lesions. When we used FFR ≤ 0.80 as the reference standard, the synthesised sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (LR+), and negative likelihood ratio (LR-) of RFR in the diagnosis of coronary ischaemia were 73%, 81%, 67%, 85%, 3.95, and 0.33, respectively. Besides, the area under the curve (AUC) was 0.8276. CONCLUSION: Using FFR as the reference standard, RFR has good diagnostic accuracy in detecting coronary ischaemic lesions and may be an effective alternative to FFR in the future, to some extent.

A meta-analysis of the relationship between circulating microRNA-155 and coronary artery disease.

OBJECTIVE: Coronary artery disease (CAD) is a leading cause of death worldwide. Many studies in China and abroad have reported an association between the expression level of microRNA-155 and CAD; however, the results remain controversial. We aimed to comprehensively investigate this association based on a meta-analysis. METHODS: We first systematically searched eight Chinese and English databases, including China National Knowledge Infrastructure, Wanfang, China Science and Technology Journal Database, PubMed, Web of Science, Embase, Google Scholar, and Cochrane Library, to identify studies concerning the relationship between microRNA-155 levels and CAD published before February 7, 2021. The quality of the literature was assessed by the Newcastle-Ottawa Scale (NOS). Meta-analysis was performed using a random-effects model to calculate the standard mean difference with a 95% confidence interval (CI). RESULTS: Sixteen articles with a total of 2069 patients with CAD and 1338 controls were included. All the articles were of high quality according to the NOS. The meta-analysis showed that the mean level of microRNA-155 was significantly lower in patients with CAD than in controls. Based on subgroup analyses, the level of microRNA-155 in the plasma of CAD patients and in acute myocardial infarction (AMI) patients was significantly lower than that in controls, whereas this level in CAD patients with mild stenosis was significantly higher than that in controls. CONCLUSION: Our study indicates that the expression level of circulating microRNA-155 in patients with CAD is lower than that in a non-CAD group, suggesting a new possible reference index for the diagnosis and monitoring of patients with CAD.

Efficacy and safety of a bridging strategy that uses intravenous platelet glycoprotein receptor inhibitors for patients undergoing surgery after coronary stent implantation: a meta-analysis.

BACKGROUND: Current guidelines indicate we can consider a bridging strategy that uses intravenous, reversible glycoprotein inhibitors for patients that required surgery following recent stent implantation. However, no strong clinical evidence exists that demonstrates the efficacy and safety of this treatment. Therefore, in this study, the efficacy and safety of a bridging strategy that uses intravenous platelet glycoprotein receptor inhibitors will be evaluated. METHODS: A meta-analysis was performed on preoperative bridging studies in patients undergoing coronary stent surgery. The primary outcome was the success rate of no major adverse cardiovascular events (MACE). The secondary outcomes were the success rate of no reoperations to stop bleeding. RESULTS: A total of 10 studies that included 382 patients were used in this meta-analysis. For the primary endpoint, the success rate was 97.7% (95% CI 94.4-98.0%) for glycoprotein IIb/IIIa inhibitors, 98.8% (95% CI 96.0-100%) for tirofiban (6 studies) and 95.8% (95% CI 90.4-99.4%) for eptifibatide (4 studies). For secondary endpoints, the success rate was 98.0% (95% CI 94.8-99.9%) for glycoprotein IIb/IIIa inhibitors, 99.7% (95% CI 97.1-100%) for tirofiban (5 studies), and 95.3% (95% CI 88.5-99.4%) for eptifibatide (4 studies). CONCLUSION: The results of this study showed that the use of intravenous platelet glycoprotein IIb/IIIa inhibitors as a bridging strategy might be safe and effective for patients undergoing coronary stent implantation that require surgery soon after.

Diagnostic performance of computed tomography-based fraction flow reserve in identifying myocardial ischemia caused by coronary artery stenosis: A meta-analysis.

BACKGROUND: As a new noninvasive diagnostic technique, computed tomography (CT)-based fraction flow reserve (FFR) has been used to identify hemodynamically significant coronary artery stenosis. This meta-analysis used invasive FFR as the standard to evaluate the diagnostic performance of FFRCT. METHODS: We searched the PubMed, Cochrane library, and EMBASE for articles published between January 2009 and January 2021. The synthesized sensitivity and specificity of invasive FFR and FFRCT were analyzed at both the patient and vessel levels. We generated a summary receiver operating characteristic curve (SROC) and then calculated the area under the curve (AUC). RESULTS: We included a total of 23 studies, including 2,178 patients and 3,029 vessels or lesions. Analysis at each patient level demonstrated a synthesized sensitivity of 88%, specificity of 79%, LR+ of 4.16, LR-of 0.15, and AUC of 0.89 for FFRCT. Analysis at the level of each vessel or lesion showed a synthesized sensitivity of 85%, specificity of 81%, LR+ of 4.44, LR-of 0.19, and AUC of 0.87 for FFRCT. CONCLUSION: Our research reveals that FFRCT has high diagnostic performance in patients with coronary artery stenosis, regardless of whether it is at the patient level or the vessel level.

Safety and efficacy of new oral anticoagulants compared to those of warfarin in AF patients with cancer: a meta-analysis of randomized clinical trials and observational studies.

BACKGROUND: Data on the efficacy and safety of nonvitamin K antagonist oral anticoagulants (NOACs) in atrial fibrillation (AF) patients with cancer are limited. Therefore, we conducted a meta-analysis to compare the efficacy and safety between NOACs and warfarin in this population. METHODS: A comprehensive search of the PubMed, Embase, and Cochrane databases for articles published through July 2020 was performed. An evaluation of each study was conducted, and data were extracted. Pooled odds ratio (OR) estimates and 95% CIs were calculated. RESULTS: Eight studies (3 randomized controlled trials (RCTs) and 5 retrospective cohort studies) involving a total of 24,665 patients were included. Among the RCTs, there were no significant differences in the rates of stroke or systemic embolism (OR=0.69; 95% CI, 0.45-1.06; P=0.09), venous thromboembolism (OR=0.91; 95% CI, 0.33-2.52; P=0.86), myocardial infarction (OR=0.74; 95% CI, 0.44-1.23; P=0.24), major bleeding (OR=0.81; 95% CI, 0.61-1.06; P=0.12), or major or nonmajor clinically relevant bleeding (OR= 0.98; 95% CI, 0.82-1.19; P=0.86) between the NOAC and warfarin groups. Among the observational studies, patients who used NOACs had a significantly lower risk than those who used warfarin. The prevalence rates of ischemic stroke (OR=0.51; 95% CI, 0.28-0.92; P=0.02), VTE (OR=0.50; 95% CI, 0.41-0.60; P<0.00001), major bleeding (OR=0.28; 95% CI, 0.14-0.55; P=0.0002), and intracranial or gastrointestinal bleeding (OR=0.59; 95% CI, 0.37-0.92; P=0.02) were significantly reduced in the NOAC group. CONCLUSION: Our meta-analysis confirms that NOACs are as safe and effective as warfarin and can be applied in the real world; this data can serve as a reference for clinical doctors for formulating treatment strategies.

[Effects of hot shock protein 70 inhibitor PFTµ on inflammatory response in lipopolysaccharide-stimulated RAW264.7 cells and mice underwent myocardial ischemia-reperfusion injury].

OBJECTIVE: To observe the effects of hot shock protein 70 (HSP70) inhibitor (PFTµ) on inflammation response in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and mice underwent myocardial ischemia-reperfusion (I/R) injury. METHODS: RAW264.7 macrophage line of mice was stimulated by LPS as an inflammatory model. These were divided into control (15 min DMSO pretreatment and LPS 2 g/L) and PFTµ treated groups (15 min PFTµ 20 µmol/L pretreatment and LPS 2 g/L). NO concentration was measured by Griess Kit. The expression of iNOS protein and mRNA were detected by Western blot and RT-PCR. Infarct size was determined on mice underwent myocardial ischemia-reperfusion (I/R) injury in the absence or presence (PFTµ 40 mg/kg, intraperitoneal injection). RESULTS: PFTµ significantly blocked the production of NO and protein and mRNA expression of iNOS (P < 0.05 vs. control). PFTµ also significantly reduced the infarct size on mice underwent I/R injury (P < 0.05 vs. control). CONCLUSION: These results suggest that PFTµ could be a potential therapeutic agent for the treatment of inflammatory diseases through inhibiting the production of NO and reducing inflammatory responses.

TGF-beta1 expression and atrial myocardium fibrosis increase in atrial fibrillation secondary to rheumatic heart disease.

BACKGROUND: Atrial fibrosis was considered a structural basis for the development and sustaining of atrial fibrillation (AF). Transforming growth factor-beta1 (TGF-beta1) was one of the main factors for accelerating collagen production. The contribution of TGF-beta1 in the pathogenesis of AF needs further investigation. HYPOTHESIS: The altered expression and distribution of TGF-beta1 will be associated with the changes in atrial fibrosis in different types of AF patients with rheumatic heart disease (RHD). METHODS: Right atrial specimens obtained from 38 RHD patients undergoing mitral valve replacement surgery were divided into 3 groups: the sinus rhythm group (n = 8), the paroxysmal AF group (pAF; n = 10), and the chronic AF group (cAF; AF lasting >/= 6 mo; n = 20). The degree of atrial fibrosis, collagen content, serum levels, messenger RNA (mRNA), and protein expression of TGF-beta1 were detected. RESULTS: The collagen content, serum level, TGF-beta1 mRNA, and protein expression of the atrial tissue increased gradually in sinus rhythm, for both pAF and cAF groups, respectively. A positive correlation between TGF-beta1 and the degree of atrial fibrosis was also demonstrated (P < 0.05). CONCLUSION: The TGF-beta1 expression in atrial tissue increased gradually in proportion to the degree of atrial fibrosis in AF and was associated with the type of AF, which suggests that TGF-beta1 is possibly involved in the pathogenesis of AF in RHD patients.

[The protective role of transient receptor potential vanilloid subtype 1 in post-myocardial infarction inflammation process.].

OBJECTIVE: To investigate the protective role of transient receptor potential vanilloid subtype 1 (TRPV1) in inflammatory process after myocardial infarction. METHODS: The survival rate, infarct size, the levels of plasma cardiac troponin I, infiltration of inflammatory cells, the levels of cytokines and chemokines, and cardiac function were monitored 3 and 7 days post-myocardial infarction in TRPV1 gene knockout (TRPV1(-/-)) and wild type (WT) mice. RESULTS: The survival rate was significantly lower in TRPV1(-/-) mice than that in WT mice (62.5% vs. 82.1%, P < 0.05). The infarct size on day 3 after MI was significantly larger in TRPV1(-/-) mice than that in WT mice (INF/AAR: 69.5% +/- 3.1% vs. 40.1% +/- 2.6%, P < 0.05). Plasma cardiac troponin I level, number of infiltrated inflammatory cells including neutrophils and macrophages were significant increased in TRPV1(-/-) mice compared to WT mice. Expressions of cytokines including TNF-alpha, IL-1beta, and IL-6, chemokines including MCP-1 and MIP-2 in the infarct area at 3 and 7 days after MI were significantly higher in TRPV1(-/-) mice than those in WT mice (all P < 0.05). Furthermore, end-systolic and -diastolic diameters were significantly increased and contractile function of the heart significantly reduced in TRPV1(-/-) mice compared to WT mice. CONCLUSION: TRPV1 gene deletion results in reduced survival rate, excessive inflammation, deteriorated cardiac function and aggravated left ventricular remodelling after MI, indicating that TRPV1 may prevent infarct expansion and cardiac injury by inhibiting inflammation and reservation cardiac function.

Combination of C-reactive protein and cardiac troponin I for predicting adverse cardiac events after sirolimus-eluting stent implantation.

AIMS: We assessed the predictive value of a combination of C-reactive protein (CRP) and cardiac troponin I (cTnI) in a 2-year prospective study in patients undergoing sirolimus-eluting stents (SES) implantation. METHODS AND RESULTS: CRP and cTnI levels were examined 1 day before and after SES implantation in 322 patients. CRP level greater than 3.0 mg/l (defining the high serum CRP levels) and cTnI level greater than 1.0 microg/l (defining the high serum cTnI levels) were considered abnormal. Major adverse cardiac events were defined as nonfatal myocardial infarction (MI), target vessel revascularization (TVR), and cardiac death. After 2+/-0.2 years of follow-up, there were 11 MI, 19 TVR, and 11 cardiac deaths. After adjustment for relevant risk factors, the combination of high CRP and cTnI remained predictive of adverse cardiac events, with the presence of both elevated CRP and cTnI associated with the highest risks of MI [relative risk (RR): 4.0, 95% confidence interval (CI): 2.3-6.4], TVR (RR: 3.3, 95% CI: 2.8-5.3), and cardiac death (RR: 4.2, 95% CI: 2.6-6.0). The presence of either a high CRP or cTnI was associated with an intermediated risk of MI (RR: 1.7, 95% CI: 1.2-2.2), TVR (RR: 1.5, 95% CI: 1.2-2.7), and cardiac death (RR: 2.8, 95% CI: 2.2-3.6). CONCLUSION: The combination of elevated CRP and cTnI increased the risk of adverse cardiac events, demonstrating the additive impacts of active inflammation and myocardial injury on prognosis after SES implantation.

[Elevated serum high sensitivity C-reactive protein and endothelial dysfunction in silent myocardial ischemia].

OBJECTIVE: To explore the association between silent myocardial ischemia (SMI) and high sensitivity C-reactive protein (hsCRP) and endothelial dysfunction. METHODS: 148 asymptomatic patients (103 men and 45 women) with known CAD were recruited. According to the results of ambulatory electrocardiography recording (AECG), patients were divided into two groups: SMI group and non-SMI group. All the patients underwent assessment of endothelial dependent flow mediated dilation (FMD) with high resolution ultrasound for the evaluation of endothelial function and 24-hour three-lead ambulatory electrocardiography recording for the detection of SMI. Serum hsCRP, blood glucose, HDL cholesterol, LDL cholesterol and triglycerides were measured. RESULTS: Sixty of the 148 patients had SMI, with a relatively high prevalence of 40.5%. The serum concentration of hsCRP in SMI group was higher than that in non-SMI group (1.86 +/- 0.52 vs 0.91 +/- 0.36, P < 0.05) and FMD was lower in SMI group than that in non-SMI group (3.02 +/- 1.46 vs 6.36 +/- 3.79, P < 0.05). In logistic regression analysis, SMI was found to be related only to FMD (beta = -0.452, P = 0.046, OR = 1.572) and hsCRP (beta = 1.233, P = 0.036, OR = 1.632). CONCLUSIONS: SMI shows a relatively high prevalence in patients with known stable CAD; it is suggested that this population still needs to be carefully evaluated with risk stratification. SMI may be caused by inflammation and endothelial dysfunction. FMD and hsCRP may serve as the surrogate markers in screening SMI in patients with known CAD.