Serum VCAM-1 and ICAM-1 measurement assists for MACE risk estimation in ST-segment elevation myocardial infarction patients.

BACKGROUND: Vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) modulate atherosclerosis by promoting leukocyte infiltration, neutrophil recruitment, endothelial cell proliferation, etc., which may directly or indirectly facilitate the occurrence of major adverse cardiac events (MACE). This study intended to investigate the value of VCAM-1 and ICAM-1 for predicting MACE in ST-segment elevation myocardial infarction (STEMI) patients. METHODS: Totally, 373 STEMI patients receiving the percutaneous coronary intervention and 50 health controls (HCs) were included. Serum VCAM-1 and ICAM-1 were detected by ELISA. Meanwhile, MACE was recorded during a median follow-up of 18 (range: 1-46) months in STEMI patients. RESULTS: Vascular cell adhesion molecule-1 and ICAM-1 were raised in STEMI patients compared with HCs (both p < 0.001). VCAM-1 (p = 0.002) and ICAM-1 (p = 0.012) high were linked with raised accumulating MACE rate in STEMI patients. Notably, VCAM-1 high (hazard ratio [HR] = 2.339, p = 0.031), age ≥ 65 years (HR = 2.019, p = 0.039), history of diabetes mellitus (DM) (HR = 2.395, p = 0.011), C-reactive protein (CRP) ≥ 5 mg/L (HR = 2.550, p = 0.012), multivessel disease (HR = 2.561, p = 0.007) independently predicted MACE risk in STEMI patients. Furthermore, a nomogram-based prediction model combining these factors was established, exhibiting an acceptable value for estimating 1, 2, and 3-year MACE risk, with AUC of 0.764, 0.716, and 0.778, respectively, in STEMI patients. CONCLUSION: This study confirms the value of VCAM-1 and ICAM-1 measurement in predicting MACE risk in STEMI patients. Moreover, VCAM-1 plus other traditional prognostic factors (such as age, history of DM, CRP, and multivessel disease) cloud further improve the predictive accuracy of MACE risk in STEMI patients.

Analysis of the Guiding Role of CYP2C19 Gene Combined With Platelet Function Detection in Antiplatelet Therapy in Patients With Complex Coronary Artery Disease After PCI.

OBJECTIVE: To explore the influence of CYP2C19 gene combined with platelet function test on clinical prognosis of patients with complex coronary artery disease receiving antiplatelet therapy after PCI. METHODS: A total of 200 patients undergoing PCI in our hospital due to complex coronary artery disease from February 2019 to February 2021 were selected and divided into the control group and the observation group according to whether CYP2C19 gene detection was performed. The control group was treated with dual antiplatelet therapy of classical aspirin combined with clopidogrel, and the observation group was treated with individual antiplatelet therapy. The patients in the two groups were followed up for 1 year after PCI, and their quality of life was assessed using the Seattle Angina Questionnaire (SAQ score). The occurrence of major adverse cardiovascular events (MACE) during the follow-up period was also recorded. RESULTS: The incidence of total MACE events in the observation group was slightly less than that in the control group, and the difference was statistically significant (P = 0.040). In particular, the observation group was superior to the control group in reducing the readmission rate of recurrent unstable angina pectoris, and the difference was statistically significant (P = 0.023). The location of coronary culprit lesions with recurrent ischemic events was commonly seen in non-interventional target lesions (interventional/non-interventional target sites: 12.9%: 77.1%). The SAQ score in the observation group was larger than that in the control group, and the difference was statistically significant (P = 0.012). There was no statistical difference in the incidence of major bleeding between the two groups (P = 0.352). CONCLUSION: Using CYP2C19 genotype combined with platelet function test to guide individualized antiplatelet therapy after complex coronary artery PCI is beneficial to reducing ischemic events in a short period (1 year), mainly due to reducing the risk of readmission for recurrent unstable angina pectoris, and improving the quality of daily life of patients without increasing the risk of massive hemorrhage, which can improve clinical prognosis.

Comparison of invasive blood pressure monitoring versus normal non-invasive blood pressure monitoring in ST-elevation myocardial infarction patients with percutaneous coronary intervention.

BACKGROUND: Hypotension post percutaneous coronary intervention (PCI) causes stent thrombosis and reduced coronary perfusion, which aggravate myocardial ischemia and lead to patient death. Therefore, the accuracy and timeliness of blood pressure monitoring (BPM) are crucial for the nursing of patients post PCI. However, it is still controversial whether invasive blood pressure monitoring (IBPM) or non-invasive blood pressure monitoring (NIBPM) should be used for patients post PCI, and the magnitude of their assistance for patients' recovery remains unclear. METHODS: A randomized controlled trial was performed in this study. 126 ST-segment elevation myocardial infarction (STEMI) patients post PCI were recruited and randomly divided into two groups (NIBPM group n = 63; IBPM group n = 63). RESULTS: Clinical characteristics and physiological outcomes of participants received different BPM methods were collected and analyzed to compare the effects of these two methods on the nursing of PCI patients. Compared to NIBPM group, IBPM assisted to shorten the time of myocardial ischemia, promote coronary reperfusion, reduce the occurrence of cardiovascular disease and other complications, and ultimately reduce the mortality of patients post PCI. CONCLUSION: The application of IBPM contributed to reduce the occurrence of complications, shorten the time of vascular reperfusion, and guide treatment of clinicians in time.

Application Analysis of Positive-Pressure Connector in Invasive Blood Pressure Monitoring in Coronary Interventional Therapy.

Background: In order to reduce the risk of invasive blood pressure monitoring and improve the safety and efficiency, this article mainly analyzes the effectiveness and safety of using positive-pressure connector for invasive blood pressure monitoring in patients with coronary artery interventional therapy, so as to improve the invasive blood pressure monitoring method. Aim: To study and analyze the application of positive-pressure connector in invasive blood pressure monitoring in coronary interventional therapy. Methods: From October 2017 to October 2019, a total of 120 patients admitted to Cangzhou Central Hospital, Cangzhou, Hebei, China, for coronary interventional therapy with invasive blood pressure monitoring were selected and divided into a control group and an experimental group by drawing lots with 60 patients in each group. Positive-pressure connector was used for invasive blood pressure detection in the experimental group, and heparin cap connector was used for invasive blood pressure detection in the control group. The effectiveness and safety of blood pressure monitoring in the two groups were compared, and the influence of different joints on invasive blood pressure monitoring was analyzed. Results: The influencing factors of puncture efficiency in the experimental group (6.67%) were significantly lower than those in the control group (30.00%) (P < 0.05). There was no significant difference in catheter bending between the experimental group and the control group (P > 0.05). The experimental group exhibited a remarkably higher puncture safety rate (93%) compared to the control group (67%) (P < 0.05). There was no significant difference in arterial blood pressure between the two groups with different indwelling time (P > 0.05). The frequency of extubation and reinsertion in the experimental group was significantly lower than that in the control group (P < 0.05). Factors influencing puncture safety in the experimental group were significantly lower than those in the control group (P < 0.05). Conclusion: The use of positive-pressure connector for invasive blood pressure monitoring in patients with coronary artery interventional therapy can greatly improve the safety of blood pressure monitoring and reduce the suffering of patients. Therefore, the application of positive-pressure connector in invasive blood pressure monitoring is worthy of promotion and application in clinical practice.

Protective effect of glycyrrhizin on coronary microembolization-induced myocardial dysfunction in rats.

Coronary microembolization (CME)-induced inflammation and cardiomyocyte apoptosis are two key factors contributing to CME-induced myocardial dysfunction. High-mobility group box-1 (HMGB1) plays essential role in progression of CME-induced injury and inhibition of HMGB1 has been shown to be protective. In present study, the potential effects of glycyrrhizin, a HMGB1 inhibitor, on CME-induced myocardial dysfunction are evaluated. Using a rat model of CME, we administrated glycyrrhizin in rats prior to CME induction. The level of HMGB1, TNF-α, iNOS, IL-6, IL-1ß, cleaved caspase-3, Bax, and Bcl-2 were measured. The serum level of cardiac troponin I, creatine kinase, was detected. The cardiac function and cardiomyocyte apoptosis were evaluated. The activation of TLR4/NF-κB signaling pathway was analyzed. Glycyrrhizin prevented CME-induced production of HMGB1, TNF-α, iNOS, IL-6, and IL-1ß. Glycyrrhizin inhibited CME-induced cardiomyocyte apoptosis and the expression of cleaved caspase-3 and Bax, while enhanced the expression of Bcl-2. Glycyrrhizin decreased cardiac troponin I and creatine kinase levels and improved cardiac function. Glycyrrhizin prevented the activation of HMGB1/TLR4/NF-κB signaling pathway. Glycyrrhizin ameliorated myocardial dysfunction in CME rats by preventing inflammation and apoptosis of cardiomyocytes.

Efficacy and safety of nebivolol in hypertensive patients: a meta-analysis of randomized controlled trials.

PURPOSE: Our meta-analysis was undertaken to evaluate the efficacy and safety of nebivolol compared with other second-generation ß blockers for hypertensive patients. METHODS: We searched PubMed, the Cochrane Library, EMBASE, and Clinical Trials.gov databases for randomized controlled trials (RCTs). The efficacy endpoints included systolic blood pressure (SBP), diastolic blood pressure (DBP), reduction of SBP and DBP, heart rate (HR), and adverse events (AEs). FINDINGS: Eight RCTs with 1514 patients met the inclusion criteria. HR was significantly lower in patients receiving other second-generation ß blockers compared with patients receiving nebivolol. There was no difference the reduction of blood pressure (SBP and DBP) or the reduction of SBP or DBP between the groups. The incidence of AEs was lower in patients taking nebivolol compared with patients taking other second-generation ß blockers. CONCLUSIONS: No significant difference was demonstrated between nebivolol and other second-generation ß blockers in the reduction of blood pressure, SBP, and DBP. The tolerability of nebivolol was significantly better compared with other second-generation ß blockers, and nebivolol was also associated with a stable HR and a lower risk of AEs compared with other second-generation ß blockers.

Circulating miR-130 and its target PPAR-γ may be potential biomarkers in patients of coronary artery disease with type 2 diabetes mellitus.

BACKGROUND: Patients of coronary artery disease (CAD) with type 2 diabetes mellitus (DM2) show increased mortality risk than CAD patients without DM2, while few biomarkers can be used to discriminate them. METHODS: Fifty-nine patients of CAD with DM2 (DM2-CAD group), 79 patients of CAD without DM2 (CAD group), and 63 healthy control subjects were recruited. Circulating miR-130 (miR-130a and miR-130b) and PPAR-γ (peroxisome proliferator-activated receptor gamma) were measured and their Pearson correlation was analyzed. 3' UTR binding prediction and luciferase assay were used to determine the target relationship between miR-130 and PPAR-γ. Receiver operating characteristics (ROC) analysis was performed to test the discrimination ability of miR-130 between DM2-CAD and CAD groups. RESULTS: miR-130a and miR-130b showed decreased expression in DM2-CAD group when compared with the CAD group and health control. Both bioinformatics and luciferase assays showed that miR-130 could bind the 3' UTR of PPAR-γ. Furthermore, miR-130 negatively correlated with PPAR-γ in both CAD and DM2-CAD group in Pearson's coefficient analysis. Both miR-130a and miR-130b were able to discriminate DM2-CAD group from CAD group and control subjects. CONCLUSION: Circulating miR-130 may regulate the expression of PPAR-γ and can be used as a biomarker to discriminate DM2-CAD from CAD.

Vitamin D Deficiency Harms Patients with Coronary Heart Disease by Enhancing Inflammation.

BACKGROUND Vitamin D (VD) deficiency and local inflammation of plaque are potential new risk factors and prevention goals for coronary heart disease (CHD). MATERIAL AND METHODS This study included 135 CHD patients and 45 chest tightness or chest pain patients (control group). Basic clinical data and serum 25-OH-VD, TNF-α, IL-6, IL-8, and IL-1ß of the 2 groups were compared by SPSS 25.0. A CHD rat model was used to explore the potential molecular mechanisms. RESULTS The serum 25-OH-VD level in the control group was significantly higher compared to the CHD group, and decreased with the worsening of the CHD condition. Logistic regression found that serum 25-OH-VD was a protective factor in the occurrence of CHD. In CHD patients, the level of serum 25-OH-VD had a negative correlation with serum TNF-α (r=-0.651, P<0.001), IL-6 (r=-0.457, P<0.001), IL-8 (r=-0.755, P<0.001), and IL-1ß (r=-0.628, P<0.001). In animal experiments, VD deficiency enhanced the level of serum TC, TG, and LDL-C. VD deficiency could increase the inflammatory response by upregulating the expression of p65 protein and reducing SIRT1 protein expression in heart tissue, thereby inducing or aggravating the state of CHD. CONCLUSIONS Serum 25-OH-VD was a protective factor in the occurrence of CHD, and VD deficiency could induce or aggravate the state of CHD by enhancing inflammation through the NF-κB pathway.

Palmatine attenuates isoproterenol-induced pathological hypertrophy via selectively inhibiting HDAC2 in rats.

This study aimed to exploit the potential therapeutic value of palmatine in treatment of cardiac hypertrophy and the underlying molecular mechanism. Rat hypertrophy model was established by intraperitoneal isoproterenol (ISO) injection. The hypertrophy was evaluated with cardiac hypertrophic parameters, hemodynamic parameters, lipid profile, and non-specific cardiac markers. The animals were intraperitoneally administrated with either palmatine or vehicle. The relative expressions of ANP, BNP, HDAC2, HDAC5, KLF4, and INPP5F transcripts were determined by real-time polymerase chain reaction (PCR). The relative protein levels of HDAC2, HDAC5, KLF4, and INPP5F were analyzed by immunoblotting. Palmatine treatment significantly attenuated ISO-induced hypertrophy in rats and elicited remarkable repressions in ANP, BNP, and HDAC2 transcriptions but not HDAC5. The downstream effector genes KLF4 and INPP5F were greatly restored in a dose-dependent manner in response to palmatine treatment. Our data demonstrated that palmatine possessed promising therapeutic potential against hypertrophy, which was mediated by modulation of HDAC2-KLF4/INPP5F pathway.

Study of coronary artery perforation during percutaneous coronary intervention in the Cangzhou Chinese population.

OBJECTIVE: Coronary artery perforation (CAP) is a rare, serious complication of percutaneous coronary intervention (PCI). Many studies have addressed the incidence, risk factors, and management of CAP in different countries except China. The aim of this study is to determine the risk factors and types of treatment for coronary perforation occurring in patients undergoing PCI and living in the Cangzhou Chinese population. METHODS AND RESULTS: A retrospective cohort of 12,113 patients who underwent PCI was used: 64 patients with CAP and 192 case-control patients were evaluated. Clinical data and findings from coronary arteriography and PCI were analysed. Logistic regression was used to evaluate candidate risk factors for CAP. The treatments were also evaluated. The incidence of CAP in patients undergoing PCI was 0.53%, and the mortality was 7.8% (5/64). Risk factors included female gender, hypertension, non-ST-elevation acute coronary syndrome (NSTE-ACS), right coronary artery (RCA) lesion, calcified lesion, and chronic total occlusion (CTO) (all P < 0.05, all OR > 1). CTO had the highest risk (OR = 5.077, P < 0.001). Patients with class I CAP underwent conservative treatment. Patients with class II CAP underwent conservative treatment or low-pressure balloon dilatation (61.1% and 22.2%, respectively). Patients with class III CAP underwent low-pressure balloon dilatation, coated-stent implantation, and emergency surgery (40.9%, 27.3%, and 22.7%, respectively). CONCLUSIONS: CAP risk factors in Cangzhou Chinese patients undergoing PCI included CTO, NSTE-ACS, hypertension, calcified and RCA lesions, and female gender. Different treatment methods should be used according to the different classes of CAP.