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Background: Mounting evidence suggests that endothelial cell-derived microparticles (EMPs) and red blood cell-derived microparticles (RMPs), which have procoagulant and vasoconstriction effects, are involved in the development of vascular acute cardiovascular events. The aim of this study was to analyze the circulating levels of EMPs and RMPs in patients with acute myocardial infarction (AMI), and to explore the correlations between EMPs and RMPs and the severity of coronary artery disease.Methods: Plasma samples from 110 patients with AMI and 57 non-coronary artery disease group (non-CAD) were collected in the present study. The flow cytometry was used to measure the EMPs (CD31) and RMPs (CD235a) qualitatively and quantitatively.Results: The levels of EMPs and RMPs in the AMI group were higher than that in the Non-CAD group, yet no significant difference was found between STEMI and non-STEMI subjects. The levels of EMPs and RMPs in multi-vessel were higher than in the single-vessel l disease. In the Thrombolysis in Myocardial Infarction (TIMI) risk assessment, the levels of EMPs in the high-risk group were higher than that in both intermediate-and low-risk group. The low-risk group had the lowest EMP levels, the difference between the groups being statistically significant (P=0.001). No significant difference in RMP levels was noted upon TIMI stratification. According to the ROC curve analysis, the areas under the curve (AUC) of EMPs and RMPs were 0.706 and 0.668, respectively. Conclusions:The circulating levels of EMPs and RMPs in patients with AMI are elevated, and the level of EMPs is related to the degree of coronary artery disease and the prognosis risk. The EMPs are more likely to be potential biomarkers than RMPs to provide diagnostic value for AMI.

IntroductionInterleukin (IL)-33 was previously shown to induce angiogenesis and inflammatory activation of endothelial Microparticles(EMPs). Tissue factor (TF) plays a central role in hemostasis and thrombosis.Material and methodsThe study analyzed the coronary blood of level of CD31+EMPs, TF protein and IL-33 protein in Acute Myocardial Infarction (AMI) and stable coronary artery disease (SCAD) patients. Human coronary artery endothelial cells (HCAECs) were treated with IL-33 to obtain EMPs. The TF activity of EMPs was tested by Thermo Fisher by adding the TF antibody. Furthermore, TF and Tissue Factor Pathway Inhibitor (TFPI) protein were tested by ELISA. Finally, NF-κB inhibitor dimethyl fumarate (DMF) and soluble extracellular domain of ST2 coupled to the Fc fragment of human IgG1 (sST2) were added to HCAECs which were treated with IL-33, and the TF protein level was also tested by ELISA.ResultsThe AMI patients had higher level of CD31+EMPs, TF protein and IL-33 protein than the SCAD patients in coronary artery. In AMI patients (N=27), the IL-33 protein positively correlated with CD31+EMPs (r=0.794, p<0.01). According to the ROC curve analysis, the AUC of CD31+EMPs, TF protein and IL-33 protein were 0.888, 0.962 and 0.778 respectively. In the cell culture, the TF activity and TF protein in EMPs increased gradually with time of intervention by the treatment of IL-33. IL-33 binding to the ST2 receptor promoted TF expression by regulating NF-κB activation in EMPs of HCAECs.ConclusionsActivated endothelial cells and EMPs they released simultaneously express TF, which is a risk factor for cardiovascular disease.

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Background and ObjectiveWhite matter lesions (WMLs) are imaging changes in MRI of cerebral small vessel disease associated with vascular risk factors, increasing the risk of dementia, depression, and stroke. Aldosterone (ALD) or activation of mineralocorticoid receptor (MR) causes cerebrovascular injury in a mouse model. We aimed to analyze the relationship between ALD and WMLs in a population with hypertension.MethodsWe conducted a retrospective review of all patients screened for causes of secondary hypertension. We enrolled 547 patients with WMLs and matched these to controls without WMLs at a 1:1 ratio. White matter lesion load was assessed by using a modified Scheltens’ scale.ResultsAmong the analytic sample (N = 1,094) with ages ranging from 30 to 64 years, 62.2% were male. We divided plasma ALD concentration (PAC), plasma renin activity (PRA), and ALD–renin ratio (ARR) into the third tertile (Q3), second tertile (Q2), and first tertile (Q1). We also analyzed them simultaneously as continuous variables. Multivariate logistic regression analysis showed that participants in Q3 (&gt;17.26 ng/dl) of PAC (OR 1.59, 95% CI 1.15, 2.19), Q3 (&lt;0.80 ng/dl) of PRA (OR 2.50, 95% CI 1.81, 3.44), and Q3 (&gt;18.59 ng/dl per ng/ml*h) of ARR (OR 2.90, 95% CI 2.10, 4.01) had a significantly higher risk of WMLs than those in Q1 (&lt;12.48) of PAC, Q1 (&gt;2.19) of PRA, and Q1 (&lt;6.96) of ARR. In linear regression analysis, we separately analyzed the correlation between the modified Scheltens’ scale score and log(PAC) (β = 2.36; 95% CI 1.30, 3.41; p &lt; 0.001), log(PRA) (β = −1.76; 95% CI −2.09, −1.43; p &lt; 0.001), and log(ARR) (β = 1.86; 95% CI 1.55, 2.17; p &lt; 0.001), which were all significantly correlated with white matter lesion load, after adjusting for confounding factors. Simple mediation analyses showed that systolic blood pressure (SBP) or diastolic blood pressure (DBP) mediated −3.83% or −2.66% of the association between PAC and white matter lesion load, respectively. In stratified analyses, there was no evidence of subgroup heterogeneity concerning the change in the risk of WMLs (p &gt; 0.05 for interaction for all).ConclusionHigher PAC, especially in PAC &gt;17.26 ng/dl, increased the risk of WMLs. PAC was positively associated with white matter lesion load independent of SBP or DBP.

Background Elevated glucose levels at admission are associated with a worse prognosis in patients with acute myocardial infarction (AMI); additionally, such elevation has a higher prognostic value for patients without diabetes. Methods We retrospectively recruited 2412 AMI patients without diabetes from 1 August 2011 to 10 January 2022. The primary outcome was all‐cause mortality during hospitalisation, and the secondary outcomes were cardiogenic shock, ventricular tachycardia, ventricular fibrillation, atrioventricular block and new stroke. Results The mean age of participants was 65 years and 78.6% were male. Of the 2412 patients, all‐cause mortality occurred in 236 patients (9.8%) during hospitalisation. In multivariate‐adjusted models that corrected for variable weights, the risk of all‐cause mortality increased with an increase in random glucose levels at admission; specifically, the risk of all‐cause mortality increased per 1 mg/dL (odds ratio [OR] 1.006, 95% confidence interval [CI]: 1.004–1.008), per 9 mg/dL (OR: 1.06, 95% CI: 1.04–1.08), and per 18 mg/dL (OR: 1.12, 95% CI: 1.07–1.16) increases in admission glucose levels. When admission glucose levels were expressed as a categorical variable, increased levels of glucose (relative to the reference glucose value <140 mg/dL) led to an increased risk of all‐cause mortality; specifically, the OR of all‐cause mortality for 140–200 mg/dL glucose was 1.55 (95% CI: 1.09–2.17) and the OR for glucose >200 mg/dL was 3.08 (95% CI: 2.00–4.62) (P for trend <0.001). The risk of cardiogenic shock also increased with glucose levels with an OR of 1.68 (95% CI: 1.21–2.31) for 140–200 mg/dL glucose and an OR of 3.72 (95% CI: 2.50–5.46) for >200 mg/dL, compared with that of glucose <140 mg/dL. In multivariate‐adjusted spline regression models, an increased risk of all‐cause mortality was observed in patients with glucose ≥122 mg/dL (OR: 1.81, 95% CI: 1.38–2.38, p < 0.001) compared with the reference cohort. Furthermore, patients with glucose ≥111 mg/dL (OR: 2.36, 95% CI: 1.80–3.12) had a higher risk of cardiogenic shock than patients with glucose <111 mg/dL. Conclusions Patients with AMI and without diabetes who had elevated random glucose levels at admission had a higher risk of all‐cause mortality and cardiogenic shock during hospitalisation. In particular, patients with glucose ≥122 mg/dL had an increased risk of all‐cause mortality, and those with glucose ≥111 mg/dL had an increased risk of cardiogenic shock.

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