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Ventricular arrhythmias (VTA) usually occur following acute myocardial infarction (AMI). However, risk factors for VTA attack after AMI have been not well-recognized. The purpose of the study is to identify risk factors associated with the incidence of VTA complicating AMI. A total of 200 patients with AMI who were admitted to our hospital from February 2018 to February 2020 were retrospectively analyzed. These 200 patients were classified into a non-VTA group ( n = 140 ) and a VTA group ( n = 60 ) based on the occurrence of VTA within 24 after AMI. Patients in the VTA group were older than those in the non-VTA group. The VTA group had more numbers of WBCs and neutrophils than the non-VTA group. The level of serum potassium was lower, but the levels of cTnT and CK-MB were higher in the VTA group than in the non-VTA group. The VTA group presented an increase in proportions of anterior MI, TpTe, and proportions of Killip classification ≥ class II but a decline in LVEF when comparable to the non-VTA group. The two groups were not significantly different concerning other variables including sex, tobacco use, alcohol consumption, diabetes mellitus, hypertension, heart rate, Scr, SUA, BUN, PTL counts, TC, TG, HDL-C, LDL-C, D-dimer, BNP, LVS, LVP, and LVEDd. The levels of hsCRP, endothelin-1, and TNF-α were remarkably higher in the VTA group than in the non-VTA group ( P < 0.001 ). Multivariate logistic regression analysis was performed, with clinical variables including age, WBCs, neutrophils, serum potassium, cTnT, CK-MB, hsCRP, endothelin-1, TNF-α, anterior MI, TpTe, proportions of Killip classification ≥ class II, and LVEF as an independent variable and with the occurrence of VTA as a dependent variable. It was revealed that serum potassium, cTnT, CK-MB, hsCRP, endothelin-1, TpTe, proportions of Killip classification ≥ class II, and LVEF were independent risk factors of VTA complicating AMI. Compared with the non-VTA group, the incidence rate of simple left heart failure, total heart failure, stroke, and dyslipidemia in the VTA group was significantly higher than those in the non-VTA group ( P < 0.05 ). It was found that the proportion of all-cause deaths within one year outside the hospital was higher in the VAT group than in the non-VAT group ( P < 0.05 ). Collectively, the study demonstrates serum potassium, cTnT, CK-MB, hsCRP, endothelin-1, TpTe, proportions of Killip classification ≥ class II, and LVEF were independent risk factors of VTA complicating AMI.

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Background: Association between plasma pentraxin-3 (PTX-3) and clinical outcomes in patients with coronary artery disease (CAD) remains not fully determined. An updated meta-analysis of cohort studies was performed to systematically evaluate the association.Methods: Cohort studies evaluating the association between plasma PTX-3 and adverse outcomes [mortality and major adverse cardiovascular events (MACEs)] in adults with CAD were identified by systematic search of PubMed, Embase, and Web of Science databases. Only studies with multivariate analysis were included. A random-effects model incorporating the potential intrastudy heterogeneity was used for the meta-analysis.Results: A total of 16 studies including 11,007 patients were included. Pooled results showed that patients with highest level of PTX-3 were independently associated with higher risk of mortality [adjusted risk ratio (RR): 2.09, 95% CI: 1.60 to 2.74, p &lt; 0.001; I2 = 50%] and MACEs (adjusted RR: 1.80, 95% CI: 1.43 to 2.28, p &lt; 0.001; I2 = 49%). Subgroup analyses showed that the associations between PTX-3 and poor prognosis in CAD were consistent in patients with ST-segment elevation myocardial infraction, non-ST-segment elevation acute coronary syndrome, and stable CAD (p &lt; 0.05 for each subgroup). Besides, the association between PTX-3 and increased incidence of mortality and MACEs were consistent in short-term (within 1 year) and long-term (over 1 year) studies and in studies with or without adjustment of C-reactive protein (CRP) (p &lt; 0.05 for each subgroup).Conclusion: Higher plasma PTX-3 is associated with poor prognosis in patients with CAD, which may be independent of the CAD subtype, follow-up durations, and adjustment of CRP.

Objective: To explore the improvement of Allicin on myocardial fibrosis and expression of MAPK1/2 and MMP-8 in rats. Methods : Dividing 30 SD rats into 3 groups, normal control, model and Allicin treatment based on model (Allicin) groups. Using 40 mg/kg streptozotocin (STZ) to make diabetes model. The the NC and Model groups' rats received daily intraperitoneal injections of saline, and those in Allicin group was given Allicin (40 mg/kg) injections. After 8 weeks, the pathologies of cardiac fibrosis were examined with HE staining and Masson staining, the proteins expressions of collagen I, MAPK1/3 and MMP-8 were analyzed with WB and IHC assay. Results: Compared with NC group, the Model rats showed increased collagen content and obvious interstitial fibrosis in the myocardial tissue with significantly increased expression levels of collagen I, MAPK1/3 and MMP-8 (P < 0 001, respectively); all the changes were obviously reversed by treatment with Allicin (P < 0 001). Collagen I, MAPK1/3 and MMP-8 expression levels and the degree of myocardial fibrosis were comparable between Allicin group and NC group (P > 0 05). Conclusion: Allicin could improve cardiac fibrosis in diabetic rats, and the mechanism might involve the inhibition of MAPK1/3/MMP-8 signal pathway.