Fatal arrhythmia associated with novel coronavirus 2019 infection: Case report and literature review.

RATIONALE: The novel coronavirus of 2019 (COVID-19) has inflicted significant harm on the cardiovascular system. Patients presenting with fatal chronic arrhythmias after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are rare, arrhythmia caused by SARS-CoV-2 infection need to be taken seriously. PATIENT CONCERNS: Three female patients were admitted to the hospital with syncopal symptoms. Previously, they had been identified to have COVID-19 infection and none of the patients had a preexisting history of arrhythmia, and upon hospital admission, no electrolyte imbalances associated with arrhythmias were observed. However, following SARS-CoV-2 infection, patients exhibit varying degrees of syncope symptoms. DIAGNOSES: A high-degree atrioventricular block was diagnosed after a comprehensive evaluation of the patient's clinical manifestations and electrocardiogram (ECG) performance. INTERVENTIONS: We performed ECG monitoring of the patient and excluded other causes of arrhythmia. The patient was discharged from the hospital after permanent pacemaker implantation and symptomatic treatment. OUTCOMES: The outpatient follow-ups did not reveal a recurrence of syncope or complications related to the pacemaker in any of the three patients. LESSONS: Some patients did not exhibit any obvious respiratory symptoms or signs following SARS-CoV-2 infection. This suggests that the cardiac conduction system may be the preferred target for some SARS-CoV-2 variants. Therefore, in addition to investigating the causes of malignant arrhythmias, special attention should be paid to SARS-CoV-2 infection in patients with developing arrhythmias. Additionally, permanent pacemaker implantation may be the most suitable option for patients who already have malignant arrhythmias.

Decreasing mitochondrial fission ameliorates HIF-1α-dependent pathological retinal angiogenesis.

Angiogenesis plays a critical role in many pathological processes, including irreversible blindness in eye diseases such as retinopathy of prematurity. Endothelial mitochondria are dynamic organelles that undergo constant fusion and fission and are critical signalling hubs that modulate angiogenesis by coordinating reactive oxygen species (ROS) production and calcium signalling and metabolism. In this study, we investigated the role of mitochondrial dynamics in pathological retinal angiogenesis. We showed that treatment with vascular endothelial growth factor (VEGF; 20 ng/ml) induced mitochondrial fission in HUVECs by promoting the phosphorylation of dynamin-related protein 1 (DRP1). DRP1 knockdown or pretreatment with the DRP1 inhibitor Mdivi-1 (5 µM) blocked VEGF-induced cell migration, proliferation, and tube formation in HUVECs. We demonstrated that VEGF treatment increased mitochondrial ROS production in HUVECs, which was necessary for HIF-1α-dependent glycolysis, as well as proliferation, migration, and tube formation, and the inhibition of mitochondrial fission prevented VEGF-induced mitochondrial ROS production. In an oxygen-induced retinopathy (OIR) mouse model, we found that active DRP1 was highly expressed in endothelial cells in neovascular tufts. The administration of Mdivi-1 (10 mg·kg-1·d-1, i.p.) for three days from postnatal day (P) 13 until P15 significantly alleviated pathological angiogenesis in the retina. Our results suggest that targeting mitochondrial fission may be a therapeutic strategy for proliferative retinopathies and other diseases that are dependent on pathological angiogenesis.

The effect of Fenton reaction using H2O2 and water control on the distribution and accumulation of As speciation within the soil-rice system.

The behavior of arsenic (As) in paddy soil is of great interest because rice is an efficient As accumulator, which can result in potential health risks to humans. In this study, we investigated the distribution and translocation of As speciation within the soil-rice system in the presence of Fenton solution (100 µM H2O2 and 100 µM Fe2+). The results showed that the iron plaque concentrations were enhanced either by the addition of Fenton solution or under flooded condition. In addition, total As, As5+, and As3+ concentrations were lower in rice tissues treated with Fenton solution than those without Fenton solution treatments. Therefore the addition of Fenton solution can reduce As speciation accumulation in rice tissue. This study revealed the function of Fenton solution on the fate of As speciation distribution within soil-rice system and the link between iron plaque and As accumulation in rice tissue under flooded and non-flooded conditions.

Exercise training restores IGFIR survival signaling in d-galactose induced-aging rats to suppress cardiac apoptosis.

INTRODUCTION: Insulin-like growth factor-I receptor (IGF1R) mediated survival signaling is a crucial mechanism for cellular endurance and a potential indicator of recuperation in deteriorating hearts. OBJECTIVE: This study evaluates the impact of long-term exercise training in enhancing cardiac survival mechanism in D-galactose-induced toxicity associated aging rats. METHODS: Forty-eight male SD-rats were segregated into 4 groups (n=9) and were named as control, exercise training groups, aging group and aging group with exercise training. Aging was induced by intraperitoneal (IP) D-galactose (150 mL/kg) injection for 8 weeks and for exercise training, the rats were left to swim in warm water for 60 min every day and 5 times/week. Western blotting of proteins from the left ventricles was performed to identify the modulations in the survival signaling. Tissue sections were analyzed to determine the extent of fibrosis and apoptosis. RESULTS: Western-blot analysis performed on the excised left ventricles (LV) showed that proteins of the cardiac survival pathway including IGF1R and Akt and the pro-survival Bcl-2 showed significant decrease in the aging group, whereas the levels were restored in the aging rats subjected to exercise training. In addition, aging groups showed increased interstitial space and collagen accumulation. Further, TUNEL assay showed higher number of apoptotic cells in the LV of aging group, which was correlated with increase in the proteins involved in FAS-FADD-dependent apoptosis. However, these aging associated effects were ameliorated upon exercise training in the D-galactose-induced aging rats that showed elevated IGF1R/Akt signaling. CONCLUSION: The results suggest that IGFIR survival signaling cascadeis elevated in following long-term exercise training and thereby provide cardio-protective benefits in D-galactose induced aging rats.

Tetramethylpyrazine reverses high-glucose induced hypoxic effects by negatively regulating HIF-1α induced BNIP3 expression to ameliorate H9c2 cardiomyoblast apoptosis.

BACKGROUND: Diabetic patients are highly vulnerable to hypoxic injury, which is associated with hypoxia induced BNIP3 expression that subsequently activate apoptosis. Our previous research show that Tetramethylpyrazine (TMP), a food flavoring agent, represses the hypoxia induced BNIP3 expression attenuate myocardial apoptosis. In this study, we evaluate the effect of TMP to provide protection against hypoxia aggravated high-glucose associated cellular apoptosis. METHODS: The cytoprotective effect of TMP against high glucose induced cellular damages was determined on embryo derived H9c2 cardiomyoblast cells that were subjected to 5% hypoxia for 24 h and subjected to different duration of 33 mM high glucose challenge. Further, the involvement of HIF-1α and BNIP3 in cellular damage and the mechanism of protection of TMP were determined by overexpression and silencing HIF-1α and BNIP3 protein expression. RESULTS: The results show that hypoxic effects on cell viability aggravates with high glucose challenge and this augmentative effect is mediated through BNIP3 in H9c2 cardiomyoblast cells. However, TMP administration effectively reversed the augmented HIF-1α levels and BNIP3 elevation. TMP improved the survival of H9c2 cells and effectively suppressed apoptosis in H9c2 cells. Further comparison on the effects of TMP on H9c2 cells challenged with high glucose and those challenged with hypoxia show that TMP precisely regulated the hypoxic intensified apoptotic effects in high-glucose condition. CONCLUSION: The results clearly show that flavoring agent-TMP attenuates cytotoxicity amplified by hypoxia challenge in high glucose condition by destabilizing HIF-1α.

Applying WCACG modified process is beneficial on reduced door-to-balloon time of acute STEMI patients.

BACKGROUND: Various systems have employed with the objective to reduce the time from emergency medical services contact to balloon inflammation for ST-elevation myocardial infraction (STEMI) patients. The WCACG message system was used to an alternative communication platform to improve confirmation of the diagnosis and movement to treatment, resulted in shorten the door-to-balloon (D-to-B) time for STEMI patients. METHODS: We collected 366 STEMI patients admitted at the Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Department of Cardiology, during the period from June 2013 to October 2015. The patients were divided into two groups one underwent the current GC processes and the other group was handled using WCACG system. We compared between two groups with several indicators including D-to-B time, duration of hospitalization, associated costs, and incidence of adverse cardiovascular events. RESULTS: The results show that the new method with WCACG system significantly reduced the average D-to-B time (from 100.42 ± 25.14 mins to 79.81 ± 20.51 mins, P < 0.05) compared to the GC processes, and also reduced the duration, costs and undesirable cardiac incidence during hospitalization. CONCLUSIONS: The modified WCACG process is an applicable system to save pieces of time and efficiently integrate the opinions of experts in emergency.

The correlation between plasma tissue factor and interleukin 18 and their significance in patients with acute coronary syndrome.

Studies suggested that the activation of the coagulation system and inflammation mutually may reinforce each other in some cases. In this study, we test the plasma tissue factor (TF) and interleukin 18 in patients with coronary heart disease (CHD) before and after treatment and aim to determine whether this relationship exists in patients with CHD. The levels of plasma TF and IL-18 from 118 patients with CHD were determined by enzyme-linked immunosorbent assay. One hundred and eighteen patients were divided into acute coronary syndrome (ACS) group (61 cases) and stable angina pectoris group (51 cases). Upon admission, patients with ACS showed significantly higher levels of plasma TF and interleukin 18 compared with those having stable angina (P < 0.01), and the levels decreased after treatment; levels of plasma TF and interleukin 18 of patients with ACS were closely and positively correlated (r = 0.74, P < 0.01); after 7 days of treatment, the correlation decreased (r = 0.53, P > 0.05); and after 1 month of treatment, no significant correlation can be detected between the two (r = 0.18, P > 0.05). The results suggest that levels of plasma TF and interleukin 18 are significantly increased in patients with ACS, and there is significant correlation between the two, indicating an interaction between inflammation and coagulation in patients with ACS and an important role of these two in the occurrence and development of such disease.

Evaluated plasma interleukin-18/interleukin-10 ratio is a risk factor for acute coronary syndromes in patients with stable angina pectoris.

BACKGROUND: Studies suggested that interleukin-18 (IL-18)/interleukin-10 (IL-10) ratio is an independent predictor of adverse cardiovascular events in patients with acute coronary syndromes (ACS). In this study we aimed to evaluate the predictive significance of IL-18/IL-10 for the occurrence of ACS in patients with stable angina pectoris (SAP) over a 40-month follow-up. METHODS: The IL-18, IL-10 levels of 257 patients with SAP were determined by Enzyme-Linked Immunosorbent Assay (ELISA). Two hundred and fifty-two patients, 42 of whom had ACS and 210 were event-free, were divided into two groups according to the presence or absence of the occurrence of ACS during the 40-month follow-up. RESULTS: Plasma IL-18 and IL-18/IL-10 ratios were both significantly higher (p = 0.001 and p = 0.044, respectively) among patients with ACS, however, IL-10 level was lower (p = 0.046) compared to the patients without ACS. The elevation of plasma IL-18/IL-10 ratio and the number of coronary artery lesions made the advantage ratio of ACS in patients with SAP increase 4.242 times and 1.942 times (p = 0.000 and p = 0.011, respectively). CONCLUSIONS: Plasma IL-18 and IL-10 levels in patients with SAP are closely related to the occurrence of ACS, elevated IL-18/IL-10 ratio has a positive predictive value for the occurrence of ACS in patients with SAP.