Analysis of the Factors Associated with Negative Conversion of Severe Acute Respiratory Syndrome Coronavirus 2 RNA of Coronavirus Disease 2019

AIM: To understand the factors associated with negative conversion of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA, targeted surveillance and control measures can be taken to provide scientific basis for the treatment of the disease and to improve the prognosis of the disease. METHODS: Using the method of retrospective cohort study, we collected the data of Coronavirus Disease 2019 (COVID-19) patients in Tongji Hospital of Wuhan, China from 10 January to 25 March, 2020. Among the data of 282 cases, 271 patients, according to whether the negative conversion happened, were divided into negative conversion group and control group. We made the quantitative variables into classification; Chi-square test single-factor and Cox regression were used in univariate analysis and extracted 30 meaningful variables, then through the collinearity diagnosis, excluded the existence of collinear variables. Finally, 22 variables were included in Cox regression analysis. RESULTS: The gender distribution was statistically significant between two groups (p < 0.05). While in the negative conversion group, the patients of non-severe group occupied a large proportion (p < 0.001). The median time for the negative conversion group was 17 days, and at the end of the observation period, the virus duration in control group was 24 days (p < 0.05). A total of 55 variables were included in univariate analysis, among which 30 variables were statistically different between the two groups. After screening variables through collinearity diagnosis, 22 variables were included in the Cox regression analysis. Last, lactate dehydrogenase (LDH), age, fibrinogen (FIB), and disease severity were associated with negative conversion of SARS-CoV-2 RNA. CONCLUSION: Our results suggest that in the treatment of COVID-19, focus on the age of more than 65 years old, severe, high level of LDH, FIB patients, and take some targeted treatment, such as controlling of inflammation, reducing organ damage, so as to provide good conditions for virus clearance in the body

Ruptured left ventricular pseudoaneurysm in the mediastinum following acute myocardial infarction: a case report

<p>Abstract</p> <p>Left ventricular pseudoaneurysm is an uncommon complication after transmural acute myocardial infarction (AMI). Here we describe the case of a 43-year-old man who presented with AMI and chest distress despite the normal appearance of his coronary artery during coronary angiography. Timely thrombolytic therapy was administered. Echocardiography, and cardiac computed tomography showed a ventricular pseudoaneurysm, and direct visualization at the time of surgery showed that it had ruptured in the mediastinum instead of the pericardium. The survival rate of patients with ventricular pseudoaneurysm rupture is low. The rupture of ventricular pseudoaneurysm in the mediastinum is rare; therefore, this case is noteworthy.</p

A new technique to salvage myocardium following the failure of thrombus aspiration in acute myocardial infarction: a case report

Abstract Background The failure of aspiration thrombectomy may negatively impact outcomes in patients with acute myocardial infarction (AMI), but the available options are limited. Case presentation A 41-year-old man with chest pain for 2 h presented with ST-segment elevation myocardial infarction. Coronary angiography revealed a large filling defect extending from the distal left main (LM) coronary artery into the proximal left circumflex (LCX) coronary artery. The whole thrombus moved and occluded the proximal left anterior descending (LAD) artery, while the guidewire crossed the lesion. Dedicated manual aspiration thrombectomy (MAT) and balloon dilation failed to reduce thrombus burden. We considered thrombus extraction as impossible when it moved forward to occlude the middle LAD. To reduce infarct size, a new balloon-pushing technique was successfully performed to move the thrombus to the terminal LAD based on the actual condition of the LAD. The final angiogram demonstrated no stenosis in the LM artery and stent deployment was not performed. A 1-week follow-up coronary angiography revealed the complete resolution of thrombus and flow restoration in the left coronary artery. Intravascular ultrasound (IVUS) showed nonsignificant residual stenosis of the LM artery. No adverse events occurred during a 12-month follow-up period. Conclusion This case suggests that the new balloon-pushing technique is a useful remedy if repeated MAT fails during AMI

A new method for the assessment of endothelial function with peripheral arterial volume

Abstract Background Currently, many methodological approaches have been developed to assess peripheral endothelial function. However, a development of the noninvasive and automated technique for routinely assessing endothelial function is still required. We evaluated the potential value of a new method to measure peripheral endothelial function with reactive hyperemia peripheral arterial volume (RH-PAV) in patients with chest pain. Methods We used a novel oximeter-like probe to detect the peripheral arterial volume (PAV) of the finger and compared it with brachial flow-mediated dilation (FMD) performed in 93 consecutive patients with chest pain. The RH-PAV index was defined as the ratio of the digital pulse volume during reactive hyperemia relative to the baseline. Results Ninety-three patients (53 men, 58 ± 5 years) completed the study, and 53 patients demonstrated coronary artery disease (CAD) following scheduled coronary angiography. There was a moderate linear relationship between PAV and FMD (r = 0.69, p < 0.01). Similar to FMD, PAV was more impaired in patients who have more cardiovascular risk factors (CRFs). The subjects with CAD had lower PAV and FMD, compared with those without CAD (1.05 ± 0.23 VS. 1.41 ± 0.37, p < 0.01; 6.7% ± 2.9% VS. 10.4% ± 2.9%, p < 0.01, respectively), and the relationships between FMD and PAV were also significant in both CAD (r = 0.54, p < 0.01) and non-CAD (r = 0.62, p < 0.01) patients. Conclusions Endothelial function of digital artery assessed with the novel PAV method demonstrated a profile similar to that of brachial artery measured with FMD. The hyperemia PAV was decreased by factors which were considered to impair endothelial function, suggesting that PAV has the potential to be a novel method to study endothelial function

Rivaroxaban, a direct inhibitor of coagulation factor Xa, attenuates adverse cardiac remodeling in rats by regulating the PAR-2 and TGF-β1 signaling pathways

Background Factor Xa (FXa) not only plays an active role in the coagulation cascade but also exerts non-hemostatic signaling through the protease-activated receptors (PARs). This study aimed to investigate whether the FXa inhibitor, Rivaroxaban (RIV), attenuates adverse cardiac remodeling in rats with myocardial infarction (MI) and to identify the underlying molecular mechanisms it uses. Methods An MI model was induced in eight-week-old, male Wistar rats, by permanent ligation of the left anterior descending coronary artery. MI rats were randomly assigned to receive RIV or protease-activated receptors 2-antagonist (PAR-2 antagonist, FSLLRY) treatment for four weeks. Histological staining, echocardiography and hemodynamics were used to assess the cardioprotective effects of RIV. Meanwhile, pharmacological approaches of agonist and inhibitor were used to observe the potential pathways in which RIV exerts antifibrotic effects in neonatal rat cardiac fibroblasts (CFs). In addition, real-time PCR and western blot analysis were performed to examine the associated signaling pathways. Results RIV presented favorable protection of left ventricular (LV) cardiac function in MI rats by significantly reducing myocardial infarct size, ameliorating myocardial pathological damage and improving left ventricular (LV) remodeling. Similar improvements in the PAR-2 antagonist FSLLRY and RIV groups suggested that RIV protects against cardiac dysfunction in MI rats by ameliorating PAR-2 activation. Furthermore, an in vitro model of fibrosis was then generated by applying angiotensin II (Ang II) to neonatal rat cardiac fibroblasts (CFs). Consistent with the findings of the animal experiments, RIV and FSLLRY inhibited the expression of fibrosis markers and suppressed the intracellular upregulation of transforming growth factor β1 (TGFβ1), as well as its downstream Smad2/3 phosphorylation effectors in Ang II-induced fibrosis, and PAR-2 agonist peptide (PAR-2 AP) reversed the inhibition effect of RIV. Conclusions Our findings demonstrate that RIV attenuates MI-induced cardiac remodeling and improves heart function, partly by inhibiting the activation of the PAR-2 and TGF-β1 signaling pathways

Genome-Wide Characterization of HSP90 Gene Family in Malus sieversii and Their Potential Roles in Response to Valsa mali Infection

Heat shock protein 90 (HSP90) is highly conservative molecular chaperon produced by plants in response to adverse environmental stresses including fungal infection. In China, canker disease, caused by Valsa mali, is the main threat for Malus sieversii, an ancestor of the cultivated apple. In this study, a total of eight HSP90 genes were identified from the M. sieversii genome and randomly distributed on eight chromosomes. According to gene structure and phylogenetic analysis, the MsHSP90s can be divided into five categories. The transcriptome analysis of M. sieversii under V. mali infection showed that the plant pathogen interaction pathway was identified as significantly enriched. RNA-seq data and qRT-PCR analysis demonstrated that the MsHSP90-6a gene was significantly repressed by V. mali infection. We further predicted cis-regulatory elements on the promotor region of MsHSP90 genes and identified canonical SHE motifs. Our results improve our understanding of the HSP90 gene family and provide a foundation for further studies of disease prevention in M. sieversii

DataSheet1_Rivaroxaban in heart failure patients with left ventricular thrombus: A retrospective study.DOCX

Background: The role of rivaroxaban in patients with heart failure (HF) combined with left ventricular (LV) thrombus remains unknown in current guideline-directed anticoagulant therapy. The aim of this study was to investigate the impact on clinical outcomes of rivaroxaban compared to vitamin K antagonists (VKAs) in patients with HF combined with LV thrombus.Methods: We retrospectively extracted clinical, echocardiographic and follow-up data of HF patients (all classifications) admitted at China-Japan Union Hospital of Jilin University from January 2017 to June 2021. A total of 198 patients with HF were identified with LV thrombus by echocardiography, 78 of them were managed with VKAs, 109 with rivaroxaban.Results: The median follow-up was 17.0 months (interquartile range: 6.0–24.0 months). High rates of major cardiovascular adverse events (MACEs) were observed in both the rivaroxaban and VKAs groups (49.5% vs. 57.7%). However, rivaroxaban versus VKAs observed a decrease in MACEs (adjusted HR:0.636; 95%CI:0.418–0.970; p = 0.035) and systemic embolism (4.6% vs. 12.8%; adjusted HR:0.318; 95%CI:0.108–0.933; p = 0.037; Gray’s test p = 0.041) but was not found to have a benefit with regard to LV thrombus resolution (59.6% vs. 70.6%; adjusted HR: 1.303; 95% CI:0.898–1.890; p = 0.163; Gray’s test p = 0.073). Additionally, there was no significant between-group difference in the rate of International Society on Thrombosis and Hemostasis (ISTH) bleeding events.Conclusion: Our data found that in populations with HF combined with LV thrombus, the overall prognosis in both the rivaroxaban and VKAs groups was catastrophic. Although rivaroxaban improved the prognosis to some extent, a considerable need remains for new treatments to improve their clinical course.</p