Outcome of Impella 2.5 use in patients undergoing Percutaneous Coronary Intervention in Henan, China: a case series.

BACKGROUND: Acute myocardial infarction (AMI) complicated by cardiogenic shock (AMI-CS) or heart failure is associated with an unacceptably high in-hospital mortality of 33%-55% and a lost chance to accept PCI (Percutaneous Coronary Intervention). AIM: The aim of the study was to find out whether percutaneous hemodynamic support device Impella 2.5 improves prognosis of high-risk PCI patients or not. METHODS: This study was a case series involving six patients who underwent a Left Ventricular Assist Device (LVAD, Impella 2.5, Abiomed, Danvers, MA) implantation after suffering from AMI with a very low ejection fraction and acute heart failure. The clinical experience and outcomes of the patients are hereby discussed. RESULTS: All PCI procedures were safely completed under LVAD support. The hemodynamic parameters of all patients improved clinically over the next 30 days and following 12 months after Impella insertion except in two patients, of which one patient (Case number 6) died 4 days post-Impella protected PCI procedure due to acute left ventricle heart failure with cardiogenic shock and pulmonary oedema; and another one died at 12 months after Impella protected PCI procedure (Case number 4) due to decompensated heart failure and infected pneumonia. CONCLUSION: Percutaneous hemodynamic support is favorable and feasible during high risk Percutaneous Coronary Intervention (PCI). A bigger study is needed to substantiate the claims of the current study.

The Effects of the SARS-CoV-2 Virus on the Cardiovascular System and Coagulation State Leading to Cardiovascular Diseases: A Narrative Review.

The novel coronavirus pandemic has led to morbidity and mortality throughout the world. Until now, it is a highly virulent contagion attacking the respiratory system in humans, especially people with chronic diseases and the elderly who are most vulnerable. A majority of afflicted are those suffering from cardiovascular and coronary diseases. In this review article, an attempt has been made to discuss and thoroughly review the mode of therapies that alleviate cardiac complications and complications due to hypercoagulation in patients infected with the SARS-CoV-2 virus. Presently a host of thrombolytic drugs are in use like Prourokinase, Retelapse, RhTNK-tPA and Urokinase. However, thrombolytic therapy, especially if given intravenously, is associated with a serious risk of intracranial haemorrhage, systemic haemorrhage, immunologic complications, hypotension and myocardial rupture. The effects of the SARS-CoV-2 virus upon the cardiovascular system and coagulation state of the body are being closely studied. In connection to the same, clinical prognosis and complications of thrombolytic therapy are being scrutinized. It is noteworthy to mention that myocardial oxygen supply/demand mismatch, direct myocardial cells injury and acute plaque rupture are the multiple mechanisms responsible for acute coronary syndrome and cardiac complications in Covid-19 infection. However, this review has limitations as data available in this context is limited, scattered and heterogenous that questions the reliability of the same. So, more multi-centric studies involving representative populations, carried out meticulously, could further assist in responding better to cardiac complications among Covid-19 patients.

LncRNA KCNQ1OT1 as a miR-26a-5p sponge regulates ATG12-mediated cardiomyocyte autophagy and aggravates myocardial infarction.

BACKGROUND: As a dominant cardiovascular disease, myocardial infarction (MI) causes a considerable mortality globally. KCNQ1 overlapping transcript 1 (KCNQ1OT1) was reported to be overexpressed in MI patients. However, the detailed mechanisms remain unclear. METHODS: We analyzed the expression of KCNQ1OT1 in the serum of MI patients, and built ischemia/reperfusion (I/R) mouse and H/R-induced cell model. TTC staining was used to evaluate infarct size in mice. TUNEL was employed to assess cell apoptosis. QRT-PCR was performed to detect the expression of KCNQ1OT1 and miR-26a-5p. The formation of autophagosomes in cells was detected by immunofluorescence. Caspase3 activity was detected by the Caspase-3 Assay Kit. Autophagy and apoptosis-related proteins were assessed by western blotting. Luciferase reporter assay was used to assess the binding relationship of KCNQ1OT1 and miR-26a-5p and miR-20a-5p/ATG12. RESULTS: KCNQ1OT1 was up-regulated while miR-26a-5p was decreased in MI patients, I/R mouse and H/R-induced cell model. KCNQ1OT1 knockdown inhibited cell autophagy and protected cardiomyocytes from apoptosis by up-regulating miR-26a-5p. Either KCNQ1OT1 knockdown or miR-26a-5p mimics caused inhibition of autophagy related 12 homolog (ATG12), which was the direct target of miR-26a-5p. In vivo, KCNQ1OT1 promoted cardiomyocytes apoptosis via miR-26a-5p/ATG12 pathway. CONCLUSION: KCNQ1OT1/miR-26a-5p/ATG12 axis regulated cardiomyocyte autophagy and apoptosis, both in vivo and in vitro. These data supported that KCNQ1OT1 inhibition might be a promising therapeutic option for protection after MI.

Knockdown of lncRNA RMST protect against myocardial infarction through regulating miR-5692 and MAGI3 axis.

AIMS: Myocardial infarction is the leading cause of death worldwide. The aim of this study was to investigate the function and mechanism of lncRNA RMST in myocardial infarction. MATERIALS AND METHODS: H/R and H2O2 models were established to assess the function of lncRNA RMST in vitro. Mouse myocardial infarction was used to analyze the function of lncRNA RMST in vivo. Bioinformatics analysis was performed to predict the potential binding target of lncRNA RMST. Rescue experiments were performed to verify the relationship between RMST and its target. RESULTS: The expression of lncRNA RMST was significantly increased with H/R or H2O2 treatment. Knockdown of lncRNA RMST improved cell death and protected mitochondria from H/R injury in vitro. In vivo, cardiac function was significantly attenuated by knockdown of lncRNA RMST. We also provided evidence that miR-5692 was a direct target of lncRNA RMST. Rescue experiments showed that knockdown of miR-5692 could restore the function of RMST. CONCLUSION: Our study is the first to prove the function and mechanism of lncRNA RMST in myocardial infarction. Thus, a deeper understanding of the role of lncRNA RMST in myocardial infarction may provide new insights for the clinical intervention of MI.

MiR-708-3p Alleviates Inflammation and Myocardial Injury After Myocardial Infarction by Suppressing ADAM17 Expression.

MicroRNAs (miRNAs) emerge as important regulators for myocardial infarction (MI). However, the function of miR-708-3p during MI is unclear. H9c2 cells were cultured in a hypoxic environment and Sprague-Dawley rats experienced surgical ligation of the left anterior descending coronary artery to establish MI models. qPCR was used to measure the expression level of miR-708-3p and ADAM17 mRNA. ELISA was used to detect inflammatory cytokines TNF-α, IL-6, and IL-1ß, and myocardial injury markers LDH, CK-MB, and cTnI. Cell apoptosis and viability were monitored by flow cytometry analysis and MTT assay. ADAM17 expression was detected by Western blot. Dual-luciferase reporter gene experiments were carried out to identify binding sites between miR-708-3p and ADAM17 3'UTR. In vivo, left ventricle functions and myocardial remodeling of the rats were measured by echocardiography. MiR-708-3p was found to be significantly decreased in H9c2 cells after hypoxia induction and in heart tissues of rats with MI or serum samples of patients with MI, while ADAM17 was upregulated. Overexpression of miR-708-3p inhibited inflammation and injury of H9c2 cells cultured in hypoxia and the heart of the rats with MI. ADAM17 was verified as a direct target of miR-708-3p and restoration of ADAM17 reversed the effects of miR-708-3p. MiR-708-3p alleviated the inflammation and injury of cardiomyocytes via targeting ADAM17.

Screening and Identification of Antipyretic Components in the Postfrost Leaves of Morus alba Based on Multivariable and Continuous-Index Spectrum-Effect Correlation.

The leaves of Morus alba (LMA) are crucial traditional Chinese medicine (TCM) of clearing heat. In ancient Chinese materia medica and the current Pharmacopoeia of the People's Republic of China, LMA are recorded to be harvested after frost for medicinal purpose. However, the reason and mechanism of this traditional usage have been still unknown so far. In this work, it was confirmed firstly that the antipyretic effect of LMA after frost was better than that of before frost significantly on feverish rats. Subsequently, the chemical profiles of LMA before and after frost were characterized by fingerprint, respectively. Then, the endemic peaks after frost and positive differential peaks were screened as the research object of spectrum-effect correlation by orthogonal signal correction partial least square discrimination (OPLS). Finally, a multivariable and continuous-index spectrum-effect correlation model coupled with OPLS was established. As a result, the antipyretic components of postfrost LMA were screened and identified as citric acid derivative and tryptophan which may be the synergistic material basis. The study can provide a scientific foundation for the enhancement of effects in the postfrost LMA. Moreover, the strategy of this research could provide a valuable reference for revealing the material basis of synergetic or antagonistic effects among other complex drug systems.

Matrine Protects Cardiomyocytes From Ischemia/Reperfusion Injury by Regulating HSP70 Expression Via Activation of the JAK2/STAT3 Pathway.

Studies have shown that matrine showed cardiovascular protective effects; however, its role and mechanism in myocardial ischemia/reperfusion (I/R) injury remain unknown. The Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway activation and elevated heat shock protein (HSP) 70 are closely related to the prevention of myocardial I/R injury. The cardioprotective effects of matrine were determined in hypoxia/reoxygenation (H/R)-treated primary rat cardiomyocytes and left anterior descending coronary artery ligation and reperfusion animal models. The molecular mechanisms of matrine in myocardial I/R injury were focused on JAK2/STAT3 pathway activation and HSP70 expression. We found that matrine significantly increased H/R-induced the suppression of cell viability, decreased lactate dehydrogenase release, creatine kinase activity, and cardiomyocytes apoptosis in vitro. Moreover, matrine notably reduced the serum levels of creatine kinase-myocardial band (CK-MB) and cardiac troponin I, lessened the infarcted area of the heart, and decreased the apoptotic index of cardiomyocytes induced by I/R in vivo. Matrine activated the JAK2/STAT3 signaling, upregulated HSP70 expression both in vitro and in vivo. The cardioprotective effects of matrine were abrogated by AG490, a JAK2 inhibitor, and HSP70 siRNA. In addition, AG490 reduced HSP70 expression increased by matrine. In conclusion, matrine attenuates myocardial I/R injury by upregulating HSP70 expression via the activation of the JAK2/STAT3 pathway.

[Optimization of stir-baking with vinegar technology for Curcumae Radix by orthogonal test].

OBJECTIVE: To optimize the stir-baking with vinegar technology for Curcumae Radix. METHOD: The intrinsic quality (the content of Curcumin) and traditional outward appearance were chosen as indexes. The best technology was determined by orthogonal test L9 (3(4)). The factors of the moistening time, stir-baking temperature and stir-baking time were investigated. RESULT: The optimal technology was as follows: the quantity of vinegar was 10%, the moistening time was 10 min, the stir-baking temperature was 130 degrees C and the stir-baking time was 10 min. CONCLUSION: The optimal stir-baking with vinegar technology for Curcumae Radix is reasonable, which can be used to guide the standardized production of Curcumae Radix stir-baked with vinegar.