scholarly journals Molecular Perspectives of Mitophagy in Myocardial Stress: Pathophysiology and Therapeutic Targets

2021 ◽  
Vol 12 ◽  
Author(s):  
Haizhe Ji ◽  
Dan Wu ◽  
O’Maley Kimberlee ◽  
Ruibing Li ◽  
Geng Qian
Keyword(s):  
Energy Supply ◽  
Myocardial Protection ◽  
Myocardial Injury ◽  
Therapeutic Targets ◽  
Cardiac Insufficiency ◽  
Regulatory Pathways ◽  
Myocardial Stress ◽  
Proper Number ◽  
Abnormal Metabolism ◽  
Species Production

A variety of complex risk factors and pathological mechanisms contribute to myocardial stress, which ultimately promotes the development of cardiovascular diseases, including acute cardiac insufficiency, myocardial ischemia, myocardial infarction, high-glycemic myocardial injury, and acute alcoholic cardiotoxicity. Myocardial stress is characterized by abnormal metabolism, excessive reactive oxygen species production, an insufficient energy supply, endoplasmic reticulum stress, mitochondrial damage, and apoptosis. Mitochondria, the main organelles contributing to the energy supply of cardiomyocytes, are key determinants of cell survival and death. Mitophagy is important for cardiomyocyte function and metabolism because it removes damaged and aged mitochondria in a timely manner, thereby maintaining the proper number of normal mitochondria. In this review, we first introduce the general characteristics and regulatory mechanisms of mitophagy. We then describe the three classic mitophagy regulatory pathways and their involvement in myocardial stress. Finally, we discuss the two completely opposite effects of mitophagy on the fate of cardiomyocytes. Our summary of the molecular pathways underlying mitophagy in myocardial stress may provide therapeutic targets for myocardial protection interventions.

scholarly journals Total Intravenous Anesthesia for Myocardial Protection and Preconditioning

2021 ◽  
Author(s):  
Minati Choudhury
Keyword(s):  
Protective Effect ◽  
Surgical Procedure ◽  
Myocardial Protection ◽  
Myocardial Injury ◽  
Volatile Anesthetic ◽  
Organ Protection ◽  
Intravenous Anesthesia ◽  
Intravenous Anesthetic ◽  
Anesthetic Agents ◽  
Anesthetic Preconditioning

AbstractPerioperative myocardial injury is common after any major surgical procedure even with best possible anesthesia and surgical management. Organ preservation during surgical procedure prevents morbidity and mortality. The effect of ischemic preconditioning on myocardial as well as other organ protection is well known. A variety of other agents also shown to have preconditioning thus protective effect on myocardium during anesthesia and surgery. The beneficial effect of volatile anesthetic preconditioning is well studied. However, the effect of intravenous anesthetic agents on this context is still way to go. This review is an attempt to look into the latest available research regarding the preconditioning and myocardial protective effect of intravenous anesthetic agents.

An infant with suspected missed diagnosis of Williams syndrome failed weaning off CPB after surgical correction of pulmonary stenosis: a case report and literature review

Perfusion ◽  
2021 ◽  
pp. 026765912110468
Author(s):  
Yuan Yuan ◽  
Ronghua Zhou
Keyword(s):  
Aortic Stenosis ◽  
Williams Syndrome ◽  
Myocardial Protection ◽  
Developmental Disorder ◽  
Pulmonary Stenosis ◽  
Surgical Correction ◽  
Supravalvular Aortic Stenosis ◽  
Cardiac Insufficiency ◽  
Valvular Stenosis ◽  
Missed Diagnosis

Williams syndrome (WS) is a rare congenital developmental disorder caused by the deletion of between 26 and 28 genes on chromosome 7q11.23. For patients with WS, in view of the particularity of the supravalvular aortic stenosis, choosing appropriate arterial cannula, maintaining higher perfusion pressure as well as strengthening myocardial protection during cardiopulmonary bypass (CPB) is essential to the clinical outcome. Here, we report a child with pulmonary artery valvular stenosis who failed to wean off CPB because of malignant arrhythmias and cardiac insufficiency after surgical correction of pulmonary valvular stenosis. With the assistance of extracorporeal membrane oxygenation (ECMO), emergency cardiac catheterization revealed supravalvular aortic stenosis (SVAS), which suggests a suspected missed diagnosis of WS. Finally, under the support of ECMO, the cardiac function gradually returned to normal, and the child was discharged 23 days after surgery.

scholarly journals Comparison between Custodiol, del Nido and modified del Nido in the myocardial protection - Cardioplegia Trial: a study protocol for a randomised, double-blind clinical trial

BMJ Open ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. e047942
Author(s):  
Adriana Silveira Almeida ◽  
Rafael Oliveira Ceron ◽  
Fernando Anschau ◽  
Luciane Kopittke ◽  
Kathize Betti Lira ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Cardiac Surgery ◽  
Clinical Outcomes ◽  
Study Protocol ◽  
Myocardial Protection ◽  
Myocardial Injury ◽  
Cardioplegic Solution ◽  
Double Blind ◽  
Related Field ◽  
Cardioplegic Solutions

IntroductionMyocardial protection is essential for successful cardiac surgery, and the search for an ideal cardioplegic solution has continued since its beginning. In this context, Custodiol, del Nido and modified del Nido are single-dose cardioplegic solutions with good safety profiles and great relevance in modern surgical practice. While these solutions have all been evaluated for their impact on patient outcomes independently, limited research exists comparing them directly. Thus, the present study aims to examine the effects of these cardioplegic solutions on myocardial protection and clinical outcomes in adult patients undergoing elective cardiac surgery. The assessment of the increase in myocardial injury biomarkers in patients submitted to all treatment methods may be considered a major strength of our study.Methods and analysisThis is a clinical trial study protocol that will compare myocardial protection and clinical outcomes among three patient groups based on which cardioplegic solution was used. Patients will be randomised to receive del Nido (n=30), modified del Nido (n=30) or Custodiol (n=30). Myocardial injury biomarkers will be measured at the baseline and 2 hours, 12 hours and 24 hours after the cardiopulmonary bypass. Clinical outcomes will be assessed during the trans operative period and the intensive care unit stay, in addition to other haematological parameters.Ethics and disseminationThis protocol and its related documents were approved by the Research Ethics Committee of the Hospital Nossa Senhora da Conceição, Brazil, registered under no. 4.029.545. The findings of this study will be published in a peer-reviewed journal in the related field.Trial registration numberRBR-7g5s66.

scholarly journals Silencing MR-1 Protects against Myocardial Injury Induced by Chronic Intermittent Hypoxia by Targeting Nrf2 through Antioxidant Stress and Anti-Inflammation Pathways

2022 ◽  
Vol 2022 ◽  
pp. 1-11
Author(s):  
Qixue Wang ◽  
Yue Wang ◽  
Jiner Zhang ◽  
Shuo Pan ◽  
Shaofeng Liu
Keyword(s):  
Oxidative Stress ◽  
Intermittent Hypoxia ◽  
Myocardial Injury ◽  
Cardiac Insufficiency ◽  
Inflammatory Factors ◽  
Chronic Intermittent Hypoxia ◽  
Heme Oxygenase 1 ◽  
Stress System ◽  
Antioxidant Stress ◽  
And Oxidative Stress

Background. Patients with obstructive sleep apnea hypopnea syndrome (OSAHS) often have cardiac insufficiency mainly due to hypoxia/reperfusion injury caused by chronic intermittent hypoxia (CIH). Inflammation and oxidative stress are involved in the cardiovascular events of OSAHS patients. Studies have found that myofibrillation regulator-1 (MR-1) participates in the pathological process of OSAHS-induced myocardial injury, but the specific mechanism is still unclear. Methods. We used a CIH-induced rat model to simulate the process of OSAHS disease. Indices of myocardial injury, inflammation, and oxidative stress were detected using quantitative PCR and enzyme-linked immunosorbent assay (ELISA). After administration of adenoassociated viral vector (AAV) encoding silencing RNA against MR-1, we examined expression of the classic antioxidant stress pathway protein NF-E2-related factor 2 (Nrf2) using western blotting. Results. We found that levels of serum inflammatory factors tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 were increased, and we further observed disturbance of the oxidative stress system, in which the content of reactive oxygen species (ROS), superoxide dismutase (SOD), reduced glutathione (GSH), and malondialdehyde (MDA) was enhanced in CIH-induced rats. Subsequently, we detected that expression of Nrf2 and heme oxygenase-1 (HO-1) was slightly increased, while the expression of Kelch-like ECH-associated protein 1 (Keap-1) was significantly increased in the CIH model. Interestingly, after administration of silencing MR-1 AAV, the elevated levels of inflammatory factors were reduced, and the disordered oxidative stress system was corrected. Additionally, the expression of Nrf2 and HO-1 was distinctly increased, but the high expression of Keap-1 was decreased. Conclusions. Our research results demonstrate that silencing MR-1 rescued the myocardium the injury from inflammatory and oxidative stress in CIH-induced rats by administration of the Nrf2 signaling pathway.

scholarly journals THE ALTERATION OF PRO- AND ANTI-INFLAMMATORY CYTOKINES IN ADRENALINE-CALCIUM INDUCED MYOCARDIAL DAMAGE AND ITS CORRECTION WITH QUERCETIN IN RATS

2018 ◽  
Author(s):  
O. V. Denefil ◽  
A. M. Мusiienko
Keyword(s):  
Myocardial Injury ◽  
Myocardial Damage ◽  
Cardiac Insufficiency ◽  
Male Rats ◽  
Tnf Alpha ◽  
Heart Damage ◽  
The World ◽  
Heart Injury ◽  
Ac Injury ◽  
Wistar Male Rats

Background. Cardiac insufficiency is one of the main causes of morbidity and mortality in the world. Objective. The aim of the study was to determine the content of interleukins in male rats with adrenaline-calcium model of myocardial injury (ACM) and under correction by quercetin.Methods. 143 Wistar male-rats aged 5-6 months were used in the experiments. The changes of interleukins (IL-1beta, IL-2, IL-4, IL-6, IL-10, TNF-alpha) content in blood serum in the development of heart injury by adrenaline and calcium (AC) and use of quercetin for protection were studied. The period of investigation was in 1, 2, 24 hours, 3, 7, 14, 21, 28 days.Results. In ACM model of myocardial injury TNF-alpha increased, IL-2, IL-4 decreased at each period of investigation. IL-1beta increased in 2 and 3 days after the injury, at all other periods (except in 1 hour and 21 days) those indices were decreased. Also we observed similar wave changes of IL-6 and IL-10 content.Injections of quercetin for 7 days caused a significant decrease of IL-2, IL-4, IL-10, and increase of IL-6. In 7 days of quercetin administration after AC-injury, decreased TNF-alpha was observed as well as increased IL-4, IL-6, and IL-1beta rates. In 14 days, the increase of TNF-alpha, normalization of IL-10 to control was evidenced. In 28 days, increased activation of IL-1beta, decreased content of TNF-alpha was fixed.Conclusions. The development of adrenaline-calcium heart damage is accompanied by bright cytokine wavelike reaction at different time points. Quercetin causes normalization of interleukins level. 

scholarly journals Glycans and Glycan-Binding Proteins as Regulators and Potential Targets in Leukocyte Recruitment

2021 ◽  
Vol 9 ◽  
Author(s):  
Franziska Krautter ◽  
Asif J. Iqbal
Keyword(s):  
Binding Proteins ◽  
Therapeutic Targets ◽  
Leukocyte Recruitment ◽  
Regulatory Pathways ◽  
Key Enzymes

Leukocyte recruitment is a highly controlled cascade of interactions between proteins expressed by the endothelium and circulating leukocytes. The involvement of glycans and glycan-binding proteins in the leukocyte recruitment cascade has been well-characterised. However, our understanding of these interactions and their regulation has expanded substantially in recent years to include novel lectins and regulatory pathways. In this review, we discuss the role of glycans and glycan-binding proteins, mediating the interactions between endothelium and leukocytes both directly and indirectly. We also highlight recent findings of key enzymes involved in glycosylation which affect leukocyte recruitment. Finally, we investigate the potential of glycans and glycan binding proteins as therapeutic targets to modulate leukocyte recruitment and transmigration in inflammation.

Nicorandil reduces myocardial injury and improves cardiac function in valve replacement surgery.

2019 ◽  
Vol 1 (4) ◽  
pp. 120-126
Author(s):  
Wael Elfeky ◽  
Mohamed Aboelnasr ◽  
Ayman Sallam ◽  
Wael Haseeb ◽  
Dalia R El-Afify
Keyword(s):  
Valve Replacement ◽  
Myocardial Protection ◽  
Myocardial Injury ◽  
Troponin I ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Replacement Surgery ◽  
Tnf Α ◽  
Valve Replacement Surgery

Background: Myocardial injury during cardiac surgery is associated with increased morbidity and mortality, and proper myocardial protection improves surgical outcomes. We aimed to study the role of preoperative nicorandil in myocardial protection during valve replacement surgery. Methods: The study included 40 patients who were randomized into two groups: control group, and nicorandil group. Preoperative, intraoperative, and postoperative data were collected. Creatine kinase- MB (CK-MB), troponin I, malondialdehyde (MDA), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were measured 24-hours before surgery then 4, 12 and 48 hours after aortic cross-clamp removal. Results: Nicorandil significantly decreased MDA (p=0.005 and 0.036), TNF-α (p< 0.001), IL-6 (p<0.001 and 0.003) 4 and 12 hours following the removal of aortic clamp compared to the control group. Additionally, It significantly reduced CK-MB (p< 0.0001 and 0.0002) and troponin-I (p= 0.0002 and < 0.0001) 4 and 12 hours after the removal of the aortic clamp, respectively. However, there was no significant difference in MDA, TNF-α, IL-6, CK-MB, and troponin-I levels between the nicorandil and the control group after 48 hours following the removal of aortic clamping (p= 0.084; 0.64; 0.12; 0.12; 0.75; respectively). Conclusions: Nicorandil reduced myocardial injury significantly in valve replacement surgery. Nicorandil decreased CK-MB and troponin I and improved postoperative left ventricular ejection fraction.

scholarly journals Improved cardiac protection with Sabax cardioplegia in Langendorff isolated rat hearts

2014 ◽  
Vol 60 (6) ◽  
pp. 254-259
Author(s):  
M. Perian ◽  
M. Mărginean ◽  
D. Dobreanu ◽  
Alina Scridon
Keyword(s):  
Myocardial Protection ◽  
Myocardial Injury ◽  
Left Ventricular ◽  
Mechanical Activity ◽  
Cardioplegic Arrest ◽  
Rat Hearts ◽  
Langendorff Perfusion ◽  
Perfusion Apparatus ◽  
Solution Methods ◽  
Male Wistar Rats

Abstract Objective: Cardioplegia is an important step to facilitate cardiac surgery while limiting intraoperative myocardial injury. Although recent advances in cardioplegic arrest methods have significantly contributed to better postoperative outcomes, there is still controversy regarding the optimal composition and temperature of the cardioplegic solution. Accordingly, we aimed to assess whether cold or lukewarm Sabax cardioplegia offer improved myocardial protection compared with the classical Krebs-Henseleit solution. Methods: The hearts of 40 male Wistar rats were isolated and submitted to constant-flow retrograde perfusion using a Langendorff perfusion apparatus. The hearts were randomly assigned to cold Krebs-Henseleit (K-H), cold Sabax, or lukewarm Sabax cardioplegia. The ECG, heart rates, and left ventricular systolic pressures (LVSP) were recorded pre- and post-cardioplegia. The time needed for cardioplegia induction and post-cardioplegia recovery were also noted. Results: Both cold and lukewarm Sabax cardioplegia insured faster induction and faster recovery following isothermic reperfusion compared to the standard K-H solution (both p< 0.01). With K-H cardioplegia, the hearts presented a 21.7% force loss after reperfusion (p< 0.001), whilst Sabax cardioplegia was associated with a slight increase in ventricular mechanical activity (3% LVSP increase with lukewarm Sabax cardioplegia, p< 0.001 and 2% LVSP increase with cold Sabax cardioplegia, p = 0.02). With Sabax cardioplegia the hearts displayed considerably less major arrhythmic events and presented less significant bradycardia. Conclusions: The present data suggest that Sabax cardioplegia may be superior to the classical cold crystalloid K-H solution in preserving mechanical activity of the heart and may provide superior protection against major arrhythmias.

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