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Journal of Cardiology Feb 2023Owing to recent advances in early reperfusion strategies, pharmacological therapy, standardized care, and the identification of vulnerable patient subsets, the prognosis... (Review)
Review
Owing to recent advances in early reperfusion strategies, pharmacological therapy, standardized care, and the identification of vulnerable patient subsets, the prognosis of acute myocardial infarction has improved. However, there is still considerable room for improvement. This review article summarizes the latest evidence concerning clinical diagnosis and treatment of acute myocardial infarction.
Topics: Humans; Myocardial Infarction; Myocardial Reperfusion; Thrombolytic Therapy; Prognosis; Percutaneous Coronary Intervention; Treatment Outcome; Myocardial Revascularization
PubMed: 35882613
DOI: 10.1016/j.jjcc.2022.07.003 -
Biochimica Et Biophysica Acta.... Jul 2020Despite major progress in interventional and medical treatments, myocardial infarction (MI) and subsequent development of heart failure (HF) are still associated with... (Review)
Review
Despite major progress in interventional and medical treatments, myocardial infarction (MI) and subsequent development of heart failure (HF) are still associated with high mortality. Both during ischemia reperfusion (IR) in the acute setting of MI, as well as in the chronic remodeling process following MI, oxidative stress substantially contributes to cardiac damage. Reactive oxygen species (ROS) generated within mitochondria are particular drivers of mechanisms contributing to IR injury, including induction of mitochondrial permeability transition or oxidative damage of intramitochondrial structures and molecules. But even beyond the acute setting, mechanisms like inflammatory signaling, extracellular remodeling, or pro-apoptotic signaling that contribute to post-infarction remodeling are regulated by mitochondrial ROS. In the current review, we discuss both sources and consequences of mitochondrial ROS during IR and in the chronic setting following MI, thereby emphasizing the potential therapeutic value of attenuating mitochondrial ROS to improve outcome and prognosis for patients suffering MI.
Topics: Apoptosis; Heart Failure; Humans; Mitochondria; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion Injury; Oxidative Stress; Reactive Oxygen Species; Ventricular Remodeling
PubMed: 32173461
DOI: 10.1016/j.bbadis.2020.165768 -
Nature Reviews. Cardiology Apr 2016The 30-year anniversary of the discovery of 'ischaemic preconditioning' is in 2016. This endogenous phenomenon can paradoxically protect the heart from acute myocardial... (Review)
Review
The 30-year anniversary of the discovery of 'ischaemic preconditioning' is in 2016. This endogenous phenomenon can paradoxically protect the heart from acute myocardial infarction by subjecting it to one or more brief cycles of ischaemia and reperfusion. Apart from complete reperfusion, this method is the most powerful intervention known for reducing infarct size. The concept of ischaemic preconditioning has evolved into 'ischaemic conditioning', a term that encompasses a number of related endogenous cardioprotective strategies, applied either directly to the heart (ischaemic preconditioning or postconditioning) or from afar, for example a limb (remote ischaemic preconditioning, perconditioning, or postconditioning). Investigations of signalling pathways underlying ischaemic conditioning have identified a number of therapeutic targets for pharmacological manipulation. Over the past 3 decades, a number of ischaemic and pharmacological cardioprotection strategies, discovered in experimental studies, have been examined in the clinical setting of acute myocardial infarction and CABG surgery. The results from many of the studies have been disappointing, and no effective cardioprotective therapy is currently used in clinical practice. Several large, multicentre, randomized, controlled clinical trials on cardioprotection have highlighted the challenges of translating ischaemic conditioning and pharmacological cardioprotection strategies into patient benefit. However, a number of cardioprotective therapies have shown promising results in reducing infarct size and improving clinical outcomes in patients with ischaemic heart disease.
Topics: Animals; Cardiovascular Agents; Humans; Ischemic Postconditioning; Ischemic Preconditioning; Ischemic Preconditioning, Myocardial; Myocardial Infarction; Myocardial Reperfusion Injury; Treatment Outcome
PubMed: 26843289
DOI: 10.1038/nrcardio.2016.5 -
Intensive Care Medicine Apr 2021The European Resuscitation Council (ERC) and the European Society of Intensive Care Medicine (ESICM) have collaborated to produce these post-resuscitation care...
The European Resuscitation Council (ERC) and the European Society of Intensive Care Medicine (ESICM) have collaborated to produce these post-resuscitation care guidelines for adults, which are based on the 2020 International Consensus on Cardiopulmonary Resuscitation Science with Treatment Recommendations. The topics covered include the post-cardiac arrest syndrome, diagnosis of cause of cardiac arrest, control of oxygenation and ventilation, coronary reperfusion, haemodynamic monitoring and management, control of seizures, temperature control, general intensive care management, prognostication, long-term outcome, rehabilitation and organ donation.
Topics: Adult; Cardiopulmonary Resuscitation; Critical Care; Heart Arrest; Humans; Myocardial Reperfusion; Resuscitation; Seizures
PubMed: 33765189
DOI: 10.1007/s00134-021-06368-4 -
Journal of the American College of... Apr 2015The damage inflicted on the myocardium during acute myocardial infarction is the result of 2 processes: ischemia and subsequent reperfusion (ischemia/reperfusion... (Review)
Review
The damage inflicted on the myocardium during acute myocardial infarction is the result of 2 processes: ischemia and subsequent reperfusion (ischemia/reperfusion injury). During the last 3 decades, therapies to reduce ischemic injury (mainly reperfusion strategies) have been widely incorporated into clinical practice. The remarkable reduction in death rates achieved with these therapies has resulted in a shift in emphasis from efforts to reduce mortality to a focus on tackling the downstream consequence of survival: post-infarction heart failure. Infarct size is the main determinant of long-term mortality and chronic heart failure, and thus, the possibility of limiting the extent of necrosis during an ST-segment elevation myocardial infarction is of great individual and socioeconomic value. After the great success of therapies to reduce ischemic injury, the time has come to focus efforts on therapies to reduce reperfusion injury, but in the recent few years, few interventions have successfully passed the proof-of-concept stage. In this review, we examine the past, present, and future therapies to reduce ischemia/reperfusion injury.
Topics: Animals; Glucagon-Like Peptide 1; Humans; Ischemic Preconditioning, Myocardial; Myocardial Reperfusion; Myocardial Reperfusion Injury; Randomized Controlled Trials as Topic
PubMed: 25857912
DOI: 10.1016/j.jacc.2015.02.032 -
Cardiovascular Research Jun 2019Mesenchymal stromal cells (MSCs) gradually become attractive candidates for cardiac inflammation modulation, yet understanding of the mechanism remains elusive....
AIMS
Mesenchymal stromal cells (MSCs) gradually become attractive candidates for cardiac inflammation modulation, yet understanding of the mechanism remains elusive. Strikingly, recent studies indicated that exosomes secreted by MSCs might be a novel mechanism for the beneficial effect of MSCs transplantation after myocardial infarction. We therefore explored the role of MSC-derived exosomes (MSC-Exo) in the immunomodulation of macrophages after myocardial ischaemia/reperfusion (I/R) and its implications in cardiac injury repair.
METHODS AND RESULTS
Exosomes were isolated from the supernatant of MSCs using gradient centrifugation method. Administration of MSC-Exo to mice through intramyocardial injection after myocardial I/R reduced infarct size and alleviated inflammation level in heart and serum. Systemic depletion of macrophages with clodronate liposomes abolished the curative effects of MSC-Exo. MSC-Exo modified the polarization of M1 macrophages to M2 macrophages both in vivo and in vitro. miRNA sequencing of MSC-Exo and bioinformatics analysis implicated miR-182 as a potent candidate mediator of macrophage polarization and toll-like receptor 4 (TLR4) as a downstream target. Diminishing miR-182 in MSC-Exo partially attenuated its modulation of macrophage polarization. Likewise, knock down of TLR4 also conferred cardioprotective efficacy and reduced inflammation level in a mouse model of myocardial I/R.
CONCLUSION
Our data indicate that MSC-Exo attenuates myocardial I/R injury in mice via shuttling miR-182 that modifies the polarization status of macrophages. This study sheds new light on the application of MSC-Exo as a potential therapeutic tool for myocardial I/R injury.
Topics: Animals; Cell Plasticity; Cells, Cultured; Disease Models, Animal; Exosomes; Gene Expression Regulation; Macrophages; Male; Mesenchymal Stem Cell Transplantation; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Knockout; MicroRNAs; Myocardial Infarction; Myocardial Reperfusion Injury; Myocardium; Phenotype; Signal Transduction; Toll-Like Receptor 4
PubMed: 30753344
DOI: 10.1093/cvr/cvz040 -
Mediators of Inflammation 2020Myocardial ischemia reperfusion syndrome is a complex entity where many inflammatory mediators play different roles, both to enhance myocardial infarction-derived damage... (Review)
Review
Myocardial ischemia reperfusion syndrome is a complex entity where many inflammatory mediators play different roles, both to enhance myocardial infarction-derived damage and to heal injury. In such a setting, the establishment of an effective therapy to treat this condition has been elusive, perhaps because the experimental treatments have been conceived to block just one of the many pathogenic pathways of the disease, or because they thwart the tissue-repairing phase of the syndrome. Either way, we think that a discussion about the pathophysiology of the disease and the mechanisms of action of some drugs may shed some clarity on the topic.
Topics: Animals; Humans; Immunity, Innate; Immunosuppression Therapy; Inflammation; Inflammation Mediators; Ischemia; Mice; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion; Myocardial Reperfusion Injury; Phenotype; Reperfusion Injury; Th1 Cells; Th2 Cells
PubMed: 32410868
DOI: 10.1155/2020/8405370 -
Clinical and Experimental Hypertension... Dec 2023Acute myocardial infarction (AMI) is the leading cause of death worldwide. Ischemia-reperfusion (I/R) injury is considered the most common contributor to AMI. Hirsutine...
Acute myocardial infarction (AMI) is the leading cause of death worldwide. Ischemia-reperfusion (I/R) injury is considered the most common contributor to AMI. Hirsutine has been shown to protect cardiomyocytes against hypoxic injury. The present study investigated whether hirsutine improved AMI induced by I/R injury and the underlying mechanisms. In our study, we used a rat model of myocardial I/R injury. The rats were given hirsutine daily (5, 10, 20 mg/kg) by gavage for 15 days before the myocardial I/R injury. Detectable changes were observed in myocardial infarct size, mitochondrial function, histological damage, and cardiac cell apoptosis. According to our findings, hirsutine pre-treatment reduced the myocardial infarct size, enhanced cardiac function, inhibited cell apoptosis, reduced the tissue lactate dehydrogenase (LDH) and reactive oxygen species (ROS) content, as well as enhanced myocardial ATP content and mitochondrial complex activity. In addition, hirsutine balanced mitochondrial dynamics by increasing Mitofusin2 (Mfn2) expression while decreasing dynamin-related protein 1 phosphorylation (p-Drp1), which was partially regulated by ROS and calmodulin-dependent protein kinase II phosphorylation (p-CaMKII). Mechanistically, hirsutine inhibited mitochondrial-mediated apoptosis during I/R injury by blocking the AKT/ASK-1/p38 MAPK pathway. This present study provides a promising therapeutic intervention for myocardial I/R injury.
Topics: Rats; Animals; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Reactive Oxygen Species; Myocardial Reperfusion Injury; Mitochondria; Myocytes, Cardiac; Myocardial Infarction; Apoptosis
PubMed: 36951068
DOI: 10.1080/10641963.2023.2192444 -
Oxidative Medicine and Cellular... 2015
Topics: Humans; Mitochondria; Myocardial Reperfusion Injury; Oxidative Stress; Reactive Oxygen Species
PubMed: 26265984
DOI: 10.1155/2015/689416 -
The Journal of Thoracic and... Jun 2021
Topics: Cardiac Surgical Procedures; Heart Ventricles; Heart-Assist Devices; Humans; Myocardial Infarction; Myocardial Reperfusion; Reperfusion Injury; Ventricular Function, Left
PubMed: 32859423
DOI: 10.1016/j.jtcvs.2020.07.078