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Trends in Cardiovascular Medicine Aug 2023Acute myocardial infarction is caused by a sudden coronary artery occlusion and leads to ischemia in the corresponding myocardial territory which generally results in... (Review)
Review
Acute myocardial infarction is caused by a sudden coronary artery occlusion and leads to ischemia in the corresponding myocardial territory which generally results in myocardial necrosis. Without restoration of coronary perfusion, myocardial scar formation will cause adverse remodelling of the myocardium and heart failure. Successful introduction of percutaneous coronary intervention and surgical coronary artery bypass grafting made it possible to achieve early revascularisation/reperfusion, hence limiting the ischemic zone of myocardium. However, reperfusion by itself paradoxically triggers an exacerbated and accelerated injury in the myocardium, called ischemia-reperfusion (I/R) injury. This mechanism is partially driven by inflammation through multiple interacting pathways. In this review we summarize the current insights in mechanisms of I/R injury and the influence of altered inflammation. Multiple pharmacological and interventional therapeutic strategies (ischemic conditioning) have proven to be beneficial during I/R in preclinical models but were notoriously unsuccessful upon clinical translation. In this review we focus on common mechanisms of I/R injury, altered inflammation and potential therapeutic strategies. We hypothesize that a dual approach may be of value because I/R injury patients are predestined with multiple comorbidities and systemic low-grade inflammation, which requires targeted intervention before other strategies can be fully effective.
Topics: Humans; Myocardial Reperfusion Injury; Myocardial Infarction; Myocardium; Heart; Inflammation; Myocardial Ischemia
PubMed: 35181472
DOI: 10.1016/j.tcm.2022.02.005 -
The American Journal of Medicine Dec 2022Mechanical complications of myocardial infarction include rupture of a papillary muscle, ventricular septum, and free wall. Since the advent of acute coronary... (Review)
Review
Mechanical complications of myocardial infarction include rupture of a papillary muscle, ventricular septum, and free wall. Since the advent of acute coronary reperfusion, there has been a significant reduction in the incidence of these complications. One must have a high index of suspicion for a mechanical complication in any patient who develops cardiogenic shock in the days following a myocardial infarction. The most important diagnostic investigation in evaluation of these complications is echocardiography. Although there is a role for mechanical circulatory support, urgent surgical repair is required in most cases. We will review the predictors, clinical features, diagnostic, and management strategies in patients with these complications.
Topics: Humans; Myocardial Reperfusion; Myocardial Infarction; Shock, Cardiogenic; Echocardiography; Ventricular Septum
PubMed: 36075485
DOI: 10.1016/j.amjmed.2022.08.017 -
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 -
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 -
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 -
Current Protein & Peptide Science 2020Heat shock proteins (HSPs) are molecular chaperones involved in a variety of life activities. HSPs function in the refolding of misfolded proteins, thereby contributing... (Review)
Review
Heat shock proteins (HSPs) are molecular chaperones involved in a variety of life activities. HSPs function in the refolding of misfolded proteins, thereby contributing to the maintenance of cellular homeostasis. Heat shock factor (HSF) is activated in response to environmental stresses and binds to heat shock elements (HSEs), promoting HSP translation and thus the production of high levels of HSPs to prevent damage to the organism. Here, we summarize the role of molecular chaperones as anti-heat stress molecules and their involvement in immune responses and the modulation of apoptosis. In addition, we review the potential application of HSPs to cancer therapy, general medicine, and the treatment of heart disease.
Topics: Animals; Antineoplastic Agents; Apoptosis; Benzoquinones; Gene Expression Regulation; Heat-Shock Proteins; Humans; Lactams, Macrocyclic; Male; Myocardial Reperfusion Injury; Oxidative Stress; Plants; Prostatic Neoplasms; Protein Refolding; Response Elements; Signal Transduction; Stress, Physiological
PubMed: 31713482
DOI: 10.2174/1389203720666191111113726 -
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 -
European Journal of Pharmacology Jan 2021Coronary heart disease (CHD) is a cardiovascular disease with high mortality and disability worldwide. The main pathological manifestation of CHD is myocardial injury... (Review)
Review
Coronary heart disease (CHD) is a cardiovascular disease with high mortality and disability worldwide. The main pathological manifestation of CHD is myocardial injury due to ischaemia-reperfusion, resulting in the death of cardiomyocytes (apoptosis and necrosis) and the occurrence of cardiac failure. Morphine is a nonselective opioid receptor agonist that has been commonly used for analgesia and to treat ischaemic heart disease. The present review focused on morphine-induced protection in an animal model of myocardial ischaemia-reperfusion and chronic heart failure and the effects of morphine on ST segment elevation myocardial infarction (STEMI) patients who underwent pre-primary percutaneous coronary intervention (pre-PPCI) or PPCI. The signalling pathways involved are also briefly described.
Topics: Animals; Cardiovascular Agents; Chronic Disease; Disease Models, Animal; Heart Failure; Humans; Morphine; Myocardial Reperfusion Injury; Myocytes, Cardiac; Percutaneous Coronary Intervention; ST Elevation Myocardial Infarction; Signal Transduction; Treatment Outcome
PubMed: 33121952
DOI: 10.1016/j.ejphar.2020.173683 -
JCI Insight Apr 2024Myocardial ischemia/reperfusion (MI/R) injury is a major cause of adverse outcomes of revascularization following myocardial infarction. Anaerobic glycolysis during...
Myocardial ischemia/reperfusion (MI/R) injury is a major cause of adverse outcomes of revascularization following myocardial infarction. Anaerobic glycolysis during myocardial ischemia is well studied, but the role of aerobic glycolysis during the early phase of reperfusion is incompletely understood. Lactylation of Histone H3 (H3) is an epigenetic indicator of the glycolytic switch. Heat shock protein A12A (HSPA12A) is an atypic member of the HSP70 family. In the present study, we report that, during reperfusion following myocardial ischemia, HSPA12A was downregulated and aerobic glycolytic flux was decreased in cardiomyocytes. Notably, HSPA12A KO in mice exacerbated MI/R-induced aerobic glycolysis decrease, cardiomyocyte death, and cardiac dysfunction. Gain- and loss-of-function studies demonstrated that HSPA12A was required to support cardiomyocyte survival upon hypoxia/reoxygenation (H/R) challenge and that its protective effects were mediated by maintaining aerobic glycolytic homeostasis for H3 lactylation. Further analyses revealed that HSPA12A increased Smurf1-mediated Hif1α protein stability, thus increasing glycolytic gene expression to maintain appropriate aerobic glycolytic activity to sustain H3 lactylation during reperfusion and, ultimately, improving cardiomyocyte survival to attenuate MI/R injury.
Topics: Animals; Mice; Heat-Shock Proteins; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocytes, Cardiac
PubMed: 38421727
DOI: 10.1172/jci.insight.169125