-
Scientific Reports Apr 2023Malignant ventricular arrhythmias (VA) after acute myocardial infarction remain a major threat. Aim of this study was to characterize the electrophysiological and...
Malignant ventricular arrhythmias (VA) after acute myocardial infarction remain a major threat. Aim of this study was to characterize the electrophysiological and autonomic sequelae of cardiac ischemia and reperfusion (I/R) in mice during the first week post incident. Left ventricular function was serially assessed using transthoracic echocardiography. VA were quantified by telemetric electrocardiogram (ECG) recordings and electrophysiological studies on the 2nd and 7th day after I/R. Cardiac autonomic function was evaluated by heart rate variability (HRV) and heart rate turbulence (HRT). Infarct size was quantified by planimetric measures. I/R caused significant myocardial scarring and diminished left ventricular ejection fraction. The ECG intervals QRS, QT, QT, and JT were prolonged in I/R mice. Both spontaneous VA scored higher and the inducibility of VA was raised in I/R mice. An analysis of HRV and HRT indicated a relative reduction in parasympathetic activity and disturbed baroreflex sensitivity up to 7 days after I/R. In summary, during the first week after I/R, the murine heart reflects essential features of the human heart after myocardial infarction, including a greater vulnerability for VA and a decreased parasympathetic tone accompanied by decelerated depolarization and repolarization parameters.
Topics: Humans; Animals; Mice; Stroke Volume; Ventricular Function, Left; Myocardial Ischemia; Electrocardiography; Coronary Artery Disease; Myocardial Infarction; Arrhythmias, Cardiac; Myocardial Reperfusion; Heart Rate
PubMed: 37029160
DOI: 10.1038/s41598-023-32346-5 -
American Journal of Physiology. Heart... Jul 2019Cell death is an important component of the pathophysiology of any disease. Myocardial disease is no exception. Understanding how and why cells die, particularly in the... (Review)
Review
Cell death is an important component of the pathophysiology of any disease. Myocardial disease is no exception. Understanding how and why cells die, particularly in the heart where cardiomyocyte regeneration is limited at best, becomes a critical area of study. Ferroptosis is a recently described form of nonapoptotic cell death. It is an iron-mediated form of cell death that occurs because of accumulation of lipid peroxidation products. Reactive oxygen species and iron-mediated phospholipid peroxidation is a hallmark of ferroptosis. To date, ferroptosis has been shown to be involved in cell death associated with Alzheimer's disease, Huntington's disease, cancer, Parkinson's disease, and kidney degradation. Myocardial reperfusion injury is characterized by iron deposition as well as reactive oxygen species production. These conditions, therefore, favor the induction of ferroptosis. Currently there is no available treatment for reperfusion injury, which accounts for up to 50% of the final infarct size. This review will summarize the evidence that ferroptosis can induce cardiomyocyte death following reperfusion injury and the potential for this knowledge to open new therapeutic approaches for myocardial ischemia-reperfusion injury.
Topics: Animals; Ferroptosis; Humans; Iron; Lipid Peroxidation; Lipid Peroxides; Myocardial Reperfusion Injury; Myocytes, Cardiac; Oxidation-Reduction; Phospholipids; Signal Transduction
PubMed: 31050558
DOI: 10.1152/ajpheart.00076.2019 -
Trends in Cardiovascular Medicine Aug 2023
Topics: Humans; Myocardial Reperfusion Injury; Myocardial Ischemia; Myocardial Infarction
PubMed: 35231615
DOI: 10.1016/j.tcm.2022.02.013 -
Journal of Cellular Physiology Aug 2019Acute myocardial infarction (AMI) is one of the leading causes of morbidity worldwide. Myocardial reperfusion is known as an effective therapeutic choice against AMI.... (Review)
Review
Acute myocardial infarction (AMI) is one of the leading causes of morbidity worldwide. Myocardial reperfusion is known as an effective therapeutic choice against AMI. However, reperfusion of blood flow induces ischemia/reperfusion (I/R) injury through different complex processes including ion accumulation, disruption of mitochondrial membrane potential, the formation of reactive oxygen species, and so forth. One of the processes that gets activated in response to I/R injury is autophagy. Indeed, autophagy acts as a "double-edged sword" in the pathology of myocardial I/R injury and there is a controversy about autophagy being beneficial or detrimental. On the basis of the autophagy effect and regulation on myocardial I/R injury, many studies targeted it as a therapeutic strategy. In this review, we discuss the role of autophagy in I/R injury and its targeting as a therapeutic strategy.
Topics: Animals; Autophagy; Cardiovascular Agents; Humans; Myocardial Reperfusion Injury; TOR Serine-Threonine Kinases
PubMed: 30807647
DOI: 10.1002/jcp.28345 -
Aging and Disease May 2024Myocardial ischemia is the most common cardiovascular disease. Reperfusion, an important myocardial ischemia tool, causes unexpected and irreversible damage to... (Review)
Review
Myocardial ischemia is the most common cardiovascular disease. Reperfusion, an important myocardial ischemia tool, causes unexpected and irreversible damage to cardiomyocytes, resulting in myocardial ischemia/reperfusion (MI/R) injury. Upon stress, especially oxidative stress induced by reactive oxygen species (ROS), autophagy, which degrades the intracellular energy storage to produce metabolites that are recycled into metabolic pathways to buffer metabolic stress, is initiated during myocardial ischemia and MI/R injury. Excellent cardioprotective effects of autophagy regulators against MI and MI/R have been reported. Reversing disordered cardiac metabolism induced by ROS also exhibits cardioprotective action in patients with myocardial ischemia. Herein, we review current knowledge on the crosstalk between ROS, cardiac autophagy, and metabolism in myocardial ischemia and MI/R. Finally, we discuss the possible regulators of autophagy and metabolism that can be exploited to harness the therapeutic potential of cardiac metabolism and autophagy in the diagnosis and treatment of myocardial ischemia and MI/R.
Topics: Humans; Autophagy; Reactive Oxygen Species; Myocardial Reperfusion Injury; Myocardial Ischemia; Animals; Oxidative Stress
PubMed: 37728583
DOI: 10.14336/AD.2023.0823-4 -
Texas Heart Institute Journal Apr 2020Warm blood cardioplegia has been an established cardioplegic method since the 1990s, yet it remains controversial in regard to myocardial protection. This review will... (Review)
Review
Warm blood cardioplegia has been an established cardioplegic method since the 1990s, yet it remains controversial in regard to myocardial protection. This review will describe the physiologic and technical concepts behind warm blood cardioplegia, as well as outline the current basic and clinical research that evaluates its usefulness. Controversies regarding this technique will also be reviewed. A long history of experimental data indicates that warm blood cardioplegia is safe and effective and thus suitable myocardial protection during cardiopulmonary bypass surgeries.
Topics: Cardiac Surgical Procedures; Heart Arrest, Induced; Humans; Intraoperative Care; Myocardial Reperfusion Injury
PubMed: 32603472
DOI: 10.14503/THIJ-18-6909 -
Resuscitation 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; Consensus; Critical Care; Heart Arrest; Humans; Myocardial Reperfusion
PubMed: 33773827
DOI: 10.1016/j.resuscitation.2021.02.012 -
International Journal of Molecular... Mar 2021Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via... (Review)
Review
Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via complex signaling networks. These networks have been an intriguing research field for decades, largely advancing our knowledge on cardiac signaling beyond the conditioning response. The centerpieces of this system are the mitochondria, a dynamic organelle, almost acting as a cell within the cell. Mitochondria comprise a plethora of functions at the crossroads of cell death or survival. These include the maintenance of aerobic ATP production and redox signaling, closely entwined with mitochondrial calcium handling and mitochondrial permeability transition. Moreover, mitochondria host pathways of programmed cell death impact the inflammatory response and contain their own mechanisms of fusion and fission (division). These act as quality control mechanisms in cellular ageing, release of pro-apoptotic factors and mitophagy. Furthermore, recently identified mechanisms of mitochondrial regeneration can increase the capacity for oxidative phosphorylation, decrease oxidative stress and might help to beneficially impact myocardial remodeling, as well as invigorate the heart against subsequent ischemic insults. The current review highlights different pathways and unresolved questions surrounding mitochondria in myocardial I/R injury and pharmacological cardiac conditioning.
Topics: Adenosine Triphosphate; Animals; Cell Death; Humans; Ischemic Preconditioning, Myocardial; Mitochondria; Mitochondrial Dynamics; Myocardial Ischemia; Myocardial Reperfusion Injury; Myocardium; Myocytes, Cardiac; Oxidative Phosphorylation; Oxidative Stress; Regeneration; Signal Transduction; Translational Research, Biomedical
PubMed: 33810024
DOI: 10.3390/ijms22063224 -
Frontiers in Endocrinology 2023The incidence of diabetes and related mortality rate increase yearly in modern cities. Additionally, elevated glucose levels can result in an increase of reactive oxygen... (Review)
Review
The incidence of diabetes and related mortality rate increase yearly in modern cities. Additionally, elevated glucose levels can result in an increase of reactive oxygen species (ROS), ferroptosis, and the disruption of protective pathways in the heart. These factors collectively heighten the vulnerability of diabetic individuals to myocardial ischemia. Reperfusion therapies have been effectively used in clinical practice. There are limitations to the current clinical methods used to treat myocardial ischemia-reperfusion injury. As a result, reducing post-treatment ischemia/reperfusion injury remains a challenge. Therefore, efforts are underway to provide more efficient therapy. Salvia miltiorrhiza Bunge (Danshen) has been used for centuries in ancient China to treat cardiovascular diseases (CVD) with rare side effects. Salvianolic acid is a water-soluble phenolic compound with potent antioxidant properties and has the greatest hydrophilic property in Danshen. It has recently been discovered that salvianolic acids A (SAA) and B (SAB) are capable of inhibiting apoptosis by targeting the JNK/Akt pathway and the NF-κB pathway, respectively. This review delves into the most recent discoveries regarding the therapeutic and cardioprotective benefits of salvianolic acid for individuals with diabetes. Salvianolic acid shows great potential in myocardial protection in diabetes mellitus. A thorough understanding of the protective mechanism of salvianolic acid could expand its potential uses in developing medicines for treating diabetes mellitus related myocardial ischemia-reperfusion.
Topics: Humans; Myocardial Reperfusion Injury; Heart; Myocardium; Diabetes Mellitus; Alkenes; Polyphenols
PubMed: 38283744
DOI: 10.3389/fendo.2023.1322474 -
International Journal of Biological... Feb 2024Reperfusion therapy is the most effective treatment for acute myocardial infarction. However, reperfusion itself can also cause cardiomyocytes damage. Pyroptosis has... (Review)
Review
Reperfusion therapy is the most effective treatment for acute myocardial infarction. However, reperfusion itself can also cause cardiomyocytes damage. Pyroptosis has been shown to be an important mode of myocardial cell death during ischemia-reperfusion. Non-coding RNAs (ncRNAs) play critical roles in regulating pyroptosis. The regulation of pyroptosis by microRNAs, long ncRNAs, and circular RNAs may represent a new mechanism of myocardial ischemia-reperfusion injury. This review summarizes the currently known regulatory roles of ncRNAs in myocardial ischemia-reperfusion injury and interactions between ncRNAs. Potential therapeutic strategies using ncRNA modulation are also discussed.
Topics: Humans; Myocardial Reperfusion Injury; Pyroptosis; MicroRNAs; RNA, Untranslated; Myocardial Infarction
PubMed: 38048927
DOI: 10.1016/j.ijbiomac.2023.128558