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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 -
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 -
Circulation Jul 2017For >4 decades, the holy grail in the treatment of acute myocardial infarction has been the mitigation of lethal injury. Despite promising initial results and decades of... (Review)
Review
For >4 decades, the holy grail in the treatment of acute myocardial infarction has been the mitigation of lethal injury. Despite promising initial results and decades of investigation by the cardiology research community, the only treatment with proven efficacy is early reperfusion of the occluded coronary artery. The remarkable record of failure has led us and others to wonder if cardioprotection is dead. The path to translation, like the ascent to Everest, is certainly littered with corpses. We do, however, highlight a therapeutic principle that provides a glimmer of hope: cellular postconditioning. Administration of cardiosphere-derived cells after reperfusion limits infarct size measured acutely, while providing long-term structural and functional benefits. The recognition that cell therapy may be cardioprotective, and not just regenerative, merits further exploration before we abandon the pursuit entirely.
Topics: Animals; Cell- and Tissue-Based Therapy; Humans; Ischemic Postconditioning; Myocardial Infarction; Myocardial Reperfusion; Myocytes, Cardiac
PubMed: 28674094
DOI: 10.1161/CIRCULATIONAHA.116.027039 -
Kardiologia Polska Oct 2019Little attention is paid to the coronary microvasculature when treating acute myocardial infarction (MI). Microvascular obstruction (MVO) contributes to... (Review)
Review
Little attention is paid to the coronary microvasculature when treating acute myocardial infarction (MI). Microvascular obstruction (MVO) contributes to ischemia-reperfusion injury, which hampers distal blood flow to the myocardium despite recanalization of the culprit epicardial vessel. One of the mechanisms behind reperfusion injury is MVO due to persistent vasoconstrictor tone during reperfusion. Arginine vasopressin (AVP) is a hormone with prominent vasoactive effects on the coronary microvessels. Its levels are elevated as part of a stress response triggered by MI, which was shown to exert vasoconstrictive effects on the coronary arteries in preclinical models, mainly in the nonepicardial vessels of the microcirculation. Circulating AVP levels are up to 100‑fold higher in MI and do not immediately decrease to baseline levels on reperfusion. This results in the so called coronary slow flow phenomenon and mediates ischemia-reperfusion injury. Recently, the C‑terminal fragment of preprovasopressin, copeptin, has emerged as a surrogate biomarker for AVP, as it is more stable in the circulation. Multiple studies have shown the predictive value of both AVP and copeptin with regards to long‑term prognoses of MI patients. We propose that both AVP and copeptin have more than just a predictive value but also play a role in the pathophysiology of adverse outcome post‑MI. Therefore, the treatment of choice for MI should not only focus on the epicardial vessel but also on targeting MVO that might pre‑exist or might directly follow reperfusion. This mandates a clinical trial with an AVP‑receptor antagonist in patients with acute MI undergoing reperfusion therapy.
Topics: Animals; Arginine Vasopressin; Humans; Myocardial Infarction; Myocardial Reperfusion
PubMed: 31553327
DOI: 10.33963/KP.14986 -
Journal of Cardiovascular Pharmacology... Nov 2021Cardiac reperfusion injury is a well-established outcome following treatment of acute myocardial infarction and other types of ischemic heart conditions. Numerous... (Review)
Review
Cardiac reperfusion injury is a well-established outcome following treatment of acute myocardial infarction and other types of ischemic heart conditions. Numerous cardioprotection protocols and therapies have been pursued with success in pre-clinical models. Unfortunately, there has been lack of successful large-scale clinical translation, perhaps in part due to the multiple pathways that reperfusion can contribute to cell death. The search continues for new cardioprotection protocols based on what has been learned from past results. One class of cardioprotection protocols that remain under active investigation is that of controlled reperfusion. This class consists of those approaches that modify, in a controlled manner, the content of the reperfusate or the mechanical properties of the reperfusate (e.g., pressure and flow). This review article first provides a basic overview of the primary pathways to cell death that have the potential to be addressed by various forms of controlled reperfusion, including no-reflow phenomenon, ion imbalances (particularly calcium overload), and oxidative stress. Descriptions of various controlled reperfusion approaches are described, along with summaries of both mechanistic and outcome-oriented studies at the pre-clinical and clinical phases. This review will constrain itself to approaches that modify endogenously-occurring blood components. These approaches include ischemic postconditioning, gentle reperfusion, controlled hypoxic reperfusion, controlled hyperoxic reperfusion, controlled acidotic reperfusion, and controlled ionic reperfusion. This review concludes with a discussion of the limitations of past approaches and how they point to potential directions of investigation for the future.
Topics: Humans; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion; Myocardial Reperfusion Injury; Oxidative Stress
PubMed: 34534022
DOI: 10.1177/10742484211046674 -
Journal of the American Heart... Jan 2023Scavenger receptors (SRs) are a structurally heterogeneous superfamily of evolutionarily conserved receptors that are divided into classes A to J. SRs can recognize... (Review)
Review
Scavenger receptors (SRs) are a structurally heterogeneous superfamily of evolutionarily conserved receptors that are divided into classes A to J. SRs can recognize multiple ligands, such as modified lipoproteins, damage-associated molecular patterns, and pathogen-associated molecular patterns, and regulate lipid metabolism, immunity, and homeostasis. According to the literature, SRs may play a critical role in myocardial infarction and ischemia/reperfusion injury, and the soluble types of SRs may be a series of promising biomarkers for the diagnosis and prognosis of patients with acute coronary syndrome or acute myocardial infarction. In this review, we briefly summarize the structure and function of SRs and discuss the association between each SR and ischemic cardiac injury in patients and animal models in detail. A better understanding of the effect of SRs on ischemic cardiac injury will inspire novel ideas for therapeutic drug discovery and disease evaluation in patients with myocardial infarction.
Topics: Animals; Myocardial Infarction; Reperfusion Injury; Myocardial Reperfusion; Biomarkers; Receptors, Scavenger
PubMed: 36645089
DOI: 10.1161/JAHA.122.027862 -
BMJ Open Sep 2022ST-segment elevation myocardial infarction (STEMI) is the most severe clinical form of acute myocardial infarction, for which the current treatment consists of effective...
INTRODUCTION
ST-segment elevation myocardial infarction (STEMI) is the most severe clinical form of acute myocardial infarction, for which the current treatment consists of effective and timely myocardial reperfusion (within 12 hours of symptom onset). However, between 10% and 15% of patients with STEMI arrive at hospital facilities 12 hours after the onset of symptoms (late presentation). Therefore, the objective of the present study will be to determine if late revascularisation (12-72 hours after the onset of symptoms) affects the indicators of cardiovascular mortality, reinfarction, recurrent infarction, hospitalisation for heart failure and post infarction angina compared with no late revascularisation in patients with STEMI.
METHODS AND ANALYSIS
A systematic literature search of PubMed, The Cochrane Library, Embase, Cumulative Index to Nursing and Allied Health Literature (CINAHL), Web of Science, Scopus and Global Health will be conducted. Publications in English, Portuguese or Spanish that report the clinical results of primary percutaneous revascularisation (primary PCI) in adult patients with STEMI 12-72 hours after the onset of symptoms will be included. Studies with participants with a diagnosis other than STEMI or patients with STEMI of >12 hours complicated by heart failure, cardiogenic shock or ventricular arrhythmias, and studies of combined interventions (pharmacoinvasive strategy) were excluded. Two independent authors will identify the relevant publications, and discrepancies will be adjudicated by a third author. Data extraction will be performed by two independent authors and verified by a third author. Risk of bias of studies will be assessed using the Cochrane 'risk of bias' tool (RoB 2) or Risk Of Bias In Non-randomised Studies - of Interventions (ROBINS-I) tool. If appropriate, a meta-analysis will be performed in order to examine the effect of late revascularisation in clinical outcomes of interest.
ETHICS AND DISCUSSION
This study will use published data only, thus, ethical approval will not be required. The results will be disseminated through peer-reviewed publication and conference presentations.
PROSPERO REGISTRATION NUMBER
CRD42021283429.
Topics: Adult; Heart Failure; Humans; Meta-Analysis as Topic; Myocardial Reperfusion; Percutaneous Coronary Intervention; ST Elevation Myocardial Infarction; Systematic Reviews as Topic
PubMed: 36104139
DOI: 10.1136/bmjopen-2021-059610 -
Med (New York, N.Y.) Jan 2024Ischemic heart disease is the greatest health burden and most frequent cause of death worldwide. Myocardial ischemia/reperfusion is the pathophysiological substrate of... (Review)
Review
Ischemic heart disease is the greatest health burden and most frequent cause of death worldwide. Myocardial ischemia/reperfusion is the pathophysiological substrate of ischemic heart disease. Improvements in prevention and treatment of ischemic heart disease have reduced mortality in developed countries over the last decades, but further progress is now stagnant, and morbidity and mortality from ischemic heart disease in developing countries are increasing. Significant problems remain to be resolved and require a better pathophysiological understanding. The present review attempts to briefly summarize the state of the art in myocardial ischemia/reperfusion research, with a view on both its coronary vascular and myocardial aspects, and to define the cutting edges where further mechanistic knowledge is needed to facilitate translation to clinical practice.
Topics: Humans; Myocardial Reperfusion Injury; Myocardial Ischemia; Myocardial Reperfusion; Myocardium
PubMed: 38218174
DOI: 10.1016/j.medj.2023.12.007 -
Journal of the American Heart... Feb 2019See Editorial by Cenko et al.
See Editorial by Cenko et al.
Topics: Female; Heart; Humans; Male; Myocardial Infarction; Myocardial Reperfusion; Thrombolytic Therapy
PubMed: 30767600
DOI: 10.1161/JAHA.118.011835 -
American Journal of Physiology. Heart... Jul 2021There is a lack of understanding in the cardiac remodeling field regarding the use of nonreperfused myocardial infarction (MI) and reperfused MI in animal models of MI....
There is a lack of understanding in the cardiac remodeling field regarding the use of nonreperfused myocardial infarction (MI) and reperfused MI in animal models of MI. This Perspectives summarizes the consensus of the authors regarding how to select the optimum model for your experiments and is a part of ongoing efforts to establish rigor and reproducibility in cardiac physiology research.
Topics: Animals; Disease Models, Animal; Heart; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion
PubMed: 34114891
DOI: 10.1152/ajpheart.00234.2021