Development of myocardial infarction

ESC CardioMed ◽  
2018 ◽  
pp. 1230-1232
Author(s):  
Pascal Vranckx
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Myocardial Ischaemia ◽  
Oxygen Supply ◽  
Myocardial Cell ◽  
Time Dependent ◽  
Collateral Flow ◽  
Complete Occlusion ◽  
Cell Layers ◽  
Artery Flow

Myocardial infarction is the irreversible myocardial cell death (necrosis) secondary to a prolonged lack of oxygen supply (ischaemia) caused by a complete occlusion of a major coronary in the absence of forward or collateral flow. Within the perfusion area of the occluded artery, flow deprivation and myocardial ischaemia are usually most severe subendocardially (apart from the innermost cell layers nourished from the cavity) and, at least in dogs, cell death progresses from the subendocardium to the subepicardium in a time-dependent fashion.

Development of myocardial infarction

ESC CardioMed ◽  
2018 ◽  
pp. 1230-1232
Author(s):  
Pascal Vranckx
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Myocardial Ischaemia ◽  
Oxygen Supply ◽  
Myocardial Cell ◽  
Time Dependent ◽  
Collateral Flow ◽  
Complete Occlusion ◽  
Cell Layers ◽  
Artery Flow

Myocardial infarction is the irreversible myocardial cell death (necrosis) secondary to a prolonged lack of oxygen supply (ischaemia) caused by a complete occlusion of a major coronary in the absence of forward or collateral flow. Within the perfusion area of the occluded artery, flow deprivation and myocardial ischaemia are usually most severe subendocardially (apart from the innermost cell layers nourished from the cavity) and, at least in dogs, cell death progresses from the subendocardium to the subepicardium in a time-dependent fashion.

scholarly journals Quantitative proteomic analyses reveal that GPX4 downregulation during myocardial infarction contributes to ferroptosis in cardiomyocytes

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Tae-Jun Park ◽  
Jei Hyoung Park ◽  
Ga Seul Lee ◽  
Ji-Yoon Lee ◽  
Ji Hye Shin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Lipid Peroxide ◽  
Enrichment Analysis ◽  
Underlying Mechanism ◽  
Myocardial Cell ◽  
Gene Set Enrichment Analysis ◽  
Neonatal Rat ◽  
Transcriptional Level ◽  
Regulated Necrosis

Abstract Ischaemic heart disease (IHD) is the leading cause of death worldwide. Although myocardial cell death plays a significant role in myocardial infarction (MI), its underlying mechanism remains to be elucidated. To understand the progression of MI and identify potential therapeutic targets, we performed tandem mass tag (TMT)-based quantitative proteomic analysis using an MI mouse model. Gene ontology (GO) analysis and gene set enrichment analysis (GSEA) revealed that the glutathione metabolic pathway and reactive oxygen species (ROS) pathway were significantly downregulated during MI. In particular, glutathione peroxidase 4 (GPX4), which protects cells from ferroptosis (an iron-dependent programme of regulated necrosis), was downregulated in the early and middle stages of MI. RNA-seq and qRT-PCR analyses suggested that GPX4 downregulation occurred at the transcriptional level. Depletion or inhibition of GPX4 using specific siRNA or the chemical inhibitor RSL3, respectively, resulted in the accumulation of lipid peroxide, leading to cell death by ferroptosis in H9c2 cardiomyoblasts. Although neonatal rat ventricular myocytes (NRVMs) were less sensitive to GPX4 inhibition than H9c2 cells, NRVMs rapidly underwent ferroptosis in response to GPX4 inhibition under cysteine deprivation. Our study suggests that downregulation of GPX4 during MI contributes to ferroptotic cell death in cardiomyocytes upon metabolic stress such as cysteine deprivation.

CD34+CXCR4+ Cell Therapy (AMR-001) for Myocardial Infarction: Preliminary Processing and Product Results of a Phase I Dose Escalation Study.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 773-773
Author(s):  
Ned Waller ◽  
Arshed Quyyumi ◽  
Douglas Vaughan ◽  
Thomas Moss ◽  
Wai S. Chan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Bone Marrow ◽  
Cell Death ◽  
Phase I ◽  
Ventricular Remodeling ◽  
Phase 1 ◽  
Myocardial Cell ◽  
Infarct Zone ◽  
St Segment ◽  
Cd34 Cells

Abstract Background: Approximately 20% of patients suffering a ST segment elevated acute myocardial infarction (AMI) have progressive peri-infarct zone myocardial cell death causing ventricular remodeling and poor cardiac outcomes in spite of large vessel revascularization and medical management. Neo-angiogenesis occurs when VEGF levels peak and endothelial precursors are mobilized and recruited to the infarct site. Stromal cell derived factor-1 (SDF-1), the ligand for the CXCR4 receptor, is expressed by CD34+ cells and plays a role in cell homing to areas of ischemic damage. CD34+ CXCR4+ cells home to areas of ischemia, rich in SDF-1, including infarcted myocardium and are capable of inducing neo-angiogenesis. Natural neoangiogenesis is present but insufficient following AMI, suggesting that direct administration of CD34+ CXCR4+ progenitors could mitigate peri-infarct zone myocardial cell death and improve ventricular function. Methods: In this phase I study, patients with an ST segment (AMI) are enrolled in cohorts of 5 to receive one of four doses (5, 10, 15, 20 x 106 of bone marrow derived CD34+ cells. Cells are harvested using a mini-bone marrow harvest (MMH) technique, acquired by Isolex selection and administered by infusion via the infarct related artery 5 to 10 day following successful coronary artery stenting post AMI. The first 10 subjects accrued as subjects on this phase 1 study included 9 males and 1 female, with a median age of 52 years (range 36–70). Results: The first ten patients (of 20 planned) underwent a MMH under conscious sedation without incident. Adequate numbers of viable, enriched CD34+ cells were obtained following Isolex selection for treatment of subjects enrolled at the first two dose cohorts (5 x 106 and 10 x 106 CD34+ cells). The mean fraction of cells expressing CD34 in the marrow product was 0.75%, with a mean recovery of 40% following Isolex selection (Table). Conclusions: Our study demonstrates the feasibility of collecting up to 409 ml of bone marrow using a MMH technique in the immediate post AMI setting, with yields up to 86 x 106 CD34+ cells. All patient cells expressed CXCR4 and had in vitro migratory capacity. However the lower than expected percentage of TNC expressing CD34 (compared with 9 healthy age matched individuals (1.49% vs. 0.75%) and a low % recovery following Isolex selection may limit successful upper (>10 x 106) cohort treatments. VEGf-2 expression on enriched CD34+ cells was variable. Processing and Product Results (N=10) mean (median) range *N=7 (technical loss of 3 samples);** N=9 (technical loss of 1 sample) MMH marrow volume (ml) 395 (396) 377 – 409 Harvest TNC content (x 109) 6.65 ( 6.73) 3.85 – 8.59 Harvest CD34+ content (x 106) 45.3 (50.2) 16.9 – 86.7 Harvest CD34+ % of TNC 0.75% (0.72%) 0.54% – 1.06% Selected CD34+ content (x 106) 17.8 (16.5) 8.4 – 28.9 Selected % CD34+ recovery 40.3% (41.9%) 30.2 – 49.7 Selected %CD34+ viability 97.1% (98.0 %) 96% – 99% Selected % CD34+ purity 82.5% (84.%) 70% – 91% Total processing time (hours) 14.2 (14.0) 11 – 17 SDF-1 induced migration (% of CD34+ cells) 20.2% (17.0%) 9.5% – 35.4% CXCR-4 expression(% of CD34+ cells)* 58.7% (52.0%) 44% – 78% VEGF-2 expression (% of CD34+ cells)** 0.82% (0.86%) 0% – 2.39%

scholarly journals Annexin V Levels as an Indicator of Myocardial Cell Death after Myocardial Infarction

2020 ◽  
Vol 19 (2) ◽  
pp. 78-84
Author(s):  
Mohammed Karem Ahmed ◽  
◽  
Adil Hassan Mohammed ◽  
Amed Medb Athab
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Plasma Concentrations ◽  
Annexin V ◽  
Myocardial Cell ◽  
Early Morning ◽  
Control Group ◽  
P Value ◽  
The Mean

Background:Myocardial ischemia is associated with apoptosis of cardiomyocyte and because of apoptotic cell death is characterized by externalization of Phosphatidylserine on the cell membrane, so it is amenable to targeting by Annexin V. Objective: To compare plasma concentrations of Annexin V in patients who had an early infarct with patients without infarction. And to analyze the plasma concentration of Annexin V in relationship to cardiovascular risk factors. Patients and Methods: A Case-control study of 100 patients (case) who are diagnosed with Myocardial Infarction (MI) and admitted to the coronary care unit of Baqubah Teaching Hospital and another 100 patients homogenous in terms of age and gender and who attended the hospital for other cause than myocardial infarction is selected as the control group during a period between the first of April and the first of July 2019. A special questionnaire used to collect the required information, an early morning blood sample is taken to measure the level of Annexin V by ELISA, Student’s t-test, ANOVA test and Chi_square test to find an association and differences between variables. Results: The results showed that The mean Annexin V level is significantly higher in cases (10.48155ng/ml) than control (1.28803ng/ml) with p-value =0.001 and a sample taken within 24 hours after MI is significantly higher in the mean level of Annexin V then the sample taken after 24 hours of MI. Conclusion: Generally, the measurement of Annexin V level has provided a good diagnostic test to evaluate myocardial infarction. Keywords: Myocardial infarction, Annexin V, Phosphatidylserine, Apoptosis

P2714Time-dependent myocardial necrosis in patients suffering from ST-elevation myocardial infarction without angiographic collateral flow visualized by cardiac magnetic resonance imaging

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Greulich ◽  
A Mayr ◽  
S Gloekler ◽  
A Seitz ◽  
S Birkmeier ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Symptom Onset ◽  
Myocardial Salvage ◽  
Collateral Flow ◽  
Area At Risk ◽  
Complete Occlusion ◽  
St Segment Elevation ◽  
Lge Cmr

Abstract Background Acute complete occlusion of a coronary artery results in progressive ischemia, moving from the endocardium to the epicardium (“wavefront”). Dependent on time-to-reperfusion and collateral flow, myocardial infarction (MI) will manifest, with transmural MI portending poor prognosis. Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging can detect MI with high diagnostic accuracy. Primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy in patients with STEMI <12 hours of symptom onset. Purpose We sought to visualize time-dependent necrosis in a ST-segment elevation myocardial infarction (STEMI) population by LGE-CMR. Methods STEMI patients with: single-vessel disease, complete occlusion with Thrombolysis in Myocardial Infarction (TIMI) score 0, absence of collateral flow (Rentrop score 0) and symptom onset <12 hours were consecutively enrolled. By LGE-CMR, area at risk (AAR) and infarct size (IS), myocardial salvage index (MSI), transmurality index, and transmurality grade (0–50%, 51–75%, 76–100%) were determined. Results 164 patients (54±11 years, 80% male) were included. Receiver-operating-characteristic (ROC)-curve (area under the curve [AUC] = 0.81) indicating transmural necrosis revealed the best diagnostic cut-off for a symptom-to-balloon time of 121 minutes, i.e. patients with >121 minutes demonstrated increased IS, transmurality index, transmurality grade (all p-values <0.01), and decreased MSI (p<0.001) vs. patients with symptom-to-balloon times ≤121 minutes. Conclusions In myocardial infarction with no residual antegrade, and no collateral flow, immediate reperfusion is vital. A symptom-to-balloon time of >121 minutes causes a high grade of transmural necrosis. In the present, pure STEMI population, time to reperfusion to salvage myocardium was less than suggested by current guidelines.

scholarly journals MicroRNA-26a/b-5p promotes myocardial infarction-induced cell death by downregulating cytochrome c oxidase 5a

2021 ◽  
Vol 53 (9) ◽  
pp. 1332-1343
Author(s):  
Seung Eun Jung ◽  
Sang Woo Kim ◽  
Seongtae Jeong ◽  
Hanbyeol Moon ◽  
Won Seok Choi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Molecular Mechanisms ◽  
Myocardial Cell ◽  
Myocardial Cells ◽  
Network Analyses ◽  
Rat Hearts

AbstractMyocardial infarction (MI) damage induces various types of cell death, and persistent ischemia causes cardiac contractile decline. An effective therapeutic strategy is needed to reduce myocardial cell death and induce cardiac recovery. Therefore, studies on molecular and genetic biomarkers of MI, such as microRNAs (miRs), have recently been increasing and attracting attention due to the ideal characteristics of miRs. The aim of the present study was to discover novel causative factors of MI using multiomics-based functional experiments. Through proteomic, MALDI-TOF-MS, RNA sequencing, and network analyses of myocardial infarcted rat hearts and in vitro functional analyses of myocardial cells, we found that cytochrome c oxidase subunit 5a (Cox5a) expression is noticeably decreased in myocardial infarcted rat hearts and myocardial cells under hypoxic conditions, regulates other identified proteins and is closely related to hypoxia-induced cell death. Moreover, using in silico and in vitro analyses, we found that miR-26a-5p and miR-26b-5p (miR-26a/b-5p) may directly modulate Cox5a, which regulates hypoxia-related cell death. The results of this study elucidate the direct molecular mechanisms linking miR-26a/b-5p and Cox5a in cell death induced by oxygen tension, which may contribute to the identification of new therapeutic targets to modulate cardiac function under physiological and pathological conditions.

scholarly journals The Significance of Troponin and Ck-Mb in Association with Q-Wave Myocardial Infarction

2018 ◽  
Vol 1 (1) ◽  
pp. 11-17
Author(s):  
Urip Harahap ◽  
Linda Margata
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Cell Damage ◽  
Myocardial Cell ◽  
Vital Role ◽  
Cardiac Markers ◽  
Cardiac Biomarker ◽  
Electrocardiogram Ecg ◽  
Myocardial Cell Damage ◽  
Q Wave

Abstract. Acute myocardial infarction (AMI) is the global main cause of morbidity and mortality. AMI describes the process of cell death due to prolonged ischemia identified by the appearance of pathological Q-wave in electrocardiogram (ECG). Myocardial cell death does not occur directly after the onset of myocardial ischemia, however, it occurs more than 6 hours after the onset. Thus, certain cardiac markers, such as cardiac troponin and creatinine kinase-MB (CK-MB) which formed in myocardial cell damage, play a vital role in diagnosing AMI. Keywords: Cardiac Biomarker, CK-MB, Diagnosis, Q-wave Myocardial Infarction, Troponin

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