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

scholarly journals Moderate hypothermia during cardiopulmonary bypass reduces myocardial cell damage and myocardial cell death related to cardiac surgery

2001 ◽  
Vol 38 (4) ◽  
pp. 1216-1223 ◽  
Author(s):  
Jaime F Vazquez-Jimenez ◽  
Ma Qing ◽  
Benita Hermanns ◽  
Bernd Klosterhalfen ◽  
Michael Wöltje ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Cell Damage ◽  
Myocardial Cell ◽  
Moderate Hypothermia ◽  
Myocardial Cell Damage

Evaluation of Myocardial Cell Damage by In-111-Monoclonal Antimyosin Antibodies in Patients Under Chronic Tricyclic Antidepressant Drug Treatment

Circulation ◽  
1995 ◽  
Vol 91 (6) ◽  
pp. 1619-1623 ◽  
Author(s):  
Vicens Martí ◽  
Manel Ballester ◽  
Claudi Udina ◽  
Ignasi Carrió ◽  
Enric Alvarez ◽  
...  
Keyword(s):  
Drug Treatment ◽  
Cell Damage ◽  
Antidepressant Drug ◽  
Myocardial Cell ◽  
Tricyclic Antidepressant ◽  
Antidepressant Drug Treatment ◽  
Myocardial Cell Damage

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.

Myocyte cell damage after administration of doxorubicin or mitoxantrone in breast cancer patients assessed by indium 111 antimyosin monoclonal antibody studies.

1993 ◽  
Vol 11 (7) ◽  
pp. 1264-1268 ◽  
Author(s):  
M Estorch ◽  
I Carrió ◽  
D Martínez-Duncker ◽  
L Berná ◽  
G Torres ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Advanced Breast Cancer ◽  
Cell Damage ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Advanced Breast ◽  
Left Ventricular Ejection ◽  
Antimyosin Antibody ◽  
Indium 111 ◽  
Myocardial Cell Damage

PURPOSE To compare myocyte cell damage induced by doxorubicin or mitoxantrone, we performed left ventricular ejection fraction (LVEF) measurements and indium 111 antimyosin antibody studies in a group of patients with advanced breast cancer who had been treated with these anthracycline derivatives. PATIENTS AND METHODS We studied 35 patients eligible to receive chemotherapy including the anthracyclines: doxorubicin or mitoxantrone (cumulative dose of doxorubicin, 500 mg/m2; or mitoxantrone, 120 mg/m2). LVEF was measured before and after 10 cycles of chemotherapy. Antimyosin uptake in the myocardium was quantified by means of a heart-to-lung ratio (HLR). RESULTS Patients treated with doxorubicin presented with a significant decrease in LVEF after chemotherapy (before, 60.4% +/- 8.92%; after, 49.8% +/- 9.71%; P = .001). Antimyosin uptake was observed in all patients with a HLR of 2.03 +/- 0.25. Seven of eight patients with a HLR greater than 2.03 had a greater than 10% decrease in LVEF. Patients treated with mitoxantrone did not present with a decrease in LVEF after chemotherapy (before, 55.4% +/- 6.25%; after, 55.8% +/- 7.25%; not significant). Antimyosin uptake was observed in 14 of 17 patients with a HLR of 1.77 +/- 0.18 (P < .05). CONCLUSION 111In antimyosin monoclonal antibodies defect myocardial cell damage produced by doxorubicin and mitoxantrone. In patients with advanced breast cancer, cumulative doses of 120 mg/m2 of mitoxantrone produce less myocardial cell damage than cumulative doses of 500 mg/m2 of doxorubicin. 111In antimyosin uptake without decrease in LVEF after treatment with mitoxantrone indicates the presence of myocyte cell damage, but not to the extent necessary to deteriorate function. These results indicate that 111In antimyosin antibody studies are useful in the noninvasive comparative assessment of cardiotoxicity produced by different anthracycline derivatives.

scholarly journals Rapid, Highly Sensitive Immunoassay for Determination of Cardiac Troponin I in Patients with Myocardial Cell Damage

1997 ◽  
Vol 43 (8) ◽  
pp. 1464-1465 ◽  
Author(s):  
Mauro Panteghini ◽  
Roberto Bonora ◽  
Franca Pagani ◽  
Francesca Buffoli ◽  
Claudio Cuccia
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Cell Damage ◽  
Myocardial Cell ◽  
Cardiac Troponin I ◽  
Highly Sensitive ◽  
Myocardial Cell Damage

scholarly journals Evaluation of myocardial cell damage in cardiac lymph during cardiopulmonary bypass

Critical Care ◽  
10.1186/cc336 ◽  
1999 ◽  
Vol 3 (S2) ◽  
Author(s):  
JF Vazquez-Jimenez ◽  
Ma Qing ◽  
OJ Liakopoulos ◽  
RG Grabitz ◽  
G von Bernuth ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Cell Damage ◽  
Myocardial Cell ◽  
Myocardial Cell Damage
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