Myocardial Infarct Localization Using Neighbourhood Approximation Forests

2016 ◽  
pp. 108-116 ◽  
Author(s):  
Héloïse Bleton ◽  
Jàn Margeta ◽  
Hervé Lombaert ◽  
Hervé Delingette ◽  
Nicholas Ayache
Keyword(s):  
Myocardial Infarct

The Quantitation of Platelet Aggregation Induced by Four Compounds: A Study in Relation to Myocardial Infarction

1966 ◽  
Vol 16 (03/04) ◽  
pp. 752-767 ◽  
Author(s):  
J. R O’Brien ◽  
F. C Path ◽  
Joan B. Heywood ◽  
J. A Heady
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Myocardial Infarct ◽  
Control Groups ◽  
The Mean ◽  
Platelet Shape

SummaryMethods for measuring and comparing day to day differences in the response of platelet aggregation in platelet-rich plasma to added ADP, 5-H.T., adrenaline and collagen are reported. Platelet aggregation induced by ADP, 5-H.T. and adrenaline was studied in patients with acute myocardial infarction and in others 3 months to 5 years after an infarct; some were receiving anti-coagulants and others not: these three groups were compared with three control groups. The mean platelet shape was rounder and the response to ADP and to 5-H.T. and one parameter of the response to adrenaline was significantly greater in all groups of patients with myocardial infarct taken together than in the controls. The platelet-rich plasma from patients with recent infarction were most responsive to ADP and 5-H.T. immediately after the infarct. Anti-coagulants had no effect on these tests. However, there was wide variation within the individuals and much overlap between groups, and these tests can only reliably distinguish between groups and not between individuals. The significance of these findings is discussed.

Modulation of Inflammatory Response Improves Myocardial Infarct Healing in Rats

2014 ◽  
Vol 20 (12) ◽  
pp. 1980-1986 ◽  
Author(s):  
A.P. Sarapultsev ◽  
O.N. Chupakhin ◽  
P.A. Sarapultsev ◽  
M.A. Rantsev ◽  
S.U. Medvedeva ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Myocardial Infarct ◽  
Infarct Healing

Analysis of the Clinical Diagnostic Value of GMFB in Cerebral Infarction

2020 ◽  
Vol 21 (10) ◽  
pp. 955-963
Author(s):  
Zhaohu Yuan ◽  
Zhiwu Yu ◽  
Yiyu Zhang ◽  
Huikuan Yang
Keyword(s):  
Myocardial Infarct ◽  
Diagnostic Value ◽  
Artery Occlusion ◽  
Response Dynamics ◽  
Stroke Patients ◽  
Ischaemic Injury ◽  
Neuronal Nuclei ◽  
Diagnosis And Prognosis ◽  
Maturation Factor ◽  
Injury And Repair

Background: Glial Maturation Factor Beta (GMFB) is a highly conserved brain-enriched protein implicated in immunoregulation, neuroplasticity and apoptosis, processes central to neural injury and repair following cerebral ischaemia. Therefore, we examined if changes in neurocellular GMFB expression and release can be used to assess brain injury following ischaemia. Methods and Results: Immunofluorescence staining, Western blotting, immunohistochemistry and ELISA were used to measure GMFB in cultured neurons and astrocytes, rat brain tissues and plasma samples from stroke model rats and stroke patients, while cell viability assays, TTC staining and micro- PET were used to assess neural cell death and infarct severity. Immunofluorescence and immunohistochemistry revealed GMFB expression mainly in astrocyte and neuronal nuclei but also in neuronal axons and dendrites. Free GMFB concentration increased progressively in the culture medium during hypoxia-hypoglycaemia treatment. Plasma GMFB concentration increased in rats subjected to middle cerebral artery occlusion (MCAO, a model of stroke-reperfusion) and in stroke patients. Plasma GMFB in MCAO model rats was strongly correlated with infarct size (R2=0.9582). Plasma GMFB concentration was also markedly elevated in stroke patients within 24 h of onset and remained elevated for more than one week. Conversely, plasma GMFB elevations were not significant in myocardial infarct patients and stroke patients without infarction. Conclusion: GMFB has the prerequisite stability, expression specificity and response dynamics to serve as a reliable indicator of ischaemic injury in animal models and stroke patients. Plasma GMFB may be a convenient non-invasive adjunct to neuroimaging for stroke diagnosis and prognosis.

scholarly journals Hydralazine protects the heart against acute ischaemia/reperfusion injury by inhibiting Drp1-mediated mitochondrial fission

2021 ◽  
Author(s):  
Siavash Beikoghli Kalkhoran ◽  
Janos Kriston-Vizi ◽  
Sauri Hernandez-Resendiz ◽  
Gustavo E Crespo-Avilan ◽  
Ayeshah A Rosdah ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Mitochondrial Fission ◽  
Vehicle Control ◽  
Myocardial Infarct Size ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Pre Treatment ◽  
Apoptotic Effects

Abstract Aims Genetic and pharmacological inhibition of mitochondrial fission induced by acute myocardial ischaemia/reperfusion injury (IRI) has been shown to reduce myocardial infarct size. The clinically used anti-hypertensive and heart failure medication, hydralazine, is known to have anti-oxidant and anti-apoptotic effects. Here, we investigated whether hydralazine confers acute cardioprotection by inhibiting Drp1-mediated mitochondrial fission. Methods and results Pre-treatment with hydralazine was shown to inhibit both mitochondrial fission and mitochondrial membrane depolarisation induced by oxidative stress in HeLa cells. In mouse embryonic fibroblasts (MEFs), pre-treatment with hydralazine attenuated mitochondrial fission and cell death induced by oxidative stress, but this effect was absent in MEFs deficient in the mitochondrial fission protein, Drp1. Molecular docking and surface plasmon resonance studies demonstrated binding of hydralazine to the GTPase domain of the mitochondrial fission protein, Drp1 (KD 8.6±1.0 µM), and inhibition of Drp1 GTPase activity in a dose-dependent manner. In isolated adult murine cardiomyocytes subjected to simulated IRI, hydralazine inhibited mitochondrial fission, preserved mitochondrial fusion events, and reduced cardiomyocyte death (hydralazine 24.7±2.5% vs. control 34.1±1.5%, P=0.0012). In ex vivo perfused murine hearts subjected to acute IRI, pre-treatment with hydralazine reduced myocardial infarct size (as % left ventricle: hydralazine 29.6±6.5% vs. vehicle control 54.1±4.9%, P=0.0083), and in the murine heart subjected to in vivo IRI, the administration of hydralazine at reperfusion, decreased myocardial infarct size (as % area-at-risk: hydralazine 28.9±3.0% vs. vehicle control 58.2±3.8%, P<0.001). Conclusion We show that, in addition to its antioxidant and anti-apoptotic effects, hydralazine, confers acute cardioprotection by inhibiting IRI-induced mitochondrial fission, raising the possibility of repurposing hydralazine as a novel cardioprotective therapy for improving post-infarction outcomes.

Effects of three types of bariatric interventions on myocardial infarct size and vascular function in rats with type 2 diabetes mellitus

Life Sciences ◽  
2021 ◽  
pp. 119676
Author(s):  
Oleg V. Kornyushin ◽  
Dmitry L. Sonin ◽  
Alexander S. Polozov ◽  
Vitaly V. Masley ◽  
Maria S. Istomina ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Infarct Size ◽  
Vascular Function ◽  
Myocardial Infarct ◽  
Myocardial Infarct Size
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