In vitro plateletutilization of (1-14C) arachidonic acid in normal humans of different age and sex and in acute myocardial infarction patients: A Comparative study for possible diagnostic purposes

1981 ◽  
Vol 7 (3) ◽  
pp. 229-243 ◽  
Author(s):  
K.C. Srivastava ◽  
K.P. Tiwari
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Arachidonic Acid ◽  
Comparative Study ◽  
Normal Humans ◽  
Age And Sex

Pharmacokinetics and Haemostatic Status During Consecutive Infusions of Recom binant Tissue-Type Plasminogen Activator in Patients with Acute Myocardial Infarction

1989 ◽  
Vol 61 (03) ◽  
pp. 497-501 ◽  
Author(s):  
E Seifried ◽  
P Tanswell ◽  
D Ellbrück ◽  
W Haerer ◽  
A Schmidt
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasminogen Activator ◽  
Peak Plasma ◽  
Peak Plasma Concentration ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Precise Control ◽  
Type Plasminogen Activator

SummaryPharmacokinetics and systemic effects of recombinant tissue type plasminogen activator (rt-PA) were determined during coronary thrombolysis in 12 acute myocardial infarction patients using a consecutive intravenous infusion regimen. Ten mg rt-PA were infused in 2 minutes resulting in a peak plasma concentration (mean ±SD) of 3310±950 ng/ml, followed by 50 mg in 1 h and 30 mg in 1.5 h yielding steady state plasma levels of. 2210±470 nglml and 930±200 ng/ml, respectively. All patients received intravenous heparin. Total clearance of rt-PA was 380±74 ml/min, t,½α was 3.6±0.9 min and t,½β was 16±5.4 min.After 90 min, in plasma samples containing anti-rt-PA-IgG to inhibit in vitro effects, fibrinogen was decreased to 54%, plasminogen to 52%, α2-antiplasmin to 25%, α2-macroglobulin to 90% and antithrombin III to 85% of initial values. Coagulation times were prolonged and fibrin D-dimer concentrations increased from 0.40 to 2.7 μg/ml. It is concluded that pharmacokinetics of rt-PA show low interpatient variability and that its short mean residence time in plasma allows precise control of therapy. Apart from its moderate effect on the haemostatic system, rt-PA appears to lyse a fibrin pool in addition to the coronary thrombus.

scholarly journals Neutrophil extracellular traps induce MCP-1 release from endothelial cells at the plaque rupture site in acute myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Ondracek ◽  
T.M Hofbauer ◽  
A Mangold ◽  
T Scherz ◽  
V Seidl ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Endothelial Cells ◽  
Plaque Rupture ◽  
Ex Vivo ◽  
Coronary Intervention ◽  
Neutrophil Extracellular Traps ◽  
Funding Source ◽  
Extracellular Traps

Abstract Introduction Leukocyte-mediated inflammation is crucial in acute myocardial infarction (AMI). We recently observed that neutrophil extracellular traps (NETs) are increased at the culprit site, promoting activation and differentiation of fibrocytes, cells with mesenchymal and leukocytic properties. Fibrocyte migration is mediated by monocyte chemoattractant protein (MCP)-1 and C-C chemokine receptor type 2 (CCR2). We investigated the interplay between NETs, fibrocyte function, and MCP-1 in AMI. Methods Culprit site and femoral blood of AMI patients was drawn during percutaneous coronary intervention. We characterized CCR2 expression of fibrocytes by flow cytometry. MCP-1 and the NET marker citrullinated histone H3 (citH3) were measured by ELISA. Fibrocytes were treated in vitro with MCP-1. Human coronary arterial endothelial cells (hCAECs) were stimulated with isolated NETs, and MCP-1 was measured by ELISA and qPCR. The influence of MCP-1 on NET formation in vitro was assessed using isolated neutrophils. Results We have included 50 consecutive AMI patients into the study. NETs and concentrations of MCP-1 were increased at the CLS. NET stimulation of hCAECs induced MCP-1 on mRNA and protein level. Increasing MCP-1 gradient was associated with fibrocyte accumulation at the site of occlusion. In the presence of higher MCP-1 these fibrocytes expressed proportionally less CCR2 than peripheral fibrocytes. In vitro, MCP-1 dose-dependently decreased fibrocyte CCR2 and reduced ex vivo NET release of healthy donor neutrophils. Conclusions NETs induce endothelial MCP-1 release, presumably promoting a chemotactic gradient for leukocyte and fibrocyte migration. MCP-1 mediated inhibition of NET formation could point to a negative feedback loop. These data will shed light on vascular healing. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Austrian Science Fund

scholarly journals Lyubertsy Study of mortality in patients with acute myocardial infarction (LIS): the analysis of anamnestic predictors of in-hospital mortality

2012 ◽  
Vol 11 (1) ◽  
pp. 45-48 ◽  
Author(s):  
S. Yu. Martsevich ◽  
M. L. Ginsburg ◽  
N. P. Kutishenko ◽  
A. D. Deev ◽  
A. V. Fokina ◽  
...  
Keyword(s):  
Physical Activity ◽  
Diabetes Mellitus ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Psychosocial Risk ◽  
Hospital Death ◽  
Hospitalised Patients ◽  
District Hospitals ◽  
The Russian Federation ◽  
Age And Sex

Aim. To identify the main anamnestic predictors of mortality in the acute phase of acute myocardial infarction (AMI). Material and methods. The study included all patients admitted to Lyubertsy District hospitals and diagnosed with AMI (n=1133). Results. Out of 1133 hospitalised patients, 172 died in the hospital; in-hospital lethality was 15,2%. Mean age of diseased patients was significantly higher than that in those survived. The risk of in-hospital death was significantly and independently associated with older age (relative risk 1,07). After adjustment for age and sex, other independent predictors of in-hospital AMI death included diabetes mellitus (DM), low physical activity, and selected psychosocial factors. Conclusion. The in-hospital lethality levels, observed in the LIS Study, were typical for the Russian Federation. The main anamnestic predictors of in-hospital death were low physical activity, DM, and psychosocial risk factors.

Ex vivo-expanded bone marrow CD34+ for acute myocardial infarction treatment: in vitro and in vivo studies

Cytotherapy ◽  
2011 ◽  
Vol 13 (9) ◽  
pp. 1140-1152 ◽  
Author(s):  
Monica Gunetti ◽  
Alessio Noghero ◽  
Fabiola Molla ◽  
Lidia Irene Staszewsky ◽  
Noeleen de Angelis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Bone Marrow ◽  
Ex Vivo ◽  
In Vivo Studies

scholarly journals Network pharmacology-based identification of major component of Angelica sinensis and its action mechanism for the treatment of acute myocardial infarction

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Xiaowei Niu ◽  
Jingjing Zhang ◽  
Jinrong Ni ◽  
Runqing Wang ◽  
Weiqiang Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Er Stress ◽  
Heart Function ◽  
Network Pharmacology ◽  
Angelica Sinensis ◽  
Peroxisome Proliferator ◽  
Multiple Targets

Background: To decipher the mechanisms of Angelica sinensis for the treatment of acute myocardial infarction (AMI) using network pharmacology analysis. Methods: Databases were searched for the information on constituents, targets, and diseases. Cytoscape software was used to construct the constituent–target–disease network and screen the major targets, which were annotated with the DAVID (Database for Annotation, Visualization and Integrated Discovery) tool. The cardioprotective effects of Angelica sinensis polysaccharide (ASP), a major component of A. sinensis, were validated both in H9c2 cells subjected to simulated ischemia by oxygen and glucose deprivation and in rats with AMI by ligation of the left anterior coronary artery. Results: We identified 228 major targets against AMI injury for A. sinensis, which regulated multiple pathways and hit multiple targets involved in several biological processes. ASP significantly decreased endoplasmic reticulum (ER) stress-induced cell death both in vitro and in vivo. In ischemia injury rats, ASP treatment reduced infarct size and preserved heart function. ASP enhanced activating transcription factor 6 (ATF6) activity, which improved ER-protein folding capacity. ASP activated the expression of p-AMP-activated protein kinase (p-AMPK) and peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α). Additionally, ASP attenuated levels of proinflammatory cytokines and maintained a balance in the oxidant/antioxidant levels after AMI. Conclusion:In silico analysis revealed the associations between A. sinensis and AMI through multiple targets and several key signaling pathways. Experimental data indicate that ASP protects the heart against ischemic injury by activating ATF6 to ameliorate the detrimental ER stress. ASP’s effects could be mediated via the activation of AMPK-PGC1α pathway.

Heterogenicity of diabetes as a risk factor for all-cause mortality after acute myocardial infarction: age and sex impact

2021 ◽  
pp. 109117
Author(s):  
Ygal Plakht ◽  
Yuval Elkis Hirsch ◽  
Arthur Shiyovich ◽  
Muhammad Abu Tailakh ◽  
Idit F Liberty ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Risk Factor ◽  
All Cause Mortality ◽  
Age And Sex

Abstract 14209: A New in vitro Methodology to Evaluate Blood Mononuclear Cells Regenerative Capacity in Diabetes Patients With Acute Myocardial Infarction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Amankeldi A Salybekov ◽  
Katsuaki Sakai ◽  
Makoto Natsumeda ◽  
Kosit Vorateera ◽  
Yuji Ikari ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cell Therapy ◽  
Mononuclear Cells ◽  
Roc Curve Analysis ◽  
Regenerative Capacity ◽  
Cd34 Cells ◽  
Blood Mononuclear Cells ◽  
M1 Type

Introduction & Hypothesis: Diabetes mellitus patients’(DMP) peripheral blood mononuclear cells (PBMNC) regenerative capacity level is impaired. An in vitro evaluation of PBMNC pre/post vasculogenic conditioning (VC) facilitates the assessment of immune cells regenerative potential (H1) and possible cell therapy for DMP with acute myocardial infarction (AMI) (H2). Materials & Methods: Eighteen DMP with the diagnosis of AMI enrolled. Blood drawn in heparin-coated syringes from AMI patients (between day 3 to 7) along with sixteen healthy control. Isolated PBMNC regenerative capability evaluated pre and post VC ( Fig 1 ) with EPCs colony formation assay/unit (EPC-CFA/U) and flow cytometry analysis. Results: An in vitro EPC-CFA revealed that DMP fresh PBMNC derived definitive EPC (DEPC) decreased compared to control. The differentiation rate of EPC, definitive vs. primitive in control groups composed equal (50%, PEPC vs. 50%, DEPC) while in DMP, PEPC prevails (70% vs. 30%). After VC, DEPC-CFU markedly increased while PEPC-CFU decreased, indicating EPC qualitatively and quantitatively improvement in DMP (Control, PBMNC vs. VC P>0.001; DMP, PBMNC vs. VC, P>0.01). DMP glycoalbumin and Hb1Ac inversely correlated with CD34+ cells (r= -0.48, P>0.03) while VC recovered CD34+ cells (r= 0.17, P<0.54). ROC curve analysis also confirmed that the CD34+ cell number is an independent risk classifier of cardiac vessel lesion (AUC=0.85, P>0.002). In contrast, VC preserved from the senescence by expansion and differentiation of CD34+ (AUC=0.54, P<0.7). Proinflammatory M1 type significantly increased in DMP compared to Control (P>0.03), while VC shifted the M1 type phenotype toward M2 type (P>0001). Conclusion: Our EPC-CFA enables us to precisely assess impaired EPC function, while VC enhanced differentiation from PEPC toward DEPC. Furthermore, these methodologies facilitate the evaluation of RACs capacities such as EPC, M1/M2, and Treg cells in DMP with AMI for cell therapy.

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