thromboplastin and Death--Sudden--Cardiac

thromboplastin has been researched along with Death--Sudden--Cardiac* in 2 studies

Other Studies

2 other study(ies) available for thromboplastin and Death--Sudden--Cardiac

Article	Year
Myeloperoxidase and plaque vulnerability. Arteriosclerosis, thrombosis, and vascular biology, 2004, Volume: 24, Issue:7 Topics: Arteriosclerosis; Coronary Thrombosis; Death, Sudden, Cardiac; Disease Progression; Endothelium, Vascular; Female; Glutathione; Humans; Hypochlorous Acid; Inflammation Mediators; Macrophages; Male; Models, Biological; Peroxidase; Rupture, Spontaneous; Thrombophilia; Thromboplastin	2004
Smoking is associated with altered endothelial-derived fibrinolytic and antithrombotic factors: an in vitro demonstration. Circulation, 2002, Aug-20, Volume: 106, Issue:8 Data about the effects of smoking on thrombo-hemostatic factors (tissue factor [TF] and tissue factor pathway inhibitor [TFPI-1]) are limited and on fibrinolytic factors (tissue plasminogen activator [t-PA] and plasminogen activator inhibitor-1 [PAI-1]) are debatable. The present study investigated the smoking-related, endothelial cell (EC)-specific responses for these factors and their relation to nitric oxide (NO) production in vitro.. Serum from 8 nonsmokers and 15 smokers were incubated with confluent (approximately 85%) human umbilical vein endothelial cells (HUVECs) in 24-well tissue-culture plates for 12 hours. After the incubation, basal NO, t-PA, PAI-1, TF, TFPI-1 production, and substance P (SP)-stimulated NO, t-PA, and PAI-1 production were determined. HUVECs treated with smokers' serum showed lower basal (P<0.02) and SP-stimulated (P=0.059) t-PA production but similar basal and stimulated PAI-1 production (P=0.9 and P=0.6) compared with nonsmokers. Basal t-PA/PAI-1 molar ratio was significantly reduced in smokers (P<0.005). TFPI-1 level in the cell culture supernatant was also significantly lower in smokers compared with the nonsmoker group (P<0.05) with no difference in TF level between both groups (P=0.5). As previously reported, both basal (P<0.001) and SP-stimulated (P<0.05) NO production were significantly reduced in smokers. Basal TFPI-1 in culture correlated positively with basal NO production (r=0.42, P=0.04) and negatively with serum cotinine level (r=-0.6, P=0.01).. These results indicate that cigarette smoking is associated with alterations in EC-derived fibrinolytic (t-PA) and antithrombotic (TFPI-1) factors. To our knowledge, this is the first demonstration that EC-derived TFPI is affected by smoking and endogenous NO or that the degree of smoke exposure may influence TFPI levels in an EC milieu. Topics: Adult; Cells, Cultured; Cotinine; Death, Sudden, Cardiac; Endothelium, Vascular; Fibrinolytic Agents; Humans; Lipoproteins; Male; Myocardial Infarction; Nitric Oxide; Plasminogen Activator Inhibitor 1; Smoking; Thromboplastin; Tissue Plasminogen Activator	2002

Article

Year

Myeloperoxidase and plaque vulnerability.

Arteriosclerosis, thrombosis, and vascular biology, 2004, Volume: 24, Issue:7

Topics: Arteriosclerosis; Coronary Thrombosis; Death, Sudden, Cardiac; Disease Progression; Endothelium, Vascular; Female; Glutathione; Humans; Hypochlorous Acid; Inflammation Mediators; Macrophages; Male; Models, Biological; Peroxidase; Rupture, Spontaneous; Thrombophilia; Thromboplastin

2004

Smoking is associated with altered endothelial-derived fibrinolytic and antithrombotic factors: an in vitro demonstration.

Circulation, 2002, Aug-20, Volume: 106, Issue:8

Data about the effects of smoking on thrombo-hemostatic factors (tissue factor [TF] and tissue factor pathway inhibitor [TFPI-1]) are limited and on fibrinolytic factors (tissue plasminogen activator [t-PA] and plasminogen activator inhibitor-1 [PAI-1]) are debatable. The present study investigated the smoking-related, endothelial cell (EC)-specific responses for these factors and their relation to nitric oxide (NO) production in vitro.. Serum from 8 nonsmokers and 15 smokers were incubated with confluent (approximately 85%) human umbilical vein endothelial cells (HUVECs) in 24-well tissue-culture plates for 12 hours. After the incubation, basal NO, t-PA, PAI-1, TF, TFPI-1 production, and substance P (SP)-stimulated NO, t-PA, and PAI-1 production were determined. HUVECs treated with smokers' serum showed lower basal (P<0.02) and SP-stimulated (P=0.059) t-PA production but similar basal and stimulated PAI-1 production (P=0.9 and P=0.6) compared with nonsmokers. Basal t-PA/PAI-1 molar ratio was significantly reduced in smokers (P<0.005). TFPI-1 level in the cell culture supernatant was also significantly lower in smokers compared with the nonsmoker group (P<0.05) with no difference in TF level between both groups (P=0.5). As previously reported, both basal (P<0.001) and SP-stimulated (P<0.05) NO production were significantly reduced in smokers. Basal TFPI-1 in culture correlated positively with basal NO production (r=0.42, P=0.04) and negatively with serum cotinine level (r=-0.6, P=0.01).. These results indicate that cigarette smoking is associated with alterations in EC-derived fibrinolytic (t-PA) and antithrombotic (TFPI-1) factors. To our knowledge, this is the first demonstration that EC-derived TFPI is affected by smoking and endogenous NO or that the degree of smoke exposure may influence TFPI levels in an EC milieu.

Topics: Adult; Cells, Cultured; Cotinine; Death, Sudden, Cardiac; Endothelium, Vascular; Fibrinolytic Agents; Humans; Lipoproteins; Male; Myocardial Infarction; Nitric Oxide; Plasminogen Activator Inhibitor 1; Smoking; Thromboplastin; Tissue Plasminogen Activator

2002