Positive Association of the β Fibrinogen H1/H2 Gene Variation to Basal Fibrinogen Levels and to the Increase in Fibrinogen Concentration during Acute Phase Reaction but not to Coronary Artery Disease and Myocardial Infarction

1997 ◽  
Vol 77 (06) ◽  
pp. 1120-1126 ◽  
Author(s):  
Andreas Gardemann ◽  
Oliver Schwartz ◽  
Werner Haberbosch ◽  
Norbert Katz ◽  
Tanja Weiß ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Acute Phase ◽  
Plasma Levels ◽  
Acute Phase Reaction ◽  
Plasma Fibrinogen ◽  
Phase Reaction ◽  
Gene Variation ◽  
Artery Disease

Summary Background: Fibrinogen has been demonstrated to be an independent risk factor of cardiovascular disease. The absence of the Haelll cutting site (H2 allele) of an H1/H2 gene variation in the promoter region of the (β fibrinogen gene was associated with increased levels of fibrinogen. Methods and Results: In the present study, the effects of the H1/H2 gene variation not only on plasma fibrinogen concentrations but also on coronary artery disease (CAD) and myocardial infarction (MI) were investigated in 923 individuals who underwent coronary angiography for diagnostic purposes. Relation of the H1/H2 genotype to fibrinogen plasma levels: A strong association was observed between the H1/H2 gene variation and fibrinogen levels. The differences in fibrinogen plasma levels between H2H2 and H1H1 homozygotes were almost threefold more pronounced within subjects with clinical chemical signs of an acute phase reaction (CRP ≥ 7.5 mg/1) than within a subgroup of subjects without these signs (CRP < 7.5 mg/1) (median of CRP distribution: 7.5 mg/1). In 207 patients who underwent aortocoronary bypass surgery plasma fibrinogen levels were almost identical directly after surgery. Two days after operation fibrinogen increased to clearly higher levels in H2H2 homozygotes than in H1H2 and H1H1 genotypes, whereas almost the same maximal increases in fibrinogen concentrations were reached 3-4 days after surgery in all individuals. Relation of the H1/H2 genotype to CAD and MI. Whereas in the total population the plasma fibrinogen concentrations were strongly associated with smoking, CAD and MI, an association of the H1/H2 gene variation to CAD and MI was not detected. However, mean age at first MI of H2H2 individuals (62.9 years) was clearly higher than of H1H2 genotypes (56.9 years) and of H1H1 subjects (56.4 years). In addition, in a subgroup of individuals with a higher risk of MI by either high apoB and/or low apoAl plasma levels the portion of MI patients was clearly smaller within H2H2 homozygotes than within H1H2 or H1H1 genotypes, although – also in these high risk groups – mean age at first MI of H2H2 individuals were higher than of the other two genotypes. Conclusions: Obviously, the H2 allele of the fibrinogen H1/H2 genotype does not only influence basal fibrinogen concentrations, but particularly also the extent of fibrinogen level increase during acute phase reaction. Whereas the fibrinogen plasma level is positively associated with coronary artery disease and myocardial infarction, the H2 allele - although exhibiting an association with elevated fibrinogen levels - was not positively associated with CAD and MI.

β Fibrinogen Gene Polymorphisms Are Associated With Plasma Fibrinogen and Coronary Artery Disease in Patients With Myocardial Infarction

Circulation ◽  
1996 ◽  
Vol 93 (3) ◽  
pp. 440-449 ◽  
Author(s):  
Isabelle Behague ◽  
Odette Poirier ◽  
Viviane Nicaud ◽  
Alun Evans ◽  
Dominique Arveiler ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Gene Polymorphisms ◽  
Plasma Fibrinogen ◽  
Artery Disease

scholarly journals Neutrophil Phenotypes in Coronary Artery Disease

2020 ◽  
Vol 9 (5) ◽  
pp. 1602
Author(s):  
Patrick Maréchal ◽  
Julien Tridetti ◽  
Mai-Linh Nguyen ◽  
Odile Wéra ◽  
Zheshen Jiang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Plasma Levels ◽  
Stable Coronary Artery Disease ◽  
St Elevation Myocardial Infarction ◽  
Multivariable Logistic Regression Analysis ◽  
Coronary Syndrome ◽  
St Elevation ◽  
Artery Disease

Clinical evidence indicates that innate immune cells may contribute to acute coronary syndrome (ACS). Our prospective study aimed at investigating the association of neutrophil phenotypes with ACS. 108 patients were categorized into chronic stable coronary artery disease (n = 37), unstable angina (UA) (n = 19), Non-ST-Elevation Myocardial Infarction (NSTEMI) (n = 25), and ST-Elevation Myocardial Infarction (STEMI) (n = 27). At the time of inclusion, blood neutrophil subpopulations were analysed by flow cytometry. Differential blood cell count and plasma levels of neutrophilic soluble markers were recorded at admission and, for half of patients, at six-month follow-up. STEMI and NSTEMI patients displayed higher neutrophil count and neutrophil-to-lymphocyte ratio than stable and UA patients (p < 0.0001), which normalized at six-month post-MI. Atypical low-density neutrophils were detected in the blood of the four patient groups. STEMI patients were characterized by elevated percentages of band cells compared to the other patients (p = 0.019). Multivariable logistic regression analysis revealed that plasma levels of total myeloperoxidase was associated with STEMI compared to stable (OR: 1.434; 95% CI: 1.119–1.837; P < 0.0001), UA (1.47; 1.146–1.886; p = 0.002), and NSTEMI (1.213; 1.1–1.134; p = 0.0001) patients, while increased neutrophil side scatter (SSC) signal intensity was associated with NSTEMI compared to stable patients (3.828; 1.033–14.184; p = 0.045). Hence, changes in neutrophil phenotype are concomitant to ACS.

scholarly journals Plasma EMMPRIN levels in acute myocardial infarction and stable coronary artery disease

2016 ◽  
Vol 39 (3) ◽  
pp. 79 ◽  
Author(s):  
Mehmet N Akkus ◽  
Adil Ormam ◽  
Sabri Seyis ◽  
Çagdas Baran ◽  
Aysegül Görür ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Plasma Levels ◽  
Stable Coronary Artery Disease ◽  
Healthy Controls ◽  
St Elevation ◽  
Artery Disease ◽  
Stable Cad

Purpose: The purpose of this study was to determine whether the plasma levels of soluble extracellular matrix metalloproteinase inducer (EMMPRIN) differed among the patients with ST-elevation myocardial infarction (STEMI), non-STEMI (NSTEMI) and stable coronary artery disease (CAD) and the healthy controls, and to identify the factors associated with the differences in plasma levels of this this protein among patients in these groups. Methods: Plasma EMMPRIN levels were compared among four age- and sex-matched groups of patients with STEMI, NSTEMI and stable CAD and healthy controls (n=44 per group), then logistic regression and correlation analyses were conducted for the whole acute myocardial infarction (AMI) patients group. Results: EMMPRIN levels were significantly higher in the STEMI (39.4±9.2ng/mL) and NSTEMI (37.1±10.5ng/mL) groups than in either the stable CAD (27.5±4.7ng/mL) or control (24.5±5.8ng/mL) groups (p

Relationships of Insulin and Intact and Split Proinsulin to Haemostatic Function in Young Men with and without Coronary Artery Disease

1995 ◽  
Vol 73 (04) ◽  
pp. 568-575 ◽  
Author(s):  
Peter Båvenholm ◽  
Anthony Proudler ◽  
Angela Silveira ◽  
David Crook ◽  
Margareta Blombäck ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Plasma Levels ◽  
Plasma Fibrinogen ◽  
Factor Vii ◽  
Premature Coronary Artery Disease ◽  
Fibrinogen Concentration ◽  
Artery Disease ◽  
Vldl Triglyceride ◽  
Pai 1

SummaryGlucose intolerance, hyperinsulinaemia, dyslipoproteinaemia and multiple disturbances of haemostatic function are characteristics of young men with premature coronary artery disease. The relations between glucose, insulin and insulin propeptides, in the fasting state, and after an oral glucose load, and haemostatic function were examined in 62 consecutive non-diabetic men with myocardial infarction before the age of 45 and in 41 age-matched healthy men. “True” hyperinsulinaemia, raised plasma concentrations of insulin propeptides, dyslipoproteinaemia, elevated plasma levels of fibrinogen, factor VII antigen (VIIag) and plasminogen activator inhibitor-1 (PAI-1) activity, and lower antithrombin activity (p <0.05-0.001) characterized the patients. PAI-1 activity was more closely associated with insulin, intact proinsulin and des 31,32proinsulin in patients than in controls, whereas the plasma levels of fibrinogen, activated factor VII (VIIa) and VIIag were stronger correlated with insulin and insulin propeptides in subjects without coronary artery disease. Very low density lipoprotein (VLDL) triglyceride was a strong determinant of VIIag and PAI-1 activity levels in both cases and controls, whereas VLDL triglyceride in controls and LDL cholesterol in patients related significantly to the plasma fibrinogen concentration. Thus, our data suggests that plasma insulin and insulin propeptides might be involved in the regulation of plasma fibrinogen concentration, factor VII level and plasma PAI-1 activity. However, apolipoprotein B-containing lipoproteins appear to influence the relationships between insulin, insulin propeptides and haemostatic factors in individuals with premature coronary artery disease.

Platelet Reactivity in Unstable Coronary Artery Disease

1987 ◽  
Vol 57 (03) ◽  
pp. 302-305 ◽  
Author(s):  
Eva Swahn ◽  
Lars Wallentin
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Acute Phase ◽  
Platelet Reactivity ◽  
Platelet Rich Plasma ◽  
Control Group ◽  
Unstable Coronary Artery Disease ◽  
Platelet Factor ◽  
Artery Disease

SummaryUnstable coronary artery disease (CAD) might be related to obstructions of coronary blood flow by platelet aggregates. In 121 men and 43 women admitted to the coronary care unit with suspected unstable CAD, blood samples for tests of platelet function were obtained within 24 hours after admission. Platelet reactivity was tested in vitro in platelet rich plasma as the aggregability towards ADP 1 μM and collagen 1 mg/ml and as the sensitivity to prostacyclin (PSP). The levels of beta-thrombo-globulin and platelet factor 4 were determined ex vivo in platelet poor plasma. Patients who developed a nontransmural myocardial infarction (n = 39) or had signs of myocardial ischemia at an exercise test performed within a week (n = 39) were considered to have unstable CAD while patients without signs of ischemia constituted the control group. In the acute phase the PSP was reduced in patients with unstable CAD without any difference between genders. The aggregability towards ADP was higher in women than men but otherwise there were no differences between groups or sexes in any other test in the acute phase. After 12 months there were no differences in PSP between the groups but women had a lower PSP than men. Thus, in the acute phase of unstable CAD, the platelet sensitivity to the inhibitory effects of prostacyclin was reduced which might contribute to the risk for further platelet aggregation, coronary occlusion and myocardial infarction.

Anticoagulants in coronary artery disease

1964 ◽  
Vol 2 (20) ◽  
pp. 77-80
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Acute Phase ◽  
Anticoagulant Therapy ◽  
Coronary Thrombosis ◽  
Myocardial Infarctions ◽  
Risk Patients ◽  
The Subject ◽  
Artery Disease

The use of anticoagulants to reduce thromboembolic complications following myocardial infarction and to prevent coronary thrombosis in patients with angina is the subject of sharp controversy. Many eminent clinicians are convinced that anticoagulant therapy during the six weeks or so of the acute phase of infarction saves many lives by reducing the risk of venous and mural thrombosis, embolism and new myocardial infarctions; some of them believe that mortality from coronary artery disease can be further reduced by giving anticoagulants for life after infarction or in patients with severe angina. Some favour anticoagulant therapy only in “high risk” patients, that is, those with severe infarction, heart failure or serious arrhythmias. Other clinicians, equally eminent, find no justification for the routine use of anticoagulants during either the acute phase of myocardial infarction or subsequently.

Modulation of Plasma Fibrinogen Levels by Ticlopidine in Healthy Volunteers and Patients with Stable Angina Pectoris

1996 ◽  
Vol 76 (02) ◽  
pp. 166-170 ◽  
Author(s):  
Moniek P M de Maat ◽  
Alf E R Arnold ◽  
Stef van Buuren ◽  
J H Paul Wilson ◽  
Cornells Kluft
Keyword(s):  
Angina Pectoris ◽  
Healthy Volunteers ◽  
Acute Phase ◽  
Stable Angina ◽  
Gene Polymorphisms ◽  
Acute Phase Reaction ◽  
Plasma Fibrinogen ◽  
Phase Reaction ◽  
Stable Angina Pectoris ◽  
Lowering Effect

SummaryElevated plasma fibrinogen levels are associated with an increased risk for cardiac events. Ticlopidine is a drug that inhibits the ADP-induced aggregation of blood platelets and it also has been described that ticlopidine can decrease the plasma fibrinogen level in patients with vascular diseases. The mechanism of this decrease has not yet been elucidated and therefore mechanisms that are known to affect fibrinogen levels were studied, viz. the acute phase reaction, total fibrin plus fibrinogen degradation (TDP) levels and the polymorphisms of the fibrinogen β-gene.The fibrinogen lowering effect of ticlopidine was studied in 26 healthy volunteers, selected on genotype of the BclI polymorphism of the fibrinogen β-gene, and in 26 patients with stable angina pectoris in a double blind, randomized cross-over study. Functional plasma fibrinogen levels were measured with the Clauss assay. Fibrinogen antigen, C-reactive protein (CRP) and TDP levels were measured using an enzyme immuno assay (EIA).In the healthy volunteers the functional fibrinogen levels had decreased by 0.20 g/l (9%, p = 0.005 using the paired Student t-test) after 4 weeks of 250 mg bid ticlopidine administration, whereas fibrinogen antigen, CRP and TDP levels were not significantly changed. In the stable angina pectoris patients the pre-treatment fibrinogen, CRP and TDP levels were significantly higher than in the volunteer group. After four weeks 250 mg bid ticlopidine administration the functional fibrinogen levels had decreased by 0.38 g/l (11%, p < 0.005), whereas the fibrinogen antigen, CRP and TDP levels were not significantly changed. The levels of functional and antigen fibrinogen, CRP and TDP did not change significantly during the placebo period in the volunteers or the patients. Neither in the volunteers nor in the patients was the effect of ticlopidine on the fibrinogen levels associated with the fibrinogen β-gene polymorphisms.Therefore, the fibrinogen lowering effect of ticlopidine is likely to be a modulation of the functionality of the molecule and unlikely to be modulated by the acute phase reaction, TDP-levels or the fibrinogen β-gene polymorphisms.

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