scholarly journals Fibrinogen as a risk factor for premature myocardial infarction in Iranian patients: A case control study

2009 ◽  
pp. 673 ◽  
Author(s):  
Mohammad Ahad Eshraghian
Keyword(s):  
Myocardial Infarction ◽  
Risk Factor ◽  
Case Control Study ◽  
Case Control ◽  
Premature Myocardial Infarction ◽  
Control Study ◽  
Iranian Patients

Helicobacter Pylori Infection and the Risk of Myocardial Infarction: Role of Fibrinogen and Its Genetic Control

1999 ◽  
Vol 82 (07) ◽  
pp. 14-18 ◽  
Author(s):  
Francesco Zito ◽  
Augusto Di Castelnuovo ◽  
Andria D’Orazio ◽  
Riccardo Negrini ◽  
Domenico De Lucia ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Genetic Control ◽  
Case Control Study ◽  
Case Control ◽  
Increased Risk ◽  
Confounding Variables ◽  
Control Study

SummaryThe contribution of Helicobacter pylori (HP) infection to the risk of myocardial infarction was evaluated. The role of fibrinogen and its genetic control as a possibile mechanism by which HP may influence myocardial infarction risk was explored in this context. A case-control study was performed in 101 patients with myocardial infarction and in 101 controls.HP infection was associated with an increased risk of myocardial infarction independently for confounding variables (OR 4.1, CI95: 1.8-9.4). HP infection was significantly associated with higher levels of fibrinogen, both in cases and in controls. Furthermore, there was an additive effect of HP infection and B2 allele of BclI fibrinogen poly-morphism in increasing fibrinogen levels. HP infection showed a stronger effect on the risk of myocardial infarction in B2 allele carriers (OR 7.6, CI95: 1.8-31.6) as compared to subjects carrying the B1B1 genotype (OR 3.3, CI95: 1.2-9.2).We showed that a previous HP infection is a risk factor for myocardial infarction. An increase in fibrinogen levels is a possible mechanism by which HP may act. Concomitant conditions, like a genetic predisposition in increasing fibrinogen levels, seem to further increase the effect of HP on myocardial infarction risk.

scholarly journals Khat chewing is a risk factor for acute myocardial infarction: a case-control study

2005 ◽  
Vol 59 (5) ◽  
pp. 574-581 ◽  
Author(s):  
A. Al-Motarreb ◽  
S. Briancon ◽  
N. Al-Jaber ◽  
B. Al-Adhi ◽  
F. Al-Jailani ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Risk Factor ◽  
Case Control Study ◽  
Case Control ◽  
Khat Chewing ◽  
Control Study

The 4G/5G Genetic Polymorphism in the Promoter of the Plasminogen Activator Inhibitor-1 (PAI-1) Gene Is Associated with Differences in Plasma PAI-1 Activity but not with Risk of Myocardial Infarction in the ECTIM Study

1995 ◽  
Vol 74 (03) ◽  
pp. 837-841 ◽  
Author(s):  
S Ye ◽  
F R Green ◽  
P Y Scarabin ◽  
V Nicaud ◽  
L Bara ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Risk Factor ◽  
Genetic Risk ◽  
Case Control Study ◽  
Plasminogen Activator Inhibitor ◽  
Case Control ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor ◽  
Pai 1 ◽  
Control Study

SummaryWe have investigated the interrelationships of plasma PAI-1 activity, the PAI-1 4G/5G polymorphism and risk of myocardial infarction (MI) in the ECTIM study, a case-control study of MI based in Belfast, Lille, Strasbourg and Toulouse. Mean PAI-1 levels in cases were similar across all centres but in controls, levels in the French centres were significantly higher. Only in Belfast were PAI-1 levels higher in cases (11.7AU/ml) than controls (10.5AU/ml). The PAI-1 4G allele frequency was similar in cases and controls (0.55 and 0.54). In all groups, 4G homozygotes had the highest mean plasma PAI-1 level (4G4G vs 5G5G; cases overall: 14.2 vs 12.1 AU/ml; controls overall: 15.0 vs 12.6AU/ml), with the heterozygotes generally intermediate. The data from Belfast are consistent with the literature implicating PAI-1 level as an MI risk factor. In ECTIM, the PAI-1 4G/5G polymorphism is not a genetic risk factor for MI but is associated with PAI-1 activity. Thus homozygosity for the 4G allele may predispose to elevated PAI-1 and impaired fibrinolysis, perhaps requiring interaction with other genetic or environmental factors to influence MI risk.

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