Increased coagulation factor XIII activity but not genetic variants of coagulation factors is associated with myocardial infarction in young patients

SummaryCoagulation factor XIII and plasma fibrinogen chromatographic assays have been performed serially in patients suffering from acute myocardial and cerebral infarction, and in others with disseminated intravascular coagulation. The findings were compared with 2 groups of “controls”; normal clinically-well subjects and hospitalized patients with cerebral infarction who exhibited minimal, stable, or improving neurological deficits. Substantial depression of factor XIII concentrations developed in the 3 patient groups, together with concomitant significant increases in the proportion and concentration of plasma high molecular weight fibrin(ogen) complexes (HMWFC). An inverse correlation (p<0.05) between coagulation factor XIII concentration and percentage of HMWFC was demonstrated in the early stages of the illness. These findings suggest that depression of coagulation factor XIII concentration in these states, is secondary to extra vascular or intravascular coagulation and may reflect its degree.

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Coagulation Factor XIII-A Val34Leu Polymorphism and the Risk of Coronary Artery Disease and Myocardial Infarction in a Chinese Han Population

Clinical and Applied Thrombosis/Hemostasis ◽

10.1177/1076029609355152 ◽

2010 ◽

Vol 17 (2) ◽

pp. 208-213 ◽

Cited By ~ 4

Author(s):

Guodong Jin ◽

Beili Feng ◽

Peng Chen ◽

Oushan Tang ◽

Jian Wang ◽

...

Keyword(s):

Myocardial Infarction ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Factor Xiii ◽

Coagulation Factor ◽

Chinese Han Population ◽

Chinese Han ◽

Han Population ◽

Coagulation Factor Xiii ◽

Artery Disease

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Epistatic and pleiotropic effects of polymorphisms in the fibrinogen and coagulation factor XIII genes on plasma fibrinogen concentration, fibrin gel structure and risk of myocardial infarction

Thrombosis and Haemostasis ◽

10.1160/th05-11-0777 ◽

2006 ◽

Vol 95 (03) ◽

pp. 420-427 ◽

Cited By ~ 28

Author(s):

Per Eriksson ◽

Carl-Göran Ericsson ◽

Anders Hamsten ◽

Angela Silveira ◽

Maria Mannila

Keyword(s):

Myocardial Infarction ◽

Factor Xiii ◽

Coagulation Factor ◽

Fibrin Clot ◽

Pleiotropic Effects ◽

Plasma Fibrinogen ◽

Fibrinogen Concentration ◽

Fibrin Gel ◽

Coagulation Factor Xiii ◽

Clot Structure

SummaryAn intricate interplay between the genes encoding fibrinogen gamma (FGG), alpha (FGA) and beta (FGB), coagulation factor XIII (F13A1) and interleukin6 (IL6) and environmental factors is likely to influence plasma fibrinogen concentration, fibrin clot structure and risk of myocardial infarction (MI). In the present study, the potential contribution of SNPs harboured in the fibrinogen, IL6 and F13A1 genes to these biochemical and clinical phenotypes was examined. A database and biobank based on 387 survivors ofa first MI and population-based controls were used. Sixty controls were selected according to FGG 9340T>C [rs1049636] genotype for studies on fibrin clot structure using the liquid permeation method. The multifactor dimensionality reduction method was used for interaction analyses. We here report that the FGA 2224G>A [rs2070011] SNP (9.2%), plasma fibrinogen concentration (13.1%) and age (8.1%) appeared as independent determinants of fibrin gel porosity. The FGA 2224G>A SNP modulated the relation between plasma fibrinogen concentration and fibrin clot porosity. The FGG-FGA*4 haplotype, composed of the minor FGG 9340C and FGA 2224A alleles, had similar effects, supporting its reported protective role in relation to MI. Significant epistasis on plasma fibrinogen concentration was detected between the FGA 2224G>A and F13A1 Val34Leu [rs5985] SNPs (p<0.001).The FGG 9340T>C and FGB 1038G>A [rs1800791] SNPs appeared to interact on MI risk, explaining the association of FGG-FGB haplotypes with MI in the absence of effects of individual SNPs. Thus, epistatic and pleiotropic effects of polymorphisms contribute to the variation in plasma fibrinogen concentration, fibrin clot structure and risk of MI.

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Genetic variants of coagulation factor XIII, postmenopausal estrogen therapy, and risk of nonfatal myocardial infarction

Blood ◽

10.1182/blood-2002-07-2308 ◽

2003 ◽

Vol 102 (1) ◽

pp. 25-30 ◽

Cited By ~ 26

Author(s):

Alexander P. Reiner ◽

Susan R. Heckbert ◽

Hans L. Vos ◽

Robert A. S. Ariëns ◽

Rozenn N. Lemaitre ◽

...

Keyword(s):

Myocardial Infarction ◽

Postmenopausal Women ◽

Factor Xiii ◽

Estrogen Therapy ◽

Coagulation Factor ◽

Nonfatal Myocardial Infarction ◽

Factor Xiiia ◽

Coagulation Factor Xiii ◽

Postmenopausal Estrogen ◽

Reduced Risk

Abstract We hypothesized that possession of either of 2 functional coagulation factor XIII polymorphisms, one within subunit A (Val34Leu) and one within subunit B (His95Arg), might modulate the prothrombotic effects of estrogen and help to explain the variation in incidence of arterial thrombotic events among postmenopausal women using hormone replacement therapy. In a population-based case-control study of 955 postmenopausal women, we assessed the associations of factor XIII genotypes and their interactions with estrogen therapy on risk of nonfatal myocardial infarction (MI). The presence of the factor XIIIA Leu34 allele was associated with a reduced risk of MI (odds ratio [OR] = 0.70, 95% confidence interval [95% CI] = 0.51-0.95). The presence of the factor XIIIB Arg95 allele had little association with MI risk. Neither factor XIII polymorphism alone significantly modified the association between the risk of MI and current estrogen use. In exploratory analyses, however, there was a significant factor XIII subunit gene-gene interaction. Compared to women homozygous for both common factor XIII alleles, the Arg95 variant was associated with a reduced risk of MI in the presence of the Leu34 variant (OR = 0.36, 95% CI = 0.17-0.75) but not in the absence of the Leu34 variant (OR = 1.11, 95% CI = 0.69-1.79). Moreover, among women who had at least 2 copies of the variant factor XIII alleles and were current estrogen users, the risk of MI was reduced by 70% relative to estrogen nonusers with fewer than 2 factor XIII variant alleles (P value for interaction = .03). If confirmed, these findings may permit a better assessment of the cardiovascular risks and benefits associated with postmenopausal estrogen therapy. (Blood. 2003;102:25-30)

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