The common Y402H variant in complement factor H gene is not associated with susceptibility to myocardial infarction and its related risk factors

2007 ◽  
Vol 113 (4) ◽  
pp. 213-218 ◽  
Author(s):  
Klaus Stark ◽  
Katharina Neureuther ◽  
Kamil Sedlacek ◽  
Wibke Hengstenberg ◽  
Marcus Fischer ◽  
...  

Recently, the genetic variant Y402H in the CFH (complement factor H) gene was associated with an increased risk for MI (myocardial infarction) in a prospective Caucasian cohort. In another nested case-control study, however, the CFH-Y402H variant did not carry susceptibility to MI. The aim of the present study was to test for an association between the CFH-Y402H variant and MI in a large case-control sample with a familial background for CAD (coronary artery disease). A total of 2161 individuals from the German MI family study were studied by questionnaire, physical examination and biochemical analyses. MI patients (n=1188; 51.4±8.6 years at first MI) were recruited from families with at least two members affected by MI and/or severe CAD. Spouses, sisters-in-law and brothers-in-law respectively, without MI/CAD were included as unaffected controls (n=973; 56.9±9.8 years). Genotyping was performed using a TaqMan assay. The common Y402H variant in the CFH gene was not associated with classical cardiovascular risk factors (diabetes, hypercholesterolaemia, hypertension, obesity, smoking and C-reactive protein serum levels). No association was found between the CFH-Y402H variant and susceptibility to MI. Separate analyses in both men and women revealed no gender-specific influence of the gene variant on cardiovascular risk factors or MI. This investigation was unable to replicate the association between the common CFH-Y402H variant and susceptibility to MI in our large Caucasian population which is enriched for genetic factors. We conclude that the CFH-Y402H variant has no relevant risk-modifying effect in our population.

2006 ◽  
Vol 47 (8) ◽  
pp. 1568-1575 ◽  
Author(s):  
Isabella Kardys ◽  
Caroline C.W. Klaver ◽  
Dominiek D.G. Despriet ◽  
Arthur A.B. Bergen ◽  
André G. Uitterlinden ◽  
...  

2008 ◽  
Vol 99 (06) ◽  
pp. 1085-1089 ◽  
Author(s):  
Marianna Politou ◽  
Christoforos Komporozos ◽  
Demosthenes Panagiotakos ◽  
Chrisoula Belessi ◽  
Anthi Travlou ◽  
...  

SummaryThere are limited and controversial data regarding the impact of factor XIII (FXIII) Val34Leu polymorphism in the pathogenesis of premature myocardial infarction (MI). We examined whether FXIII Val34Leu polymorphism is associated with the development of early MI.We recruited 159 consecutive patients who had survived their first acute MI under the age of 36 years (mean age=32.1 ± 3.6 years, 138 were men). The control group consisted of 121 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease (CHD). FXIII Val34Leu polymorphism was tested with polymerase chain reaction and reverse hybridization. There was a lower prevalence of carriers of the Leu34 allele in patients than in controls (30.2 vs. 47.1%, p=0.006). FXIII Val34Leu polymorphism was associated with lower risk for acute MI after adjusting for major cardiovascular risk factors (odds ratio [OR] = 0.51, 95% confidence interval [CI] 0.27–0.95, p=0.03). Subgroup analysis according to angiographic findings (“normal” coronary arteries [n=29] or significant CHD [n=130]) showed that only patients with MI and significant CHD had lower prevalence of carriers of the Leu34 allele compared to controls after adjusting for major cardiovascular risk factors (OR = 0.42, 95% CI 0.22–0.83, p=0.01). Our data indicate that FXIII Val34Leu polymorphism has a protective effect against the development of MI under the age of 36 years, particularly in the setting of significant CHD.


2017 ◽  
Vol 135 (10) ◽  
pp. 1037 ◽  
Author(s):  
Eveline Kersten ◽  
Maartje J. Geerlings ◽  
Anneke I. den Hollander ◽  
Eiko K. de Jong ◽  
Sascha Fauser ◽  
...  

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