Mayer, B.* ; Lieb, W.* ; Götz, A.* ; König, I.R.* ; Kauschen, L.F.* ; Linsel-Nitschke, P.* ; Pomarino, A.* ; Holmer, S.* ; Hengstenberg, C.* ; Döring, A. ; Loewel, H. ; Hense, H.W.* ; Ziegler, A.* ; Erdmann, J.* ; Schunkert, H.*
     
 
    
        
Association of a functional polymorphism in the CYP4A11 gene with systolic blood pressure in survivors of myocardial infarction.
    
    
        
    
    
        
        J. Hypertens. 24, 1965-1970 (2006)
    
    
    
		
		
			
				OBJECTIVE: Survivors of myocardial infarction (MI) are known to have a high prevalence of arterial hypertension which, at the same time, imposes a major risk to such patients. Genetic variants of the arachidonic acid monooxygenase CYP4A11 may result in decreased synthesis of 20-hydroxyeicostatetraenoic acid (20-HETE), experimental hypertension and elevated blood pressure levels in humans. The present study aimed to investigate the impact of the functionally relevant T8590C polymorphism of this gene on blood pressure and the prevalence of hypertension in MI patients. METHODS: Survivors of MI from the MONICA Augsburg MI registry (n = 560) were studied after a mean of 5.6 years after the acute event. Participants were examined by standardized anthropometric and echocardiographic measurements, as well as genotyping for CYP4A11 T8590C allele status. RESULTS: Genotype frequencies in MI patients (TT = 71.8%, CT = 26.2%, CC = 2.0%) did not differ from those in population-based controls (n = 1363; TT = 75.4%, CT = 22.5% and CC = 2.1%, P = 0.22). MI survivors with the CC genotype displayed higher systolic blood pressure levels (CC: 143.4 ± 4.9 mmHg versus CT: 134.5 ± 1.3 mmHg and TT: 131.1 ± 0.8 mmHg; P = 0.02) and a non-significant trend towards higher diastolic blood pressure levels (CC: 88.4 ± 3.0 mmHg versus CT: 84.9 ± 0.8 mmHg and TT: 83.9 ± 0.5 mmHg; P = 0.17) in multivariate models. Accordingly, the C allele was related to elevated odds ratios for hypertension in a recessive [4.14; 95% confidence interval (CI) = 1.07-15.96, P = 0.04] and in a dominant model (1.50; 95% CI = 1.03-2.20, P = 0.04), respectively. No blood pressure-independent association of the T8590C polymorphism with echocardiographic parameters of left ventricular function and/or geometry was found. CONCLUSION: The data obtained in the present study strengthen the evidence of an association of the CYP4A11 T8590C polymorphism with blood pressure levels and hypertension prevalence. Particularly, the risk of arterial hypertension is substantially higher in MI patients homozygous for the CC allele. By contrast, no evidence was obtained for an association between this genotype and MI. © 2006 Lippincott Williams & Wilkins.
			
			
				
			
		 
		
			
				
					
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        Publikationstyp
        Artikel: Journalartikel
    
 
    
        Dokumenttyp
        Wissenschaftlicher Artikel
    
 
    
        Typ der Hochschulschrift
        
    
 
    
        Herausgeber
        
    
    
        Schlagwörter
        association; CYP4A11; genetics; hypertension; left ventricular structure; myocardial infarction; polymorphism
    
 
    
        Keywords plus
        
    
 
    
    
        Sprache
        englisch
    
 
    
        Veröffentlichungsjahr
        2006
    
 
    
        Prepublished im Jahr 
        
    
 
    
        HGF-Berichtsjahr
        0
    
 
    
    
        ISSN (print) / ISBN
        0263-6352
    
 
    
        e-ISSN
        1473-5598
    
 
    
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        Konferenzort
        
    
 
	
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	    Band: 24,  
	    Heft: 10,  
	    Seiten: 1965-1970 
	    Artikelnummer: ,  
	    Supplement: ,  
	
    
 
  
        
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            Verlag
            Lippincott Williams & Wilkins
        
 
        
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        Begutachtungsstatus
        Peer reviewed
    
 
    
        Institut(e)
        Institute of Epidemiology (EPI)
    
 
    
        POF Topic(s)
        
30202 - Environmental Health
    
 
    
        Forschungsfeld(er)
        
Genetics and Epidemiology
    
 
    
        PSP-Element(e)
        G-503900-004
G-504090-001
    
 
    
        Förderungen
        
    
 
    
        Copyright
        
    
 	
    
    
    
        Erfassungsdatum
        2006-12-31