' '
Deutsch | English    

Forschungsdatenbank PMU-SQQUID

Lack of association of the Glu298Asp polymorphism of endothelial nitric oxide synthase with manifest coronary artery disease, carotid atherosclerosis and forearm vascular reactivity in two Austrian populations.
Schmoelzer, I; Renner, W; Paulweber, B; Malaimare, L; Iglseder, B; Schmid, P; Schallmoser, K; Wascher, TC;
EUR J CLIN INVEST. 2003; 33(3): 191-198.
Originalarbeiten (Zeitschrift)


Iglseder Bernhard
Paulweber Bernhard
Schallmoser Katharina


Objective Conflicting data exists about the possible contribution of the homozygous Asp/Asp genotype of the Glu298Asp polymorphism of endothelial nitric oxide synthase to human atherosclerotic vascular disease. We investigated the polymorphism in two independent study populations: a case-control study including patients with angiographically verified coronary artery disease (CAD) on the one hand and a cross-sectional epidemiological study on the other hand. Methods The Glu298Asp polymorphism was determined by PCR-RFLP as established. In the case-control study (240 patients and 248 controls) a possible association between the polymorphism and CAD, and age of onset of CAD and myocardial infarction was investigated. In the cross-sectional epidemiological study (932 subjects) intima-media thickness (IMT) of the carotid artery as well as morphological plaque burden and forearm vascular reactivity (peak postischemic reactive hyperaemia, determined by venous occlusion plethysmography) were measured. Results In the case-control study genotype distribution (Glu/Glu; Glu/Asp; Asp/Asp) was not different between the CAD patients (43/46/11%) and the controls (49/41/10%, P = NS). No association of the polymorphism with age of onset of CAD or myocardial infarction was found. In the epidemiological study no influence of the genetic variant on IMT was observed after correction for classical determinants of IMT (average IMT: Asp/ Asp: 0.077 +/- 0.011 mm; Glu/Glu and Glu/Asp: 0.080 +/- 0.012 mm, P = NS). Forearm vascular reactivity was also not different between homozygous Asp/Asp subjects and Glu/Glu and Glu/Asp subjects (peak-reactive hyperaemia 20.1 +/- 7.3 mL min(-1) 100 mL(-1) vs. 20.0 +/- 6.5 mL min(-1) 100 mL(-1) , P = NS). Conclusions Our results suggest that there is no association of the Glu298Asp polymorphism with coronary or carotid atherosclerosis or forearm vascular reactivity in these populations recruited in a country with a rather high risk for atherosclerosis. We suggest additional investigations to be performed in populations at different risk for coronary events to further elucidate the possible contribution of this polymorphism to vascular disease.

Useful keywords (using NLM MeSH Indexing)






Carotid Artery Diseases/epidemiology

Carotid Artery Diseases/genetics*

Case-Control Studies

Cohort Studies

Coronary Disease/epidemiology

Coronary Disease/genetics*

Cross-Sectional Studies






Middle Aged

Nitric Oxide Synthase/genetics*

Polymorphism, Genetic

Tunica Intima/pathology*

Find related publications in this database (Keywords)

carotid artery
coronary artery disease
intima-media thickness
nitric oxide synthase
reactive hyperaemia