January 1, 2001ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam)
Relationship between the G894T polymorphism (Glu298Asp variant) in endothelial nitric oxide synthase and nitric oxide-mediated endothelial function in human atherosclerosis
Why the study?
Does the eNOS Glu298Asp variant affect NO-mediated endothelial vasomotor function in patients with coronary artery disease?
Population
104 patients with coronary artery disease and identified risk factors for atherosclerosis
Comparison
Presence of the eNOS Glu298Asp polymorphic variant vs Absence of the eNOS Glu298Asp variant
Design
Cross-sectional
Authors
Discussion
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Member takes
Implication
Modifiable risks impair endothelial function in CAD; leaves open any Glu298Asp role in larger or longitudinal cohorts.
Structured PICO
Does the eNOS Glu298Asp variant affect NO-mediated endothelial vasomotor function in patients with coronary artery disease?
P
Population
104 patients with coronary artery disease and identified risk factors for atherosclerosis (human saphenous veins obtained from these patients)
I
Intervention
Presence of the eNOS Glu298Asp (G894T) polymorphic variant
C
Comparator
Absence of the eNOS Glu298Asp variant
O
Outcome
Endothelium-dependent vasorelaxations to different agonists (acetylcholine, bradykinin, calcium ionophore) and relaxations to sodium nitroprussidesurrogate
The eNOS Glu298Asp polymorphism does not have a major direct functional effect on vascular eNOS activity in human atherosclerosis, whereas clinical risk factors strongly impair endothelial function.
Cite This Study
Guzik et al. (2001) studied this question.