Endothelial nitric oxide synthase in bicuspid aortic valve disease.
BACKGROUND
The pathogenesis of ascending aortic dilatation in the presence of a bicuspid valve is discussed controversially. Recent experimental evidence suggests that the expression of endothelial nitric oxide synthase (eNOS) may have an influence on aortic valve anatomy and aneurysmal dilatation of the aorta. We investigated the relationship among eNOS expression, valve anatomy, and aortic dilatation in the human aortic wall.


METHODS
Aortic wall specimens from 39 patients with aortic valve disease (bicuspid, n = 17; tricuspid, n = 22) were studied. The functional aortic valve pathology was regurgitation (n = 22), stenosis (n = 10), and combined aortic valve disease (n = 7). The specimens were obtained intraoperatively from the aortic wall above the noncoronary sinus. The eNOS protein expression was quantified by western blot analysis after immunoprecipitation from tissue lysates. The eNOS levels were analyzed for correlation with valve anatomy and ascending aortic diameters.


RESULTS
The eNOS protein expression of aortic endothelial cells was significantly lower in patients with bicuspid as compared with tricuspid aortic valves (4,615 +/- 489 vs 6,275 +/- 442; p = 0.017). In bicuspid aortic valves there was a significant correlation between eNOS expression and maximum aortic diameter (r = -0.530; p = 0.029) or sinotubular diameter (r = -0.520; p = 0.033). In patients with tricuspid aortic valves, no significant correlation between aortic size and eNOS expression was found.


CONCLUSIONS
Our results show an association between eNOS levels and aortic valve anatomy as well as aneurysm formation in patients with bicuspid aortic valves.
Aicher
Diana
D
Department of Thoracic and Cardiovascular Surgery, University-Hospital, Homburg/Saar, Germany. dianaaicher@gmx.de
Urbich
Carmen
C
Zeiher
Andreas
A
Dimmeler
Stefanie
S
Schäfers
Hans-Joachim
HJ
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001021:Aortic Valve / Q000201:enzymology* / Q000473:pathology*; D001022:Aortic Valve Insufficiency / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D001024:Aortic Valve Stenosis / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D015415:Biomarkers / Q000032:analysis; D004108:Dilatation, Pathologic; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000201:enzymology; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D011336:Probability; D011379:Prognosis; D012494:Sampling Studies; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D046509:Tissue Culture Techniques; D014261:Tricuspid Valve / Q000201:enzymology
D015415:Biomarkers; D052250:Nitric Oxide Synthase Type III