The effect of myocardial bridging of the coronary artery on vasoactive agents and atherosclerosis localization.
The relationship between alterations in the immunohistochemical expression of three vasoactive agents [endothelial nitric oxide synthase (eNOS), endothelin-1 (ET-1), and angiotensin-converting enzyme (ACE)] and the occurrence human atherosclerosis was investigated in relation to the myocardial bridge (MB) of the left anterior descending coronary artery (LAD), an anatomical site that experiences increased shear stress. Five millimetre cross-sections of LADs with MB from 22 autopsied cases were taken from the left coronary ostium to the cardiac apex and were immunohistochemically stained with antibodies against eNOS, ET-1, and ACE. The extent of atherosclerosis in each section was calculated using the atherosclerosis ratio (intimal cross-sectional area/medial cross-sectional area) determined by histomorphometry. The results were analysed according to their anatomical location relative to the MB, either proximal, beneath, or distal. The extent of atherosclerosis was significantly lower beneath the MB, compared with proximal and distal segments. The expression of eNOS, ET-1, and ACE was also significantly lower beneath the MB. The expression of these agents correlated significantly with the extent of atherosclerosis. Because nitric oxide, after its production by eNOS, is believed to be degraded by superoxide radicals, the effect of eNOS expression on atherosclerosis remains controversial. However, the present findings clearly indicate that the expression of ET-1 and ACE is directly related to the development of human coronary atherosclerosis in vivo through shear stress.
Masuda
T
T
Department of Pathology, Toho University School of Medicine, 5-21-16 Ohmori-nishi, Ohta-ku, Tokyo 143-8540, Japan. masudatk@med.toho-u.ac.jp
Ishikawa
Y
Y
Akasaka
Y
Y
Itoh
K
K
Kiguchi
H
H
Ishii
T
T
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002317:Cardiovascular Agents / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D003330:Coronary Vessel Anomalies / Q000150:complications* / Q000378:metabolism; D019332:Endothelin-1 / Q000378:metabolism; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D008297:Male; D008875:Middle Aged; D019001:Nitric Oxide Synthase / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D013314:Stress, Mechanical
D002317:Cardiovascular Agents; D019332:Endothelin-1; D019001:Nitric Oxide Synthase; D007703:Peptidyl-Dipeptidase A