Background: Longstanding compressive-relaxing effect of the myocardial bridge (MB) may produce endothelial dysfunction through direct stress to endothelium. Therefore, we assessed the hypothesis that MB would alter the endothelial function and subsequently, influence the extent of atherosclerotic plaque. Methods: In 128 patients with typical angiographic systolic milking effects with > 30 % reduction (54.7짹10.9 yr, 42 men) and 231 control patients without bridgings and overt coronary artery disease (54.1짹13.2 yr, 111 men), endothelial function was estimated by incremental acetylcholine infusion (ACh: 20 µg, 50 µg and 100 µg/min) into the left coronary ostium. In 74/128 patients with MB and 64/231 control patients, intracoronary ultrasound (ICUS) assessments were obtained after nitroglycerin (200 µg) administration. Results: The mean percent change of MB segments was 44.01짹16.55 %. Coronary vasoconstriction to ACh was seen in 114/128, 89 % of MB group and 81/231, 35.1 % of controls (p < 0.001). In MB group, vasoconstriction in response to ACh was dominantly at the bridge segments (123/128, 88.3 %). The mean vasoconstriction response to ACh at MB segments was more pronounced than that in controls (-71.91짹24.49 vs -37.83짹35.44, p < 0.001). By ICUS, there was a typical half-moon phenomenon in 71/74 (95.9 %) cases of MB group. The atherosclerotic plaques at MB segments were absent in 67/74 (90.5 %) and only mild in 7/74 (9.5 %) cases as compared with those of matched segments of LAD in controls (plaque burden 5.91짹1.37 vs 24.71짹24.21 %, p < 0.001). The plaques at MB segments were all eccentric. There were no significant correlations between plaque burden and bridging severity or vasoconstriction in response to ACh (p=0.34, 0.45, respectively). Conclusions: Despite the prominent relationship between MB and endothelial dysfunction, the MB segments were spared from the atherosclerotic plaques. These results suggest that there may be another protective mechanism to development of atherosclerosis at MB segment.