The longstanding compression-relaxation effects of myocardial bridging may produce endothelial dysfunction by direct stress on the endothelium. We tested the hypothesis that myocardial bridging induces endothelial dysfunction and subsequently increases the risk of coronary spasm and investigated the symptomatic response to medication in patients with documented myocardial bridging and coronary spasm. In 81 patients with myocardial bridging (44 men; mean age 57.2 years) and 195 control patients without bridging and atherosclerotic lesions confirmed by angiography (97 men; mean age 58.4 years), spasm provocation testing was done by incremental acetylcholine infusion into the left coronary artery. Spasm was documented in 62 of 81 patients with bridging and in 31 of 195 controls (p <0.001). A focal spasm was limited to the bridging segments compared with controls (p <0.001). In conclusion, the results of this study showed that myocardial bridging increased the risk of coronary spasm by endothelial dysfunction in the bridging segment.