Purpose: 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. Methods:: In 81 patients with myocardial bridging (males 44, mean age 57.2 years), and 195 control patients without bridging and atherosclerotic lesions confirmed by angiography (males 97, mean age 58.4 years), spasm provocation test was done by incremental acetylcholine infusion into the left coronary artery. Based on the control state of the patient during one year after starting medication, we estimated the efficacy of medications. Therapeutic responders were patients with the disappearance of chest pain attacks for at least six months after starting medication. Results: Spasm was documented in 62 of 81 patients with bridging and in 31of 195 controls (76.5 vs. 16.0 %, p < 0.001). A focal spasm was limited to the bridging segments as compared to controls (64.1 vs. 7.6 %, p < 0.001). At one year, a combination of a calcium antagonist and isosorbide dinitrate suppressed chest pain more effectively than a calcium antagonist alone (p=0.02, Table). Conclusions: The results of this study showed that myocardial bridging increased the risk of coronary spasm via endothelial dysfunction in the bridging segment and the combination of a calcium antagonist and nitrate effectively controlled the chest pain in patients with myocardial bridging and spasm.