Shear stress alteration has been recognized as a predisposing factor for the impairment of endothelial function. Myocardial bridging is a congenital condition associated with alteration in shear stress, however, its impact upon vasoreactivity remains undetermined. This was a case-control designed study with 29 patients with myocardial bridging and 58 patients without myocardial bridging. Endothelium-dependent and endothe-lium-independent changes in coronary artery diameters, blood flow and wall shear stress were determined after intracoronary infusion of acetylcholine(ACH, 10-6-10-4 mol/L) and nitroglycerine (NTG, 200 μg). Coronary flow velocity reserve (CFVR) was determined after intracoronary injection of adenosine (18-36 μg). In response to ACH, there was more epicardial vasoconstriction at the myocardial bridging site compared with the proximal and distal segments(-29.6±21.7 vs. -9.6±22.5 and -17.4±21.5%, p< 0.05) and compared with the control group(-29.6±21.7 vs. -5.9±36.5%, p< 0.001). The response to NTG and CFVR was the same in the case and the control group. Wall shear rate(WSR) was higher in the MB site at baseline and in response to ACH. MB is characterised by enhanced WSR and impairment in endothelium-dependent vasorelaxation. These functional alterations may add to the severity of structural lumen compression and thus to the clinical presentation of this congenital abnormality. Shear stress alteration has been recognized as a predisposing factor for the impairment of endothelial function. Myocardial bridging is a congenital condition associated with alteration in shear stress, however, its impact upon vasoreactivity remains undetermined. This was a case-control designed study with 29 patients with myocardial bridging and 58 patients without myocardial bridging. Endothelium-dependent and endothe-lium-independent changes in coronary artery diameters, blood flow and wall shear stress were determined after intracoronary infusion of acetylcholine (ACH, 10-6-10-4 mol / Coronary flow velocity reserve (CFVR) was determined after intracoronary injection of adenosine (18-36 μg). In response to ACH, there was more epicardial vasoconstriction at the myocardial bridging site compared with the proximal and distal segments (-29.6 ± 21.7 vs. -9.6 ± 22.5 and -17.4 ± 21.5%, p <0.05) and compared with the control group (-29.6 ± 21.7 vs. -5.9 ± 36.5% , p <0.001). The response to NTG and CFVR was the same in the case and the control group. Wall shear rate (WSR) was higher in the MB site at baseline and in response to ACH. MB is characterised by enhanced WSR and impairment in endothelium-dependent vasorelaxation. These functional alterations may add to the severity of structural lumen compression and thus to the clinical presentation of this congenital abnormality.