We report on a 46-year-old male with unstable angina pectoris due to a total proximal occlusion of the left circumflex artery. At the side of a plaque rupture there was a thrombotic occlusion. With PTCA recanalization was possible, but a dissection occurred, therefore coronary stents were implanted. Besides an optimal morphological result and recurrent applications of nitroglycerin, the baseline blood flow velocity declined from initial 16 cm/s to 11 cm/s after PTCA down to 8.4 cm/s after stent implantation. Because peak flow velocity remained almost unchanged, the low baseline velocity ("slow flow phenomenon") did not lead to an impaired coronary flow velocity reserve (CFVR). Only after application of 1 mg verapamil, a sustained flow velocity on a higher baseline level was reached (17 cm/s), at the same time typical signs of ischemia in the ECG (ST-segment depressions) improved. Additionally, in the non-treated LAD there was an increase in coronary blood flow velocity from 10 cm/s up to 25 cm/s. The reduction in coronary blood flow velocity with increasing manipulations might be due to an impairment of the coronary microcirculations with increasing alpha-adrenergic vasoconstriction, a distribution of vasoactive agents and peripheral microembolizations. Only after administration of verapamil, a calcium channel blocker with non-specific anti-adrenergic effects, the slow flow was removed and ECG signs of ischemia improved. The blood flow velocity in the non-treated LAD was low at baseline and improved after verapamil. This phenomenon leads to the conclusion that mechanisms with vasoconstrictive effect are present in the whole coronary system, but these mechanisms are less pronounced in non-treated vessels.