IMMEDIATE AND LONG-TERM EFFECT OF BALLOON ANGIOPLASTY OR STENT IMPLANTATION ON THE ABSOLUTE AND RELATIVE CORONARY BLOOD-FLOW VELOCITY RESERVE

Background-There is controversy regarding the immediate and long-term effects of PTCA on the coronary flow reserve. Methods and Results-A to tal of 54 patients with 1-vessel disease and normal left ventricular f unction were studied after balloon angioplasty (n=34) or stent implant ation (n=20). Distal coronary blood flow velocity reserve (CFR) was de fined as the ratio of adenosine-induced hyperemic versus baseline bloo d flow velocity with a 0.014-in Doppler guidewire. The relative CFR wa s defined as the ratio of the distal CFR and the reference CFR measure d in the normal adjacent coronary artery. Hemodynamic and angiographic measurements were performed before and directly after balloon angiopl asty or stent implantation and at B-month follow-up. CFR after PTCA le ss than or equal to 2.5 was defined as an impaired CFR. Immediately af ter PTCA, CFR improved toward the range of the reference artery CFR. I n both the balloon-treated and the stent-treated groups, initial high CFR values decreased and impaired CFR values increased at follow-up to ward the values of the reference CFR in patients without restenosis. I mpaired CFR after balloon angioplasty (33%) or stent implantation (58% ) in patients without restenosis was related to an increased baseline now velocity that normalized at follow-up. Patients with an increase o f CFR after stenting were characterized by an unaltered baseline flow velocity and an increased adenosine-induced hyperemic flow velocity. C onclusions-An impaired CFR (less than or equal to 2.5) is a frequent f inding after balloon angioplasty or stent implantation as a result of a high baseline flow velocity. Normalization of impaired CFR at follow -up in patients without restenosis was associated with a decline of th e baseline flow velocity after both balloon angioplasty and stent impl antation, supporting the contention that this phenomenon relates to a slow recovery of autoregulation of the microvascular bed.