The importance of acute luminal diameter in determining restenosis after coronary atherectomy or stenting.

BACKGROUND: We evaluated native coronary arteries treated by directional coronary atherectomy or balloon-expandable stent placement in an effort to derive a quantitative geometric model relating the luminal diameter immediately after intervention to that present 6 months later. The minimal luminal diameter of each lesion was measured before and immediately after intervention in 102 single Palmaz-Schatz stents and 134 directional atherectomies, 192 (81%) of which had repeat angiographic measurement of minimal luminal diameter 6 months after the intervention. The immediate enlargement in luminal diameter produced by the intervention (acute gain) and the subsequent reduction in luminal diameter from the time of intervention to 6 months of follow-up (late loss) were calculated. METHODS AND RESULTS: Luminal diameter increased from 0.69 +/- 0.40 mm to 3.11 +/- 0.64 mm (acute gain, 2.41 +/- 0.64 mm) after intervention, providing an immediate postprocedure residual stenosis of 1 +/- 14% relative to a reference diameter of 3.13 +/- 0.65 mm. At 6-month follow-up, the late luminal diameter was 1.97 +/- 0.92 mm (late loss, 1.13 +/- 0.89 mm), yielding a late diameter stenosis of 36 +/- 26%. The restenosis rate (according to the traditional definition of diameter stenosis > or = 50%) was 30%. Multivariable analysis demonstrated that late luminal diameter (p = 0.02), late percent stenosis (p = 0.04), and restenosis (according to a > 50% definition, p = 0.04) were each strongly associated with the luminal diameter present immediately after the procedure. Whereas late luminal diameter was also influenced by reference artery size and the vessel treated (left anterior descending versus right coronary artery), reference vessel size was rejected by the multivariable models of late percent stenosis and binary restenosis after they were adjusted for the effect of postprocedure luminal diameter. Once adjusted for postprocedure luminal diameter, neither late luminal diameter nor late loss was found to be independently determined by which device was used (atherectomy versus stents). Rather, late loss was determined independently by the immediate postprocedure luminal diameter (p = 0.005) and the postprocedure percent stenosis (p = 0.02). Although late loss thus increased with acute gain, the net beneficial effect of increased acute gain was maintained: Late loss was only a fraction (0.47) of acute gain, so the ability of a larger postprocedure luminal diameter to reduce the probability of subsequent restenosis was preserved. CONCLUSIONS: This quantitative model demonstrates that the late coronary lumen diameter and the probability of restenosis after Palmaz-Schatz stenting or directional atherectomy are influenced strongly by the lumen diameter present immediately after the procedure rather than by the specific device used. Although the influence of a larger acute result on reduced restenosis appears to be well established in this treatment population, the interplay among the multiple other biological influences on restenosis limits the ability to predict the probability of restenosis for the individual patient based on a large acute result alone. Future studies of restenosis, however, can further refine this multivariable quantitative model by adjusting for the effects of other clinical variables, mechanical interventions, or drug therapies in addition to the clear effect of postprocedure luminal diameter.