FREQUENCY AND CONSEQUENCES OF INTIMAL HYPERPLASIA IN SPECIMENS RETRIEVED BY DIRECTIONAL ATHERECTOMY OF NATIVE PRIMARY CORONARY-ARTERY STENOSES AND SUBSEQUENT RESTENOSES

Although intimal hyperplasia is a frequent occurrence after arterial interventional procedures, the overall frequency and significance of intimal hyperplasia in primary coronary lesions has not been previously addressed. The incidence of intimal hyperplasia was therefore examined using standard light microscopy in specimens obtained from native coronary arteries of patients undergoing directional coronary atherectomy. The associated clinical history, angiographic results and clinical outcomes were also tabulated. Intimal hyperplasia was identified in 51 of 55 Patients (93%) treated with directional coronary atherectomy for restenosis after a prior intervention. These restenosis lesions had less acute gain in lumen diameter after directional coronary atherectomy, a smaller late lumen diameter, more severe late stenosis (p < 0.04), and tended to have more restenosis defined as late stenosis greater-than-or-equal-to 50% (restenosis rate 40% for prior restenosis vs 26% for primary lesions). Surprisingly, however, intimal hyperplasia was also identified in 45 of 102 (44%) primary stenoses. Primary lesions (n = 45) with intimal hyperplasia were more likely to occur in younger patients and in the left anterior descending artery than were either primary lesions without intimal hyperplasia (n = 57) Or prior restenosis lesions. There were otherwise no differences in the baseline characteristics, angiographic findings or clinical outcome of primary lesions with or without intimal hyperplasia (restenosis rate 28 and 24%, respectively). The event-free survival (72% at 12 months) was similar in all 3 groups. Thus, even though intimal hyperplasia is an almost universal finding in restenosis lesions, intimal hyperplasia is not specific for restenosis since histologically identical hyperplasia may be found in nearly half of primary coronary artery stenoses. The finding of intimal hyperplasia in primary coronary stenoses, however, does not predict a different outcome from that seen in primary stenoses without intimal hyperplasia.