Restenosis and InStent Restenosis

New insights into the pathophysiology of restenosis have emerged concurrently with developments in coronary stenting. Early animal studies suggested that intimal proliferation after arterial injury is the predominant cause of restenosis. As a result, several clinical trials tested the effect of various antiproliferative agents on coronary restenosis. These trials, however, showed no significant beneficial effect in preventing restenosis (122).

The results of several recent studies have challenged the theory that intimal proliferation is the sole or predominant mechanism of restenosis following conventional PTCA. For instance, molecular studies using immunohistochemical labeling of proliferating cell nuclear antigens in human atherectomy specimens, revealed minimal evidence of cellular proliferation in both primary as well as restenotic lesions following conventional PTCA (123). In addition, serial IVUS imaging studies have shown intimal proliferation to be a minor contributor (30%) to late diameter loss and have demonstrated that shrinkage of the dilated segment (measured as a reduction in the cross-sectional area of the vessel subtended by the external elastic lamina) is a major contributor to lumen loss following conventional PTCA (124). With respect to in-stent restenosis, serial IVUS studies have demonstrated that neo-intimal proliferation, through the stent struts, accounts for almost all of the late diameter loss, with almost no evidence of vessel shrinkage or stent collapse (125). Three large randomized trials comparing stenting (using Palmaz-Schatz stents) with conventional PTCA for the treatment of focal de novo native vessel lesions including the Benestent-I and Benestent-II (55,169) and the STRESS-I (56) studies, revealed larger acute lumen diameters and a 25-30% relative reduction in the rate of restenosis after stenting compared with conventional PTCA (Table 5). Thus, coronary stenting is associated with reduced restenosis rates because it maintains expanded lumen diameters and prevents pathologic remodeling.

Although current stenting techniques have reduced restenosis, they have not eliminated it. Recently, much attention has been focused on stent designs with better scaffolding properties that may be able to minimize intimal injury and prevent subsequent restenosis. The rate of restenosis at 6 mo using aspirin (without ticlopidine) with the ACS multilink stent (West European Stent Trial [WEST]-II trial) was lower (10%) than that when using the Palmaz-Schatz stent (Multicenter Ultrasound Stenting in Coronar-ies trial [MUSIC]) (13%), despite the inclusion of smaller vessels and a greater number of patients with unstable angina in the WEST-II trial (126). Brachytherapy, the use of local radiation, has emerged as a viable option for the prevention of recurrent ISR, and

Table 5

Multicenter Randomized Trials Comparing Conventional PTCA with Stenting

Table 5

Multicenter Randomized Trials Comparing Conventional PTCA with Stenting

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