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J Am Coll Cardiol, 2003; 42:396, doi:10.1016/S0735-1097(03)00633-8
© 2003 by the American College of Cardiology Foundation
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LETTER TO THE EDITOR

Reply

Ron Waksman, MD*

* Washington Hospital Center, 110 Irving Street, NW, Suite 4B-1, Washington, DC 20010, USA

ron.waksman{at}medstar.net


We thank Drs. Almeda and Schaer for their interesting comments. We have previously reported that ostial in-stent restenotic lesions treated with intracoronary radiation have equivalent clinical outcomes to nonostial irradiated in-stent restenotic lesions and have significantly reduced recurrent restenosis compared to in-stent restenotic ostial lesions treated with conventional percutaneous interevention alone (1). We did not find that postprocedural minimal luminal diameter correlated with subsequent failure, although smaller vessels (based on reference vessel diameter) have higher restenosis rates. Intracoronary radiation therapy reduces angiographic restenosis in all sized vessels, with the effect seen predominantly in small vessels (<2.5 mm) (2). In the current analysis, these factors did not influence clinical outcomes.

The initial enthusiasm for the cutting balloon as an interventional strategy for in-stent restenosis has not been supported by reduced event rates in clinical trials. There is no evidence showing the cutting balloon to be superior over conventional angioplasty with adjunctive intracoronary radiation.

Our ongoing analysis suggests the time to first target vessel revascularization in the majority of patients is between 6 to 12 months, suggesting there is a "delay" in recurrent restenosis compared to conventional angioplasty. Recurrent restenosis beyond 12 months has been infrequent in the majority of published Washington Radiation for In-stent restenosis Trial (WRIST) series.

The overall use of glycoprotein (GP) IIb/IIIa inhibitors in the current analysis was 22% and did not influence clinical outcomes. Integrilin WRIST was a randomized trial addressing whether the treatment of eptifibatide (small-molecule competitive GPIIb/IIIa inhibitor) would improve both the procedural and the long-term outcomes in patients undergoing treatment for in-stent restenosis with intracoronary radiation therapy. That study (submitted for publication) did not detect differences in major clinical events with use of GPIIb/IIIa inhibitors. However, at any end point of the study there was nonsignificant reduction of creatine phosphokinase release in the eptifibatide group when compared to control, and these findings may stimulate a larger study to detect benefit of GPIIb/IIIa inhibitors in the setting of intracoronary radiation therapy.


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 References
 
1. Ajani AE, Waksman R, Cheneau E, et al. Impact of intracoronary radiation on in-stent restenosis involving ostial lesions. Catheter Cardiovasc Interv. 2003;58:175–180[Medline]

2. Ajani AE, Waksman R, Kim H-S, et al. The impact of lesion length and reference vessel diameter on angiographic restenosis and target vessel revascularization in treating in-stent restenosis with radiation. J Am Coll Cardiol. 2002;39:1290–1296[Abstract/Free Full Text]





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