Brachytherapy in total coronary occlusions: Quidquid agis, prudenter agas, et respice finem

Abstract

In the study by Jain et al. presented in this issue, vascular brachytherapy was performed, applying a betaradiation source (BetaCath TM) to reduce restenosis rates after PTCA of chronic total occlusions (CTOs). The outcome of radiotherapy after percutaneous revascularization of 82 CTOs were analyzed from the RENO registry database, which contains 1,098 consecutive patients undergoing brachytherapy. The results were comparable with those known for brachytherapy of nonocclusive in-stent restenosis with respect to prevention of new restenosis. Why is this finding remarkable?It has become general knowledge that treating chronic coronary occlusions by conventional PTCA is a "different animal" compared with PTCA of plain coronary artery stenosis [1]. Many studies have shown that restenosis rates are extremely high in patients with CTO, even when stenting is performed [2]. Some institutions leave treatment of symptomatic CTOs primarily to the cardiac surgeon. Revascularization of CTO is favorable over medical treatment at least when treated surgically [3]. Therefore, it is important to realize from the report by Jain et al. that restenosis rates of PTCA in CTO have been reduced dramatically using vascular brachytherapy. However, there is the problem of thrombotic vessel occlusion increasing MACE rates, which needs to be understood and acted on. Brachytherapy was plagued from the beginning with the occurrence of late and "late late" thrombosis [4]. Yet only half of all patients of the RENO registry were kept on the combined antiplatelet therapy of aspirin and clopidogrel for a period of 6 months. In addition, new stents were implanted, which tended to reocclude the coronary arteries. What are the lessons we learn from this report? In the words of Gesta Romanorum: "Quidquid agis, prudenter agas, et respice finem." Whatever you do, do it thoughtfully, and kept in mind the goal.Brachytherapy of chronic coronary occlusions requires special attention to the increased risk of thrombotic vessel occlusion. Potential means for reducing the risks of MACE are as follows: apply aspirin and clopidogrel for a minimum period of 12 months (perhaps as lifelong addition of clopidogrel to aspirin medication); use a minimum of new stents to reduce foreign-body activation of platelets; study an increased loading and maintenance dose of clopidogrel in a randomized fashion in the setting of CTO; and, most importantly, remember that CTO patents only benefit from revascularization if viable myocardium is present [5].Mixed results were obtained by other investigators in two recent studies applying brachytherapy in CTO. One group reported similar efficacy and complication rates with intracoronary brachytherapy of occluded in-stent restenosis using a gamma-emitter (Ir-192) compared with irradiation for nonocclusive in-stent restenosis [6]. The other group, however, clearly pointed out that radiotherapy of total occlusions from in-stent restenosis causes increased MACE rates compared with brachytherapy of plain in-stent restenosis [7]. In summary, m...

Intracoronary Brachytherapy and Drug-Eluting Coronary Stents

“…20 A recent editorial recommends using aspirin and clopidogrel for a minimum of 12 months after brachytherapy for chronic coronary occlusions. 26 In addition, the late effects of radiation on the vasculature remain to be defined. Finally, at present, the logistic requirement of specialized equipment and a multidisciplinary team, including a radiation oncologist and a physicist, has limited brachytherapy to a few specialized centers.…”

“…One editorial suggested continuing antiplatelet therapy for a full year after brachytherapy. 26 Different trials of DESs have used 3 to 6 months of antiplatelet therapy, often corresponding to the duration of the study follow-up period. In the absence of long-term follow-up data, it is difficult to say whether 3 to 6 months of antiplatelet therapy would be sufficient or a longer period is necessary to minimize in-stent thrombosis after placement of a DES.…”