Sidebranch Patency During Main Branch Stenting: Try to Keep the Branch Open Immediate and Long-Term!

The study presented by Timurkaynak et al. in this issue of the Journal discusses a contemporary topic, which is direct stenting.1 It is interesting that the evaluation of this technique is performed in the setting of coronary bifurcations or in the presence of a sidebranch (> 1 mm) at the site of the lesion. The authors included 151 patients with 185 sidebranches in this report originating at the level of the lesion. Eighty-eight patients (110 sidebranches) underwent direct stenting, while 63 patients (75 sidebranches) underwent stenting with balloon predilatation (conventional stenting). The decision to perform either technique was left at the discretion of the operator. See Timurkaynak et al. on pages 497–501 There was no much difference in clinical variables among the patients treated with the either technique. The decision to use direct stenting versus predilatation was left to the physician and this finding may support the appropriate judgment of each operator. Regarding the lesion characteristics, there was a significantly higher prevalence of B2 lesions in the group treated with predilatation (9.1 vs. 34.7%; p = 50% diameter stenosis) was similar in the two groups, and reported in about one-fourth of cases. The type of disease in the main branch and in the sidebranch was evaluated according to the Duke classification.2 In both groups, most of the lesions involved the main branch, with only one-third of the narrowing involving the ostium of the sidebranch (type D). Following stent implantation, thirty-eight sidebranches occluded, while 147 maintained patency. Overall, there were more (24%) sidebranch occlusions in the conventional stenting group compared to the direct stenting group (18.2% sidebranch occlusions). Among the important findings of this study, the authors report a comparison between the lesion characteristics of sidebranches which occluded upon stent placement (n = 38) compared to ones which maintained patency (n = 147). The most important characteristic of the sidebranches which occluded was the presence of disease at their origin (type D of the Duke classification). Among the sidebranches, which occluded the incidence of type D morphology was 55.3% compared to 22.4% in those, which maintained patency (p 12 ATM) did not increase risk of sidebranch occlusion.3,4 This article adds further support to the concept, already reported by other authors, that each sidebranch with significant narrowing at the ostium needs to be carefully protected due to the risk of occlusion during treatment of the narrowing in the main branch.4–10 It is interesting to notice that the fact that the operator used direct stenting or even high pressure did not per se correlate with the risk of occlusion, while the amount of narrowing in the sidebranch was the only element of importance. We cannot dismiss the fact that the operator made the decision to use direct stenting versus predilatation, a fact that does not allow to conclude that direct stenting is equally safe as predilatation in preserving sidebranches. How do we translate this information into our clinical practice? First of all, no matter what strategy the operator is planning to do, a careful assessment needs to be done about the amount of disease present at the sidebranch (type D morphology). Even if the sidebranch is not diseased, the presence of significant narrowing in the main branch near the ostium of the sidebranch (type C) should be seriously considered as a potential risk for sidebranch compromise. Therefore, the operator needs to wire the sidebranch and predilate this vessel. Then, if considered feasible, direct stenting can be applied to the main branch, while removing (or not) the wire from the sidebranch. In case the operator decides to trap the wire underneath the stent, it is important to avoid initial high-pressure inflation. Further decisions concerning re-dilatation of the sidebranch or kissing inflations are taken upon behavior of the narrowing at the ostium of the sidebranch. The fact that, in this study, the authors did not report an increase in risk of sidebranch occlusion when the morphology was type E and F, is due to the low representation of these types of sidebranch compromise in the subset of lesions reported. No matter what strategy the operator decides to undertake (direct stenting vs. predilatation), the important message of this study is that sidebranch occlusion during stenting of the main vessel can be a significant problem. As a matter of fact, the 18.2% sidebranch occlusion with direct stenting and the 24% sidebranch occlusion with predilatation are potential complications which should not be dismissed and need to be avoided. Little comfort for the operator should be the fact that at late follow-up, high proportion of the sidebranches will reopen again. Temporary occlusion is what matters to cause enzyme elevation and myocardial necrosis. Although a higher incidence of in-hospital myocardial infarctions following sidebranch occlusion is reported,9,11,12 it seems that sidebranch compromise or occlusion do not influence late major adverse events, including death, myocardial infarction, or need for repeat revascularization.4,10 The recent advent of intracoronary brachytherapy and drug-eluting stents reduced significantly the incidence of restenosis; however, there are only few reports addressing the evolution of the sidebranches in those clinical scenarios.13,14 Cottin et al. reported that the rates of sidebranch occlusion were similar between the irradiated and control groups.13 However, in the control group, fifty percent of the sidebranch occlusions that occurred after the procedure were patent at 6-month follow-up. In contrast, in the irradiated group, the incidence of sidebranch occlusion even increased from 9–15%. Authors concluded that the absence of restoration patency following brachytherapy is most likely a consequence of a delayed healing process. The issue may be different when implanting drug-eluting stents. A subanalysis from the RAVEL trial investigated the fate of the occluded sidebranches and found the trend (p = 0.15) toward higher rate of reopening in the sirolimus stent group compared to uncoated stents (92% versus 67%), a finding which certainly warrants further investigation. A possible role should also be given to protection with IIb/IIIa infusion. Even if not clearly demonstrated, a number of studies have shown a trend towards a lower incidence of sidebranch occlusion in patients treated with IIb/IIIa inhibitors versus placebo.15,16 The recipe for immediate and sustained patency should be: evaluate the amount of compromise of the ostium of the sidebranch and dilate it if necessary, use IIb/IIIa agents when not contraindicated, use direct stenting following careful evaluation of the anatomical situation of the main and sidebranch, and perform kissing inflation in most of the cases. By the way, do not forget to implant a drug-eluting stent!

1. Timurkayanak T, Ciftci H, Ozdemir M, et al. Sidebranch occlusion after coronary stenting with or without balloon predilatation: Direct versus conventional stenting. J Invas Cardiol 2002;14:497–501. 2. Lansky AJ, Popma JJ. Qualitative and quantitative angiography. In: Topol E (ed). Textbook of Interventional Cardiology. 3rd Edition. Philadelphia: W.B. Saunders, 1998: pp. 725–747. 3. Yilmaz H, Demir I, Belgi A, et al. Sidebranch occlusion in direct intracoronary stenting: Predictors and results. J Invas Cardiol 2001;13:578–581. 4. Aliabadi D, Tilli FV, Bowers TR, et al. Incidence and angiographic predictors of side branch occlusion following high-pressure intracoronary stenting. Am J Cardiol 1997;80:994–997. 5. Meier B, Gruentzig AR, King SB III, et al. Risk of side branch occlusion during coronary angioplasty. Am J Cardiol 1984;53:10–14. 6. Nakamura S, Hall P, Maiello L, Colombo A. Techniques for Palmaz-Schatz stent deployment in lesions with a large side branch. Cathet Cardiovasc Diagn 1995;34:353–361. 7. Cho GY, Lee CW, Hong MK, et al. Effects of stent design on side branch occlusion after coronary stent placement. Cathet Cardiovasc Intervent 2001;52:18–23. 8. Boxt LM, Meyerovitz MF, Taus RH, et al. Side branch occlusion complicating percutaneous transluminal coronary angioplasty. Radiology 1986;161:681–683. 9. Arora RR, Raymond RE, Dimas AP, et al. Side branch occlusion during coronary angioplasty: Incidence, angiographic characteristics, and outcome. Cathet Cardiovasc Diagn 1989;18:210–212. 10. Bhargava B, Waksman R, Lansky AJ, et al. Clinical outcomes of compromised side branch (stent jail) after coronary stenting with the NIR stent. Cathet Cardiovasc Intervent 2001;54:295–300. 11. Talasz H, Genser N, Mair J, et al. Side-branch occlusion during percutaneous transluminal coronary angioplasty. Lancet 1992;339:1380–1382. 12. Cho GY, Lee CW, Hong MK, et al. Side-branch occlusion after rotational atherectomy of in-stent restenosis: Incidence, predictors, and clinical significance. Cathet Cardiovasc Intervent 2000;50:406–410. 13. Cottin Y, Lansky AJ, Kim HS, et al. Intracoronary brachytherapy not associated with changes in major side branches. Cathet Cardiovasc Intervent 2000;51:154–158. 14. Tanabe K, Degertekin M, Sousa JE, et al. Fate of side branches after sirolimus-eluting stent implantation (Abstr). J Am Coll Cardiol 2002;39:1149–1115. 15. Blankenship JC, Tasissa G, O'Shea JC, et al. Effect of glycoprotein IIb/IIIa receptor inhibition on angiographic complications during percutaneous coronary intervention in the ESPRIT trial. J Am Coll Cardiol 2001;38:653–658. 16. Almeda FQ, Nathan S, Calvin JE, et al. Frequency of abrupt vessel closure and side branch occlusion after percutaneous coronary intervention in a 6.5-year period (1994 to 2000) at a single medical center. Am J Cardiol 2002;89:1151–1155.