Sidebranch Compromise During Percutaneous Coronary Interventions

Neeraj Prasad, MD and *Peter H. Seidelin, MD

Neeraj Prasad, MD and *Peter H. Seidelin, MD

Sidebranches are within the vicinity of the angioplasty site in over 50% of cases and although many are unaffected, a considerable proportion are compromised by the procedure. In this article, we systematically review the current literature concerning the fate of sidebranches during coronary angioplasty and stenting and develop an approach toward sidebranch compromise. Our discussions in this review concern sidebranches from native coronary arteries and not aorto-ostial lesions.

Classification of coronary sidebranches

Assessing the importance of a sidebranch prior to beginning coronary angioplasty is valuable because a planned strategy can be followed if branch compromise occurs during the procedure. Examining branch factors such as vessel size and the myocardial territory served, as well as predictors of poor outcome such as branch ostial disease, can influence the planned therapeutic strategy. Before an approach to the management of sidebranches can be developed, a definition and classification of sidebranches that allows the comparison between studies must be proposed.

Vessel size and myocardial territory. Vessel size is used in revascularization decisions for both surgical and percutaneous endoluminal procedures. The diameter of a vessel can readily be assessed by visual estimation or measured by quantitative coronary analysis (QCA) during coronary angiography. The existing literature has varied in the way sidebranch size has been classified (Tables 1–3),1–12 i.e., < 1 mm, > 1 mm, > 1.8 mm or just “moderate size and would be bypassed.” From the present literature, it is really only possible to discuss sidebranches that are less than or greater than 1 mm in diameter.

The size of the myocardial territory that the branch supplies is also likely to be important and should be taken into consideration. The territory can be assessed as suggested for terminating vessels by Alderman et al. for the BARI Investigators (small = < 1/3 base to apex distance; medium = 1/3–2/3 base to apex distance; large = > 2/3 base to apex distance).13 The territory served by the branch has not been evaluated in the existing literature. The vessel size is only one factor in a complex decision-making process to decide if the planned procedure is appropriate or is technically feasible. The current technical limitation for surgical revascularization is vessel size of less than 1 mm. In the field of coronary stenting, lesions in vessels less than 2.5 mm are not routinely being stented and good follow-up data from randomized trials on 2.5–3.0 mm vessels are not encouraging (see section on “stenting small vessels”). The role of balloon angioplasty in branches less than 2.5 mm is still not clear; although it is technically possible, balloon angioplasty is not currently practiced in vessels less than 1.5 mm. With these considerations in mind, sidebranches from native coronary arteries may be classified by size as it may dictate the current therapeutic options (Table 4).

Sidebranch ostial disease and branch relationship to parent vessel lesion. Another factor that is very important when considering sidebranches is the presence of ostial disease in the branch vessel. The presence of atheromatous plaque in the sidebranch can determine its fate during balloon angioplasty of the parent vessel. If ostial disease is present in the branch vessel, there is a five- to ten-fold increase in the possibility of sidebranch compromise.1,2 The definition of ostial disease has been diverse within the existing reports (Table 1–3), from a categorical classification ostial stenosis > 50%, < 50% or 20–99%, as well as various terms such as “originating in the lesion”. Assessing the branch vessel ostia narrowing in terms of 0%, < 50%, and >= 50% occurring within 2 mm of the origin is a simple acceptable classification (Table 4). Added factors altering the fate of sidebranches may be the position of the sidebranch take-off in relation to the parent vessel lesion, i.e., before, within or after the lesion and the angle of the sidebranch take-off from the parent vessel. To date, the importance of the branch take-off in relation to the parent lesion or the angle in relation to the parent vessel lesion has not been reported. Often, if the branch take-off is within the parent vessel lesion, the origin of the branch is likely to be diseased and to have a worse prognosis; however, most reports have not defined the relationship of the branch take-off relative to the lesion. Our own data indicate that if a branch originates within the lesion, it is more likely to be compromised with subsequent cardiac enzyme rise (unpublished).

Sidebranch compromise. The assessment of sidebranch compromise has been variable, including terms such as “occlusion”, “decrease in branch ostia”, “compromise” or “TIMI flow deterioration” (Tables 1–3). This can lead to confusion when research data are evaluated between studies. One of the many useful definitions given in the BARI study involved sidebranch narrowing. The minimum change in sidebranch narrowing defined in the BARI study was 20% based on the variability of caliper measurements and angiographer visual assessment that the change is definite based on side-by-side review of the serial studies.13 In addition, TIMI flow changes and symptoms are both important factors. We propose a definition based on visual detectable change and symptoms to guide therapeutic interventions and allow assessment in clinical research (Table 4).

The effect of balloon angioplasty and stenting of the parent coronary vessel on a sidebranch
When balloon angioplasty is performed in native coronary arteries, sidebranches within the vicinity are covered by the inflated balloon. This intervention in the parent vessel could cause one of four pathogenic processes: 1) plaque shift into the sidebranch; 2) intimal dissection that covers or involves the branch vessel; 3) thrombus that occludes the branch; or 4) coronary spasm which may occur in the sidebranch. All these pathogenic processes may compromise blood flow. The relative importance and occurrence of each of these pathogenic mechanisms of sidebranch compromise have not been evaluated. Clinical reports support some of these possible mechanisms. For example, plaque shift into the ostium of the branch is often identifiable at the time of angioplasty and a debulking strategy such as rotational atherectomy prior to coronary stenting may prevent sidebranch occlusion.14 If branch blood flow is reduced after angioplasty, this may improve after intra-coronary injection of nitrate (suggesting that spasm may be a factor).15 Dissection in the parent vessel causing flow obstruction in the branch can also be implicated as a mechanism because it can be temporally related to the sidebranch compromise1,4 and by indirect evidence with the observation that some branches compromised after ballooning improve after stent deployment in the parent vessel.9 This could indicate that intimal dissections which were compromising flow to the branch may have been tacked down.

The possible pathogenic mechanisms of sidebranch compromise during coronary artery stent placement are the same as those discussed for balloon angioplasty. In addition, there is a possibility that a stent strut is across the opening of the branch (so called “stent jail”), which can also compromise blood flow. The majority of compromised sidebranches seem to occur after initial balloon inflation with some further vessel compromise after stent placement9 and high-pressure dilatation.12

The risk of sidebranch compromise can be assessed from the existing reports. Compromise of sidebranches less than 1 mm will occur in 15–20% after balloon angioplasty or stenting.2,9–11 In branches greater than 1 mm, approximately 19% will be compromised if they have branch ostial disease and only 4% will become compromised if there is no branch ostial disease after balloon angioplasty.1–3,5 After coronary stenting, 25% of branches with ostial disease but only 3% with no ostial disease will be compromised.8–11 Many of the sidebranches that are compromised after coronary angioplasty or stenting can improve.8,9,11 However, factors predictive of spontaneous recovery of sidebranches have not been evaluated. If compromise does occur in the branch, the degree of compromise (including total occlusion) does not appear to be predictive of whether they will spontaneously improve.

Clinical consequences of sidebranch compromise

Compromising a sidebranch during angioplasty is potentially important because the presence of myocardial ischemia may cause chest pain or electrocardiographic changes, which may necessitate further intervention. In some cases, a CK rise occurs after sidebranch compromise. Tables 1–31–12 summarize the reported clinical consequences of sidebranch compromise after balloon angioplasty and stenting. Of the sidebranches compromised that were less than 1 mm in diameter, only 6% had chest pain and none had an observed cardiac enzyme rise; electrocardiographic changes are not detailed in these reports. In sidebranches greater than 1 mm in diameter, approximately 15% had chest pain and 12% had enzymatic evidence of myocardial infarction (MI); the reporting of electrocardiographic changes was variable. Not surprisingly, the compromise of larger branch vessels leads to more frequent symptoms and cardiac enzyme rises.

Cardiac enzyme rises after intervention are associated with a worse long-term prognosis. A recent consensus document about cardiac enzyme rises post-intervention states that “the risk of adverse outcome increases with any elevation of CK or CK-MB”.16 Where intervention has been successfully undertaken on a compromised sidebranch, the cardiac enzyme rise is smaller than in those where the attempted opening of the branch has been unsuccessful.17 Intervening to reopen the branch after compromise has occurred may be appropriate with the aim of treating symptoms (if present) and avoiding cardiac enzyme rises.

Management of sidebranch compromise

Before considering the literature on intervention when sidebranches are compromised, it is necessary to consider interventions in small vessels and ostial lesions because this information is pertinent to sidebranch intervention.

Angioplasty and coronary stenting in small vessels. The clinical efficacy of coronary angioplasty and stenting has been demonstrated;18,19 however, these studies were intending to evaluate reference vessels > 3.0 mm. Recently, several retrospective studies have reported preliminary results on various aspects of small vessel angioplasty and stenting (Table 5).20–32 These studies report on vessels between 2.3–3.0 mm.

Procedural success rates for both balloon angioplasty and stenting are high and comparable to intervention in larger vessels. In contrast, the restenosis rates for both balloon angioplasty and stenting are higher compared to larger vessels. A few of these studies have reported observational data comparing restenosis after angioplasty or stenting in small vessels. These have shown either that angioplasty is equal to stenting or that there may be a slight advantage for coronary stenting with regard to restenosis. The indication for which the coronary artery was stented may be another factor in the higher restenosis rate in small vessels. For example, coronary stenting for threatened closure in small vessels was found to have a very high restenosis rate (66%).22 We need to probably adapt a provisional stent strategy in small coronary results with the current available data.
Ostial coronary angioplasty. Balloon angioplasty of ostial branch lesions from native coronary arteries has lower initial procedural success (74%), a higher in-hospital complication rate (13%) and a higher rate of restenosis (68%).36 Coronary stenting and/or rotational atherectomy in aorta-ostial lesions can improve long-term results compared to balloon angioplasty alone. However, these techniques in the branch ostial situation have not been evaluated. In addition, it is important to recognize that intervention in ostial branch lesions may affect the parent vessel, either by plaque shift, dissection or stent distortion. These issues again need further evaluation.

Sidebranch angioplasty

Sidebranch angioplasty is a complex situation because the vessels are small and the lesions are ostial in location. If sidebranch compromise occurs after parent vessel stenting, the patient may develop ischemic symptoms or an ischemic electrocardiogram. To date, there are no data about lengthening of hospital stay or long-term morbidity if sidebranch compromise occurs with or without overt ischemia. In this situation, one can protect the integrity of the parent vessel and sacrifice the branch, giving analgesia for chest pain (sidebranch sacrifice). As mentioned earlier, many of these compromised sidebranches may improve even if occluded, so not all will have cardiac enzyme rises. Our own data suggest that sidebranch TIMI flow reduction after parent vessel stenting is associated with cardiac enzyme rises in 40% of cases (unpublished). The alternative is to attempt angioplasty of the sidebranch. If ischemia is not overtly present, there can still be a desire to complete the revascularization based on the premise that despite not knowing the long-term consequences of sidebranch compromise, it is reasonable to presume that optimizing myocardial blood flow without increasing procedural risk will benefit the patient by preserving myocardial function. An early report suggests that sidebranch occlusion is associated with a worse outcome with a higher 6-month target vessel revascularization rate (22% in patients with sidebranch occlusion versus 10% in those without sidebranch occlusion).37 The issues to consider are the technical feasibility of the branch rescue, the acute closure rate and the restenosis or revascularization rate after the intervention in both the sidebranch and the parent vessel.

Single balloon angioplasty of a sidebranch. The most simple strategy for intervention after the occurrence of sidebranch compromise is to attempt balloon angioplasty. The sidebranch can often be wired by the parent vessel wire and a balloon can then be introduced and inflated in the sidebranch. After balloon angioplasty of the parent vessel, if the sidebranch becomes occluded, Arora et al. report a 75% success rate in reopening the sidebranch.4 The success after parent vessel stenting might be expected to be worse because traversing into the sidebranch can be hampered by a stent strut.

However, Caputo et al. report successfully dilating branches “jailed” by stenting in 84% with minimal complications and observed a reduced cardiac enzyme rise post-procedure compared to those who had an unsuccessful angioplasty attempt.17 If the sidebranch is difficult to access or the balloon cannot cross the ostia, it is often worth attempting to pass a fixed wire system (e.g., the ACE balloon; Boston Scientific, Scimed, Inc., Maple Grove, Minnesota), which has been shown to be successful in an in vitro model35 and in a few in vivo cases.17 The ACE balloon has a short, fixed wire tip to guide it into the vessel. It has a low profile and can often traverse through the side of a stent. Our own experience suggests that the use of the ACE balloon is often possible with good initial results, including resolution of the ischemia without parent vessel compromise. However, there is some evidence that simple balloon angioplasty of a branch lesion may have a high restenosis rate (Table 1)5 and a suggestion that stent distortion can occur, causing distal stent stenosis in the parent vessel.39 Thus, if a patient is overtly ischemic, this strategy may be useful for improving the immediate clinical course and if the branch vessel has reduced TIMI flow this strategy may prevent cardiac enzyme rise. However, sidebranch balloon angioplasty is limited by the possibility of parent vessel stent distortion and poor long-term outcome.

Kissing balloon angioplasty. Kissing balloon angioplasty can also be performed to reopen a compromised sidebranch. The advantage of this technique is that by placing two balloons (one in the sidebranch and the other in the parent vessel) and simultaneously inflating them, plaque shifting between the vessels may be prevented and the sidebranch could be optimally remodeled. Also, with a balloon in the parent vessel, stent distortion may be minimized. The “kissing” balloon inflation technique is performed by placing guidewires in both the parent vessel and the adjacent branch vessel. Two balloons (one on each wire) are then positioned in each vessel across the lesion and bifurcation. Both balloons are simultaneously inflated for a short time (30–90 seconds). The effective perimeter of the double balloon combination in the parent vessel is less than the sum of the two and can be calculated by the following formula (Table 6):40 Where cosa = (R1–R2)/(R1+R2). Balloon sizing should be chosen to avoid excessive oversizing in the parent vessel — a potential concern with this technique (Table 6). The kissing balloon technique is potentially an improvement on simple balloon angioplasty when sidebranch compromise occurs. In general, this technique has been reported to be safe,41–45 but needs more extensive evaluation.

Stenting a compromised sidebranch

Stenting a compromised sidebranch can be considered when the branch is larger in caliber. Often, a large sidebranch in the vicinity of the parent vessel angioplasty may not be affected. However, one should plan a strategy for the event of a large sidebranch becoming compromised since there are likely to be clinical manifestations. If there is a true bifurcation lesion with a large sidebranch, stenting both branches at the outset is possible with a variety of techniques, i.e., “T” stenting, inverted “Y” stenting, “V” stenting and the Culotte technique.46,47 These techniques need more formal evaluation and randomized comparisons to coronary bypass grafting or standard balloon angioplasty. However, if sidebranch compromise has occurred after parent vessel stenting, one is limited to stenting through a stent with a modification of the “T” stenting technique or a variation of the Culotte technique.

A debulking strategy may be logical prior to parent vessel stenting to help prevent sidebranch compromise by reducing the potential plaque shift. However, there has only been one short report of the benefits of this strategy and therefore it requires further evaluation.14 A potentially useful approach to protect a sidebranch during parent vessel stenting has been described by Foley and Serruys.43 This involves placing a “ten” (0.010´´) wire into the sidebranch prior to parent vessel stenting and leaving it in place during the stent deployment. If sidebranch occlusion occurs, then a third wire can be guided through the side of the stent, with the “ten” wire helping to mark the ostium of the occluded branch. The “ten” wire can then be removed while using caution that the guide catheter is not pulled in during the process. Foley and Serruys report that this has not resulted in wire stripping or fracture or any damage to the stent in their experience. Once the sidebranch has been accessed through the side of the stent, a balloon can be introduced to dilate the ostium. The sidebranch stent can then be deployed so that the proximal end of the stent just covers the ostium of the sidebranch (the “T” technique). Alternatively, a longer stent from the parent vessel into the sidebranch can be deployed after withdrawing the parent vessel wire (the “Y” technique). At the end, a “kissing balloon” inflation is used to open and stretch the struts extending across the lumen of the parent vessel. Both of these sidebranch stenting methods have been reported to have a very high procedural success rate (> 90%).48,49 Longer-term results have shown a significantly higher one-year adverse cardiac event rate (i.e., death, MI or repeat revascularization) with “Y” stenting (86.3%) than “T” stenting (30.4%).49 Long-term results of adverse cardiac events where sidebranches have just had balloon angioplasty after parent vessel stenting versus stenting sidebranches (“T” or “Y” stenting procedures) are similar.49 Thus, if a reasonable result is achieved with balloon angioplasty of a sidebranch, this may be an acceptable result. In general, the problems with sidebranch stenting after parent vessel stenting relate to: 1) wiring of the sidebranch (the “ten” wire technique suggested by Foley and Serruys may help this problem); 2) balloon crossing into the ostium of the sidebranch (sometimes helped by predilating with a fixed wire balloon such as the ACE balloon and then crossing with an over-the-wire or rapid exchange balloon); and 3) the ability of the stent to cross into the sidebranch (this may be affected by the parent vessel stent geometry as well as the profile of the intended sidebranch stent).

The early promise that has been shown with coated stents [sirolimus (rapamycin), a potent immunosuppressive agent used in renal transplant] in reducing restenosis to 0%50 may significantly alter the way we approach small vessels and bifurcation lesions. If the problems of stent deployment in bifurcation lesions can be overcome, then restenosis could be reduced significantly.
Conclusion. Sidebranch compromise during coronary balloon angioplasty and coronary stent placement is a recurring issue for interventional cardiologists. Assessment of the jeopardized sidebranch for the risk of compromise can be made by evaluating the sidebranch diameter, the myocardial territory supplied, the relationship to the parent vessel lesion and the presence of ostial disease. This can help in the decision-making process of the proposed intervention, allowing a strategy to be pre-planned in the event of sidebranch compromise. Sidebranch compromise associated with TIMI flow reduction in a branch vessel that is of medium or large diameter and serving moderate or large territory is often associated with a cardiac enzyme rise. A variety of balloon angioplasty and stenting techniques are used for sidebranch compromise with some short-term success in preserving the myocardium. However, there is no current “ideal” intervention and this important issue needs formal randomized evaluation with regard to both the short- and long-term results for both the branch vessel and the parent vessel.

Acknowledgment. The authors would like to thank Dr. P. Mazieka for his constructive help in the preparation of this manuscript.


1. Meier B, Gruentzig AR, King SB, et al. Risk of side branch occlusion during coronary angioplasty. Am J Cardiol 1984;53:10–14. 2. Vetrovec GW, Cowley MJ, Wolfgang TC, Ducey KC. Effects of percutaneous transluminal coronary angioplasty on lesion associated branches. Am Heart J 1985;109:921–925. 3. Boxt LM, Meyerovitz MF, Taus RH, et al. Side branch occlusion complicating percutaneous transluminal coronary angioplasty. Radiology 1986;161:681–683. 4. 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. 5. Ciampricotti R, Gamal ME, van Gelder B, et al. Coronary angioplasty of bifurcational lesions without protection of large side branches. Cathet Cardiovasc Diagn 1992;27:191–196. 6. Zack PM, Ischinger T. Experience with a technique for coronary angioplasty of bifurcational lesions. Cathet Cardiovasc Diagn 1984;10:433–443. 7. Myler RK, Shaw RE, Stertzer SH, et al. Lesion morphology and coronary angioplasty: Current experience and analysis. J Am Coll Cardiol 1992;19:1641–1652. 8. Fischman DL, Savage MP, Leon MB, et al. Fate of lesion related side branches after coronary artery stenting. J Am Coll Cardiol 1993;22:1641–1646. 9. Mazur W, Grinstead C, Hakim AH, et al. Fate of side branches after intra-coronary implantation of the Gianturco-Roubin flex-stent for acute or threatened closure after percutaneous transluminal coronary angioplasty. Am J Cardiol 1994;74:1207–1210. 10. Iniguez A, Macaya C, Alfonso F, et al. Early angiographic changes of side branches arising from a Palmaz-Schatz stented coronary segment: Results and clinical implications. J Am Coll Cardiol 1994;23:911–915. 11. Pan M, Medina A, Lezo JS, et al. Follow-up patency of side branches covered by intracoronary Palmaz-Schatz stent. Am Heart J 1995;129:436–440. 12. 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. 13. Alderman EL, Stadius M. The angiographic definitions of the Bypass Angioplasty Revascularization Investigation. Coron Artery Dis 1992;3:1189–1207. 14. Sharma SK, Bhalla N, Dangas G, et al. Rotational atherectomy prior to coronary stenting prevents side branch occlusion. J Am Coll Cardiol 1997;29:498A. 15. Shiu MF, Singh A. Spontaneous recanalisation of side branches occluded during percutaneous transluminal coronary angioplasty. Br Heart J 1985;54:215–217. 16. Califf RM, Abdelmeguid AE, Kuntz RE, et al. Myonecrosis after revascularization procedures. J Am Coll Cardiol 1998;31:241–251. 17. Caputo RP, Chafizadeh ER, Stoler RC, et al. Stent jail: A minimum-security prison. Am J Cardiol 1996;77:1226–1229. 18. Fischman DL, Leon MB, Baim DS, et al, for the Stent Restenosis Study Investigators. A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med 1994;331:496–501. 19. Serruys PW, de Jaegere P, Kiemeneij F, et al., for the BENESTENT Study Group. A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med 1994;331:489–495. 20. De Cesare NB, Bartorelli AL, Galli S, et al. Acute and long-term results of Palmaz-Schatz stent placement in small diameter (< 3 mm) coronary vessels. Eur Heart J 1995;16:335. 21. Keane D, Azar AJ, Serruys PW, et al., on behalf of the BENESTENT Study Group. Outcome following elective stent implantation in small coronary vessels. Eur Heart J 1995;16:335. 22. Chan CNS, Tan ATH, Koh TH, et al. Intracoronary stenting in the treatment of acute or threatened closure in angiographically small coronary arteries (< 3.0 mm) complicating transluminal coronary angioplasty. Am J Cardiol 1995;75:23–25. 23. Roberts DK, Arthur A, Bellinger RL, et al. Reduced anticoagulation protocol for stenting (RAPS) in smaller coronary vessels using intravascular ultrasound guidance. 30 procedural results. J Am Coll Cardiol 1996;77:393A. 24. Savage MP, Fischman DL, Rake R, et al., for the STRESS Investigators. Efficacy of coronary stenting versus balloon angioplasty in coronary arteries: Results from STRESS. J Am Coll Cardiol 1998;31:307–311. 25. Nunes G, Pinto I, Mattos L, et al. Coronary stent implantation in vessels smaller than 3 mm is associated with higher restenosis rates. Eur Heart J 1996;17;173. 26. Romero M, Suarez de Lezo J, Medina A, et al. Elective stenting for the treatment of lesions located in small coronary arteries. Eur Heart J 1996;17:217. 27. Morice MC, Valeix B, Dumas P, et al. Coronary stenting of small coronary arteries. Preliminary results of a pilot study with a 2.5 mm microstent AVE. Eur Heart J 1996;17;217. 28. Kawagishi N, Tsurumi Y, Ishii Y, et al. Palmaz-Schatz stenting in ultra small coronary arteries (< 2.5 mm). Circulation 1997;96:I-274. 29. Fernandez-Ortiz A, Vizcayno MP, Goicolea J, et al. Should we stent small coronary vessels? Comparison with balloon angioplasty. Circulation 1997;96:I-274. 30. Chevalier B, Lefévre T, Meyer P, et al. French registry of seven cell NIR stent implantation in 2.5 mm coronary arteries. Circulation 1997;96:I-274. 31. Fischman DL, Savage MP, Penn IM, et al. Have current stenting techniques improved the long term outcome of coronary stents in smaller vessels? Circulation 1997;I-275. 32. Abizaid AS, Mehran R, Saucedo J, et al. Small vessel stenting is associated with high event rate at late follow-up: A comparison study. Am J Cardiol 1997;80:2S. 33. Park SW, Lee CW, Hong MK, et al. Randomized comparison of coronary stenting with optimal balloon angioplasty for treatment of lesions in small coronary arteries. Eur Heart J 2000;21:1785–1789. 34. Kastrati A, Schomig A, Dirschinger J, et al. A randomized trial comparing stenting with balloon angioplasty in small vessels in patients with symptomatic coronary artery disease. ISAR-SMART Study (Intracoronary Stenting or Angioplasty for Restenosis Reduction in Small Arteries) Investigators. Circulation 2000;102:2593–2598. 35. Schalij MJ, Doucet S, Hilton D, et al. The SISA study: A randomized comparison of balloon angioplasty and stent to prevent restenosis in small arteries: Six month angiographic and 12 month clinical outcome (Abstr). Circulation 2000;102:II-663. 36. Mathias DW, Mooney JF, Lange HW, et al. Frequency of success and complications of coronary angiography of a stenosis at the ostium of a branch vessel. Am J Cardiol 1991;67:491–495. 37. Abizaid AS, Popma JJ, Lansky AJ, et al. The clinical impact of side branch occlusion and side branch narrowing after elective coronary stent placement in STARS. J Am Coll Cardiol 1998;31–32(Suppl):18A. 38. Guarneri EM, Sklar MA, Russo RJ, et al. Escape from stent jail: An in vitro model. Circulation 1995;92:688. 39. Ormiston JA, Webster MWI, Ruygrok RN, et al. Stent distortion during simulated side branch dilatation. J Am Coll Cardiol 1998;31–32:18A. 40. Yeager SB. Balloon selection for double balloon valvotomy. J Am Coll Cardiol 1987;9:467–468. 41. Meier B. Kissing balloon coronary angioplasty. Am J Cardiol 1984;54:918–920. 42. DiSciascio G, Goudreau E, Vetrovec GW. Coronary angioplasty of bifurcational stenoses: A new approach utilizing a single guide, double probe technique. Angiology 1990;41:145–150. 43. Pinkerton CA, Slack JD. Complex coronary angioplasty: A technique for dilatation of bifurcation stenoses. Angiology 1985;36:543–548. 44. den Heijer P, Bernink PJ, van Dijk RB, et al. The kissing balloon technique with two over the wire balloon catheters through a single 8 French guiding catheter. Cathet Cardiovasc Diagn 1991;42:187–190. 45. Myler RK, McConahay DR, Stertzer SH, et al. Coronary bifurcation stenoses: The kissing balloon probe technique via a single guiding catheter. Cathet Cardiovasc Diagn 1989;16:267–278. 46. Foley DP, Serruys PW. Bifurcation lesion stenting. Thoraxcenter J 1996;8:32–36. 47. Schampaert E, Fort S, Adelman AG, Schwartz L. The V-stent: A novel technique for coronary bifurcation stenting. Cathet Cardiovasc Diagn 1996;39:320–326. 48. Lefévre T, Louvard Y, Morice MC, et al. Stenting of bifurcation lesions: Classification, treatments, and results. Cathet Cardiovasc Diagn 2000;49:274–283. 49. Al Suwaidi J, Berger PB, Rihal CS, et al. Immediate and long-term outcome of intracoronary stent implantation for true bifurcation lesions. J Am Coll Cardiol 2000;35:929–936. 50. Sousa JE, Costa MA, Abizaid A, et al. Lack of neointimal proliferation after implantation of sirolimus-coated stents in human coronary arteries: A quantitative coronary angiography and three-dimensional intravascular ultrasound study. Circulation 2001;103:192–195.