Sidebranch Occlusion After Coronary Stenting With or Without Balloon Predilation: Direct Versus Conventional Stenting

Sidebranch occlusion (SBO) is a challenging problem during interventional procedures.1–5 Although occlusion of branches smaller than 2 mm was reported to be of little clinical importance, this may lead to angina or myocardial infarction. Sidebranches with ostial lesions were observed to occlude more than the ones without any lesion. Plaque shift, plaque embolization, spasm, thrombus formation, design of the stent struts and high-pressure balloon predilation (> 10 atm) are reported to be the mechanisms responsible for SBO.6,7 Direct stenting (DS; stenting without balloon predilation) is a novel approach in percutaneous treatment of coronary artery lesions. Stenting without previous balloon dilation may decrease trauma, incidence of dissection and distal embolization, leading to a better outcome.8–11 However, the data evaluating SBO after stenting without balloon predilation are scarce.12 The aim of this study was to evaluate the impact of DS, a novel percutaneous coronary intervention (PCI) technique, on sidebranch occlusion and compare it to conventional stenting with balloon predilation (CS). METHODS Study population. We retrospectively reviewed our institutional interventional database from February 1998 through May 2001 and identified all patients who underwent stent implantation. A total of 151 patients had sidebranches (> 1 mm) covered by stents. Patients were then divided into two groups: the CS group consisted of patients who had undergone conventional stenting (n = 63 patients) and the DS group consisted of those who had undergone direct stenting (n = 88 patients). Stenting procedure. PCI was performed after obtaining two orthogonal views of the lesion. After crossing the lesion with a 0.014´´ guidewire, interventionist preference determined the procedure to be performed. Initial balloon dilation in the CS group was carried out with undersized PTCA balloons inflated at nominal pressures (6–8 atmospheres). Multiple balloon inflations were done if needed. The majority of the stenting in both groups was accomplished with the use of second-generation preloaded tubular stents (Jostent and ACS Multi-Link). The stent to artery ratio was 1.1/1. Direct stenting was accomplished using a delivery balloon with a high-pressure single inflation. Procedural success was defined as optimal angiographic result (residual diameter stenosis 3 times normal associated with elevation of CK-MB. Q-wave infarction was diagnosed in the presence of new Q-waves in two contiguous leads. In-hospital death (due to any cause), recurrent MI, target vessel reintervention and coronary artery bypass operation were also noted. Troponin T, creatine kinase and CK-MB measurements were routinely taken immediately after, at 6 hours and 16 hours post-intervention. A second-generation commercial ELISA cTnT assay (Boehringer Corporation, Mannheim, Germany) was used to measure cTnT with a cut-off of 0.1 ng/dl. Total CK (normal, 300 seconds. Ticlopidine (500 mg loading dose, 250 mg twice daily for 30 days) or clopidogrel (300 mg loading dose, 75 mg/day for 30 days) plus aspirin (300 mg, indefinitely) and beta blocker (if not contraindicated) therapy were started after the procedure. Glycoprotein IIb/IIIa receptor antagonists were not used in any patient. Angiographic evaluation. Angiograms were reviewed and graded by two independent film readers to identify vessels with major sidebranches (> 1 mm in diameter) covered by stents. Parent vessel and sidebranch percent diameter stenosis, minimal lumen diameter and reference diameter were analyzed before and after stenting. Quantitative coronary angiography (QCA) was performed with the use of an automatic edge-detection system (General Electric DLX Angiographic Systems, GE Medical Systems Europe, Sedex, France). SBO was defined as persistent reduction in TIMI flow grade Statistical analysis. Data were expressed as means ± standard deviation for continuous variables and as frequencies for categorical variables. Continuous variables were compared by Student’s t-test and categorical variables by Chi-square test. A p-value 2.5 mm. Stenting was successful in all patients. In 2 patients (2.2%), the lesions could not be directly crossed over with the stent. However, stenting was accomplished successfully after balloon predilation. There was no stent loss or imprecise stent placement in the DS group. Patient and angiographic variables of the two groups are listed in Tables 1 and 2. There was no significant difference between the two groups regarding the baseline clinical characteristics. Incidence of AHA/ACC type A and B2 morphology of the parent vessel was higher in the DS group (p 0.05) (Table 3). Of all the variables analyzed, most of the SBOs were observed in cases with type D sidebranch morphology (p = 50% (p = 0.019) (Table 4). Logistic regression analysis failed to show any other clinical and angiographic variables predicting the SBO. Of the 151 patients, eleven experienced post-procedural chest pain, but only 3 developed cardiac enzyme elevation due to SBO (non-Q wave MI). DISCUSSION Stenting has become the mainstay of therapy for coronary lesions in the last years. An important potential complication of stenting is sidebranch occlusion due to mechanical obstruction or thrombosis.3,4,14,15 Depending on the design, stents usually cover 10–20% of the vessel surface area. SBO, which complicates the procedure, could be quite troublesome. Although sidebranch protection is accomplished with an extra guidewire, the incidence of SBO is quite high, ranging between 12–41%.3,16–18 There is also the risk of inability to cross the stent struts after the occlusion or entrapment of the balloon in these struts. Although a variety of techniques are proposed for protection of the sidebranch, including kissing balloon, T-stenting, Y-stenting, and the culotte technique, SBO is still an important problem.19–22 Occlusion of branches smaller than 2 mm is reported to be of little clinical importance. Although SBO after stent placement is reported in many studies, several reports revealed that the majority regained their patency at 6-month control.1,23,24 Sidebranches with ostial lesions were observed to occlude more than those without any lesion. The “snow plow” effect, where the atheromatous plaque is shifted toward the ostium of the sidebranch, is reported to be the responsible mechanism after stenting.7 Cho et al. reported that besides type D and F morphology, plaque volume of the parent vessel is a major determinant of SBO.25 Other mechanisms involved in this process include spasm of the sidebranch, embolization of the atherosclerotic material, thrombus formation and stent material itself. The authors also reported that the presence of an ostial lesion in the sidebranch is the most powerful predictor of SBO after rotational atherectomy of in-stent restenosis.6 We also observed in this study that SBO was seen in patients with type D morphology and sidebranch ostial lesions > 50%.6 Recently, Cho et al. investigated the effect of stent design on SBO after stenting and reported that specific stent design did not influence immediate and late SBO.25 Herz et al. reported a very low incidence of SBO (5%) after direct stenting.9 The authors reported that by eliminating balloon predilation, atherosclerotic plaque shift to sidebranches decreases.9 However, the incidence in our patient population undergoing DS is quite high (18.2%) and this was not statistically different than the CS group (24%) (p > 0.05). Since the study by Herz et al. was not designed for analyzing SBO, we don’t have the detailed descriptive analysis of the sidebranches in their patient cohort. The only data so far regarding SBO after DS were recently reported by Yilmaz et al.12 The authors evaluated 86 patients with 111 sidebranches who underwent direct stenting; they reported a SBO incidence of 8.1%.12 The major predictor of SBO was reported to be the ostial involvement of the sidebranch (> 50% ostial narrowing) arising within or just beyond the diseased portion of the vessel, high-pressure and multiple inflations (> 2 times). We also used high-pressure stenting in the DS patient cohort which might have led to this high incidence of SBO. The higher incidence of SBO in our DS cohort could be due to the higher incidence of thrombus at the lesion site (31.8% vs. 8.0%) and higher amount of patients with acute coronary syndrome (86.4% vs. 30.2%) in our DS cohort compared to the cohort of Yilmaz et al.12 Although we speculate that the difference in plaque composition might also be an important factor for the fate of the sidebranch, since soft, fragile thrombus may increase the plaque shift and thrombus propagation leading to SBO, the presence of thrombus did not seem to increase SBO (p = 0.8). However, although not statistically significant, there was a trend for SBO in patients presenting with acute coronary syndromes (p = 0.079). Glycoprotein IIb/IIIa receptor blockers were reported to improve the results after PCI in high-risk patients with thrombus.26 Use of these agents before or during the procedure may improve flow patterns by preventing embolization and decreasing the thrombus burden.27 Platelet inhibitors may play an important role in this setting by decreasing thrombus burden and avoiding propagation to the sidebranch, resulting in improved clinical outcome. Conclusion. To the best of our knowledge, this is the first report comparing incidence of SBO between two different PCI methods, CS versus DS. Although the incidence of SBO was low in the DS group compared to the CS group, this difference was not statistically different. Study limitations. This is a single-center, retrospective and non-randomized study with small numbers of patients. Since follow-up coronary angiogram was not performed, the long-term fate of SBO could not be evaluated. Randomized studies with larger patient populations should be conducted.

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