TEACHING COLLECTION

Treatment of a Giant Coronary Aneurysm with a Novel Technique: Scaffolding (Tunnel) Stenting to Support PTFE-Covered Stents: Ins

Mauricio López-Meneses, MD, Fernando Alfonso, MD, PhD, Antonio Fernández-Ortíz, MD, PhD, Javier Escaned, MD, PhD, Alex Flores, MD, Pablo García, MD, Jaime Arias, MD, Manel Sabaté, MD, PhD, Rosana Hernández, MD, PhD, Camino Bañuelos, MD, PhD, Carlos Macaya, MD, PhD
Mauricio López-Meneses, MD, Fernando Alfonso, MD, PhD, Antonio Fernández-Ortíz, MD, PhD, Javier Escaned, MD, PhD, Alex Flores, MD, Pablo García, MD, Jaime Arias, MD, Manel Sabaté, MD, PhD, Rosana Hernández, MD, PhD, Camino Bañuelos, MD, PhD, Carlos Macaya, MD, PhD
Coronary artery aneurysm (CAA) is an uncommon condition with a natural history and prognosis still obscure.1 Aneurysmal coronary artery disease is defined as coronary dilatation that exceeds the diameter of the adjacent reference vessel by 1.5 times or more.1,2 Management of these patients is a therapeutic challenge and most published recommendations are based on anecdotal experience.3,4 If asymptomatic, the time period for the eventual progression or rupture is poorly defined. Patients can be symptomatic due to ischemia secondary to embolism, spasm, thrombus, dissection or associated arterial lumen narrowing. Surgery has been advocated for selected patients with large CAA in view of the potential risk for thrombosis and rupture, especially in saccular forms. However, there are no data available comparing medical or interventional management with surgical intervention in these patients.1–4 Coronary stents have significantly improved the results of coronary interventions. In the case of CAA, the use of covered stents is an attractive therapeutic alternative. There are several reports describing the use of covered stents for the obliteration of CAA.5–10 In the following case report, we describe a patient with a giant CAA, treated with a long stent that was used as a scaffolding device to support the subsequent implantation of two stent grafts. Case Report. A 77-year-old male with a history of cigarette smoking presented in June 1999 with stable angina; he had a positive exercise test. At that time, a coronary angiography revealed 80% stenosis in the proximal right coronary artery (RCA) and a giant CAA in its distal segment that extended close to the origin of the posterior descending coronary artery (PDA) (Figure 1A). Moderate narrowing at both CAA edges was also appreciated. The left anterior descending coronary artery (LAD) and circumflex coronary artery (CX) had only minor irregularities. Left ventricular angiography revealed normal systolic function with an ejection fraction of 70%. In the first procedure, the severe lesion of the proximal RCA was treated successfully with two Nir Primo stents (3.5 x 16 mm and 3.5 x 9 mm; Boston Scientific/Scimed, Inc., Maple Grove, Minnesota). At that time, the CAA was not treated because the symptoms were attributed to the proximal RCA lesion. Four months later, however, the patient underwent a new coronary angiography for persistent stable angina despite medical treatment. The 2 stents on the proximal RCA maintained a good angiographic result and the CAA had similar dimensions, but the stenosis located at its distal edge now appeared more severe (70% lumen narrowing) (Figure 1B). Since the patient had severe angina, a coronary intervention was designed to exclude the CAA from the vessel lumen using covered stents. The patient was pretreated with 8,000 units of heparin, 325 mg of aspirin, and 500 mg of ticlopidine. An 8 French (Fr) multipurpose guide catheter (Cordis Corporation, Miami Lakes, Florida) was placed at the ostium of the RCA and a 0.014´´ BMW guidewire (Guidant Corporation, Santa Clara, California) was used to cross the CAA and the distal stenosis. On intravascular ultrasound (IVUS) with a 3.2 Fr, 30 MHz transducer (Ultracross, Boston Scientific/Scimed, Inc.), the CAA was thin walled (mean diameter, 12 mm; maximal cross sectional area, 113 mm2) and significant stenoses at both CAA edges were also visualized (Figures 2A and 2B). The stenosis at the proximal edge was caused by a fibrotic plaque (residual lumen area, 3 mm2; total vessel area, 17 mm2); the stenosis at the distal edge was caused by a fibrocalcific plaque (minimal lumen area, 2.6 mm2; total vessel area, 14.9 mm2). The lesion was predilated using a 4 x 30 mm Worldpass balloon (Cordis Corporation) at 10 atmospheres (atm). A 3.5 x 38 mm Multi-Link stent (Guidant Corporation) was then delivered at 14 atm, covering the complete length of the CAA and also the 2 edge stenoses (the stent length was selected according to the length of the CAA as determined by the motorized IVUS pullback). This stent was implanted with the intention to provide scaffolding, bridge or tunnel to allow subsequent delivery of the two covered stents. A 3 x 19 mm JoStent coronary stent graft (Jomed Implantate GmbH, Unterschleissheim, Germany) was mounted and crimped onto a 4 x 30 mm Worldpass balloon and deployed at 14 atm (over the previous stent) to cover the distal lesion and partially the CAA. A second 3 x 19 mm JoStent stent graft was then deployed at 14 atm covering the proximal part of the CAA and slightly overlapping the more distal stent graft. Immediately after this procedure, a minor endovascular leak (where the 2 covered stents overlapped) allowed a slow and partial filling of the CAA. Both stents were then dilated to 16 atm using a 4 x 10 mm Tacker balloon (Cordis Corporation). The final angiogram showed an incomplete exclusion of the CAA and TIMI 2 flow in the PDA branch, which emerged precisely from the distal stent edge, where a 30% residual stenosis was seen (Figure 1C). This aspect of the stent was not post-dilated to prevent total occlusion of the PDA branch. The patient had recurrent chest pain 12 hours later, and a new angiogram showed completed exclusion of the CAA but also a total occlusion of the PDA (Figure 1D). He remained asymptomatic and hemodynamically stable, but had a maximal creatine kinase elevation of 470 IU/l. No electrocardiogram changes were detected. He was discharged on the seventh hospital day. Two months later, the patient presented with recurrent exertional chest pain. A new coronary angiogram showed focal severe restenosis confined to the distal edge of the distal covered stent, where the mild residual lesion was previously documented. The proximal and mid segments of the stents showed excellent angiographic appearance and complete exclusion of the CAA was also visualized (Figure 1E). Using an 8 Fr JR4 guide catheter (Cordis Corporation), a 0.014´´ BMW guidewire was used to cross the focal in-stent restenosis. A 3.2 Fr, 30 MHz Ultracross IVUS catheter was advanced. Severe stent underexpansion localized precisely at the distal part of the stent was then recognized (Figure 2C). At this point, the IVUS catheter was nearly occlusive (3.5 mm2). The bodies of this covered stent and also the proximal covered stent, however, had no significant intimal thickening on IVUS. A 3 x 20 mm Gemini balloon (Guidant Corporation) at 20 atm followed by a 4 x 10 mm Tacker balloon at 22 atm were then used to dilate the restenotic segment. The final angiogram showed no residual stenosis and TIMI 3 flow (Figure 1F). The IVUS study was repeated, confirming the correct expansion of the distal edge of the stent (minimal lumen area, 17.5 mm2 with a lumen area of 18 mm2 in the proximal stent) (Figure 2F). The patient had an uneventful clinical evolution. At 6-month follow-up exam, a new coronary angiography demonstrated an excellent result without residual stenosis on the distal RCA, which was also confirmed by repeated IVUS interrogation. One year after the last coronary intervention, he was asymptomatic and had a negative exercise test. Discussion. The most appropriate therapy for patients with CAA is unknown due to the low prevalence of this condition. Controversy still persists regarding the use of surgical or medical management. Published guidelines have been based on anecdotal experience rather than systematic studies.1–4 Surgically implantable tissue prostheses have been used for decades as vascular conduits and more recently, investigational devices such as tissue-covered stents have been used in peripheral vessels to treat aneurysmal dilatations or to seal vessel ruptures.5 Recently, polytetrafluoroethylene (PTFE) stent grafts have become available for implantation into human coronary arteries. The main indications are bail-out procedures (coronary perforation and rupture during percutaneous transluminal coronary angioplasty and also acute or threatened closure due to extensive dissections). Furthermore, these devices have been used in the treatment of degenerated saphenous vein grafts and the closure of CAA and pseudoaneurysms.4–11 PTFE is a biocompatible polymer that may be manufactured in the form of microporous distensible membranes. The JoStent Coronary Stent Graft consists of 2 coaxially aligned stainless-steel stents (surgical 316 L) that encompasses a microporous PTFE membrane between them in a sandwich-like configuration. This stent has ideal mechanical properties since this membrane can be expanded 4–5 times without laceration or shrinkage. Moreover, the negative charge of the polymer prevents blood protein coagulation on the tissue surface and limits platelet activation and thrombus formation. The stent graft is currently available in lengths from 9–26 mm. The maximum achievable diameter is 5.0 mm.5 In our patient, we tried first to occlude the giant CAA, and second to cover the significant stenoses at both CAA edges. The unique approach that we selected was designed because a stent with a minimum length of 35 mm was deemed necessary. IVUS findings were very useful to accurately select the stent length. Taking into consideration that the maximal length available for covered stents was 26 mm, we used a conventional long stent as a bridge to support the subsequent deployment of 2 covered stent grafts and also to treat the lesions at the CAA margins. We found that the apposition of the stent graft over the underlying stent was easily achieved using high pressures. Another potential advantage of IVUS in this setting is the differentiation between true CAA and pseudoaneurysm.9,10,12 In our patient, IVUS was diagnostic of a thin-walled, giant CAA. IVUS was also helpful to clarify the presence and severity of the 2 stenoses located at the CAA edges that appeared ambiguous on angiography. Indirect findings of a significant narrowing at the entrance of the CAA were also evident, namely a striking image of mobile negative contrast streaming on the echogenic blood at the proximal aspect of the CAA (Figures 2B and 2D). This procedure was complicated by the occlusion of the PDA, fortunately enough, without any clinical sequelae. Such adverse events are not unusual with the use of stent grafts, and therefore special care should be taken in identifying all relevant sidebranches in jeopardy before the procedure. In this regard, the use of IVUS may also be of potential benefit to accurately identify the ostium of the sidebranch and facilitate precise stent deployment, which may be critical in some patients.13 In addition, our patient developed restenosis at the distal edge of the stent. Previous reports indicate that neointimal proliferation in coronary PTFE stents occurs predominantly at the edges not covered by the PTFE membrane.5 In contrast, proliferation in conventional stents is longitudinally uniformly distributed. In our case, however, IVUS provided a different explanation for this phenomenon. A suboptimal expansion of the stent was probably underestimated on angiography at the time of the initial procedure, when the major concern was the impending occlusion of the PDA. However, IVUS imaging revealed severe underexpansion of the distal stent edge supporting that “pseudo” in-stent restenosis was in fact the main pathophysiological mechanism in our patient.14 The contrast medium surrounding the stent may explain why severe underexpansion of the stent was initially unrecognized. This phenomenon was readily recognized at follow-up using IVUS, which was also very useful in guiding the repeat intervention. In summary, exclusion of giant CAA can be done with the technique described. This strategy appears to be feasible and useful, allowing a percutaneous intervention to be performed in those cases where the CAA length exceeds that of the currently available covered stents. Thus, this technique provides an attractive alternative to surgical intervention in patients with giant CAA.
References
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