CASE REPORTS

Acute Stent Recoil in the Left Main Coronary Artery Treated with Additional Stenting

Kais Battikh, MD, Riadh Rihani, MD, Jean Michel Lemahieu, MD
Kais Battikh, MD, Riadh Rihani, MD, Jean Michel Lemahieu, MD
Left main coronary artery (LMCA) disease is found in 3–5% of patients undergoing cardiac catheterization for ischemic chest pain, congestive heart failure or cardiogenic shock.1 Revascularization by coronary artery bypass grafting (CABG) has been shown to improve survival, whereas conventional balloon angioplasty was associated with a poor long-term prognosis. Elective stenting of LMCA stenosis should provide a reduction of abrupt closure risk, greater acute gain with a larger minimum lumen diameter (MLD), and a lower restenosis rate at follow-up compared to balloon angioplasty. The increased fibrous cellularity and calcification of the aorto-ostial lesions can cause arterial strain leading to stent recoil. Although stent collapse is an unusual finding, its occurrence should modulate the lesion approach and the choice of stent design in cases of hard and ostial lesions. We report a case of acute stent collapse occurring after LMCA angioplasty and treated with additional stenting. Case Report. A 77-year-old male patient with a history of hypertension, hypercholesterolemia and coronary artery disease was admitted in September 2000 for unstable angina. Four years ago, he was investigated for chronic stable angina with coronary angiography revealing triple-vessel disease with severe calcification of the left coronary artery, a 55% ostial stenosis of the LMCA and a severe narrowing of the proximal left anterior descending coronary artery (LAD) and the left circumflex artery (LCX). The right coronary artery (RCA) was occluded in its middle segment. The patient underwent CABG; a sequential saphenous vein graft was performed on the obtuse marginal (OM) and the distal RCA, while both the LAD and the diagonal artery were grafted with the left internal mammary artery (LIMA). Surgical revascularization was successful and the patient remained free from angina until September 2000, when he experienced an episode of rest angina with electrocardiographic changes in the postero-lateral leads and troponin I elevation. An angiographic control was then performed that showed a critical and calcified stenosis at the ostium of the LMCA with a thrombotic filling defect in its middle segment (Figure 1). The LCX ostium was severely narrowed and the proximal LAD and RCA were occluded. There was moderate stenosis at the anastomosis of the LIMA graft with normal flow to the LAD, while the venous sequential graft was occluded in its proximal portion. Ventricular angiography showed a normal ejection fraction. Since the LMCA and native LCX supplied the perfusion of the two OMs and the distal RCA through the distal patent part of the venous sequential graft, we decided to perform angioplasty of the LMCA. An 8 French (Fr) guiding catheter could not engage the LMCA and was positioned just in front of the left coronary ostium because of the severe stenosis. Since the first check angiogram, the LMCA appeared heterogeneous with a suspicious aspect of thrombus in addition to the major calcifications (Figure 1). Because of this angiographic appearance, we avoided the use of rotational atherectomy and instead preferred to begin with the administration of an intra-venous bolus of 0.25 µg/kg abciximab and 200,000 U intracoronary urokinase. The stenosis was crossed with a 0.014´´ Crossit 100 wire and the LCX was reached up to its third OM. Angioplasty was then attempted in order to dilate the calcified lesion using subsequent balloon sizes ranging from 2.5–4.0 mm and inflated at high pressure (18–19 atmosphere [atm]). The result remained unsatisfactory with important recoil after balloon deflation, leading us to implant a stent at the LMCA lesion. Initially we planned to use the Multi-link Ultra stent, but this device could not reach the proximal LCX because of the severe bend at the distal LMCA bifurcation. Therefore, a 4.0 x 18 mm Multi-Link Tetra stent was placed successfully in order to cover the ostium of the LMCA and the proximal part of the LCX. Despite the acceptable expansion of the stent inflated at 18 atm, acute and severe recoil occurred at the LMCA ostium after balloon deflation. Thus, additional inflation was done within the stent using a short, 4.5 mm-diameter Chubby balloon with an increased pressure reaching 18 atm to obtain full expansion. Immediately after, angiography again showed recoil of the LMCA ostial stent with a residual stenosis of 50%. When comparing the final diameter of the stent to the fully inflated balloon diameter, we concluded that the stent collapsed (Figures 2 and 3). We chose to implant an additional stent at the site of the focal collapse and performed the procedure by deploying a 4.5 x 13 mm Multi-Link Ultra stent at 18 atm, post-dilated with a 5.0 mm Bypass Speedy balloon. The latter was inflated at 16 atm and positioned to flare the proximal end of the stent across the aortic ostium. Finally, the procedure yielded an acceptable angiographic result with a residual stenosis of 18% (Figure 4). The hospital course was uneventful and the patient was discharged on the fourth day with aspirin and clopidogrel. He remained free from angina, without evidence of ischemia at exercise tolerance test 6 months later. Discussion. Initial studies of LMCA balloon angioplasty reported poor long-term prognosis.2 The high concentration of elastic fibers in the aorto-ostial and proximal segments of the LMCA has been proposed as a possible mechanism of elastic recoil and high restenosis rate after balloon angioplasty at these sites.3,4 In addition, the presence of ostial calcification contributes to further lesion rigidity.5 New studies suggest that a lesion-specific approach including rotational ablation, adjunctive dilatation and coronary stents produces excellent immediate angiographic results and low procedural complications in patients with protected or unprotected LMCA disease.6 Silvestri et al.7 confirmed the feasibility and safety of stent-supported angioplasty of the LMCA leading to an acceptable morbidity, with a 6-month target lesion revascularization rate of 17%. The 6-month angiographic restenosis rate was 23%, with a better result in proximal lesions (17% in ostial lesions, 23% in mid-portion lesions and 20% in distal lesions). Rotational atherectomy facilitates balloon expansion and stent passage and optimizes the initial diameter gain,7 especially in calcified lesions, but it was not used in our case because of the presence of thrombus. The main causes of small in-stent lumen after high-pressure dilatation are focal stent collapse, under-expansion due to lesion hardness or plaque prolapse through the stent mesh. The latter is recognized when we detect an endoluminal defect in a well-expanded stent. Such cases have been well described by Kahn8 as the result of a dissection flap or bulky atheromatous material protruding through the stent mesh or its articulation. On the other hand, stent under-expansion is commonly seen as a persistent indentation despite high-pressure inflation because of lesion hardness. We were able to conclude that the stent collapsed in our patient by comparing the stent shape before and after balloon deflation using quantitative angiography (Figures 2 and 3). In order to allow meticulous study of the edges, the stent should be sufficiently radio-opaque. The use of IVUS can be helpful in detecting and understanding inadequate stenting as in the case of a focal stent collapse,7–9 under-expansion or plaque prolapse. Moreover, it also detects incomplete stent apposition, which is frequent with LMCA stenting even after angiographic optimization (19% LMCA versus 1% non-LMCA; p in vivo study by Danzi,14 the mean angiographic acute recoil assessed by QCA was minimal for the NIR Royal stent (8 ± 7%), intermediate for the Multi-Link Duet stent (14 ± 7%) and higher for the Paragon stent (21 ± 11%). In the literature, few authors2,4,5,15,16 have reported stent recoil occurring immediately or many days after stenting of calcified lesions, with only 3 cases of aorto-ostial lesions. All reported cases were treated with additional stenting leading to an acceptable angiographic result and good outcome. To our knowledge, no previous cases of acute stent recoil were reported in the LMCA (Table 1). To avoid stent recoil during LMCA angioplasty, it is mandatory to use tubular stents that generate strong radial force.7 In calcified lesions, the use of rotational ablation may be helpful to achieve a good angiographic result. If there is a limitation of rotational atherectomy, as in our case, one must choose a stent with sufficient resistance against arterial strain. According to the comparative studies carried out by Danzi14 and Garcia,13 the NIR royal stent could be highly attractive for hard and calcified ostial lesions. However, in the former report,14 the 2 cases of LMCA stented with the NIR royal where achieved with 17.3% elastic recoil. Because it provides a greater radial force and a more optimal angiographic result, the biliary stent was also proposed for use in large vessels (> 4 mm), where adequate ostial tissue ablation might not be achieved.16 The Multi-Link Ultra is a tubular stent with more cells than the Multi-Link Tetra stent, and is specifically designed for vein graft angioplasty. Since this stent can be expanded > 6 mm in diameter, it appears to be the device of choice for treating large vessel lesions such as those in the LMCA. However, because of its rigidity, some difficulty may occur while attempting to cross tight bends as in our case. When acute stent recoil occurs, the addition of a second stent can provide the necessary radial support to achieve a large and stable stent lumen after a final high-pressure balloon inflation.2 This combination provided procedural success in reported cases2,4,5,15,16 and was reported in the experimental study of Yamamoto, with a reduction of stent recoil to Conclusion. Stenting provides a reduction in immediate elastic recoil, which commonly occurs at the LMCA due to the high concentration of elastic fibers in the vessel wall and frequent calcifications. Although most stents generate a sufficiently strong radial force to overcome arterial strain, stent collapse can occur (especially in case of aorto-ostial and calcified lesions). The optimal approach to this complex lesion subset often involves decalcification or tissue ablation followed by optimal deployment of an adequate stent. Nevertheless, when stent crush does occur, it can be treated with an additional overlapping stent with a good angiographic result and outcome.
References
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