From *Mumbai University, Seth G. S. Medical College and KEM Hospital, Mumbai, India, and §McMaster University, Hamilton Health Sciences, Hamilton General Hospital, Hamilton, Ontario, Canada. The authors report no conflicts of interest regarding the content herein. Manuscript submitted November 7, 2008, provisional acceptance given February 17, 2009, final version accepted February 20, 2009. Address for correspondence: Charan Lanjewar, MD, DM, Associate Professor, Cardiology, Seth G.S.Medical College and KEM Hospital, Parel(E), Mumbai, India. E-mail: firstname.lastname@example.org
_______________________________________________ ABSTRACT: Late stent malapposition (LSM) within a coronary artery aneurysm is an unusual intravascular ultrasound (IVUS) finding at follow up, and has been reported to be more common after drug-eluting stent implantation than after bare-metal stenting. We describe a case of LSM with coronary artery aneurysm 6 months after paclitaxel-eluting stent implantation. This unusual case was successfully managed under IVUS guidance.
J INVASIVE CARDIOL 2009;21:E87–E90 Key words: Late stent malapposition, persistent restenosis, coronary aneurysm, drug-eluting stent The incidence of late coronary aneurysm with bare-metal stents (BMS) is 0.2%, compared to 1.4% with drug-eluting stents (DES).1 DES, which locally elute antiproliferative drugs, dramatically reduce restenosis,2,3 but at the same time may cause coronary aneurysms.4 Late stent malapposition (LSM) has been observed more frequently after DES implantation as a cause of coronary aneurysm in 8–10% of patients.2,5 Intravascular ultrasound (IVUS) is an invaluable tool for managing coronary aneurysms, since it provides exact etiologic information, i.e., hemorrhage, ulcer, coronary dissection and LSM. It also allows precise assessment of the size of the aneurysm and can assist in guiding treatment and evaluation of outcomes.5 We present the case of a patient who underwent IVUS assessment of a coronary aneurysm which was noted 6 months after DES implantation in the right coronary artery (RCA). Case Report. A 56-year old hypertensive male presented with acute coronary syndrome. The electrocardiogram (ECG) was suggestive of evolved inferior wall myocardial infarction. The patient underwent coronary angiography and revascularization, which revealed near-total occlusion of the proximal RCA, with no significant lesions in the left anterior descending or left circumflex arteries (Figure 1A). The lesion in the RCA was crossed with a 0.014 inch Balance MiddleWeight™ (BMW) guidewire (Guidant Corp., Santa Clara, California) and dilated with a 2 x 20 mm Voyager™ balloon (Abbott Vascular, Abbott Park, Illinois) at a pressure of 12 atm. There was no dissection after balloon angioplasty. Subsequently, a 2.75 x 32 mm Taxus® DES (Boston Scientific Corp., Natick, Massachusetts) was deployed in the proximal RCA at a pressure of 14 atm, resulting in thrombolysis in myocardial infarction (TIMI) 3 flow (Figure 1B), yielding a satisfactory PCI result. The patient was readmitted 6 months later with unstable angina despite being on regular dual antiplatelet agent. The ECG showed minor ST-T changes in the inferior leads. Coronary angiography showed no progression of disease in the left system, while the RCA revealed a saccular aneurysm measuring 4.5 mm at the site of the previous stent, with proximally tight, focal, persistent restenosis (Figure 2). IVUS evaluation revealed giant gaps between the stent struts and vessel wall, which was filled with blood specks. The localized dilatation exceeded 1.5 times the diameter of the adjacent segment, and the LSM was found to be predominant in the proximal part of the stent. Quantitative IVUS measurement showed significant enlargement of the external elastic membrane cross-sectional area (CSA) and marked positive vessel remodeling at the site of the LSM and aneurysm. Under IVUS guidance, direct stenting of the proximal RCA was performed with a 3 x 15 mm Vision BMS, which covered only the restenotic lesion. The stent was placed just before the aneurysm (Figure 3), thus not overlapping it. The stent was minimally overlapped and was postdilated with a 3.5 x 10 Mercury balloon (Abbott Vascular, Abbott Park, Illinois) at 16 atm. The patient was advised to remain on lifelong dual antiplatelet therapy and to undergo close follow up with repeat angiography and IVUS to assess for potential progression of the malapposition. Discussion. Following PCI, coronary artery aneurysms can form via several mechanisms. Aneurysms are known to form acutely due to coronary artery dissection and perforation that may result from the use of oversized balloons or high-pressure dilatation causing intimal and medial tearing. Gradual formation of a coronary artery aneurysm can occur due to residual small tears of the artery uncovered by the proximal end of the stent or dissection within the layers of the arterial wall leading to thinning and remodeling of the arterial wall.2,3 In addition, in the case of DES deployment, a coronary artery aneurysm may result from delayed and incomplete endothelialization, inflammatory changes of the medial wall or hypersensitivity reactions to the drug/polymer.4 Several histological studies have shown extensive inflammation consisting primarily of eosinophils and lymphocytes with a focal giant-cell reaction around the stent struts and surrounding the polymer after DES implantation.4 Virmani et al4 presented an autopsy case with aneurysmal dilation of stented arterial segments with a severe localized hypersensitivity reaction consisting predominantly of T-lymphocytes and eosinophils through all layers of the vessel wall. An additional phenomenon that has been observed after DES implantation as a cause of coronary aneurysm is stent malapposition.6–8 Stent malapposition is defined as a separation of at least one stent strut from the intimal surface that is not overlapping a side branch and had IVUS evidence of blood speckles behind the strut.9 Stent malapposition is defined as acute, if present immediately after the index procedure; as late, if present at 9-month follow up; as resolved, if present after stent implantation but not at follow up; as persistent, if present both after stent implantation and at follow up; and as acquired, if present at follow up, but not after stent implantation.9 The RAVEL trial reported a 21% incidence of LSM in SES at follow up.10 In the SIRIUS trial, which had serial IVUS both at implantation and follow up, LSM was seen in 8.7% of SES versus none in the control cohorts. A meta analysis of the TAXUS-IV, V and VI trials also showed a higher rate of LSM in paclitaxel-eluting stents (PES) than in control stents (8.4% versus 3.5%; p
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