Subacute Development of a Coronary Artery Pseudoaneurysm After Primary Angioplasty and Stenting for Acute Myocardial Infarction

The pharmacological and mechanical coronary angioplasty environment extensively enhances the immediate outcome so much that acute procedural complications seem to belong to the past. Other than restenosis, the management of which is now well codified and the future of which might be “compromised” by rapamycine and/or paclitaxel coated stents, long-term post-angioplasty results are now essentially dependent on atherosclerosis progression. Nevertheless, rare complications such as pseudoaneurysm can still occur. Case Report. A 76-year-old woman was admitted during hour 5 of an acute anterior wall myocardial infarction following 24 hours of unstable, but neglected, angina pectoris. Her only risk factor was treated hypercholesterolemia. Due to the delay since the onset of symptoms, the persistence of the chest pain and the importance of the left ventricular dysfunction, primary angioplasty was performed rather than thrombolysis. The coronary angiogram revealed double-vessel disease, including an abrupt left anterior descending (LAD) occlusion poorly supplied by the right coronary artery and a strong stenosis in the middle part of a marginal branch of the circumflex artery. An Intermediate guidewire (Boston Scientific/Scimed, Inc., Maple Grove, Minnesota) cleared the LAD occlusion and a 2.5 x 20 mm balloon inflated for 72 seconds at 12 atmospheres (atm) reopened the artery without angiographic dissection. The result was achieved with implantation of a 3.0 x 18 mm Seaquest stent (Nycomed Amersham, Paris, France) for 37 seconds at 12 atm in the proximal part of the LAD. Because of severe left ventricular dysfunction, we also treated the marginal branch with direct stenting with a 3.0 x 8 mm Tristar RX stent (Guidant Corporation, Temecula, California) for 26 seconds at 10 atm. The result was satisfactory, with anterograde TIMI III flow on both treated arteries without obvious complications on angiogram. The evolution was favorable after an initial congestive heart failure controlled with diuretics. She was discharged from the unit on the tenth day on aspirin, ticlopidine, beta-blockers, ACE inhibitors, lipid-lowering treatment and diuretics. Because of recurrent post-percutaneous transluminal coronary angioplasty angina, the patient was referred for control coronary angiography during the third month. The exploration showed severe marginal in-stent restenosis (measured at 85% on off-line quantitative coronary angiography) and, above all, a picture of an aneurysm in the LAD stent without significant restenosis (Figures 1 and 2). After a medico-surgical consultation, we opted for a surgical strategy based on the 2 internal mammary artery grafts on the marginal and LAD coronary arteries associated with proximal LAD exclusion. Surgical examination of the first part of the LAD led to the diagnosis of a pseudoaneurysm. Six months after the double coronary artery bypass graft surgery, the patient is still alive without angina pectoris or symptoms of heart failure. Discussion. Morgagni described the first coronary aneurysm in 1761.1 The major spontaneous etiologies are atherosclerotic (about one-half) and congenital (about one-fifth). Others are inflammatory, infectious and traumatic,2,3 but more and more are related to transcatheter coronary revascularization.4 Lell and Kitzis report a frequency of 5% of coronary artery aneurysms in angiographic studies, about 3.9–5% (with an average delay of 4 months) in post-PTCA area1,3 and a vexed correlation between post-PTCA coronary artery dissection and aneurysm formation (aneurysm on angiographic control, 9% in case of coronary artery dissection versus 2.9% without dissection).5 Non-iatrogenic aneurysms are classically true and those associated with atherosclerosis usually follow the wash-out of a large lipid core from a large plaque. On the other hand, arterial barotraumatism induced by the balloon inflation can promote two sorts of lesions leading to an angiographic picture of aneurysm: the true and the false aneurysm. The difference between both was dependent on visual and histologic examination before the use of intravascular ultrasound (IVUS); it depends on the presence or absence of coronary arterial wall overlying the aneurysmal formation.6 The mechanism leading to the formation of a true or false aneurysm is imperfectly known. For Lell et al., a coronary artery wall dissection or a perforation that concerns only the media, without crossing the adventitia, induces a true aneurysm formation due to a local increase of arterial wall compliance.1 On the other hand, a complete perforation that also concerns the adventitia can evolve either toward a disastrous complication such as tamponade7 or toward a relatively benign outcome such as pseudoaneurysm formation.1 The post-PTCA risk factors for aneurysm formation are under debate. Some authors report the influence of oversized balloons, high-pressure inflation or the use of atherectomy devices.3,8 Hill et al.9 associate post-PTCA dissections with the development of coronary artery aneurysms, whereas Slota et al.10 do not. Nevertheless, the prognosis for true aneurysms is reported to be benign and to require no specific treatment.1,11–13 On the other hand, the prognosis for pseudoaneurysms is hazardous due to the difficulty evaluating the risk of complications including thrombosis, distal embolization, mechanical luminal obstruction and mainly, rupture.1 Lell et al. believe that the lack of intravascular ultrasound examination of post-PTCA aneurysmal angiographic pictures should require an interventional or surgical approach to prevent the risk of rupture of a potential pseudoaneurysm.1 The best treatment for a pseudoaneurysm is not codified between a surgical treatment with resection or exclusion associated with coronary bypass grafting, and an interventional treatment either with “classical”4 or covered stent approach.3,14,15 The purpose is to cover the collar of the pseudoaneurysm in order to reduce the blood flow and promote thrombosis, thus preventing the expansion and subsequent rupture of the pseudoaneurysm.4 In our patient, the choice of a surgical treatment was guided by several factors. The first was the localization of the pseudoaneurysm at the ostial part of the LAD (which is considered to be an interventional contraindication by Lell et al.), making the implantation of a covered stent difficult and an eventual subacute in-stent thrombosis hazardous.1 The second was the lack of intravascular ultrasound, which was unavailable to us and therefore could not help us manage the patient by differentiating between a true and false aneurysm. Finally, this patient had early severe restenosis on the marginal branch, double vessel disease including the ostial LAD, of which the long-term prognosis after CABG is known to be better. Even though the mechanism leading to the development of a post-PTCA pseudoaneurysm is probably multifactorial and not completely understood, the main risk factors are well known. Surprisingly, we did not find any of these risk factors in this clinical report; we did not use any atherectomy devices, oversized balloons or high-pressure inflations during balloon angioplasty or stent implantation. Given the lack of usual risk factors, we debated two hypotheses to explain this aneurysm formation. The first concerns the role of a wall perforation caused by the guidewire when it cleared the occlusion. This punctual arterial perforation could have promoted local extravascular bleeding, which was enhanced with the use of antiplatelet and heparin therapy. The second depends on the arterial wall fragility following a plaque rupture which, aggravated by the balloon inflation and stent implantation, could have promoted a non-angiographically visible dissection leading to aneurysm formation. However, since primary angioplasty to treat cases of acute myocardial infarction is frequent and pseudoaneurysm formation quite scarce, we would rather incriminate the guidewire in this case. Conclusion. Post-angioplasty coronary artery aneurysm or pseudoaneurysm formation represents a rare but non-negligible mid delay complication. The formation mechanism is not completely known. Review of the literature leads one to treat only pseudoaneurysms because of their low but uncompressible complication risks.

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