Case Report

Mechanical Intervention and Coronary Artery Aneurysm

Shalima R. Gautam, MD, Deepak Mishra, MD, B.K. Goyal, MD

Shalima R. Gautam, MD, Deepak Mishra, MD, B.K. Goyal, MD

ABSTRACT: Coronary artery aneurysms after intervention are rare, and most are pseudoaneurysms rather than true aneurysms. Stent infection has been associated with mycotic aneurysm formation, as is the use of drug-eluting stents (DES). The antiproliferative and immunomodulatory properties of DES may reduce the local host defense mechanism and thus increase the chance of infection and contribute to aneurysm formation. Mechanical factors during implantation also play an important role in aneurysm formation. We report 3 cases of complications of mechanical interventions in coronary arteries.
J INVASIVE CARDIOL 2010;22:E213–E215
Coronary artery aneurysms after percutaneous coronary intervention (PCI) are rare (0.3–0.6%). Most are actually pseudoaneurysms, rather than true aneurysms. Mycotic aneurysms at the site of sirolimus-eluting stents are rarer still. Mechanical factors, infection and inflammation all play a role. We report three cases of coronary artery aneurysm as a complication of PCI.

Case Reports

Patient #1. A 56-year-old, non-diabetic but hypertensive female was admitted with complaints of angina on exertion (Class 2). The treadmill test was positive for inducible myocardial ischemia. Two-dimensional echocardiogram showed an ejection fraction of 55%. Coronary angiography revealed a 90% lesion in the mid segment and a long, diffuse lesion of the distal segment of the right coronary artery (RCA) (Figure 1). The other arteries were normal. She was given ecosprin and clopidogrel 600 mg 12 hours before the procedure. Percutaneous transluminal coronary angioplasty (PTCA) with stenting to the RCA was done after predilating the lesion with a 2.5 x 12 mm Sprinter balloon (Medtronic, Minneapolis, Minnesota) at 12 atm, followed by deploying 3 x 28 mm and 2.75 x 33 mm Pronova sirolimus-eluting stents (Eucatech AG, Germany) in an overlapping fashion at 14 atm for 30 seconds with good TIMI 3 flow (Figure 2). The activated clotting time (ACT) during the procedure was 290 seconds. Three weeks after the procedure, the patient had an episode of fever with chills along with severe precordial chest pain at rest for 15 minutes. She was treated with antimalarials and nitroglycerine, along with other cardiac medications. Peripheral smears for malarial parasites and blood cultures were negative. Electrocardiogram revealed sinus tachycardia with ST depression in leads 2, 3 and aVF. CPK-MB and troponinT were negative. She continued to have pain and hence was subjected to coronary angiography, which showed a giant mycotic aneurysm at the proximal stented segment (Figure 3). She was sent for surgery and is doing well at clinical follow-up. Patient #2. A 53-year-old, hypertensive, non-diabetic male with a known case of coronary artery disease presented with complaints of angina on exertion Class III of 1 month’s duration. He had undergone coronary angioplasty and stent implantation of the left anterior descending (LAD) coronary artery 18 months prior with the Cypher Select 2.5 x 33 mm sirolimus-eluting stent (Cordis, Miami, Florida). Angiography was planned and it showed total occlusion of the stent (Figure 4). It was decided to revascularize and the lesion was crossed with the Cross-IT 200 guidewire (Abbott Vascular, Abbott Park, Illinois) and predilated sequentially with 1.5 x 6 mm and 2.5 x 10 mm Sprinter balloons at 12 atm. The vessel revealed significant disease distal to the previously stented segment; hence, 2 Cypher sirolimus-eluting stents (2.5 x 33 mm and 2.75 x 33 mm) were deployed in an overlapping fashion at 14 atm. The overlapping segment was postdilated (Figure 5). Two months later, the patient presented again with chest pain and New York Heart Association Class III. Blood culture showed no growth and the total leukocyte count was 11,000/cubic millimeter. Electrocardiogram revealed ST-segment depression in the anterior precordial leads. Coronary angiography was done, and showed a coronary aneurysm arising from the overlapped segment of the stented portion of the artery with TIMI 2 flow distal to it, while the rest of the vessels were normal (Figure 6). The patient was sent for bypass grafting to the LAD and is doing well after the surgery. Patient #3. A 50-year-old, non-diabetic, non-hypertensive, non-smoking male with normal cardiac valves and good left ventricular function on two-dimensional echocardiogram presented with complaints of breathlessness and NYHA Class III symptoms. He had a known case of coronary artery disease and had undergone PTCA with implantation of a Pronova 3 x 23 mm stent to the LAD 40 days prior. Examination showed raised jugular venous pressure B/L basal crepitations over lung fields, soft S1 and an early diastolic murmur grade 3 in the aortic area. His TLC was 26,000/cubic millimeters and blood culture was positive for staphylococcus aureus (after 48 hours). Two-dimensional echocardiogram showed a large, mobile vegetation (10 x 10 mm) on the aortic valve freely moving in and out of the left ventricular outflow tract accompanied with severe aortic regurgitation (Figures 7 and 8). CT angiography was planned, but the patient collapsed and could not be revived. Discussion. PCI-related aneurysms are usually detected at the time of repeat angiography for recurrent symptoms or as part of routine angiography at follow-up. Coronary aneurysms have been reported from 3 days to 4 years after DES implantation. These stents do inhibit neointimal growth by eluting the drug locally, but at the same time may delay re-endothelialization, aggravate inflammation and elicit hypersensitivity reactions, thereby favoring the development of coronary aneurysms.1,2,8 Mechanical factors, such as residual dissections, arterial wall injury caused by oversized balloons and stents, high-pressure inflations, and atherectomies, have all been associated with aneurysm formation after percutaneous interventions.1,4 Coronary stent infection can present as mycotic aneurysm, pseudoaneurysm, myocardial abscess, and pericarditis with pericardial effusion. Development of mycotic aneurysm is rare in those who do not have infective endocarditis prior to PCI. Postulated mechanisms include embolic occlusion of the vasa-vasorum, immune complex injury and direct bacterial invasion in the setting of infective endocarditis.2,5 Apart from mechanical and infective risk factors for aneurysm formation that are observed for both bare-metal stents (BMS) and DES, the inflammatory and allergic reactions of nickel and molybdenum have been reported for BMS implantation. Allergic and inflammatory responses with DES are more complex. There are 3 components: the drug; the polymer; and the stent platform. Several histological studies have shown them to provoke eosinophilic, lymphocytic infiltration with focal giant cell reaction around the stent struts and polymer after DES implantation.3,6,7,9 Finally, the delayed healing response (such as incomplete endothelialization around DES struts) may reduce restenosis at the cost of being a precursor to aneurysm formation. Patient #2 had 3 long, drug-eluting coronary stents placed in the LAD on two separate occasions. Repeated application of antiproliferative agent or the excess of metal might have predisposed the patient to aneurysm formation in this case. Patient #3 had a large vegetation and severe AR of the aortic valve post-stent implantation and died suddenly before he could be evaluated properly, but positive blood culture (staphylococcus aureus), which came 48 hours later, is a pointer toward the infective etiology of a possible stent aneurysm in this case. In conclusion, our case reports illustrate coronary aneurysm as a complication of PCI, with contributions from mechanical, infective and inflammatory factors. The antiproliferative and immunomodulatory properties of DES may reduce the local host defense mechanism and increase the chance of infection, thereby contributing to aneurysm formation. Meticulous care to avoid iatrogenic stent infection should be practiced and future investigations are required to determine the pathophysiology and best therapy for DES-associated aneurysms.


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From the Department of Cardiology, Bombay Hospital Institute of Medical Sciences, Mumbai, India. The authors report no conflicts of interest regarding the content herein. Manuscript submitted February 3, 2010, provisional acceptance given March 23, 2010, final version accepted April 28, 2010. Address for correspondence: Dr. Shalima Gautam, Department of Cardiology, Bombay Hospital, 12 New Marine Lines, Mumbai 400020, India. E-mail: