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Year : 2021  |  Volume : 5  |  Issue : 2  |  Page : 166-168

Giant Right Coronary Artery Aneurysm Following Percutaneous Transluminal Coronary Angioplasty

1 Department of Cardiology, AMRI Hospital, Salt Lake, Kolkata, West Bengal, India
2 Department of Cardiology, IPGME and R-SSKM Hospital, Kolkata, West Bengal, India
3 Department of Medicine, BMCH, Burdwan, West Bengal, India
4 Department of Cardiology, ICVS, IPGME and R-SSKM Hospital, Kolkata, West Bengal, India

Date of Submission16-Aug-2020
Date of Decision14-Oct-2020
Date of Web Publication24-Mar-2021

Correspondence Address:
Dr. Sudeb Mukherjee
4/28 A, Jadavgarh, Dr B. C. Roy Road, Kolkata - 700 078, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jiae.jiae_46_20

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Coronary artery aneurysm following percutaneous coronary angioplasty (PTCA) is rare in interventional cardiology. Several factors may contribute to the development of such complication following PTCA that include stent size, improper apposition, nature of vascular disease, and operative technique. Here, we report a case of giant right coronary artery in-stent restenosis and aneurysm following PTCA stenting within 1-month duration. The operative technique, underlying diseased segment of coronary artery, and associated comorbidities are contributing factors for such complications. Bedside echocardiography may detect aneurysm and expedite the process of treatment.

Keywords: Aneurysm, in-stent restenosis, right coronary artery

How to cite this article:
Mukherjee S, Datta S, Ghosh S, Mandal SC. Giant Right Coronary Artery Aneurysm Following Percutaneous Transluminal Coronary Angioplasty. J Indian Acad Echocardiogr Cardiovasc Imaging 2021;5:166-8

How to cite this URL:
Mukherjee S, Datta S, Ghosh S, Mandal SC. Giant Right Coronary Artery Aneurysm Following Percutaneous Transluminal Coronary Angioplasty. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2021 [cited 2021 Nov 29];5:166-8. Available from: https://www.jiaecho.org/text.asp?2021/5/2/166/311857

  Introduction Top

The incidence of coronary artery aneurysms (CAAs) ranges widely from 0.3% to 5.3% of the population, and a pooled analysis reports a mean incidence of 1.65%.[1],[2] A study from India reported an incidence of 10%–12%, the highest in the literature to date, perhaps reflecting a specific genetic and/or environmental predisposition.[3] Coronary Artery Surgery Study (CASS) registry, which analyzed consecutive angiograms from over 20,000 patients performed to evaluate suspected coronary artery disease, revealed a 4.9% incidence of coronary aneurysms.[4] It was found that the patients with aneurysms were more likely to have three-vessel disease (TVD) and a history of myocardial infarction. In the Taxus-V trial, CAAs were more prevalent after implantation of paclitaxel-eluting stents than bare metal stents (1.4% vs. 0.2%), though this trend did not quite achieve statistical significance (P = 0.07).[5] A lot of factors may play a role in the development of a CAA. Atherosclerosis and Kawasaki disease have been known to be the most common causes of CAAs in adult and pediatric populations. Reports of development of aneurysms following percutaneous coronary angioplasty (PTCA) are rare. Here, we report such a case of CAA which developed after PTCA.

  Case Report Top

A 50-year-old gentleman with controlled hypertension (on medication) and nonsmoker for the last 8 years, was admitted with a diagnosis of unstable angina. He underwent coronary angiogram (CAG) which revealed TVD. He was advised for coronary artery bypass grafting (CABG), but the patient opted for multi-vessel percutaneous coronary intervention with the understanding of prognostic implications. Preoperative transthoracic echocardiogram (TTE) revealed left ventricular ejection fraction (LVEF) of 54% and no other structural abnormalities. He underwent successful PTCA with stenting with drug (everolimus)-eluting stent (DES) to right coronary artery (RCA), obtuse marginal (OM) artery, and left anterior descending (LAD) artery. RCA was stented with two overlapping stents from proximal to distal segment. He was kept on dual-antiplatelet therapy with aspirin and ticagrelor along with other medications in accordance with the current standard guidelines. The patient was discharged after 4 days in a stable condition. After 10 days, the patient came back with dyspnea without any chest pain or fever. TTE evaluation revealed 8-mm pericardial effusion. Chest X-ray posteroanterior view revealed bilateral pleural effusion. Renal function parameters and serum electrolytes were normal at that time. Complete blood count revealed total leukocyte count of 12,800/cumm (80% neutrophils, 13% lymphocytes) and erythrocyte sedimentation rate 100 mm in the first hour. Pleural fluid aspiration study was suggestive of exudative nature. Culture sensitivity did not show any pathogenic growth. Tuberculosis polymerase chain reaction came to be negative. Pericardial fluid was not drained at that time due to minimal amount and the patient's refusal. All autoimmune markers (antinuclear antibody profile) were negative. He was started on intravenous piperacillin tazobactam and oral linezolid antibiotics. He improved clinically and was discharged after the completion of 7 days course of antibiotics. At the time of discharge, he had only a minimal pericardial effusion and minimal pleural effusion.

After 1 month, he came back to our department for routine checkup. On examination, he was found to be mildly dyspneic and had bilateral pedal edema. TTE was done and it revealed an echogenic structure obscuring the right ventricle view [Figure 1]. CAG was done which revealed normal left main vessel, patent stent in the LAD with good distal flow, diagonals normal, and patent stent in OM with normal flow in the left circumflex (LCX) artery. Two stents were noted in the proximal and mid-RCA. The proximal RCA stent was patent, but there was severe stenosis of the RCA beyond the proximal stent and at the beginning of the second mid-RCA stent almost totally occluding the vessel. A pseudoaneurysm partially filled with thrombus was seen at mid-RCA involving proximal one-third of the mid-RCA stent [Figure 2] and [Figure 3]. The mid-RCA stent showed total in-stent occlusion. The in-stent occlusion extended into the lower mid-RCA. He was referred to the cardiothoracic department for further management. Cardiac computed tomography was done which revealed a large-sized hematoma seen surrounding the pseudoaneurysm measuring approximately 80 mm × 75 mm × 70 mm in the atrioventricular groove indenting the right atrium and the right ventricle. The interventricular septum was displaced to the left with right atrial and superior vena cava dilatation, suggestive of localized tamponade. He was planned for CABG with aneurysm repair. RCA pseudoaneurysm was repaired by direct pledgeted sutures and hemostasis achieved. CABG was not done because of sufficient collaterals to distal RCA, posterior descending artery, and jeopardized anatomy. The patient was discharged after 7 days. He has been doing well till date.
Figure 1: Echogenic structure obscuring the right ventricle view. Arrowed structure is the aneurysmal dilatation of the right coronary artery

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Figure 2: The right coronary artery aneurysm in the left anterior oblique view

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Figure 3: Right coronary artery aneurysm in the right anterior oblique view

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  Discussion Top

The first pathologic description of a CAA was reported in 1761[6] and the first case series in 1929.[7] CAA is defined as a localized dilatation of coronary artery more than 50% diameter of the adjacent normal segment. The definition of giant CAA is still controversial. It is defined as a dilatation that exceeds the reference coronary artery diameter by four times or has a diameter more than 8 mm. The diameter of giant CAAs in adults varies from 50 to 150 mm in various publications, and only a few cases have been described in the literature. This rare entity shows male predominance. It may be fusiform or saccular. CAA is rare, but giant aneurysm is rarer still. The incidence of giant CAA in patients with atherosclerosis is as few as 0.02%. The incidence of giant CAAs according to various literature is reported to be around 52.2% in the RCA, 19.4% in the LAD, 7.4% in the LCX, 13.4% in the left main coronary artery, and 4.5% in combined RCA and LAD.[8] Though in patients with coronary artery disease, CAAs are associated with atherosclerosis, diabetes and chronic hypertension are also contributing factors. The advancement in DES implantation also increases the incidence of CAA as found in this present case report. The DES contains immunoproliferative agents such as sirolimus and paclitaxel, which inhibit cell proliferation with the sole intention to preserve intraluminal stent diameter and patency for longer duration than bare metal stents. The polymer of DES in which drug is embedded may cause hypersensitivity reaction and vasculitis that can erode the vessel wall and weaken the wall, resulting in subsequent dilatation of the segment of coronary artery. Turbulence of blood flow and balloon angioplasty may also injure the vessel wall, which can lead to subsequent CAA formation. This did not appear to be due to differences in pressure during deployment or stent size, suggesting that aneurysms may be the result of an inflammatory reaction to the drug-coated stent. In our case, the development of such CAA may have been due to tissue prolapse in the overlapping stent segment of the RCA. Improper apposition and underlying native nature of the atherosclerotic process may also have aggravated the process of the aneurysm formation. Although covered stent application could have been an option in the management of aneurysm, surgical resection was chosen in this case.

  Conclusion Top

CAA may develop following PTCA due to a lot of factors starting from stent deployment to underuse of medications, improper apposition, length and nature of stents, and missed overlapping segments. High degree of suspicion and proper imaging technology must be used for proper diagnosis and appropriate management.


We thank the patient for giving us consent to report this case.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Markis JE, Joffe CD, Cohn PF, Feen DJ, Herman MV, Gorlin R. Clinical significance of coronary arterial ectasia. Am J Cardiol 1976;37:217-22.  Back to cited text no. 1
Hartnell GG, Parnell BM, Pridie RB. Coronary artery ectasia. Its prevalence and clinical significance in 4993 patients. Br Heart J 1985;54:392-5.  Back to cited text no. 2
Sharma SN, Kaul U, Sharma S, Wasir HS, Manchanda SC, Bahl VK, et al. Coronary arteriographic profile in young and old Indian patients with ischaemic heart disease: A comparative study. Indian Heart J 1990;42:365-9.  Back to cited text no. 3
Principal Investigators of CASS and their Associates: National heart, lung, and blood institute coronary artery surgery study. Circulation 1981;63 Suppl II: Il-1.  Back to cited text no. 4
Stone GW, Ellis SG, Cannon L, Mann JT, Greenberg JD, Spriggs D, et al. Comparison of a polymer-based paclitaxel-eluting stent with a bare metal stent in patients with complex coronary artery disease: A randomized controlled trial. JAMA 2005;294:1215-23.  Back to cited text no. 5
Morgagni JB: De Sedibus et Causis Morborum. Vol 1, book 2, epist 27, art 28. Venice, 1761.  Back to cited text no. 6
Packard M, Wechsler H. Aneurysms of coronary arteries. Arch Intern Med 1929;43:1.  Back to cited text no. 7
Villines TC, Avedissian LS, Elgin EE. Diffuse nonatherosclerotic coronary aneurysms: An unusual cause of sudden death in a young male and a literature review. Cardiol Rev 2005;13:309-11.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3]


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