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Normal to Normal: A Method of Treatment of Coronary Aneurysms with Deployment of Bare-Metal Stents

Ioannis Iakovou, MD¬ß,  Antonios Dimopoulos, MD¬ß,  George Dangas, MD‚Ć

May 2011

ABSTRACT: Coronary artery aneurysm (CAA) is defined as a coronary dilatation that exceeds the diameter of normal adjacent segments or the diameter of the patient’s largest coronary vessel by 1.5 times. The presence of a CAA is not always without complications. Thrombosis with myocardial infarction, formation of arteriovenous fistulae, vasospasm, and even rupture, may occur especially with very large aneurysms. These complications dictate the need for medical, surgical or percutaneous therapy. The latter consists mainly of the use of polytetrafluoroethylene (PTFE)-covered stents. Compared to PTFE-covered stents, bare-metal stents (BMS) have better flexibility, making implantation in tortuous vessels easier, and permitting access to sidebranches when a bifurcation lesion is involved. Their use in treatment of CAA has rarely been reported. We present three cases with CAA that have been treated with BMS with excellent post-procedure angiographic results and complete exclusion of the aneurysm at mid-term angiographic follow-up.

J INVASIVE CARDIOL 2011;23:E121–E125

Key words: aneurysm, bifurcations, stents

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Coronary artery aneurysm (CAA) is defined as a coronary dilatation that exceeds the diameter of normal adjacent segments or the diameter of the patient’s largest coronary vessel by 1.5 times.1 This is an uncommon disease that has been diagnosed with increasing frequency since the advent of coronary angiography. The incidence varies from 1.5–5%, with male dominance and a predilection for the right coronary artery.1 History of coronary artery disease (CAD), previous myocardial infarction (MI) and presence of aortic aneurysm seems to be significantly more frequent in patients with CAA.2 Atherosclerotic CAD is considered the major cause of their formation3 and congenital or inflammatory origins are also found in 20–30% and 10–20% of cases, respectively.4

The presence of CAA is not always without complications. Thrombosis with MI, formation of arteriovenous fistulae, vasospasm, and even rupture, may occur especially with very large aneurysms.1 These complications dictate the need for medical, surgical or percutaneous therapy. The latter consists mainly of the use of polytetrafluoroethylene (PTFE)-covered stents. Compared to PTFE-covered stents, bare-metal stents (BMS) have better flexibility, making implantation in tortuous vessels easier and permitting access to sidebranches when a bifurcation lesion is involved. Their use in treatment of CAA has rarely been reported.5 We present three cases of CAA treated with BMS, with careful anchoring of the stent edges to “normal” proximal and distal to the lesion segments, with excellent post-procedure angiographic results and complete exclusion of the aneurysms at mid-term angiographic follow-up.

Patient #1. A 71-year-old, male hypertensive with a prior history of triple bypass surgery [left internal mammary to left anterior descending artery (LAD), and saphenous vein grafts (SVG) to circumflex (LCX) and right coronary artery (RCA)] was referred to our department due to angina and clinically positive exercise stress test, with ischemia in the inferior wall in the thallium stress test. The patient underwent coronary angiography, which showed total occlusion of the LAD and circumflex and severe stenosis at the proximal part of the RCA with post-stenotic aneurysm and TIMI-I flow distally (Figure 1A); LIMA and SVG at the LAD and LCX, respectively, were patent and well functioning, while the SVG to the RCA was totally occluded. An ad-hoc percutaneous coronary intervention (PCI) at the RCA was performed. An AL1 guide catheter was used in order to cannulate the artery and after placement of one BMW middleweight and one BMW heavyweight 0.014˝ wire at the distal end of the artery (“buddy” wire technique) and predilation with a 3.0 x 15 mm Maverick balloon (Boston Scientific Corporation, Natick, Massachusetts) at 14–18 atm and a 3.0 x 15 mm Quantum Maverick balloon at 16–26 atm, an attempt was made to advance a 3.0 x 19 mm PTFE-covered Jostent (Abbott Vascular, Abbott Park, Illinois). However, the stent could not be advanced due to lesion severity and pre-stenotic tortuousity. The lesion was then treated with placement of a 3.0 x 18 mm Driver stent (Medtronic, Minneapolis, Minnesota) at 16 atm, which was carefully anchored distally to the aneurysm. The final angiographic result was excellent with no residual stenosis, and normal flow (TIMI-3), while stagnation of the dye at the site of the aneurysm was observed (Figure 1B). A scheduled angiographic follow-up was performed at 4 months, and showed hemodynamically significant in-stent restenosis at the proximal part of the implanted stent, but also complete exclusion of the artery (Figure 1C). The restenotic lesion was treated with predilatation, implantation of a 3.5 x 23 mm Cypher stent (Cordis Corporation, Warren, New Jersey) at 14 atm and post-dilatation with a 3.5 x 8 mm Quantum Maverick balloon at 16–26 atm (Figure 1D). At 2-year follow-up, the patient was asymptomatic with no ischemia at the myocardial scintigraphy.

Patient #2. A 62-year-old female with history of hypertension, diabetes mellitus, systemic lupus erythematosous and recent non-ST elevation MI presented with exertional angina that had worsened over the course of the preceding month and ischemia at the anterolateral wall in the scintigraphy. Coronary angiography revealed aneurysm at the ostium and critical post-aneurysmatic stenosis at the proximal part of the first diagonal branch. There were no additional hemodynamically significant stenoses in the coronary tree (Figures 2A and 2B). A PCI at the bifurcation of the first diagonal branch with wire protection at the LAD was performed. After predilatation with a 2 x 10 mm Sprinter balloon (Medtronic) at 12–16 atm, careful anchoring of a 2.5 x 14 mm Driver stent at 16 atm to the distal non-diseased segment was performed. The final angiographic result was excellent, with dye stagnating inside the aneurysm and the patient was discharged uneventfully the following day (Figure 2C). At 6-month angiographic follow-up, significant in-stent restenosis and complete abolition of the aneurysm was observed (Figure 2D). The restenostic lesion was treated with placement of a 2.5 x 18 mm Cypher stent at 16 atm. After 12 months, the patient was asymptomatic and the myocardial scintigraphy showed no ischemia at the anterolateral wall.

Patient #3. A 56-year-old female with history of hypertention and a mixed connective tissue disease presented with ischemia in the anterior wall (myocardial scintigraphy) and unstable angina. The baseline coronary angiogram revealed a significant stenosis at the proximal LCX artery as well as a sacular aneurysm at the distal LAD artery (Figure 3A). The LAD aneurysm was treated by direct stenting of a 2.5 x 15 mm Tsunami stent (Terumo Corporation, Somerset, New Jersey) at 16 atm which was anchored carefully to the proximal and distal non-diseased segments (Figure 3B). The LCX stenosis was treated with direct implantation of a 3.5 x 13 mm Cypher stent at 14 atm. At 6-month angiographic follow-up, the aneurysm was totally excluded with no evidence of significant restenosis; at 24-month clinical follow-up, the patient was asymptomatic with negative exercise stress tests (Figures 3C and 3D).

Discussion. In this series of three cases, large symptomatic coronary aneurysms have been treated with implantation of BMS with careful anchoring of the stents at the non-diseased segments of the artery. In these cases, the use of PTFE-covered stents was either problematic (i.e., highly calcified proximal lesion, tortuosity) or not indicated (bifurcation lesion). In all 3 cases, the immediate result was stagnation of the dye at the site of the aneurysm. At mid-term angiographic follow-up (4–6 months), all 3 aneurysms had been completely abolished. Two of the 3 patients had target lesion revascularization triggered by in-stent restenosis, which was treated by standard methods and implantation of DES.

The mechanisms responsible for CAA formation during the atherosclerotic process are largely unknown. The matrix metalloproteinases (MMPs) and particularly the MMP-3 5A allele seem to play some role through increased proteolysis of extracellular matrix proteins.5,6 A rare but appreciable cause of CAA is iatrogenic formation after coronary interventions, with a reported incidence of 0.3–6.0%. Residual dissection and deep arterial wall injury (rupture or resection of the vessel media) caused by oversized balloons or stents, high-pressure balloon inflations, atherectomy, and laser angioplasty have all been associated with this complication.7–10

The type of stent implanted seems to play a major role. The incidence of late coronary aneurysm with BMS is 0.2%, compared to 1.4% with DES.11 Late stent malapposition has been observed more frequently after DES implantation and is considered to be a significant cause of coronary aneurysms in 8–10% of cases.12 Alfonso et al analyzed 1,197 consecutive patients with late angiographic evaluation after DES implantation. Coronary aneurysms developed in 1.25% of patients during follow-up. Predictors of aneurysm formation included implantation during acute MI, stent length, and incomplete stent apposition.13

The impetus for the treatment of CAA is predicated on the host of complications associated with these lesions. Angina, MI, and sudden death have been reported even in the absence of CAD.14–16 Other adverse events include thrombosis, thromboembolism, and formation of arteriovenous fistulae, vasospasm, and rupture.1 These complications may be related to turbulent flow associated with aneurysms, though they could also be attendant features of severe coronary artery disease. It has also been postulated that patients with aneurysms and angina can experience a paradoxical worsening of ischemia after using nitroglycerin via a mechanism termed “dilated coronaropathy.”17 Based on these data and the additional need for prolonged dual antiplatelet therapy, we do not think that the exclusion of coronary aneurysms with DES is advisable.

Treatment options consist of surgical, percutaneous, and medical therapy. Controversies persist regarding the use of these three options and the ideal approach has not yet been formally studied. Medical therapy is indicated for the majority of patients and consists of antiplatelet and anticoagulant medication. Surgical or percutaneous CAA repair has been recommended for those patients who are symptomatic or develop complications.18,19

The largest experience in adults has been with surgical management, which typically includes bypass surgery. It seems to be a good approach, especially when aneurysms involve all three coronary vessels or they are too large.20 Based on a CASS substudy, no difference in survival after bypass surgery was noted between patients with CAD and aneurysms (over 500 patients) and CAD alone. Surgical therapy except bypass grafting may also include aneurysm ligation, resection, or marsupialization with interposition graft.21

The percutaneous approach consists of the use of PTFE-covered stents, with very promising results. Szalat et al retrospectively compared outcomes in a series of patients treated with either surgery (n = 18) or PTFE-covered stents (n = 24).22 No deaths were reported in either group. Stent length and aneurysmal size (diameter > 10 mm) were independent risk factors for future restenosis in the percutaneous approach. Important considerations associated with use of PTFE-covered stents include: 1) decreased flexibility, making implantation in tortuous vessels complex; and 2) they are not suitable because of their lack of permeability (they block access to sidebranches when bifurcation lesions are treated).

To overcome these complexities, the use of uncovered BMS has been introduced alone or in combination with PTFE-covered stents. Orlic et al reported a case with a large RCA aneurysm that was sealed with two PTFE-covered stents together with a BMS, using a sequential technique.23 Previously, we used a custom-made bifurcation system to treat a large aneurysm of the proximal LAD involving bifurcation with a diagonal branch. A PTFE-covered stent was used for the main branch and a BMS for the sidebranch, with excellent clinical and angiographic results at 5-month follow-up.24 Ohtsuka et al presented the reduction of the size of a coronary aneurysm after stenting on the proximal stenosis without covering the whole length of the aneurysm, suggesting two possible mechanisms by which stenting might cause this reduction: 1) attenuation of hydrodynamic wall stress on the aneurysm; and 2) the improvement of the degradation of the extracellular matrix structure through the regulation of MMPs.5 We believe that the most probable mechanism is the creation of a laminar stream flow pathway that excludes the aneurysm from most of the blood flow. Thereby, there is low, turbulent flow inside the aneurysm that promotes mural thrombosis, which cannot propagate inside the stent due to the opposite effect of the fast flowing blood.25

Conclusion. Successful percutaneous intervention for the treatment of CAAs can be achieved with the use of a BMS in situations when advancement of PTFE-covered stents is problematic or not indicated. The operator should deploy these devices with special attention to achieve careful anchoring of the stent edges to “normal” proximal and distal to the lesion segments.

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______________________________

From the §1st Cardiology Department, Onassis Cardiac Surgery Center, Athens, Greece, and Cardiovascular Research Foundation, New York, New York.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted July 28, 2010, provisional acceptance given September 13, 2010, final version accepted October 4, 2010.
Address for correspondence: Ioannis Iakovou, MD, 1st Cardiology Department, Onassis Cardiac Surgery Center, 356 Syggrou Ave., 17674, Athens, Greece. Email: iako@hol.gr


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