Sudden Cardiac Death Due to Large Coronary Aneurysm Successfully Treated with a Covered Stent and ChromaFlo Guidance

ABSTRACT: We present the case of a gentleman who presented to our hospital with recurrent episodes of sudden cardiac death treated initially with cardioversion. Immediate coronary angiography revealed a 7 mm aneurysm in the proximal left coronary artery. Using intravascular ultrasound and ChromaFlo™ technology, the aneurysm was successfully treated with a polytetrafluoroethylene-covered stent and the patient had no further episodes of sudden cardiac death.

Coronary artery aneurysms (CAA) are defined as dilatation of a coronary artery greater than 1.5 times the diameter of the adjacent normal segment.¹ CAA has an incidence of 1.4–4.9% in diagnostic coronary angiography² with atherosclerosis accounting for 50% of all cases.³ The remainder of cases may be caused by Kawasaki disease, cocaine, polyarteritis nodosa, sarcoidosis,⁴ infection, dissection, surgical trauma, congenital etiologies and due to angiography and coronary artery stenting.⁵ CAA often present with symptoms of myocardial infarction, angina,⁶ or sudden cardiac death (SCD), with most case reports attributing the sudden death to rupture or thrombosis of the aneurysm.⁷ We present the case of a patient with SCD due to a large proximal left anterior descending (LAD) artery aneurysm that was treated with a covered stent using the guidance of intravascular ultrasound (IVUS) and ChromaFlo™.

Case Report. An 83-year-old gentleman with a history of triple-vessel coronary artery bypass grafting 8 years prior (left internal mammary to the LAD, saphenous vein graft to the obtuse marginal branch of the left circumflex artery, and a saphenous vein graft to the posterior descending artery) suddenly lost consciousness while at home doing the dishes. His wife called 911 and emergency medical services found the patient to be in ventricular tachycardia (Figure 1). He was successfully cardioverted with 100 Joules (synchronized).

While being transported to the hospital, he had 2 more episodes of cardiac arrest with ventricular fibrillation and was successfully defibrillated. Upon arrival at the hospital, he was emergently taken to the cardiac catheterization laboratory. An electrocardiogram obtained after cardioversion (Figure 2A) showed normal sinus rhythm with left bundle branch block. QT was noted to be 484 msec. No prior ECGs were available for comparison.

The arterial and venous grafts were widely patent, but the patient was noted to have a large aneurysm, estimated to be at least 7 mm in diameter, in the proximal portion of the LAD (Figure 2B).

Based on the patient’s clinical presentation, the diagnosis of SCD secondary to CAA was made. In light of published case reports of CAA causing SCD7 and no other apparent etiology for ventricular tachycardia, we elected to percutaneously manage and exclude this aneurysm with a 3.5 mm x 16 mm JoStent™ polytertafluroethylene (PTFE)-covered, balloon-expandable stent (Abbott Vascular, Santa Clara, California).⁸ The institutional review board was notified of our intention to use this device under a humanitarian exemption.

After the patient received anticoagulation with bivalirudin (Angiomax, The Medicines Company, Parsipanny, New Jersey) and antiplatelet therapy with clopidogrel 600 milligrams, coronary intervention was performed. After documenting that the activated clotting time was 350 seconds, a 7 French (Fr) JL4 guide catheter (Cordis Corporation, Miami, Florida) was engaged in the left main coronary artery and a 0.014 inch, 300 centimeter, Asahi Prowater wire (Abbott Vascular) was placed in the distal LAD. Intravascular ultrasound (IVUS) was performed with an Eagle Eye Gold™ IVUS catheter with the addition of ChromaFlo™ imaging (Volcano Corporation, San Diego, California) to document the size and length of the CAA to aid in performing the coronary intervention. The use of ChromaFlo images documented the intraluminal differences between the specific segments in the LAD. The images obtained in the normal component of the LAD (Figure 3A) contrast with the images obtained in the aneurismal segment (Figure 3B).

The lesion proximal to the aneurysm was dilated with a 2.0 mm x 12 mm Maverick balloon (Boston Scientific, Natick, Massachusetts) at 12 atmospheres (atm) followed by a second balloon dilatation with a 2.5 mm x 12 mm Maverick balloon at 12 atm. Attempts were made to place a 3.5 mm x 16 mm JoStent (Abbott Vascular) in the LAD, but due to heavy calcification of the artery, the stent could not be advanced. A 0.014 inch x 182 cm PT2 coronary wire (Boston Scientific) was placed into the first diagonal branch and placement of this wire facilitated passage, via the “buddy wire” technique, of the 3.5 x 16 mm JoStent which was deployed at 14 atm without complications. Repeat angiography revealed patent flow without thromboembolic complications and a sealed aneurysm (Figure 4).

Repeat IVUS demonstrated adequate stent apposition and no blood flow around the stent edges (Figure 5). The patient tolerated the procedure well and had no further episodes of SCD. Given his presenting symptoms, he had an ICD placed and was discharged home on hospital day 3 without any complications. Laboratory evaluation demonstrated normal electrolyte levels with elevated cardiac biomarkers (troponin T, 0.14 ng/ml; reference range

Discussion. This is the first reported case of a native CAA secondary to atherosclerosis causing SCD successfully treated with a covered stent and ChromaFlo. Case reports of SCD due to CAA have been reported in Kawasaki’s disease and are typically related to thrombosis.⁹ In adult cases of sudden death in the setting of CAA, these typically involve rupture of the aneurysm.¹⁰ In this case, there was no evidence of rupture of the aneurysm, but the left bundle branch block on the ECG suggestive of profound LAD ischemia implicated the aneurysm as the thrombus source. This thrombus embolized possibly to the mid LAD, resulting in ventricular tachycardia and SCD. Published reports have documented the presence of large aneurysm arising from saphenous vein grafts,¹¹ but this gentleman had no aneurysms of his SVGs.

The optimal treatment of CAA is controversial due to the various sizes of these lesions as well as the absence of controlled trials. Management is largely based on case reports and operator experience. Surgery, either resection or ligation, is the preferred option for patients with giant aneurysms, defined as more than 2 cm in diameter.¹² Because of the risk of thrombosis and resultant ischemia associated with these lesions, antiplatelet or anticoagulant medication has been advocated in the medical management of CAA.¹³ Surgical and percutaneous coiling of the aneurysms has also been proposed.¹⁴ Although CAA have been increasingly reported as a hypersensitivity reaction complicating drug-eluting stents,¹⁵ PTFE-covered stents have been shown to be effective in the management of CAA.¹⁶ PTFE-covered stents have more traditionally been used in the treatment of perforations of the coronary arteries in the setting of angiography. By placing a long covered stent across the aneurysm, flow into the aneurysm is halted. However, PTFE stents are associated with a higher rate of stent thrombosis and in-stent restenosis compared to non-covered stents¹⁷ and thus the use of antiplatelet therapies and close clinical follow up is warranted. Given that this particular patient presented without any other reason for his multiple SCDs, we emergently treated the aneurysm as the likely culprit in this case. Despite having several SCDs prior to stent placement, he subsequently had no further arrhythmias during his hospitalization.

IVUS can serve as a useful tool in evaluation of CAA due to the detailed images it provides.¹⁸ IVUS also is helpful to distinguish true aneurysms from false aneurysms.¹⁹ In true aneurysm, there is continuity of the medial tissue from the normal coronary segment to the adjacent aneurysm. In contrast, in false aneurysm, the border of the aneurysm wall is seen as adventitial tissue. In this particular case, we utilized a novel imaging technique, ChromaFlo, which elucidated flow patterns and diameter of the vessel. The use of ChromaFlo in this case demonstrated that the aneurysm was not thrombosed which guided management in favor of stenting with an PTFE stent rather than anticoagulation. ChromaFlo is an integrated IVUS-based imaging technology that allows in vivo characterization of blood movement with resultant output as non-directional color-flow images. The ChromaFlo technology captures up to 30 grayscale IVUS frames/second and generates serial comparative assessments of sequential axial images. Differences in the position of echogenic blood particles between images are colorized and represented in real-time as movement of blood. ChromaFlo is a motion detection process; it detects the low intensity moving components (blood) with respect to other stationary ones (the vessel). It is using a signal filtering process (not Doppler) to estimate motion and associate a color intensity (red) according to the level of motion of the tissue at a specific location within the image. The higher the motion or blood flow, the more yellowish the pixel (block) is tinted.²⁰ Both cross-sectional and longitudinal reproductions of this data are captured and displayed. ChromaFlo imaging has been validated both in coronary²¹ and peripheral imaging applications²² and is useful in delineation of dissection planes, differentiation of soft atheroma from blood speckle, assessment of aneurysms and in improving reproducibility of luminal measurements.²³

After stent deployment, IVUS with ChromaFlo demonstrated not only that the stent had good apposition, but that there was no longer any flow in the aneurysm or any blood flow around the stent. This additional imaging confirmed that the aneurysms had been successfully treated. Review of the literature yielded no prior instances when ChromaFlo was used to document successful sealing of a CAA

Conclusion. This is the first reported case of the use of ChromaFlo to guide the evaluation and management of a lethal CAA and ensured optimum approximation of the PTFE-covered JoStent with demonstrable effacement of the aneurysm. This report may help guide future treatment strategies regarding the optimal therapy of CAA.

References

1. Swaye PS, Fisher LD, Litwin P, et al. Aneurysmal coronary artery disease. Circulation 1983;67:134–138.

2. Groenke S, Diet F, Kilter H, et al. Charakterisierung der dilatativen Koronaropathie bei Patienten mit und ohne stenosierende koronare Herzkrankheit. Dtsch Med Wochenschr 2005;130:2375–2379.

3. Nichols L, Lagana S, Parwani A. Coronary artery aneurysm: A review and hypothesis regarding etiology. Arch Pathol Lab Med 2008;132:823–828.

4. Barton JH, Tavora F, Farb A, et al. Unusual cardiovascular manifestations of sarcoidosis, a report of three cases: Coronary artery aneurysm with myocardial infarction, symptomatic mitral valvular disease, and sudden death from ruptured splenic artery. Cardiovasc Pathol 2009;5:1–10.

5. Virmani R, Robinowitz M, Atkinson JB, et al. Acquired coronary arterial aneurysms: An autopsy study of 52 patients. Hum Pathol 1986;17:575–583.

6. Syed M, Lesch M. Coronary artery aneurysm: A review. Prog Cardiovasc Dis 1997;40:77–84.

7. Fineschi V, Reattelli LP, Baroldi G. Coronary artery aneurysms in a young adult: A case of sudden death. A late sequelae of Kawasaki disease? Int J Legal Med 1999;112:120–123.

8. Fineschi M, Gori T, Sinicropi G, Bravi A. Polytetrafluoroethylene (PTFE) covered stents for the treatment of coronary artery aneurysms. Heart 2004;90:490.

9. Kristensen IB, Kristensen BO. Sudden death caused by thrombosed coronary artery aneurysm. Int J Leg Med 1994;106:277–280.

10. Walsh J, Siklos P, Al-Rufaie HK. Massive aneurysm of the right coronary artery causing sudden death. Int J Cardiol 1998;64:213–214.

11. Puri R, Dundon BK, Leong DP, et al. Giant saphenous vein graft pseudoaneurysm rupture presenting with cardiac tamponade. Heart Lung Circ 2009;18:52–54.

12. Jha N, Ouda H, Khan J, et al. Giant right coronary artery aneurysm: Case report and literature review. J Cardiothorac Surg 2009,4:18.

13. Khan IA, Dogan OM, Vasavada BC, Sacchi TJ. Nonatherosclerotic aneurysm of the left circumflex coronary artery presenting with accelerated angina pectoris: Response to medical management: A case report. Angiology 2000;51:595–598.

14. Rath PC, Panigrahi NK, Agarwala MK, et al. Coil embolization of a giant atherosclerotic coronary artery aneurysm. J Invasive Cardiol 1999;9:559–562.

15. Stabile E, Escolar E,Weigold G, et al. Marked malapposition and aneurysm formation after sirolimus-eluting coronary stent implantation. Circulation 2004;110:E47.

16. Fineschi M, Gori T, Sinicropi G, Bravi A. Polytetrafluoroethylene (PTFE) covered stents for the treatment of coronary artery aneurysms. Heart 2004;90:490.

17. Indolfi C, Achille F, Tagliamonte G, et al. Polytetrafluoroethylene stent deployment for a left anterior descending coronary aneurysm complicated by late acute anterior myocardial infarction. Circulation 2005;112:E70–E71.

18. Eshtehardi P, Cook S, Moarof I, et al. Giant coronary artery aneurysm: Imaging findings before and after treatment with a polytetrafluoroethylene-covered stent. Circ Cardiovasc Interv 2008;1:85–86.

19. Pahlavan P, Niroomand F. Coronary artery aneurysm: A review. Clin Cardiol 2006;29:439–443.

20. Written conversation with Dr. Sandra Weiss.

21. Eshtehardi P, Cook S, Moarof I, et al. Giant coronary artery aneurysm: Imaging findings before and after treatment with a polytetrafluoroethylene-covered stent. Circ Cardiovasc Interv 2008;1:85–86.

22. Irshad K, Reid DB, Millar PH, et al. Early clinical experience with color 3-dimensional intravascular ultrasound in peripheral interventions. J Endovasc Ther 2001;8:329–338.

23. Weiss, S, Shah J, Shah F, et al. Addition of non-directional, color-flow significantly improves grayscale intravascular ultrasound diagnostic precision in critical coronary trunk vessel and left main coronary artery stenoses during percutaneous coronary intervention. Abstract presentation at SCAI Annual Scientific Sessions, San Diego, CA, May 7, 2010.

From the University of Chicago, Pritzker School of Medicine, Department of Medicine, Division of Cardiology, Chicago Illinois. The authors report no conflicts of interest regarding the content herein. Manuscript submitted April 20, 2010, provisional acceptance give May 11, 2010, final version accepted May 18, 2010. Address for Correspondence: Atman P. Shah, MD, 5841 South Maryland, MC 6080, Chicago IL 60608. E-mail: ashah5@uchicago.edu