2/2012
vol. 8
Successful percutaneous management of occluded ”woven” coronary artery: a case report
Postep Kardiol Inter 2012; 8, 2 (28): 168–172
Online publish date: 2012/07/17
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IntroductionWoven coronary artery is a rare congenital abnormality defined as branching of the epicardial coronary arteries into multiple thin channels at any segment which then cross each other and fuse again to form distal reanastomosis [1]. There have been only a few case reports about patients with this morphology [1-8]. We describe a patient with woven left anterior descending (LAD) and circumflex (Cx) coronary arteries.
Case reportA 60-year-old man with the coronary risk factors of hypertension and a history of cigarette use was admitted to our outpatient clinic with resting chest pain. His physical examination was unremarkable. The resting 12-lead electrocardiography was within normal limits. Transthoracic echocardiography revealed left ventricular hypertrophy, mild diastolic dysfunction and hypokinesia of the posterolateral wall with an ejection fraction of 55%.
The patient had undergone exercise stress testing one week ago which demonstrated 2 mm horizontal ST depression in leads V4-6. Coronary angiography was performed and revealed dissected plaques in the proximal segments of the LAD and Cx and total occlusion of the distal segment of the Cx. The other coronary arterial segments were angiographically normal. No interventional therapy was performed; the clinicians had decided to perform revascularization with bypass surgery but the patient refused the surgery.
When we reconsidered the coronary angiogram, we saw a total occlusion in the distal segment of the Cx and a significant ostial stenosis in the second obtuse marginal branch (OM2). The coronary angiogram also showed that the Cx and LAD were subdivided into thin channels with a normal flow rate, which fused again (Figure 1). We described the distal Cx, the proximal segment of the OM2 and mid-LAD artery as woven coronary artery anomaly. Some of the channels forming braid segment in the Cx were occluded with retrograde filling from the LAD. We planned to perform percutaneous coronary intervention (PCI) for the lesions in the distal Cx and ostial OM2.
We performed the sequential Culotte approach for both bifurcation lesions using three stents. This technique could be described as initial stenting of the side branches. The main vessel is wired, dilated and stented through the struts of the first and second stents. Finally, the first and second stents are rewired and sequential final kissing inflations are performed. A 7 Fr Extra back up 3.75 guiding catheter (Launcher, Medtronic Inc, Minneapolis, MN, USA) was used to cannulate the left main artery. Road-map angiograms in right anterior oblique/caudal view revealed occlusion of the channels forming braid segment in the mid Cx with retrograde filling from the LAD (Figure 1). Firstly, the OM2 was wired with a hi-torque Whisper® LS guidewire (Abbott Laboratories, Abbott Park, IL, USA). Another Whisper® LS guidewire was placed in the third OM. A hi-torque Pilot® 150 (Abbott Laboratories, Abbott Park, IL, USA) guidewire was negotiated through the total occlusion. A 1.25 mm × 10 mm over-the-wire angioplasty system (Ryujin Plus®, Terumo, Japan) was used for crossing through the lesion. Some of the thin channels were occluded in the braid segment of Cx so we passed the guidewire through an open channel with the help of an over-the-wire balloon. After passing the occlusion, we performed a puncture and the guidewire re-entered the true lumen in the distal Cx. The coronary angiogram showed immediate dissection spreading OM3 after the puncture. We negotiated another guidewire (a hi-torque Whisper® LS guidewire, Abbott Laboratories, Abbott Park, IL, USA) to recanalize the true lumen. After confirming the second guidewire in the true lumen, the lesion was predilated with subsequent dilatations with a 2.0 mm × 20 mm Maverick® (Boston Scientific, Boston, MA, USA) balloon using 12-14 atm for 15 s to 30 s. A Biolimus-eluting stent (Biomatrix®, Biosensors International GRO, Singapore) 3.0 mm × 18 mm was deployed in the OM3 lesion (Figure 2 A). About 3 mm of the proximal segment of the stent was left protruding into the Cx. The OM2 ostial lesion was predilated with a 2.0 mm × 20 mm Maverick® (Boston Scientific, Boston, MA, USA) balloon. A 2.75 mm × 36 mm Biolimus-eluting stent (Biomatrix Flex®, Biosensors International GRO, Singapore) was advanced across the OM2 ostium and deployed (Figure 2 B). About 5 mm of the proximal segment of the stent was left protruding into the Cx. A hi-torque Pilot® 50 (Abbott Laboratories, Abbott Park, IL, USA) guidewire was passed through the protruding stent struts from the OM2 and OM3 to the distal Cx. Then stent struts were dilated with a 2.0 mm × 20 mm Maverick® (Boston Scientific, Boston, MA, USA) balloon using 14 atm for 15 s. Using the Culotte technique, a 3.5 mm × 36 mm Biolimus-eluting stent (Biomatrix Flex®, Biosensors International GRO, Singapore) was deployed in the Cx trunk with maximum inflation pressure of 10 atm (Figure 2 C). Post-stent dilatation was performed with a 3.0 mm × 15 mm non-compliant balloon (Quantum Maverick®, Boston Scientific, Boston, MA, USA) in both obtuse marginal branches and with a 3.5 mm × 15 mm non-compliant balloon (Quantum Maverick®, Boston Scientific, Boston, MA, USA) in the Cx with maximum inflation pressure of 20 atm. Finally, simultaneous kissing balloons were inflated in the OM3 and the Cx using two non-compliant balloons (3.5 mm × 15 mm and 3.0 mm × 15 mm Quantum Maverick®, Boston Scientific, Boston, MA, USA) with maximum inflation pressure of 12 atm in both (Figure 3 A). The same procedure was performed for OM2 and Cx bifurcation (Figure 3 B). The final angiogram demonstrated an excellent angiographic result without any residual stenosis or dissection in the Cx (Figure 4).
His further stay in the hospital was uneventful, and he was discharged after 2 days on dual anti-platelet therapy with aspirin, and clopidogrel for at least a year, as well as an angiotensin-converting enzyme inhibitor, a -blocker and a statin.
DiscussionWoven coronary anomaly is an uncommon congenital malformation characterized by the branching of a major epicardial artery into thin channels, which then merge again in order to form the main lumen after twisting along the coronary artery axis [4-6]. The distance of the abnormal segment is limited so the downstream coronary blood flow distal to the woven segment is absolutely normal. This morphology has been previously described only in a few patients [1-7]. In most of the cases, the right coronary artery is affected but it could be visualized in the LAD and Cx. Because of its common misinterpretation as intracoronary thrombus, spontaneous coronary dissection or bridging collaterals of chronic total coronary arterial occlusion, the frequency of this anomaly is underestimated [5]. The etiology is unknown and it is generally accepted as a benign condition and medical surveillance is recommended for these cases [6]. On the other hand, Martuscelli et al. postulated that the coronary blood could be reduced to form an intracoronary thrombus [1]. Also, we speculated that increased shear stress in the narrow braid segments could accelerate atherosclerosis. The present case had unstable angina despite optimal medical therapy so we performed PCI for the stenotic lesions in the Cx artery.
In conclusion, although it is an uncommon malformation, the case reported above shows that woven coronary artery anomaly can be misdiagnosed by interventional cardiologists. So, clinicians performing angiography should obtain multiple projections to discriminate malformation and anomalies from pathological conditions and be very careful in interpreting angiograms. Also, thrombotic lesions could develop in the braid segment of this anomaly and PCI could be performed successfully in case of ischemia.
Acknowledgments
Published with the written consent of the patient. No external funding and no competing interests declared. The authors would like to thank Prof. Dr. Omer Goktekin for all his input and guidance on this case report.
References 1. Martuscelli E, Romeo F, Giovannini M, et al. Woven coronary artery: differential diagnosis with diffuse intracoronary thrombus. Ital Heart J 2000; 1: 306-307.
2. Sane DC, Vidaillet HJ Jr. "Woven" right coronary artery: a previously undescribed congenital anomaly. Am J Cardiol 1988; 61: 1158.
3. Berman AD, Kim D, Baim DS. "Woven" right coronary artery: case report and therapeutic implications. Cathet Cardiovasc Diagn 1990; 21: 258-259.
4. Gregorini L, Perondi R, Pomidossi G, et al. Woven left coronary artery disease. Am J Cardiol 1995; 75: 311-312.
5. Kursaklioglu H, Iyisoy A, Celik T. Woven coronary artery: a case report and review of literature. Int J Cardiol 2006; 113: 121-123.
6. Iyisoy A, Celik T, Yuksel UC, et al. Woven right coronary artery: a case report and review of the literature. Clin Cardiol 2010; 33: E43-45.
7. Kaya D, Kilit C, Onrat E. An uncommon congenital anomaly of coronary arteries misdiagnosed as intracoronary thrombus: woven coronary artery disease. Anadolu Kardiyol Derg 2006; 6: 383-384.
8. Yildirim A, Og˘uz D, Olguntürk R. Woven right and aneurysmatic left coronary artery associated with Kawasaki disease in
a 9-month-old patient. Cardiol Young 2010; 20: 342-344.
Copyright: © 2012 Termedia Sp. z o. o. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License ( http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
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