Ann Thorac Surg 2012;93:2065-2067. doi:10.1016/j.athoracsur.2011.10.068
© 2012 The Society of Thoracic Surgeons
Case Reports
Histopathology of the Longest-Lived Saphenous Vein Graft in a Patient With Kawasaki Disease
Satoru Domoto, MDa,*,
Kiyoharu Nakano, MDa,
Kojiro Kodera, MDa,
Ryota Asano, MDa,
Mariko Fujibayashi, MDb,
Yasuo Takeuchi, MDc
a Department of Cardiovascular Surgery, Tokyo Women's Medical University Medical Center East, Tokyo, Japan
b Department of Surgical Pathology, Tokyo Women's Medical University Medical Center East, Tokyo, Japan
c Department of Cardiovascular Surgery, Nishiarai Heart Center Hospital, Tokyo, Japan
Accepted for publication October 25, 2011.
* Address correspondence to Dr Domoto, Department of Cardiovascular Surgery, Tokyo Women's Medical University, Medical Center East, 2-1-10 Nishiogu, Arakawa-ku, Tokyo, Japan (Email: domoca{at}dnh.twmu.ac.jp).
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Abstract
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The patency rate of saphenous vein grafts (SVGs) for children with Kawasaki disease (KD) tends to decline during the early years after coronary artery bypass grafting (CABG). Although degenerative changes have been considered the main cause of SVG occlusion, there have been no reports on the histopathologic features of the SVG in patients with KD. We herein describe a redo off-pump total arterial revascularization in a 43-year-old man with KD, 34 years after the first CABG using SVG. The histopathologic examination of the longest-lived SVG demonstrated that graft occlusion was mainly caused by the diffuse intimal hyperplasia.
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Introduction
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Coronary artery bypass grafting (CABG) for children with Kawasaki disease (KD) has been performed in Japan since 1974, and saphenous vein grafts (SVGs) were mainly used at the beginning. However the patency rate of SVG has been reported to be less than ideal [1]. Although degenerative changes have been considered the main cause of SVG occlusion [2], there have been no reports on the histopathologic features of the SVG in patients with KD. We herein describe a case of redo off-pump total arterial revascularization in a 43-year-old man with KD 34 years after the first operation, which is probably the longest reported period of SVG patency and the longest interval from the first operation to reoperation. In this report we describe histopathologic findings on the longest-lived SVG in a patient with KD.
A 5-year-old Japanese boy was found to have KD. At the age of 9 years, his echocardiogram showed anterior- and inferior-wall ischemia. Coronary angiography revealed complete occlusion of the right coronary artery, a saccular aneurysm of the proximal left anterior descending artery (LAD) with distal critical stenosis, and a fusiform aneurysm of the left circumflex artery without stenosis. In November 1977, at the age of 9 years (height, 139 cm; weight, 40 kg), our patient underwent CABG using a SVG to the LAD in our institution. Blood transfusion was carried out during this operation, and the patient acquired hepatitis C virus infection. Follow-up coronary angiography performed 7 and 20 years after the operation showed excellent patency with excellent runoff and no obvious growth failure of the SVG [3]. The LAD had undergone complete proximal occlusion, and the cardiac blood supply was dependent on SVG flow.
In April 2011, at the age of 43 years, the patient experienced chest oppression. Coronary computed tomography revealed that the SVG was patent; however distal flow of native LAD from the SVG was not detected (Fig 1). In May 2011, coronary angiography revealed that the SVG was occluded and the distal LAD and distal right coronary arterial branches were opacified by the collateral circulation from the left circumflex artery (Fig 2); therefore we decided to perform a reoperation.
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Fig 2. Coronary angiography showing a saccular aneurysm of the proximal left anterior descending (LAD) artery with (A) distal total occlusion and (B) the occluded saphenous vein graft (SVG).
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On this admission, the patient was 173 cm tall and weighed 122 kg and had hypertension, hyperlipidemia, and a long history of smoking. He also had liver cirrhosis with esophageal varices; therefore we chose the radial artery and not the gastroepiploic artery as the arterial graft to avoid abdominal manipulation. Through a median sternotomy, the left internal thoracic artery was taken down and the left radial artery was harvested. Surgical findings showed that the SVG adapted to the growth of the host by an increase in length and diameter. The left internal thoracic artery was anastomosed to the distal LAD, and the radial artery was anastomosed to the right coronary artery as the aortocoronary bypass.
The postoperative course was uneventful. In the histopathologic examination of the SVG, a diffuse intimal hyperplasia was observed, and luminal occlusion was caused by partial fresh intimal hyperplasia with old thrombosis. The vascular smooth muscle cells in the tunica media were atrophic and had converted to collagen fiber. No obvious migration of vascular smooth muscle cells from the tunica media to the intima and no inflammation or atherosclerotic plaque were seen (Fig 3).
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Fig 3. (A) Resected saphenous vein graft (SVG). (B) Histopathologic findings demonstrate a diffuse intimal hyperplasia and partial fresh intimal hyperplasia (arrow) with old thrombosis (hematoxylin and eosin; x20). (C) The vascular smooth muscle cells (arrow) in the tunica media were atrophic and had converted to collagen fiber. No obvious migration of vascular smooth muscle cells from the tunica media to the intima was observed (elastica van Gieson stain; x40).
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Comment
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Coronary artery bypass grafting for children with KD has been performed in Japan since 1974, and SVGs were mainly used as the graft until the early 1980s. However the patency rate of SVGs for children with KD tends to decline during the early years after CABG. When the patient was younger than 10 years at operation, the patency rate declined more sharply [1]. Therefore some patients have required repeated revascularization using arterial grafts in the follow-up period.
Degenerative changes, which might progress more frequently and more rapidly in small children, and growth failure of the SVG have been considered the main causes of occlusion [2, 4, 5]. Wakisaka and colleagues [2] demonstrated the degenerative changes of the SVG in a patient with KD by measuring the changes in the ratio of the maximum to minimum diameter of the SVG by coronary angiography and evaluating the SVG lumen by intravascular ultrasonographic imaging. In their study, a high ratio of the maximum to minimum diameter of the SVG indicated the likelihood of graft occlusion in the late period, and a major luminal defect with suspected lipid plaque evaluated by intravascular ultrasonographic imaging in the late period was found in a patient with obesity and hyperlipidemia. They also suggested that when SVG patency exceeds 1 year after operation and there is no wall irregularity, it may be possible to preserve long-term patency provided that coronary risk factors such as obesity, hyperlipidemia, hypertension, and smoking are controlled. However they did not report on the histopathologic features of the SVG.
In adults without KD, reports on the SVG histopathologic features indicated that degenerative changes include intimal hyperplasia and subsequent accelerated atherosclerosis [6, 7]. Intimal hyperplasia is defined as abnormal hypertrophy, proliferation, and migration of vascular smooth muscle cells from the tunica media to the intima, with associated deposition of an extracellular connective tissue matrix. Intimal hyperplasia is considered to be caused by the endothelial damage resulting from mechanical injury during operation and hemodynamic stress [6]. The predisposing factors for subsequent atherosclerosis are similar to those in native coronary arteries, including cigarette smoking, hypertension, diabetes mellitus, and hyperlipidemia [7].
Our histopathologic examination of the SVG in a patient with KD demonstrated that the graft occlusion was mainly caused by diffuse intimal hyperplasia and atrophic vascular smooth muscle cells in the tunica media. Although there was no obvious atherosclerosis and migration of vascular smooth muscle cells from the tunica media to the intima, the histopathologic findings for the SVG were similar to those reported in adults without KD. In addition, there was no inflammation and nothing special was used to grow the SVG itself.
These findings suggested that the long-term patency of SVG is not affected by KD but by acquired coronary risk factors. It is also suggested that if the SVG can be manipulated with minimum endothelial damage during the operation and if intimal hyperplasia can be avoided during the early years after CABG, long-term graft patency is possible in patients with KD. In our patient, the first operation was performed at 9 years of age, and follow-up coronary angiography performed 20 years after the operation showed excellent patency and no obvious growth failure of the SVG. However excessive obesity and other coronary risk factors could have had a negative impact on the patency.
In conclusion, we performed a histopathologic examination of the longest-lived SVG in a patient with KD, which demonstrated that graft occlusion was mainly caused by diffuse intimal hyperplasia. We believe that if intimal hyperplasia does not occur during the early years after CABG, long-term patency of the SVG is possible in patients with KD provided that coronary risk factors are properly controlled.
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References
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- Kitamura S, Tsuda E, Kobayashi J, et al. Twenty-five-year outcome of pediatric coronary artery bypass surgery for Kawasaki disease Circulation 2009;120:60-68.[Abstract/Free Full Text]
- Wakisaka Y, Tsuda E, Yamada O, Yagihara T, Kitamura S. Long-term results of saphenous vein graft for coronary stenosis caused by Kawasaki disease Circ J 2009;73:73-77.[Medline]
- Suda Y, Takeuchi Y, Ban T, Ichikawa S, Higashita R. Twenty-two-year follow-up of saphenous vein grafts in pediatric Kawasaki disease Ann Thorac Surg 2000;70:1706-1708.[Abstract/Free Full Text]
- Yoshikawa Y, Yagihara T, Kameda Y, et al. Results of surgical treatments in patients with coronary-arterial obstructive disease after Kawasaki disease Eur J Cardiothorac Surg 2000;17:515-519.[Abstract/Free Full Text]
- Kitamura S. Invited commentary: El-Khouri HM, Danilowicz DA, Slovis AJ, Colvin SB, Artman M: Saphenous vein graft growth 13 years after coronary bypass in a child with Kawasaki disease Ann Thorac Surg 1998;65:1127-1130.[Abstract/Free Full Text]
- Yamada T, Itoh T, Nakano S, Tokunaga O. Time-dependent thickening of the intima in aortocoronary saphenous vein graft: clinicopathological analysis of 24 patients Heart Vessels 1995;10:41-45.[Medline]
- Safian RD. Accelerated atherosclerosis in saphenous vein bypass grafts: a spectrum of diffuse plaque instability Prog Cardiovasc Dis 2002;44:437-448.[Medline]
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Abstract
Introduction
