Coronary artery bypass grafting in a patient with antiphospholipid syndrome

Coronary artery bypass grafting in a patient with antiphospholipid syndrome

Ann Thorac Surg 1996;61:739-40 CASE REPORT SAKAKIBARAET AL CABG IN ANT1PHOSPHOLIPIDSYNDROME 739 Coronary Artery Bypass Grafting in a Patient With A...

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Ann Thorac Surg 1996;61:739-40

CASE REPORT SAKAKIBARAET AL CABG IN ANT1PHOSPHOLIPIDSYNDROME

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Coronary Artery Bypass Grafting in a Patient With Antiphospholipid Syndrome Naoki Sakakibara, MD, Michio Kawasuji, MD, Yasushi Matsumoto, MD, Hirofumi Takemura, MD, a n d Yoh Watanabe, MD Department of Surgery (I), Kanazawa University School of Medicine, Kanazawa, Japan

We report a 32-year-old female patient with antiphospholipid syndrome including severe coronary artery disease and multiple arterial and venous thrombosis. The patient had occlusion of the right internal thoracic artery, diffuse stenosis of the left internal thoracic artery, and occlusion of the left saphenous vein. The patient underwent successful coronary artery bypass grafting using the right gastroepiploic artery and a segment of the right saphenous vein. Antiphospholipid syndrome should be considered in young patients with myocardial infarction. (Ann Thorac Surg 1996;61:739-40) A

clinical s y n d r o m e with w i d e s p r e a d arterial a n d venous thrombosis, associated with antibodies directed against phospholipids, was initially described as anticardiolipin s y n d r o m e in 1983 [1] a n d is now called a n t i p h o s p h o l i p i d syndrome. Although association with mitral valve involvement is striking in a n t i p h o s p h o l i p i d s y n d r o m e [2], a characteristic association b e t w e e n increased concentrations of a n t i p h o s p h o l i p i d antibodies a n d recurrent cardiovascular events in y o u n g survivors of myocardial infarction was also r e p o r t e d [3]. Here we report a case of severe coronary artery disease with a n t i p h o s p h o l i p i d s y n d r o m e , w h i c h was successfully m a n a g e d by myocardial revascularization using the gastroepiploic artery (GEA). A 32-year-old w o m a n h a d s u d d e n chest pain and consciousness loss in January 1994. The patient h a d no history of venous thrombosis or recurrent abortion a n d there were no clinical features of systemic lupus erythematosus. Electrocardiogram showed acute inferior myocardial infarction. Life-threatening arrhythmias and cardiac arrest occurred. During cardiac resuscitation, hypotension, hypoxemia, a n d severe respiratory acidosis were p r o l o n g e d a n d multifocal cerebral infarction developed, from which the patient recovered by rehabilitation. Brain magnetic resonance imaging showed a t r o p h y of the h i p p o c a m p u s and multiple lacunar lesions in the Accepted for publication Aug 1, 1995. Address reprint requests to Dr Sakakibara, Department of Surgery (1), Kanazawa University School of Medicine, 13-1 Takaramachi, Kanazawa 920, Japan.

© 1996 by The Society of Thoracic Surgeons Published by Elsevier Science lnc

Fig 1. Preoperative angiogram showing a diffuse irregularity up to 50% stenosis of the left internal thoracic artery (left) and a totally occluded right internal thoracic arte~ (right).

corticocerebral layer. Technetium-99m and iodine-123 J3-methyl i o d o p h e n y l pentadecaoic acid myocardial scintigram s h o w e d d e c r e a s e d perfusion in the anteroseptal a n d inferior wall of the heart. The e c h o c a r d i o g r a m showed no a b n o r m a l findings of the mitral valve. Coronary a n g i o g r a p h y d e m o n s t r a t e d complete occlusion of the right coronary artery, and the left circumflex artery, and a 75% stenosis in the left anterior d e s c e n d i n g artery. The left internal thoracic artery h a d a diffuse irregularity with up to 50% stenosis, whereas the right internal thoracic artery was totally occluded (Fig 1). Laboratory data were negative for antilupus erythematosus antibody. The a n t i - D N A antibody level was 3.9 IU/mL and the positive-anticardiolipin antibody (immunoglobulin G) level was 170 GPL units (normal; <20 GPL units), whereas activated partial thromboplastin time was prolonged to 39.4 seconds and thrombocyte a n d s e r u m lipid levels were normal. The patient u n d e r w e n t coronary artery bypass grafting on May 25, 1994. Because both internal thoracic arteries were not available, the right GEA was used for the left anterior d e s c e n d i n g coronary artery. The right GEA was 2.0 m m in d i a m e t e r a n d had a good free flow. The left greater s a p h e n o u s vein was totally thrombosed. A segm e n t of the right s a p h e n o u s vein was used for the left circumflex coronary artery. The right coronary artery was not graftable. After discontinuation of c a r d i o p u l m o n a r y bypass, the flow, m e a s u r e d by a transit-time ultrasonic blood flowmeter (Transonic, Ithaca, NY), was 38 m L / m i n in the right GEA and 23 m L / m i n in the s a p h e n o u s vein graft. The patient s h o w e d an uneventful recovery and was free of symptoms. Coronary a n g i o g r a p h y 1 month

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CASE REPORT SAKAKIBARA ET AL CABG IN A N T I P H O S P H O L I P I D SYNDROME

Fig 2. Postoperative angiogram of right gastroepiploic artery (GEA), which bypassed the left anterior descending artery (LAD). after the operation showed a patient right GEA (Fig 2) a n d s a p h e n o u s vein graft. Histologic examination of the ascending aorta s h o w e d m i l d arteriosclerosis, a n d that of the occluded s a p h e n o u s vein s h o w e d thrombophlebitis. A s e g m e n t of the GEA s h o w e d mild intimal thickening. Comment The original description of anticardiolipin s y n d r o m e included arterial a n d venous thrombosis, stroke, migraine, livedo reticularis, r e c u r r e n t abortion, a n d occasional t h r o m b o c y t o p e n i a [1]. The major heart complication is valvular disease (particularly mitral valve involvement) and myocardial infarction [2]. H a m s t e n a n d co-workers [3] found that one fifth of all y o u n g patients with myocardial infarction had increased a n t i p h o s p h o l i d a n t i b o d y levels a n d a large proportion of patients with high a n t i p h o s p h o l i p i d a n t i b o d y levels experienced additional cardiovascular events during a follow-up of 3 to 5 years. Morton and co-workers [4] d e s c r i b e d a correlation between p r e o p e r a t i v e anticardiolipin a n t i b o d y levels a n d the incidence of late vein graft occlusion. However, another study d e m o n s t r a t e d no correlation b e t w e e n the prevalence and significance of coronary artery disease a n d anticardiolipin a n t i b o d y levels [5]. A recent study s u g g e s t e d that a subset of a n t i p h o s p h o l i p i d antibodies reacted with a complex of p h o s p h o l i p i d s a n d the s e r u m protein ]32-glycoprotein I, the cofactor that inhibits factor XII activation, platelet activation, and p r o t h r o m b i n a s e activity [6]. This interference m a y cause a potent predisposition to prothrombotic diathesis.

A n n Thorac Surg 1996;61:739-40

Vasculopathy in a n t i p h o s p h o l i p i d s y n d r o m e was rep o r t e d to be acute, w i d e s p r e a d , n o n i n f l a m m a t o r y vascular occlusion, a n d m a y be associated with intimal thickening a n d medial h y p e r t r o p h y of large a n d mediu m - s i z e d vessels due to endothelial d a m a g e [7]. Because the p r e s e n t patient was y o u n g a n d had a t e n d e n c y t o w a r d thrombosis, arterial grafts, which have a high p a t e n c y rate for the long-term period, are preferable. A l t h o u g h the internal thoracic artery is r e g a r d e d as the first choice for grafting the left anterior d e s c e n d i n g coronary artery, both internal thoracic arteries were unavailable in the p r e s e n t case. Fortunately, the right GEA was not diseased a n d was used as an alternative conduit for the left anterior d e s c e n d i n g coronary artery. The GEA was used as an in situ arterial conduit to b y p a s s the distal right coronary artery a n d left circumflex system. The distal left anterior d e s c e n d i n g artery is a possible target for GEA grafting. Mild proximal stenosis of the coronary artery m a y affect graft flow a n d long-term patency. As the p r e s e n t case s h o w e d 75% stenosis of the left anterior d e s c e n d i n g coronary artery, careful observation for graft prognosis is necessary in addition to anticoagulation against thrombosis. Although low-dose aspirin is the logical first-line medication, there is little d o u b t that patients with high anticardiolipin antibody concentrations a n d previous major thrombosis require long-term, possibly life-long anticoagulation [8]. References 1. Hughes GRV. Thrombosis, abortion, cerebral disease, and the lupus anticoagulant. Br Med J 1983;287:1088-9. 2. Cervera R, Khamashta MA, Font J et al. High prevalence of significant heart valve lesions in patients with the "primary' antiphospholipid syndrome. Lupus 1991;1:43-8. 3. Hamsten A, Norberg R, Bjorkholm M, De Faire U. Antibodies to cardiolipin in young survivors of myocardial infarction: an association with recurrent cardiovascular events. Lancet 1986; 8473:113-5. 4. Morton KE, Gavaghan TP, Krilis SA, et al. Coronary artery bypass graft failure--an autoimmune phenomenon? Lancet 1986;8520:1353- 6. 5. Tsakiris DA, Marbet GA, Burkart F, Duckert F. Anticardiolipin antibodies and coronary heart disease. Eur Heart J 1992;13:1645-8. 6. McNeil HP, Simpson RJ, Chesterman CN, Krilis SA. Antiphospholipid antibodies are directed against a complex antigen that includes a lipid-binding inhibitor of coagulation: /32 1 (apolipoprotein H). Proc Natl Acad Sci USA 1990;87: 4120-4. 7. Harris EN. An acute disseminated coagulopathy-vasculopathy associated with the antiphospholipid syndrome. Arch Intern Med 1991;151:231-2. 8. Hughes GRV. The antiphospholipid syndrome: ten years on. Lancet 1993;342:341-4.