Atherosclerotic aneurysm formation in an in situ saphenous vein graft

Transcription

1 CASE REPORT Atherosclerotic aneurysm formation in an in situ saphenous vein graft J. Jeffrey Alexander, MD, and Yao-Chang Liu, MD, Cleveland, Ohio Nonanastomotic aneurysm formation in autogenous vein grafts, although rarely described, has been uniformly associated with advanced atherosclerotic change of the vein wall. In the case reported, histologic examination of an in sitka vein graft aneurysm demonstrates obliteration of normal vessel wall architecture by penetrating atherosclerotic plaque. Although these findings do not prove a causal relationship, they do provide additional support for atherosclerosis as an etiologic factor in aneurysm disease. (J VASC SURG 1994;20:660-4.) Histologic changes in autogenous vein grafts placed in the arterial system have been recognized since the development of this technique} These changes are characterized by endothelial disruption and subendothelial transformation consisting of medial necrosis, loss of elastic elements, and fibrous proliferation? More advanced atherosclerotic degeneration has been reported as a later finding~ 36 frequently in conjunction with hyperlipidemia 3,6,7 and hypertension. 8.Adthough the pathophysiology of these processes remains obscure, it may be related to the marked alteration in hemodynamic forces to which the arterialized vein is exposed. Manipulation and distention of the vein during harvest may play an additional role, resulting in a loss of endothelial integrity and an increase in cellular proliferation, matrix production, and lipid infiltration. 9,1 It has therefore been postulated that use of in situ venous grafting for arterial reconstruction might reduce fibrointimal and atherosclerotic degeneration of the vein wall.i1 True aneurysm formation is another, although rarely documented, abnormality of vein grafts. In an angiographic follow-up study of 377 autogenous vein grafts to popliteal or infrapopliteal arteries, From the Department of Surgery and the Department of Pathology (Dr. Liu), Case Western Reserve University, Metro- Health Medical Center, Cleveland. Reprint requests: L Jeffrey Alexander, MD, MetroHealth Medical Center, 2500 MetroHealth Dr., Ckveland, OH Copyright 1994 by The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter /94/$ /4] Szilagyi et al. lz found aneurysmal change in 10 of 260 (3.8%) patent grafts. Most of these were mild, and although progressive dilation was seen in 50%, reoperation was not required in any case. In a similar study of 109 femoropopfiteal bypass procedures with saphenous vein grafts, Vanttinen ~3 noted a single nonanastomotic graft aneurysm, which was resected and replaced with an interposition vein graft. This report describes a patient with multiple peripheral arterial aneurysms in whom a true aneurysm developed in the mid portion of an in situ femoral-dorsalis pedis bypass that had been placed 3 years previously forthe treatment of a thrombosed poptiteal artery aneurysm. The finding of advanced atherosclerosis at the aneurysm site suggests that this process was etiologically responsible. CASE REPORT A 65-year-old man was admitted in November 1993 with a 4 cm painless, pulsatite mass in the medial aspect of the right thigh directly above the knee, which was contiguous with an in sire femoral-dorsafis pedis bypass graft. He denied local trauma or infection. His medical history included hypertension, type II diabetes mellitus, a remote inferior wall myocardial infarction, and a one-packper-day smoking habit, which he had discontinued in The patient had previously undergone ligation of a ruptured fight internal iliac artery aneurysm and subsequent elective repair of a fight common femoral artery aneurysm in He did well until 1990, when he was evaluated for right foot rest pain. At that time, he was found to have a thrombosed poptiteat artery aneurysm and a 2.5 cm superficial femoral artery aneurysm, which were surgically excluded and bypassed with a femoral-dorsalis pedis in situ graft. He returned in 1992 with an enlarging

2 JOURNAL OF VASCULAR SURGERY Volume 20, Number 4 Alexander and Liu 661 Fig. 1. Vein graft aneurysm with dilation and gross atherosclerotic involvement of proximal vein (right) and mural thrombus within aneurysm. left popliteal artery aneurysm, which was treated by ligation and arterial reconstruction with an in situ femoral-posterior tibial artery bypass. On present evaluation, the patient was found to be 185 cm in height and 96.6 kg in weight, with a blood pressure of 170/90 mm Hg. A 4 cm pulsatile mass was both visible and readily palpable in the right medial thigh directly above the knee. There was a widening of the pulse in the groin and an easily palpable pulse along the in situ vein graft to the ankle. Laboratory findings included a fasting serum glucose level of 306 mg/dl, creafinine level of 1.4 mg/dl, triglycerides of 238 mg/dl, serum albumen of 3.5 g/dl, serum leukocyte count of /mm 3, and hematocrit of 41.9%, Color-flow duplex scanning of the mass confirmed the presence of a graft aneurysm with intratuminal thrombus. The vein graft appeared to be normal below the knee. At surgical exploration, the patient was found to have diffuse enlargement of the proximal vein graft with extensive aneurysmal widening at the proximal anastomosis and with a true saccular aneurysm containing thrombus at the midportion of the graft above the knee (Fig. 1). This entire segment was replaced with a prosthetic graft. A distal thromboembolectomy was required because of embolization of mural thrombus during manipulation of the aneurysm, but the patient otherwise had an uneventful recovery and was discharged the following week with a palpable dorsalis pedis pulse. Histologic examination of the proximal autogenous vein revealed extensive intimal fibroplasia and moderate to severe atherosclerotic change (Fig. 2). The thickened intima was extensively altered by cholesterol deposits, calcification, ulceration, hemorrhage, and focal thrombus formation (Fig. 3). The medial layer was fragmented, atrophic, and focally separated from the overlying atheromatous plaque by proliferating fibrous connective tissue. The proximal graft wall, immediately adjacent to the aneurysm demonstrated atrophy of the media, with a rim of fibrous tissue extending from the atheromatous mass and replacing the media itself. The adventitial elastic tissue was largely obliterated. Sections from the wall of the aneurysm demonstrated complete replacement of the media and adventitia by dense, avascular connective tissue. The overlying atheroma showed profuse ulceration, thrombus formation, and hemorrhage into the dense connective tissue. These findings suggest an obfiteration of the structural architecture of the vessel wall by invading atherosclerotic plaque, which may be responsible for its weakening and aneurysmal dilation. DISCUSSION Increasing evidence implicates gene-linked variations in connective tissue composition or alterations in metalloproteinase or enzyme activity in the development of some arterial aneurysms. 14,1s However, atheroscterotic degeneration of the arterial wall has traditionally been cited as a primary mechanism of this disease and continues to be promoted by some investigators as a causative factor Aneurysms of arterialized vein grafts occur infrequently and are not necessarily equivalent to their arterial counterparts, but may provide additional insight regarding the pathophysiologic condition of aneurysm formation. A review of previous reports of adequately documented nonanastomotic, nonmycotic vein graft aneurysms demonstrates their occurrence primarily in middle-aged men (78%) with a history of hypertension (71%) and smoking (83%, Table I) Few of these patients had hypercholesterolemia (22%). Three (33%) had a history of arterial aneurysms. Most vein graft aneurysms were discovered as an

3 662 Alexander and Liu JOURNALOF VASCULARSURGERY October 1994 Fig. 2. Graft vessel demonstrates severe atherosclerotic change. Overlying atheromatous plaque shows focal calcification and is covered by a fibrous cap. (Movat's stain; original magnification 20.) Fig. 3. Thickened intima is extensively altered by cholesterol deposits, calcification, and focal thrombus formation. Fragmented and atrophic medial layer is separated from atheromatous plaque by proliferating fibrous connective tissue. (Movat's stain; original magnification 30.)

4 JOURNAL OF VASCULAR SURGERY Volume 20, Number 4 Alexander and Liu 663 Table I. Nonanastomatic aneurysms O f autogenous vein bypass grafts First Patient Cholesterol Size Years to author Age Sex Smoking Hypertension (mg/dl) (cm.) occurrence Graft Davidson is 62 M Yes Yes FP,RSVG De la Rocha I9 63 M NA NA NA FP,RSVG Friedman 2 74 F NA Yes FP,RSVG DeWeese zl 62 M NA NA NA NA 9 FP,RSVG Denton z2 58 M Yes Yes Normal 8 5 FP,RSVG 63 M Quit No Normal 3 6 FP,Cephalic vein Cloud 2s 58 F Yes Yes High FP,RSVG Kelly M No No FP,RSVG Present 61 M Quit Yes 159 ' 4 3 F-DP,In situ FP, Femoropopliteal bypass; RSVG, reversed saphenous vein graft; F-DP, femoral-dorsalis pedis bypass. asymptomatic pulsatile mass, although aneurysmal enlargement with skin ulceration, 24 acute rupture, 22 and thrombosis 22 have also been described. The mean time from initial graft placement to recognition of the aneurysm was 7.4 years; three aneurysms (33%) occurred within 4 years of the original bypass procedure. Characteristic of all vein graft aneurysms was the presence of advanced atherosclerotic change, with subendothelial cholesterol deposition, foamy macrophages, obliteration of the elastic lamina and fibromuscular thickening of the intima. 19,22 It has been suggested that such changes are primarily responsible for weakening of the vascular wall, allowing its aneurysmal dilation in response to arterial pressure. These findings are evident in this case where histologic examination of the resected aneurysm shows progressive obliteration of normal vessel wall structure. In particular, there is destruction of the elastic and connective tissue elements of the media and adventitia because of penetrating atherosclerotic plaque. Although a cause and effect relationship cannot be established on the basis of this examination, aneurysm formation might be attributed to these changes. The history of multiple peripheral artery aneurysms in this patient, all of which were reported to have a similar histologic pattern, would underscore the diffuse nature of this process. It is interesting to note, however, that the patient had not been smoking since his original bypass procedure. His serum cholesterol level was not elevated, his hypertension was medically controlled, and he had shown no recent fluctuation in weight. Use of the in sire technique for arterial reconstruction would theoretically minimize endothelial trauma by reducing operative manipulation, preserving vasovasorum, and eliminating the pressure-induced endothelial desquamation that has been associated with mechanical distention of reversed vein grafts during their harvest. These factors failed to protect this patient from early atherosclerotic degeneration and aneurysm formation of the vein graft. REFERENCES 1. Carrel A, Guthrie CC. Results of bi-terminal transplantation of veins. Am J Med Sci 1906;132: Jones M, Conkle DM, Ferrans VJ, et al. Lesions observed in arterial autogenous vein grafts: light and electron microscopic evaluation. Circulation 1973;48(Suppl 3): Beebe HG, Clark WF, DeWeese JA. Atherosclerotic change occurring in an autogenous venous arterial graft. Arch Surg 1970;101:85-8, 4. Ejrup B, Hiertonn T, Moberg A. Atheromatous changes in autogenous venous grafts. Acta Chir Scand 1961;121: Penn I, Schenk E, Rob C, DeWeese J, Schwartz SJ. Evaluation of the development of athero-arteriosclerosis in autogenous venous grafts insertion into the peripheral arterial system. Circulation 1965;3 l(suppl I): Wyatt AP, Gonzales IE. Atheromatous lesions in arterialized vein grafts. Br J Surg 1969;56: Scott HW Jr, Morgan CV, Bolasny BL, Lanier VC, Younger RK, Butts W. Experimental atherosclerosis in autogenous vein grafts. Arch Surg 1970;101: Wyatt AP, Taylor GW. Vein grafts: changes in the endothelium of autogenous free vein grafts used as arterial replacements. Brit J Surg 1966;53: Bush HL, ~[akubowski JA, Curl GR, Deyldn D, Mabseth DC. The natural history of endothelial structure and function in arterialized vein grafts. Vase Surg 1986;2: Sako Y. Susceptibility of autologous vein grafts to atheromatous degeneration. Surg Forum 1961;12: Buchbinder D, Singh JK, Karmody AM, Leather RP, Shah DM. Comparison of patency rate and structural changes of in situ and reversed vein arterial bypass. J Surg Res 1981;30: Szilagyi DE, Elliott JP, Hageman JI-I, Smith RF, Dall'olmo CA. Biologic fate of autogenous vein implants as arterial substitutes: clinical, angiographic and histopathologic observations in femoro-popliteal operations for atherosclerosis. Ann Surg 1973;178:

5 664 Alexander and Liu JOURNAL OF VASCULAR SURGERY October Vanttinen E. Postoperative changes in bypass vein grafts and collateral arteries after femoropopliteal arterial reconstructive surgery. Acta Chir Scand 1975;141: , Tilson MD. Status of research on abdominal aortic aneurysm disease. J VASC SURG 1989;9: Tilson MD. Atherosclerosis and aneurysm disease. J VAsc SUttG 1990;12: Zarins CK, Glagov S, Vesselinovitch D, Wissler RW. Aneurysm formation on experimental atheroscterosis: relationship to plaque evolution. J VASC SURG 1990;12: Reed D, Reed C, Stenmaerman G, Hayashi T. Are aortic aneurysms caused by atherosclerosis? Circulation 1992;85: Davidson ED, DePalma RG. Atherosclerotic aneurysm occurring in an autogenous vein graft. Am J Surg 1972; 124: De la Rocha AG, Peixoto RS, Baird KJ, Atherosclerosis and aneurysm formation in a saphenous vein graft. Br J Surg 1973;60: Friedman SA, Cerruti MM, Gerstmann KE, Washor H. Aneurysm formation: a late compfication of venous by-pass grafting. Am Heart j 1975;89:366-8, 21. DeWeese JA. Aneurysms of venous bypass grafts in the lower extremities. J Cardiovasc Surg 1975;5: Denton MJ, McCowan MA, Scott DF. True aneurysm formation in femoro-popliteal autogenous vein bypass grafts: two cases. Aust N Z J Surg; 1983;53: Cloud W, Handte G, Kron IL. Atherosclerotic aneurysm formation on a femoro-popliteal saphenous vein graft. South Med J 1984;77: Kelly PH, Julsrud JM, Dyrud PE, Blake DP. Aneurysmal rupture of a femoro-popliteal saphenous vein graft. Surgery 1990;107: Submitted Feb. 9, 1994; accepted April 17, 1994.