Operative balloon angioplasty in the treatment of internal carotid artery fibromuscular dysplasia

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1 Operative balloon angioplasty in the treatment of internal carotid artery fibromuscular dysplasia Louis L. Smith, M.D., Douglas C. Smith, M.D., J. David Killeen, M.D., and Anton N. Hasso, M.D., Loma Linda, Calif. Seven patients with symptomatic fibromuscular dysplasia have had eight internal carotid arteries treated by operative balloon dilatation. This technique is described in detail and provides three distinct advantages over conventional graduated intraluminal dilatation-- atraumatic passage of the catheter through the affected vessel with fluoroscopic guidance; precise dilatation of the involved segment of the internal carotid artery; and the appfication of a radial force against the arterial wall rather than a longitudinal shear force, thereby making intimal damage less likely. There were no treatment complications in this group of patients. This technique of balloon angioplasty is compared with the results of treatment in eight patients with fibromuscular dysplasia of the internal carotid artery, who had percutaneous transfemoral angioplasty. Long-term follow-up revealed the resolution of symptoms in all patients. (J VAse St3R6 1987;6:482-7.) The usual surgical procedure used in the management of symptomatic fibromuscuiar dysplasia (FMD) of the internal carotid artery is graduated intraluminal dilatation with calibrated metal probes. We believe that this procedure is somewhat "blind" and prone to injure the blood vessel wall, particularly in those high lesions adjacent to the base of the skull. Intimal damage and false passage with subintimal dissection are real possibilities. We have used operative balloon dilatation to minimize these complications. This procedure allows accurate placement of the dilating instrument with fluoroscopic guidance and applies the dilating force radimly against the vessel wall, thereby reducing the chance, of complications. The dilatation is performed with the carotid bifurcation exposed and opened, which provides a back flush after dilatation to minimize the likelihood of cerebral embolization. This article describes our operative management of internal carotid artery FMD and reports the longterm follow-up in these patients. PATIENTS AND FINDINGS Eight internal carotid artery dilatations were performed in seven patients and form the basis of this From the Departments of Surgery and Radiation Sciences, School of Medicine, Loma Linda University. Presented at the Second Annual Meeting of the Western Vascular Society, Tucson, Ariz., Jan , Reprint requests: Louis L. Smith, M.D., Department of Surgery, Loma Linda University, Loma Linda, CA article. All patients had symptomatic FMD of the internal carotid artery; Table I summarizes the important data from these cases. The average age of these patients was 60 years and all were female. The presenting symptoms were hemispheric transient ischemic attacks (TIAs) in six patients and nonhemispheric TIAs in one. The one patient who had bilateral carotid dilatations appeared first with left hemispheric symptoms that were relieved by percutaneous balloon angioplasty; right hemispheric symptoms developed 5 years later, which required operative balloon angioplasty of the opposite side. Each patient in this series had bilateral carotid bruits. One of the seven patients had a neurologic deficit at the initial physical examination, which consisted of loss of fine coordination of the hand with persistent difficulty in writing after an initial mild upper extremity monoparesis. The potential for cerebral embolization from these irregular arteries seems probable and in this case the focal nature of the preoperative stroke suggests this origin. None of the remaining patients had neurologic deficits when examined. Carotid dilatation was performed with the patient under general endotracheal anesthesia. The carotid bifurcation was exposed through a flexion crease incision. Silicone rubber (Silastic) vascular loops were placed around the common, external, and internal carotid vessels. The G-arm fluoroscope was then positioned about the patient's neck, after which a small longitudinal incision was made in the internal carotid

2 Volume 6 Number 5 November 1987 Balloon angioplasty to treat internal carotid artery FMD 483 Table I. Summary of seven patients with fibromuscular dysplasia of the internal carotid artery treated by operative balloon angioplasty Age Patient (yr) Sex Symptoms and signs Angiographic findings Operative treatment Follow-up duration 1 50 F Rt hemiparesis, aphasia, Bilat. ICA FMD Lt ORD 1971 Recurrent symptoms bilat, bruits Rt ORD Rt hemiparesis Recurrent high Lt FMD Lt OBD 3/30/81 with short segmental (68 mo) Bilat. carotid bruits dissection from previous graduated intraluminal dilatation Rt amaurosis fugax Lt Recurrent FMD Rt ICA Rt OBD 2/10/86 Aymptomatic hemiparesis Resected 1.8 cm CCA (9 mo) 2 62 F Residual Rt upper FMD both ICA Lt OBD 8/18/81 extremity monoparesis (64 mo) with difficulty writing; Subsequent Rt transfemoral Lt hemiparesis, bilat, balloon dilatation carotid bruits 2/17/ F Lt amaurosis fugax, Rt Bilat. ICA FMD-high Lt OBD 3/31/83 hemiparesis and numbness Rt hand; bilat. carotid bruits 4 69 F Rt arm and leg weakness; Bilat. ICA FMD Lt OBD 2/8/82 with visual "gray out"; Lt resection 2 cm CCA carotid bruit 5 76 F Numbness with weakness; Bilat. ICA FMD Lt OBD 10/5/84 Rt side of body; Resected 2 cm CCA bilat, carotid bruits 6 50 F Lt hemiparesis with Lt Bilat. ICA FMD; bilat. Rt OBD 12/10/84 facial weakness and dys- renal artery FMD phasia; bilat, carotid hypertension bruits 7 54 F Bilat. irregular lines in Bilat. ICA FMD Rt OBD 3/13/86" vision; bilat, carotid Percutaneous angioplasty bruits (45 mo) (58 mo) (26 too) (24 mo) (9 mo) ICA = internal carotid artery; CCA = common carotid artery; OBD = operative balloon dilatation; FMD = fibromuscular dysplasia; ORD = operative rigid dilatation. *The nondominant ICA was empirically dilated in this patient with nonhemispheric symptoms. bulb. A standard mm angiographic guide wire was then inserted into the internal carotid artery while the common and external carotid vessels were occluded with vascular clamps and the internal carotid vascular loop was tightened. After precise placement of the guide wire to the base of the skull, a 7F Gruentzig balloon catheter was inserted over the guide wire and placed in accurate position for internal carotid dilatation. The balloon was inflated until it achieved a tubular, nonindented configuration. The pressure balloon inflation was between 5 and 7 atm. After this shape was maintained for 15 to 45 seconds, the balloon was deflated. A second similar inflationdeflation process was immediately performed. The Silastic snubbers were then relaxed and the catheter was removed. Brisk back-bleeding allowed washout of any debris that might otherwise have embolized into the cerebral circulation. Additional technical details are described elsewhere.1 In those cases in which the dysplastic segment was longer than the dilating balloon, the catheter was repositioned in an overlapping fashion for a second dilatation. The arteriotomy incision was closed with a 6-0 polypropylene (Prolene) suture. Angiography was routinely performed after dilatation to document the adequacy of the procedure after a satisfactory angiogram. The neck incision was closed. No arteriotomy incision in this series had to be reopened for further dilatation. Fig. 1 shows a typical preoperative angiogram demonstrating internal carotid FMD. The postoperative on-table angiogram is shown in Fig. 2 and demonstrates satisfactory disruption of fibrous septa. FMD was associated with a redundant internal carotid artery and kinking in three patients. Each of these patients required resection and anastomosis of a segment of the common carotid artery (see Table I for operative details). Fig. 3 shows an angiogram of a representative patient with this problem. Operative balloon dilatation as described earlier was

3 484 Smith et al. Journal of VASCULAR SURGERY i i~i! Fig. 1. Arteriogram reveals typical "beaded" appearance of fibromuscular dysplasia involving upper cervical portion of the internal carotid artery (arrows). followed by resection of a 2 cm segment of the terminal common carotid artery. Reanastomosis followed, with 5-0 Prolene sutures. Fig. 4 shows the postoperative angiogram in this patient. The only operative complication was a temporary subintimal dissection produced by contrast injection during ontable angiography. There were no postoperative neurologic complications in these patients. DISCUSSION We do not believe that FMD is a benign disease in the symptomatic patient. Effeney et al.2 in their large series of 86 patients reported a 22% incidence of completed strokes when the patients came for treatment. Stewart et al. 3 took a more conservative approach and have evaluated 14 patients who initially had focal ischemia and who were not treated surgically; all became asymptomatic with the exception of one patient. These authors reported that most of Fig. 2. After operative balloon dilatation the internal carotid artery appears smoother. these patients were treated with platclet inhibitors. Regardless of the threat of stroke, one must consider the stress and inconvenience caused by the focal symptoms. Each patient in this series either had disabling visual deficits or transient paralysis. Relief of symptoms of this severi~ seems to us to be adequate justification for the operative dilatation hercin described. Only symptomatic patients with what appeared to be flow-limiting disease were selected for the operation described herein. Operative balloon dilatation offers three advantages over graduated intraluminal dilatation. With the aid of fluoroscopic monitoring, the guide wire and subsequent balloon catheter can atraumatically traverse the entire dysplastic arterial segment. Fluoroscopic monitoring allows dilatation to occur at precisely the correct location, a crucial consideration for lesions at the base of the skull. The dilating force is applied radially rather than as a longitudinal shear

4 Volume 6 Number 5 November 1987 Balloon angiqolasty to treat internal carotid artery FB'U) 485 Fig. 3. Arteriogram reveals not only typical "beads" and "webs" offibromuscular dysplasia (arrows) but a prominent kink at the level of C-2 and C-3. force and is therefore less likely to produce intimal damage. The longitudinal shear force of the rigid metal dilator and the tortuous dysplastic internal carotid artery makes perforation a hazard during graduated intraluminal dilatation. Krupski et al.4 reported such a case occurring during this procedure. Effeney et al.2 reported the case of a 47-year-old man who had a right-sided hemiparesis 2 months after graduated intraluminal dilatation. An arteriogram obtained at that time showed what appeared to be an intimal tear high in the internal carotid artery thought to be the source of an embolus. We noted a false passage on a cerebral angiogram in patient 7 (Table I); she had graduated intraluminal dilatation at another hospital 10 years previously. One of us (A. N. H.) has previously reported percutaneous transfemoral angioplasty of internal carotid artery FMD in eight patients. One patient had transient middle cerebral ischemia during the pro- Fig. 4. After operative balloon dilatation dysplastic defbrmities have resolved. Prominent kink is no longer present after segmental resection of the distal common carotid artery. cedure but recovered completely in 20 minutes, s He no longer advises the percutaneous transfemoral approach but recommends the operative technique herein described. Jooma, Bradshaw, and Griffin s have reported intimal dissection of the internal carotid artery complicating a transfemoral balloon angioplasw done to treat FMD. There was one technical error of no serious consequence in our series. The surgeon shif[ed the 18- gauge catheter (Intracath) for the postdilatation angiogram from a retrograde direction in the common carotid artery to an antegrade position within the internal carotid artery in an effort to obtain better opacification of this vessel. The subsequent injection produced a subintimal dissection (Fig. 5). The patient awakened from anesthesia without symptoms. One week later, during a bilateral renal

5 486 Smith et al. Journal of VASCULAR SURGERY Fig. 5. A prominent dissection (arrowheads) resulted from antegrade placement of the Intracath into the internal carotid artery for the operative arteriogram. Irregularity over its proximal 2 cm is also evident. angiogram performed because of hypertension, a selective carotid angiogram was obtained (Fig. 6). There was no evidence of residual intimal injury. It is the policy of our angiography team never to make any injection directly into a recently dilated artery because of the presence of postdilatation intimal fissures and the likelihood of an injection producing a subintimal dissection. The prcsence of a trained angiographer to pass a guide wire through the tortuous dysplastic internal carotid segment has been of great benefit to the surgical team. Some of these vessels can present a real challenge to negotiate and properly position the guide wire for subsequent dilatation. We believe in the "team approach" in the management of this disease. Open internal carotid artery dilatation for FMD as described has been safe and effective in this small Fig. 6. Spontaneous healing of the internal carotid artery is shown at 1 week. series of patients. Each patient became asymptomatic after dilatation of the internal carotid artery, appropriate to the hemispheric symptoms, and has remained so to date with a mean follow-up time of 42 months (range 9 to 68 months). It is hoped that more centers dealing with this curious disease will heed the suggestion made by Effeney et al.2 and pool information in a national registry on the natural history of asymptomatic patients and the results of therapy in symptomatic patients to provide a better understanding of this significant internal carotid artery disease. REFERENCES 1. Smith DC, Smith LL, Hasso N. Fibromuscular dysplasia of the internal carotid artery treated by operative bauoon angioplasty. Radiology 1985;155: Effeney JD, Ehrenfeld WK, Stoney RJ, Wylie EJ. Why operate on carotid fibromuscular dysplasia? Arch Surg 1980;115: Stewart MT, Moritz MW, Smith RB III, Fulenwider Jr, Per-

6 Volume 6 Number 5 November 1987 Balloon angioplasty to treat internal carotid artery FMI) 487 due GD. The natural history of carotid fibromuscular dysplasia. J VAsc SURG 1986;3: Kmpski WC, Effeney DJ, Ehrenfeld WK. Fibromuscular dysplasia, aneurysms, and carotid artery. In: Bergan JJ, Yao JST, eds. Cerebrovascular insufficiency. New York: Grune & Stratton, Inc, 1983: Hasso AN, Bird CR. Percutaneous translummal angioplas W of carotid and vertebral arteries. In: Jang GC, ed. Angioplasty. New York: McGraw-Hill Book Co., 1986: Jooma R, Bradshaw JR, Griffin HB. Intimal dissection fbllowing percutaneous transluminal carotid angioplas9' for fibromuscular dysplasia. Neuroradiology 1985;27: LIEBIG FOUNDATION AWARD FOR VASCULAR SURGICAL RESEARCH, 1988 The Liebig Foundation announces the seventh annual competitive award of $fi000 for the best essay on a problem in general vascular surgery. The investigative work shall be: 1. Clinical or experimental research 2. Original and unpublished 3. Performed by a house officer in the United States, Canada, or Mexico with senior collaborators acting in a consultive capacity 4. Submitted in English (6 copies of typed manuscript and 6 copies of glossy prints of illustrations) 5. Accompanied by a signed letter from the essayist's superior confirming the status of the essayist Previous winners were: 1987, Peter D. Cahill, M.D., Stanford University School of Medicine, Stanford, Calif.; 1986, Axel W. Joob, M.D., University of Virginia Medical Center. The winning essay will be judged for presentation at the June 1988 meeting of the North American Chapter, International Society for Cardiovascular Surgery and will be considered for publication in the Joum'~AL. Further inquiries may be directed to the same address to which the essays must be sent, postmarked before Dec. 31, 1987: Dr. Richard J. Turner Award Committee Secretary 112 Bauer Drive Oakland, NJ USA (201)

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