Vascular Medicine and Endovascular Interventions - part 9 pptx

CHAPTER 26 Renal and Mesenteric Arterial Stenosis 263 Renal function at the time of stent placement strongly predicts patency and expected survival after intervention. In patients with normal renal function, 3-year survival is 94%, 74% if serum creatinine is between 1.5 and 2.0 mg/ dL, and 52% if serum creatinine is greater than 2.0 mg/ dL. • The cure rate with angioplasty for renal artery fi bromuscular dysplasia is approximately 25%, and some improvement can be expected in approximately 40% • Stent placement is now the preferred treatment for most patients with atherosclerotic renal artery disease • The technical success rate for renal artery stent placement for atherosclerotic stenosis is >90% • The restenosis rate is 15%-20% after renal artery angioplasty and stenting; improvement in blood pressure control can be expected in >50% and stabilization or improvement in >60% Imaging the Renal Arteries Conventional angiography is still considered the best anatomic study for evaluating patients with renal artery stenosis. Duplex ultrasonography can be very helpful and should be the fi rst imaging study in patients suspected of having renal artery stenosis. The quality of renal ultrasonography depends on the operator and on other vari- ables such as body habitus, but even so, the sensitivity of duplex scanning has been reported to be 98%, with 98% specifi city and high positive and negative predictive val- ues. In many practices, computed tomography angiography (CTA) is now replacing conventional angiography as the anatomic test of choice for evaluating renal arteries. The images are comparable to those of conventional angiography, vessels can be evaluated in three dimensions, and CTA offers options for clarifying anatomy which may be better than with conventional angiography. Exposure of the patient to radiation from renal CTA is comparable to that from catheter angiography. Magnetic resonance angiography (MRA) is also a good test to evaluate the anatomy of the renal arteries. It has lower resolution than CTA or conventional angiography but is excellent for patients with impaired renal function because the contrast agent (gadolinium) is relatively non- nephrotoxic. Mesenteric Arterial Occlusive Disease This discussion will focus on atherosclerotic lesions, which are responsible for more than 90% of all cases of chronic mesenteric ischemia. It is crucial to understand the basic vascular supply to the bowel. The supply from the stom- ach to the distal rectum is provided by 3 major vessels: the celiac artery, the superior mesenteric artery, and the inferior mesenteric artery. A rich collateral vascular bed exists between these three vessels. Asymptomatic stenosis of one or more of the three arteries is not uncommon; one angiographic study showed more than 50% stenosis of either the celiac or superior mesenteric artery in 27% of asymptomatic patients. The usual symptom of chronic mesenteric ischemia is abdominal pain, which typically starts 30 minutes after food intake (postprandial pain) and may last for up to 3 hours. Patients exhibit “food fear” with resultant weight loss. Epidemiology Chronic mesenteric ischemia is rare, with an incidence of only 2 to 4 patients per 100,000, and affects mostly elderly women. Acute mesenteric ischemia accounts for approximately 0.1% of all hospital admissions. Estimates suggest that only 20% to 50% of these patients have underlying mesenteric artery stenosis. Most patients with atherosclerotic mesenteric artery stenosis have classic symptoms of chronic mesenteric ischemia before acute occlusion develops. This allows for corrective intervention—either surgical or endovascular—on the mesenteric vessels, thus averting an acute event. • Chronic mesenteric ischemia is more common in elderly women • The incidence of chronic mesenteric ischemia is low (2-4 per 100,000 patients) Etiology The cause of chronic mesenteric ischemia in most cases (>90%) is atherosclerosis, but many other causes have been associated with the condition (Table 26.2). Approxi- mately half of patients with chronic mesenteric ischemia also have signifi cant coronary artery disease and peripheral vascular disease. • Atherosclerotic changes in the central mesenteric arteries are the most common causes of chronic mesenteric ischemia • A large proportion of patients with chronic mesenteric ischemia have coronary or carotid artery disease Natural History Even less is known about the natural history of chronic mesenteric ischemia than about that of renal artery stenotic disease. The disease is progressive, and some patients with mesenteric artery stenosis eventually have symptoms of chronic mesenteric ischemia. In a 1998 study Vascular Medicine and Endovascular Interventions 264 of 60 patients with severe angiographic mesenteric stenosis, four (7%) had development of mesenteric ischemia, one of whom presented with acute mesenteric ischemia and subsequently died. These four patients belonged to a cohort of 15 (27%) that had three-vessel disease (superior mesenteric, celiac, and inferior mesenteric artery). None of the other patients had symptoms of mesenteric ischemia during the study period. The mortality rate for patients with asymptomatic mesenteric arterial stenosis is high. Over a mean follow-up of 2.6 years, 40% of the patients in one study (29 of 72, 12 with less severe disease) died from other causes and only one from acute mesenteric ischemia. Although highly controversial, the practice of prophylactic intervention in asymptomatic patients with signifi cant three-vessel mesenteric artery stenosis is recommended by the authors of this study. They also suggest that patients with asymptomatic one- or two-vessel disease be followed up closely. • Patients with silent mesenteric arterial stenosis of two or more arteries should be followed up on a regular basis; there are currently no data to support intervention in asymptomatic patients • Patients with mesenteric artery stenosis have a high mortality rate from other causes Endovascular Treatment Surgical management has traditionally been the treatment of choice for chronic mesenteric ischemia, but endovascular therapy (angioplasty alone or with stent placement) has become commonplace in the management of these patients. The outcomes are highly variable, with frequent complications (19%-54%) and signifi cant mortality (0%- 17%) after surgical repair. Surgical options include endarterectomy and bypass using synthetic or autologous conduits. Most atherosclerotic lesions occur in the ostium or the fi rst two to three centimeters of the vessel but can extend into the more distal aspects in some patients (Fig. 26.4). Initial technical success after endovascular repair is typically greater for ostial lesions (95%) than for more distal lesions. Most reports indicate technical success rates between 88% and 100%, with long-term symptom relief in the range of 61% to 91%. The restenosis rate is relatively low, with primary patency rates of 60% to 85% and secondary patency rates up to 100%. Recurrence rates are higher for celiac intervention, possibly because of the cru- ciate ligament, which may compress a stent in the celiac artery. Angioplasty and stent placement are not advocated for the treatment of celiac artery stenosis caused by compression by the median ligaments. A recent paper on stenting the superior mesenteric and/ or celiac artery in 14 patients reported technical success in 17 of 18 treated arteries (94%). No perioperative deaths or major morbidity was reported; mean hospital stay was 2 days. The mean length of follow-up was 13 months, during which restenosis developed in 8 patients (57%), with a mean of 9 months from the initial procedure to the time of reintervention. Seven patients were treated with repeat angioplasty or placement of an additional stent. Subse- quent fatal acute mesenteric ischemia developed in one of the patients. A recent abstract from Mayo Clinic reported outcomes of surgical and endovascular treatment for chronic mesenteric ischemia in 229 consecutive patients. Surgical revascularization was performed in 146 patients (265 vessels) and endovascular revascularization with either angioplasty alone or angioplasty and stent placement was performed in 83 patients (105 vessels). Surgical revascularization resulted in higher early morbidity and longer hospitalization but no greater mortality than in the endovascular group. Incidences of recurrent symptoms and restenosis were signifi cantly higher, and reintervention was needed more commonly, in the endovascular group than in the surgically treated group. The recommendation was that surgical revascularization should be offered to “good risk” patients, whereas endovascular revascularization should be reserved for patients who were at high surgical risk. • Surgical bypass is the preferred therapy for most patients with low surgical risk and chronic mesenteric ischemia Cause Affected segment Incidence, % Atherosclerosis Ostium and fi rst portion 90 Median arcuate ligament compression syndrome Ostium celiac >> superior mesenteric artery <5 Fibromuscular dysplasia Main artery <5 Takayasu arteritis Ostium and proximal part of artery <1 Giant cell arteritis (temporal arteritis) Main artery <1 Radiation All <1 Thromboangiitis obliterans All <1 Mesenteric vein thrombosis Venous <1 Table 26.2 Causes of Chronic Mesenteric Arterial Occlusion CHAPTER 26 Renal and Mesenteric Arterial Stenosis 265 • Clinical success for mesenteric artery angioplasty and stenting is in the range of 60%-90% Imaging the Mesenteric Arteries Angiography is still regarded as the gold standard for arterial imaging of the mesenteric arteries. Over the past 5 to 10 years, considerable progress has been made in both CTA (with introduction of multislice scanners) and MRA. Ultrasonography with Doppler should still be the fi rst imaging study for suspected chronic mesenteric arterial disease. Color Doppler can identify narrow areas of the vessels, but Doppler peak-velocity measurements give an accurate indication of the severity of the vascular disease. For mesenteric arterial disease, a peak systolic velo city of more than 275 cm/s, either in the celiac or superior mesenteric artery, predicts a 70% stenosis with a sensitivity of 92% and a specifi city of 96%. Like renal duplex ultrasonography, this technique is dependent on operator experience and patient body habitus. In recent years, CTA has become an excellent tool for anatomic evaluation of the mesenteric circulation. This is largely due to the multislice CT scanners that can cover the entire body in less than 10 seconds and obtain sub-mil- limeter resolution. MRA is also a good study for anatomic evaluation but does not have the resolution of CTA or conventional angiography and may therefore be somewhat less predictable. Questions 1. Which statement regarding fi bromuscular dysplasia is true? a. It is more common in men. b. The renal arteries are the only affected visceral arteries. c. It can be seen in the iliac arteries. d. Fibromuscular dysplasia usually resolves by age 20 years. 2. Which of the following can cause renal artery stenosis? a. Neurofi bromatosis b. Radiation c. Trauma d. Takayasu arteritis e. All of the above 3. Which statement is true? a. Aneurysms are common complications of fi bromuscular dysplasia. b. Atherosclerosis constitutes approximately 10% of all renal artery stenoses, and fi bromuscular dysplasia, 90%. c. Atherosclerotic stenoses are most common in the main body of the main renal artery rather than at the ostium. Fig. 26.4 Preprocedural and postprocedural images of angioplasty and stent placement for mesenteric artery stenosis. A, Lateral aortography showing tight stenosis of the celiac axis origin and the superior mesenteric artery origin caused by atherosclerosis. (The head is toward the top of the image.) B, After placement of balloon-expandable stents across both ostial stenoses, a good lumen was restored with subsequent good clinical response. BA Vascular Medicine and Endovascular Interventions 266 d. “String of beads” is a phrase often used for angiographic changes seen with neurofi bromatosis. 4. Which statement is true regarding endovascular treatment of renal artery stenosis? a. For renal artery stenosis caused by atherosclerosis, angioplasty alone is usually suffi cient treatment. b. After angioplasty for renal artery stenosis caused by fi bromuscular dysplasia, hypertensive cure can be expected in more than 95% of cases. c. Atherosclerotic stenosis of the renal artery ostium is now almost uniformly treated with stent placement. d. Three-year survival cannot be predicted by preprocedural creatinine value in patients undergoing renal artery intervention. 5. Regarding chronic mesenteric ischemia, which statement is true? a. The majority of patients with chronic mesenteric ischemia are women. b. An important artery for chronic mesenteric ischemia is the inferior epigastric artery. c. Coronary disease is rare in patients with chronic mesenteric ischemia. d. Almost no collateral circulation exists between the major mesenteric arteries. 6. Which is not true of chronic mesenteric ischemia and its management? a. Most mesenteric artery stenoses are central or ostial. b. Stent placement is not indicated for median arcuate ligament compression syndrome. c. Clinical success can be expected in 60%-90% of patients treated with angioplasty and stenting for chronic mesenteric artery ischemia. d. Patients with chronic mesenteric ischemia rarely die from other causes. Suggested Readings Alhadad A, Mattiasson I, Ivancev K, et al. Revascularisation of renal artery stenosis caused by fi bromuscular dysplasia: ef- fects on blood pressure during 7-year follow-up are infl uenced by duration of hypertension and branch artery stenosis. J Hum Hypertens. 2005;19:761-7. Brown DJ, Schermerhorn ML, Powell RJ, et al. Mesenteric stenting for chronic mesenteric ischemia. J Vasc Surg. 2005;42:268-74. Caps MT, Perissinotto C, Zierler RE, et al. Prospective study of atherosclerotic disease progression in the renal artery. Circula- tion. 1998;98:2866-72. Caps MT, Zierler RE, Polissar NL, et al. Risk of atrophy in kid- neys with atherosclerotic renal artery stenosis. Kidney Int. 1998;53:735-42. Chobanian AV, Bakris GL, Black HR, et al, National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National High Blood Pressure Education Program Coordi- nating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treat- ment of High Blood Pressure: the JNC 7 report. JAMA. 2003 May 21;289:2560-72. Epub 2003 May 14. Erratum in: JAMA. 2003;290:197. Cleveland TJ, Nawaz S, Gaines PA. Mesenteric arterial ischaemia: diagnosis and therapeutic options. Vasc Med. 2002;7:311-21. Mounier-Vehier C, Lions C, Jaboureck O, et al. Parenchymal consequences of fi bromuscular dysplasia renal artery stenosis. Am J Kidney Dis. 2002;40:1138-45. Razavi M, Chung HH. Endovascular management of chronic mesenteric ischemia. Tech Vasc Interv Radiol. 2004;7:155-9. Safi an RD, Textor SC. Renal-artery stenosis. N Engl J Med. 2001;344:431-42. Salifu MO, Haria DM, Badero O, et al. Challenges in the diagnosis and management of renal artery stenosis. Curr Hypertens Rep. 2005;7:219-27. Sharafuddin MJ, Olson CH, Sun S, et al. Endovascular treatment of celiac and mesenteric arteries stenoses: applications and results. J Vasc Surg. 2003;38:692-8. Slovut DP, Olin JW. Fibromuscular dysplasia. N Engl J Med. 2004;350:1862-71. Tan KT, van Beek EJ, Brown PW, et al. Magnetic resonance angiography for the diagnosis of renal artery stenosis: a meta- analysis. Clin Radiol. 2002;57:617-24. Thomas JH, Blake K, Pierce GE, et al. The clinical course of asymptomatic mesenteric arterial stenosis. J Vasc Surg. 1998;27:840- 4. van de Ven PJ, Kaatee R, Beutler JJ, et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomised trial. Lancet. 1999;353:282-6. van Jaarsveld BC, Krijnen P, Pieterman H, et al, Dutch Renal Ar- tery Stenosis Intervention Cooperative Study Group. The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. N Engl J Med. 2000;342:1007-14. Watson PS, Hadjipetrou P, Cox SV, et al. Effect of renal artery stenting on renal function and size in patients with atherosclerotic renovascular disease. Circulation. 2000;102:1671-7. Zalunardo N, Tuttle KR. Atherosclerotic renal artery stenosis: current status and future directions. Curr Opin Nephrol Hy- pertens. 2004;13:613-21. 267 27 Endovascular Therapy for Brachiocephalic Vessels David P. Slovut, MD, PhD, FACC J. Michael Bacharach, MD, MPH, FACC fi bromuscular dysplasia, giant cell arteritis, and radiation- induced arteriopathy. Atherosclerosis is the most common cause of large vessel stenosis. Occasionally, small vessel obstruction occurs as ulcerated plaques from the large vessel stenoses shower emboli to the digits, producing painful focal discoloration of the fi ngertips, splinter hemorrhages, or livedo reticular- is. Atherosclerosis affects the left subclavian artery three to fi ve times more often than the right. Most lesions are proximal to the origin of the vertebral artery, whereas 10% involve the artery both proximal and distal to the vertebral artery and 10% are found distal to the origin of the vertebral artery. Takayasu arteritis (also known as aortic arch arteritis and “pulseless disease”) is a chronic, idiopathic vascu- litis involving the aorta, great vessels, and coronary and pulmonary arteries. It occurs predominantly in women, with higher prevalence rates reported in Asian and South American countries. Fibromuscular dysplasia is a non- atherosclerotic, non-infl ammatory vascular disease that most commonly affects the renal and internal carotid arteries. In the upper extremities, fi bromuscular dysplasia is identifi ed most frequently in the subclavian arteries but has been described in the brachial and axillary arteries. Giant cell arteritis, also referred to as temporal arteritis, predominates in women older than 60 years. The disease produces a spectrum of symptoms including headache, vision loss, and intermittent jaw and tongue claudication. Giant cell arteritis involves the subclavian, axillary, or brachial arteries in 15% of cases. Other causes of upper extremity ischemia include drugs (e.g., cocaine, ergotamine, methamphetamine), collagen vascular disease, iatrogenic injury, and thoracic outlet syndrome (TOS), which may present as a neurologic syndrome diagnosed by electromyography. In less than 5% of cases, TOS results from a vascular abnormality caused by compression of the subclavian artery or vein. Patients are often young and may report arm ache and fa- Subclavian and Innominate Artery Intervention Anatomy The aortic arch typically gives rise to three great vessels: the brachiocephalic trunk, which bifurcates into the right subclavian artery and right common carotid artery; the left common carotid artery; and the left subclavian artery. In 20% to 30% of the population, the brachiocephalic trunk and left common carotid artery share a common origin. In 7% of persons, the left common carotid artery arises as a branch off the innominate artery, a variant known as a bo- vine arch. Arch anomalies include left arch with aberrant right subclavian artery (0.4%-2.0% incidence), right arch with aberrant left subclavian artery (the most common type of right arch and a frequent cause of symptomatic vascular ring), and right arch with mirror-image branch- ing (associated with cyanotic congenital heart defects). • In 20%-30% of cases, the brachiocephalic trunk and left common carotid artery share a common origin • Upper extremity occlusive disease accounts for only 5%-6% of all cases of limb ischemia, much less frequent than lower extremity ischemia Etiology of Occlusive Disease Upper extremity occlusive disease occurs much less frequently than disease of the lower extremity, accounting for only 5% to 6% of all cases of limb ischemia. Several types of subclavian artery occlusive disease (with different causes) are amenable to percutaneous revascularization, including that due to atherosclerotic disease, Takayasu arteritis, © 2007 Society for Vascular Medicine and Biology Vascular Medicine and Endovascular Interventions 268 tigue, particularly when raising the arm above the head. Patients with proximal thrombosis or distal embolization may present with Raynaud syndrome, ulceration of the digits, or gangrene. Non-invasive testing with thoracic outlet maneuvers can provoke symptoms or signs of arterial compression. TOS is not amenable to percutaneous revascularization; cervical or fi rst rib resection is required to relieve the compression. • In less than 5% of cases, TOS results from a vascular abnormality caused by compression of the subclavian artery or vein • TOS is not amenable to percutaneous revascularization; cervical or fi rst rib resection is required to relieve the compression Indications for Intervention Patients with upper extremity ischemia may report symptoms such as arm or hand claudication, arm paresthesias, or rest pain. Lower limb ischemia is sometimes seen in patients who have undergone extra-anatomic bypass such as axillofemoral bypass grafting. Infl ow disease is an uncommon but important cause of late graft failure. Up to 25% of patients who undergo axillofemoral bypass grafting have signifi cant atherosclerotic disease in the infl ow arteries. In vertebral-subclavian steal syndrome, upper extremity exertion leads to retrograde vertebral fl ow and neurologic symptoms including vertigo, syncope, ataxia, diplopia, motor defi cits, and intermittent arm claudication. In coronary-subclavian steal syndrome, blood is diverted from the coronary circulation to the arm via the internal mammary artery graft during arm exercise. Symptoms include angina or infarction. The syndrome can be diagnosed by an image-based stress test (nuclear, echocardiographic, or magnetic resonance imaging [MRI]) after arm exercise. • In vertebral-subclavian steal syndrome, upper extremity exertion leads to retrograde vertebral fl ow and neurologic symptoms including vertigo, syncope, ataxia, diplopia, motor defi cits, and intermittent arm claudication • In coronary-subclavian steal syndrome, blood is diverted from the coronary circulation to the arm via the internal mammary artery graft during arm exercise Subclavian artery stenosis is associated with a favorable natural history. Many patients with high-grade stenosis and mild upper extremity claudication become asymptomatic as collaterals develop. In asymptomatic patients, subclavian intervention may be performed before coronary artery bypass grafting using the internal mammary artery or extra-anatomic bypass grafting, or to preserve infl ow to the internal mammary artery in patients who may undergo bypass in the future. In patients with other brachiocephalic lesions, especially concomitant carotid artery disease, it may be reasonable to revascularize the subclavian artery. To date, no prospective, multicenter, randomized trials of subclavian artery intervention have been performed. Retrospective case series have demonstrated reasonable durability, with patency rates of 75% to 85% at 35- to 60-month follow-up. Patient Assessment and Treatment Subclavian artery stenosis is considered signifi cant if the pressure difference between arms is more than 20 mm Hg. Segmental arm pressures and Doppler waveforms can be measured above the elbow, below the elbow, and above the wrist while insonating the radial artery at the wrist. Abnor- mal waveforms and decreased pressures at the above-elbow cuff site indicate subclavian or axillary artery occlusive disease. Digital plethysmography may show a peaked waveform in vasospasm and a damped waveform in occlusive disease. Elevated velocities in the stenotic segment and a peak velocity ratio of more than 5.5 by duplex ultrasonography are consistent with greater than 75% diameter stenosis. Several specifi c ultrasonographic fi ndings are seen in steal syndrome: reversal of vertebral fl ow throughout the cardiac cycle, bidirectional vertebral fl ow (forward in systole, retrograde in diastole), and normal fl ow with the patient at rest. In the latter two situations, inducing arm hyperemia by infl ating a blood pressure cuff to suprasystol- ic pressure for 5 minutes may unmask steal phenomenon. With cuff defl ation, patients with steal have fl ow reversal or biphasic vertebral fl ow. Computed tomography angiography (CTA), magnetic resonance angiography (MRA), or invasive angiography of the aortic arch and great vessels can be used to determine the extent of brachiocephalic artery involvement and aid in planning revascularization. During invasive angiography, the left anterior oblique view is useful for delineating the left subclavian artery, whereas the right anterior oblique view with caudal angulation permits visualization of the innominate bifurcation. Before the advent of percutaneous transluminal angioplasty, surgical revascularization was the primary therapeutic modality for patients with symptomatic subclavian artery occlusive disease. Commonly used extrathoracic methods for subclavian artery revascularization include carotid-subclavian, carotid-axillary, or axillo-axillary bypass using polytetrafl uoroethylene or polyethylene terephthalate grafts and subclavian-carotid transposi- tion. Surgical repair produces excellent long-term patency (>90%) with low morbidity and mortality. For catheter-based therapy, arterial access is obtained via the femoral artery in most cases. The brachial approach or combined femoral and brachial approach can be useful in treating patients with total subclavian artery occlusion. After access is achieved, heparin should be administered CHAPTER 27 Endovascular Therapy for Brachiocephalic Vessels 269 until the activated clotting time is greater than 250 seconds; alternatively, bivalirudin can be used. Although it has not been reported specifi cally for subclavian intervention, bivalirudin has been associated with a low rate of ischemic events and bleeding in patients undergoing renal, iliac, and femoral artery intervention. The stenotic lesion is crossed with a 0.035-in guidewire. If the brachial approach is used, the guidewire can be advanced into the abdominal aorta, snared, and exteriorized via a groin sheath, a maneuver that permits the use of a smaller brachial artery sheath. A 7F guiding sheath is positioned across the stenosis. Lesions may be treated with balloon angioplasty alone or stenting, although long-term patency is greater with stenting (Fig. 27.1). If possible, the stent should be positioned to avoid covering the vertebral artery. Balloon-expandable stents are preferable for use with ostial lesions, whereas self-expanding nitinol stents are favored for tortuous vessels and lesions distal to the vertebral artery where stent compression is possible. Va- sospasm is treated with intra-arterial nitroglycerin (200 µg) or papaverine (10-40 mg). Antiplatelet therapy should consist of aspirin, 325 mg orally per day indefi nitely, and clopidogrel, 300 mg loading dose followed by 75 mg orally for 4 weeks after stenting. • Subclavian artery stenosis is considered signifi cant if a pressure gradient >20 mm Hg is found between brachial artery measurements Fig. 27.1 Angiographic images of balloon angioplasty and stenting of upper extremity arteries. A, Composite image shows contrast injection via the left main coronary artery with dye traveling retrograde up the internal mammary artery graft to fi ll the distal left subclavian artery. B, Selective injection of the left subclavian artery shows critical stenosis. The vertebral artery, but not the internal mammary artery, is seen in this injection. C, After balloon angioplasty, wide luminal patency is re-established. The internal mammary artery graft now fi lls antegrade. C B A Vascular Medicine and Endovascular Interventions 270 • Retrograde vertebral artery fl ow persists briefl y after dilating subclavian artery lesions, which protects the posterior circulation from emboli; consequently, use of embolic protection devices is not warranted • Technical success rates for treating stenotic lesions are >90%, whereas the rate for total occlusions is 50%-60% in most series; the rate for major adverse events (e.g., stroke and death) is 2% Distal embolic complications are infrequent. Retrograde vertebral artery fl ow can persist briefl y after dilating subclavian artery lesions, which may protect the posterior circulation from emboli. Consequently, use of embolic protection devices is usually not warranted. In general, the vertebral artery remains patent if it originates from a non- stenotic segment of the subclavian artery. If associated vertebral artery stenosis is present, or if the subclavian lesion encroaches on the vertebral artery, the artery should be protected with a guidewire during subclavian artery dilatation. If the vertebral artery is compromised, simultane- ous infl ation using kissing technique may be performed. Treatment of ostial right subclavian stenoses merits placement of a safety wire in the common carotid artery. For restenotic lesions, balloon angioplasty, cutting balloon angioplasty, or repeat stenting may be performed. Technical success rates for treating stenotic lesions are greater than 90%, and the rate for total occlusions is 50% to 60% in most series. Major adverse events (e.g., stroke and death) occur in less than 2%. Minor complications include transient ischemic attack, distal embolization to the arm or hand, reperfusion edema with or without compartment syndrome, and access-related brachial artery thrombosis. Long-term results are excellent, with primary patency rates higher than 90% at 1 year and secondary patency rates of 80% to 90% at 5 years. In Takayasu arteritis, medical therapy consists of cor- ticosteroids and antiplatelet agents. Revascularization is indicated for severe cerebral or upper extremity ischemia. Ideally, revascularization is performed during the quies- cent phase of the disease. In patients with active disease (e.g., fever, musculoskeletal pain, or elevated erythrocyte sedimentation rate), prednisone (1 mg/kg per day) should be administered before intervention and continued for 6 months. Methotrexate (7.5 mg/wk) may be added in patients who are unresponsive to prednisone. Compared with patients with atherosclerosis, those with Takayasu arteritis are younger, more likely to be female, and present with upper extremity claudication rather than gangrene. In contrast to atherosclerotic disease, Takayasu arteritis produces diffuse transmural fi brotic arterial lesions that typically require higher infl ation pressures to dilate. Al- though long-term symptomatic relief is excellent, restenosis occurs in 26% of patients. Disease activity should be controlled strictly with immunosuppressive therapy. In patients with giant cell arteritis, case reports suggest excellent immediate and long-term outcome with upper extremity balloon angioplasty. Innominate Artery Occlusive Disease Innominate artery occlusive disease is seen infrequently. When present, it is often accompanied by carotid or subclavian artery stenosis. In contrast to carotid artery occlusive disease, the natural history of innominate artery occlusive disease is poorly understood. Patients may present with an asymptomatic blood pressure disparity between arms, or with upper extremity claudication, cerebrovascular steal, transient ischemic attack, or stroke. Transthoracic surgical repair consists of aorto-innominate bypass or aortocarotid bypass with reimplantation of the subclavian artery. In- nominate endarterectomy and cervical reconstruction are used less commonly. Transthoracic operation is preferred in patients with embolic disease who require exclusion of the embolic source and revascularization of the distal innominate artery. Graft patency is excellent. The combined stroke and death rate is up to 16%. Overall patient survival after transthoracic reconstruction is 73% at 5 years and 52% at 10 years. Percutaneous revascularization with balloon angioplasty alone or stenting provides excellent medium-term patency (>90%) with low morbidity and mortality. Aneurysmal Disease Aneurysms of the subclavian and axillary arteries are seen in atherosclerotic disease, trauma, vasculitides, and TOS. Covered stents have been used for more than a decade to treat abdominal aortic aneurysms and have been used suc- cessfully to exclude subclavian artery aneurysms. Trauma, whether blunt or penetrating, can produce a spectrum of injuries ranging from intimal tear to pseu- doaneurysm to complete transection. Traditionally, most vascular injuries to the head and neck warrant surgical repair. An aneurysm is seen in 60% of patients with an aberrant subclavian artery (Kommerell diverticulum). The abnormality may be discovered incidentally or during investi- gation for symptoms such as cough and progressive dysphagia for solids (dysphagia lusoria). Surgical treatment is indicated because of the risk of rupture. Vertebral and Basilar Artery Intervention Anatomy The blood supply to the medulla, pons, and mid brain is derived from the vertebrobasilar system. The vertebral CHAPTER 27 Endovascular Therapy for Brachiocephalic Vessels 271 artery is divided into four segments: V1 (extraosseous, extending from its origin to the transverse foramen of C 6 ), V2 (foraminal, extending from the transverse foramen of C 6 to C 1 ), V3 (extraspinal, extending from the exit of the transverse foramen of C 1 to the foramen magnum), and V4 (intradural, extending from the foramen magnum to the basilar artery) (Fig. 27.2). The left vertebral artery is domi- nant in 75% of the population and arises directly from the aorta in 1% to 5%; pronounced tortuosity of the V1 segment is observed in 40%. The basilar artery arises from the confl uence of the vertebral arteries. The posterior inferior cerebellar artery (PICA) typically originates from the intradural segment of the vertebral artery but can arise from the extracranial vertebral artery 5% to 18% of the time. In 0.2% of cases, the vertebral artery has an anomalous end- ing at the PICA. In rare cases, the PICA is absent and the ipsilateral anterior inferior cerebellar artery supplies the territory. • The blood supply to the medulla, pons, and mid brain is derived from the vertebrobasilar system • Symptoms of posterior circulation ischemia include diplopia, blurred vision, vertigo, gait disturbance, episodic perioral numbness, or drop attacks Extracranial Vertebral Artery Occlusive Disease In general, vertebrobasilar territory ischemia results from luminal compromise of both vertebral arteries or their infl ow vessels (i.e., synchronous innominate and left subclavian artery lesions). Mechanisms of vertebrobasilar ischemia include embolization from the aorta or heart, thrombotic cerebral ischemia from ulcerated plaque, and low-fl ow states, in which symptoms develop when blood fl ow is inadequate to support neuronal function. Potential causes of low-fl ow states include atherosclerosis of the vertebral arteries or small intracranial branches, steal syndromes, vasculitides, fi bromuscular dysplasia, and vertebral artery impingement. Symptoms of posterior circulation ischemia include diplopia, blurred vision, vertigo, gait disturbance, episodic perioral numbness, or drop attacks. Stereotypical movements such as extend- Fig. 27.2 Angiographic images showing the segments of the vertebral artery. A, The extracranial vertebral artery segments, V1-V4. B, The intracranial vertebral artery segments. PCA, posterior cerebral artery; PICA, posterior inferior cerebellar artery. B A Vascular Medicine and Endovascular Interventions 272 ing the neck or turning the head in a particular direction may provoke symptoms. Non-specifi c symptoms include headache, nausea, vomiting, and tinnitus. Initial therapy consists of platelet inhibitors or anticoagulation. Revascu- larization is indicated if symptoms persist despite medical management. Doppler examination of the vertebral arteries in vertebrobasilar ischemia shows reversal of fl ow or bidirectional fl ow. MRA, CTA, or invasive 4-vessel cerebral angiography using digital subtraction provides more defi nitive imaging when revascularization is being contemplated. An anteroposterior view with 20° cranial angulation typically provides good visualization of the entire extracranial vertebral artery. Multiple orthogonal views, including anteroposterior and lateral views, should be obtained to fully evaluate the high cervical and intracranial vertebrobasilar circulation. Surgical treatment of the vertebral artery can be techni- cally challenging. Approaches to surgical revascularization include vertebral to common carotid artery trans- position, vertebral endarterectomy, vertebral vein patch angioplasty with or without suture plication of the artery, and bypass from the subclavian artery to the vertebral artery. Complications—including Horner syndrome, lymphocele, recurrent laryngeal nerve palsy, immediate thrombosis, and chylothorax—after proximal vertebral artery reconstruction occur in up to 15% of cases. In some series, the rate of vertebral artery thrombosis approaches 9%. Catheter-based intervention has gained favor for treatment of symptomatic vertebral artery lesions. Before the procedure, patients should receive aspirin, 325 mg orally, and a loading dose of clopidogrel (300 mg orally followed by 75 mg orally once daily for 4 weeks). Femoral artery access is favored, although the brachial approach may be used. Heparin, 50 to 70 U/kg, is administered to achieve an activated clotting time greater than 250 seconds. A 6F Judkins right, headhunter, vertebral artery, or internal mammary artery catheter is used to engage the subclavian artery. A 6F or 7F guiding catheter is advanced to the stenosis over a 0.035-in wire. A buddy wire may be positioned in the distal subclavian artery to provide additional stability for the guiding catheter. The lesion is traversed with a 0.014-in steerable guidewire. Predi- lation is performed with a balloon that is undersized compared with the reference vessel diameter. For ostial lesions, low-profi le balloon-expandable coronary stents are preferred. The proximal portion of the stent is positioned with 1 or 2 cells protruding into the subclavian artery to prevent prolapse of subclavian artery plaque into the vertebral artery. For distal vertebral artery lesions, balloon-expandable or self-expanding stents may be used. Additional dilatation of the stent can be required to produce complete stent expansion. Oversizing the postdilation balloon is inadvisable because of the risk of perforation, dissection, or extrusion of plaque through the stent struts. Distal embolic protection devices have been used rarely in the vertebral artery. Compared with the internal carotid artery, the vertebral artery is smaller and more tortuous, which can make fi nding an adequate landing zone for the embolic protection device problem- atic. Placement of an embolic protection device should be considered if the vertebral artery diameter is larger than 3.5 mm, if the distal landing zone is relatively free of tortuosity, and if the target lesion is ulcerated. Mini- mal sedation is given during the procedure to facilitate neurologic monitoring. Neurologic status should be as- sessed after each major procedural step (e.g., placement of the guiding catheter, balloon dilation, and stent de- ployment). Only anecdotal data exist regarding the use of glycoprotein IIb/IIIa inhibitors in vertebral artery intervention. Procedural success is achieved in more than 90% of vertebral artery interventions; most patients improve or become asymptomatic. Long-term angiographic follow- up shows moderate to severe in-stent restenosis in up to 43% of cases, but most patients with restenosis remain asymptomatic. Drug-eluting stents have not been tested or approved for use in the vertebral artery. Close follow-up including duplex ultrasonography is warranted to moni- tor these patients. Repeat intervention is performed for symptom recurrence. • Placement of an embolic protection device should be considered if the vertebral artery diameter is larger than 3.5 mm, if the distal landing zone is relatively free of tortuosity, and if the target lesion is ulcerated • Procedural success is achieved in more than 90% of vertebral artery interventions; most patients improve or become asymptomatic Vertebral Artery Dissection The source of a vertebral artery dissection is usually an intimal tear, which allows pressurized blood to enter the artery wall and form an intramural hematoma. Subintimal dissection usually leads to stenosis of the arterial lumen; subadventitial dissection can produce aneurysmal dilatation of the artery. Dissection may occur spontaneously after blunt trauma or chiropractic manipulation, which can stretch the vertebral artery over the lateral mass of the second cervical vertebra. Spontaneous dissection is seen more commonly in fi bromuscular disease, Marfan syndrome, Ehlers-Danlos type IV syndrome, and cystic me- dial necrosis. Patients may report sudden pain in the back of the neck or head. Physical examination may indicate signs of posterior circulation ischemia. [...]... ischemia: definition and natural history Curr Drug Targets Cardiovasc Haematol Disord 2004;4:21 9- 2 5 O’Hare AM, Katz R, Shlipak MG, et al Mortality and cardiovascular risk across the ankle-arm index spectrum: results from the Cardiovascular Health Study Circulation 2006;113:38 8 -9 3 Pokrajac B, Potter R, Wolfram RM, et al Endovascular brachy- 283 Vascular Medicine and Endovascular Interventions therapy... registry Radiology 199 9;211:3 9- 4 9 Erratum in: Radiology 199 9;213 :93 0 Ouriel K, Gray B, Clair DG, et al Complications associated with the use of urokinase and recombinant tissue plasminogen activator for catheter-directed peripheral arterial and venous thrombolysis J Vasc Interv Radiol 2000;11: 29 5-8 Ouriel K, Katzen B, Mewissen M, et al Reteplase in the treatment of peripheral arterial and venous occlusions:... comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia J Vasc Surg 199 4; 19: 102 1-3 0 2 89 Vascular Medicine and Endovascular Interventions were numerous methodologic flaws in the trial Randomization and analysis were based on “intention to treat.” However, many patients who were randomly assigned to thrombolysis were never treated... Surg 2005;30:30 0-6 Howell MA, Colgan MP, Seeger RW, et al Relationship of severity of lower limb peripheral vascular disease to mortality and morbidity: a six-year follow-up study J Vasc Surg 198 9 ;9: 691 6 Krueger K, Zaehringer M, Bendel M, et al De novo femoropopliteal stenoses: endovascular gamma irradiation following angioplasty: angiographic and clinical follow-up in a prospective randomized controlled... intravenous recombinant tissue plasminogen activator and intra-arterial streptokinase in peripheral arterial thrombolysis Br J Surg 199 1;78 :98 8 -9 5 Comerota AJ, Aldridge SC Thrombolytic therapy for acute deep vein thrombosis Semin Vasc Surg 199 2;5:7 6-8 1 Comerota AJ, Aldridge SC Thrombolytic therapy for deep venous thrombosis: a clinical review Can J Surg 199 3;36:35 9- 6 4 Dayal R, Bernheim J, Clair DG, et al Multimodal... & Wilkins; 199 9 Qureshi AI, Ziai WC, Yahia AM, et al Stroke-free survival and its determinants in patients with symptomatic vertebrobasilar stenosis: a multicenter study Neurosurgery 2003;52:103 3 -9 Schievink WI Spontaneous dissection of the carotid and vertebral arteries N Engl J Med 2001;344: 89 8 -9 06 275 Vascular Medicine and Endovascular Interventions SSYLVIA Study Investigators Stenting of Symptomatic... Disease Treatment 12-mo patency, % Angioplasty With claudication With critical limb ischemia Cryoplasty 5 0-7 5 4 0-6 0 70 Cutting balloon angioplasty Laser Mechanical atherectomy Stent Drug-eluting stent Covered stent Brachytherapy No data 6 0-8 0 80 6 0-8 0 8 0-1 00 6 0-8 0 6 0-8 0 TASC, TransAtlantic Inter-Society Consensus 280 Notes TASC A and B lesions TASC A and B lesions Lesions . percutaneous revascularization, including that due to atherosclerotic disease, Takayasu arteritis, © 2007 Society for Vascular Medicine and Biology Vascular Medicine and Endovascular Interventions 268 tigue,. 2.54 Cerebrovascular disease 2.42 Congestive heart failure 1.20 Any cardiovascular disease 2. 69 Advanced age 2 .9 Elevated fi brinogen 1.4 Elevated body mass index 1.2 Vascular Medicine and Endovascular Interventions 278 area. 2003;52:103 3 -9 . Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. 2001;344: 89 8 -9 06. Figure for Question 5. (Courtesy of S. Ramee, MD, Ochsner Clinic.) Vascular Medicine

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