- •Vascular Surgery
- •SECTION AND BOARD OF VASCULAR SURGERY
- •Foreword to the First Edition
- •Preface to the First Edition
- •Preface to the Second Edition
- •Preface to the Third Edition
- •Contents
- •Contributors
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •1.1 Commentary
- •1.2 Beta-Adrenergic Antagonists
- •1.3 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors (Statins)
- •1.4 Percutaneous Revascularization
- •1.5 Coronary Artery Bypass Grafting
- •References
- •2: Abdominal Aortic Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •2.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •Question 12
- •Question 13
- •Question 14
- •3.1 Commentary
- •3.2 Case Analysis Quiz
- •References
- •4: Ruptured Abdominal Aortic Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •4.1 Commentary
- •References
- •5: Thoracoabdominal Aortic Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •5.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •Question 12
- •Question 13
- •6.1 Commentary
- •References
- •7: Aortic Dissection
- •7.1 Dissection: Stanford A
- •Question 1
- •Question 2
- •Question 3
- •7.2 Dissection: Stanford B
- •Question 4
- •Question 5
- •7.3 Commentary
- •References
- •8: Popliteal Artery Aneurysms
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •8.1 Popliteal Artery Aneurysm
- •References
- •9: Renal Artery Aneurysm
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •9.1 Commentary
- •References
- •10: Anastomotic Aneurysms
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •10.1 Commentary
- •10.2 Indications for Intervention
- •10.3 Treatment for Anastomotic Aneurysms
- •10.4 Infection in Anastomotic Aneurysms
- •10.5 Outcome
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •11.1 Commentary
- •References
- •12: Acute Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •12.1 Commentary
- •References
- •13: Arterial Embolism
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •13.1 Commentary
- •References
- •14: Blast Injury to the Lower Limb
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •14.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •15.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Smoking
- •Antiplatelet Agents
- •Blood Pressure (BP)
- •Glucose Status
- •Lipids
- •Emerging Risk Factors
- •Question 4
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •17.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •18.1 Commentary
- •18.2 Clinical Assessment
- •18.3 Imaging Techniques
- •18.4 Revascularization Options
- •18.5 Aortobifemoral Bypass
- •18.6 Iliac Angioplasty and Stenting
- •18.7 Iliac Stenting Combined with Profunda Femoris Artery Revascularization
- •18.8 Rationale for Angioplasty of “Donor” Iliac Artery Prior to Femorofemoral Crossover Bypass
- •18.10 Supervision and Follow-up of the Patient
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •Question 12
- •19.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •20.1 Commentary
- •References
- •21: Bypass to the Popliteal Artery
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •21.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •22.1 Commentary
- •References
- •23: Popliteal Artery Entrapment
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •23.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •24.1 Commentary
- •References
- •25: The Obturator Foramen Bypass
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •25.1 Commentary
- •25.2 Preoperative Measures
- •25.3 The Concept of the Obturator Foramen Bypass
- •25.4 Obturator Foramen Bypass Technique
- •References
- •26: Diabetic Foot
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •26.1 Commentary
- •References
- •27: Chronic Visceral Ischemia
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •27.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •28.1 Commentary
- •References
- •29: Renovascular Hypertension
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •29.1 Commentary
- •29.4 Intra-arterial Angiography
- •29.5 Duplex Ultrasonography (DU)
- •29.6 Treatment
- •29.6.1 Medical Treatment
- •29.6.2 Revascularization
- •29.7 Prognosis
- •References
- •30: Midaortic Syndrome
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •30.1 Commentary
- •References
- •31: Management of Portal Hypertension
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •31.1 Commentary
- •31.2 General Considerations
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •32.1 Commentary
- •References
- •33: The Carotid Body Tumor
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •33.1 Commentary
- •33.2 Clinical Presentation
- •33.3 Treatment
- •33.4 Summary
- •References
- •Question 1
- •Question 2
- •Question 3
- •34.1 Commentary
- •34.2 Vertebrobasilar Ischemia: Low-Flow Mechanism
- •Question 1
- •Question 2
- •34.3 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •35.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •36.1 Commentary
- •References
- •37: Acute Axillary/Subclavian Vein Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •37.1 Commentary
- •References
- •38: Raynaud’s Phenomenon
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •38.1 Commentary
- •References
- •39: Aortofemoral Graft Infection
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •39.1 Commentary
- •References
- •40: Aortoenteric Fistulas
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •40.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •41.1 Commentary
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Questions 7 and 8
- •Question 9
- •Question 10
- •Comment
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •42.1 Commentary
- •References
- •43: Amputations in an Ischemic Limb
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •43.1 Commentary
- •References
- •44: Congenital Vascular Malformation
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •44.1 Clinical Evaluation
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •44.2 Commentary
- •References
- •45: Klippel-Trenaunay Syndrome
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •45.1 Commentary
- •Clinical Presentation
- •Evaluation
- •Treatment
- •References
- •46: Deep Venous Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •46.1 Commentary
- •References
- •47: Endoluminal Ablation of Varicose Veins
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •47.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •48.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •50.1 Commentary
- •References
- •51: Iliofemoral Venous Thrombosis
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •50.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •Question 11
- •52.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •Question 6
- •Question 7
- •Question 8
- •Question 9
- •Question 10
- •53.1 Commentary
- •References
- •Question 1
- •Question 2
- •Question 3
- •Question 4
- •Question 5
- •54.1 Commentary
- •References
- •Index
29 Renovascular Hypertension |
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29.6 Treatment
One of the major priorities in the management of ARVD is to improve blood pressure to reduce cardiovascular burden and prevent renal decline. However, the treatment of ARVD has been the subject of much debate in recent years, particularly because of the possibility that renal revascularization therapy might improve patient outcomes. In the past there has been limited high-quality evidence regarding outcomes after revascularization, but in the latter part of 2009 the initial results of the ASTRAL trial were published, a study which recruited over 800 patients.17
29.6.1
Medical Treatment
ARVD is part of a diffuse vascular disease process and extra-renal vascular pathology is the major contributor to poor outcome. Cardiovascular protection forms the mainstay of treatment. Lifestyle changes include smoking cessation. Patients should receive an anti-platelet agent and a statin.18 Anti-hypertensive medication should be titrated aiming for a blood pressure of <130/80, although this can be a hard target to achieve given the long-standing nature of the hypertension and arterial stiffness seen in some cases. Patients often require combinations of several antihypertensive drugs for effective blood pressure control. Where possible, the addition of RAB is recommended. This may appear controversial as guidelines recommend caution with ACE-I/ARB use in patients with bilateral RAS or a solitary functioning kidney with RAS because potentially an acute reduction in GFR may occur due to an ACE-I/ARB – induced reduction of glomerular hydrostatic pressure. However, with careful titration of doses and checking of renal function (7–10 days post ACE-I/ARB introduction and after each dose increment), such serious complications can be detected early. An increase of creatinine of >25%overbaselinewouldberegardedasareasontostopthedrugs.Revascularization is emerging a means of allowing continuation of these beneficial drugs when renal functional deterioration is observed, although studies are still awaited in this regard. Other benefits to RAB include reduction of proteinuria19 and left ventricular hypertrophy,20 both significant independent predictors of mortality in ARVD (as in patients with other causes of CKD).
29.6.2 Revascularization
Renal revascularization procedures are performed in 16% of newly diagnosed ARVD cases.1 Over the course of the last 2 decades the availability of endovascular techniques has increased accessibility of patients to revascularization, and now <2% of all procedures are
300 |
C. Chrysochou and P.A. Kalra |
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surgical (compared to 35% in 199221). There are certain indications for renal revascularization procedures which have a wide consensus of support (albeit, non-evidence-based). These include:
•Prevention or treatment of life threatening flash pulmonary oedema22–24
•Relief of critical stenosis in order to preserve renal mass
•Acute occlusion that has resulted in acute kidney injury (AKI)25,26 (Fig. 29.3a and b)
•Renovascular hypertension resistant to multiple medications27
a
b
Fig. 29.3 (a) Left main renal artery pre-revascularization. (b) Post-angioplasty/stent insertion with restoration of renal artery patency and flow (Courtesy of Dr. Nicholas Chalmers, Radiology Department, Manchester Royal Infirmary)
29 Renovascular Hypertension |
301 |
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Outside of these indications, studies have shown a variable benefit of revascularization over conservative medical management, in terms of hypertension control and especially renal functional outcome. Until recently there has been a lack of adequately powered randomized controlled trials to detect a difference, and in other studies the patient phenotype has been inconsistent. The Angioplasty and Stent for Renal Arterial Lesions (ASTRAL) 17trial reported its initial findings in 2009, it being the largest randomized control trial to datecomparingmedicaltreatmenttorevascularizationwithmedicaltherapyin806patients with anatomically significant ARVD. Over an average follow-up period of 34 months, no renal functional (the primary end-point), systolic or diastolic blood pressure, cardiovascular event or mortality benefit was provided by revascularization with medical therapy, compared to medical therapy alone, in a clinically relevant, but relatively asymptomatic ARVD population. Within this population there is no doubt that some patients will have shown improvements in renal function and blood pressure control, and further analyses will be directed at assessing whether a series of clinical and investigational characteristics would reliably identify this subgroup. The minority of patients who do improve in this way after revascularization are classed as having a “functionally significant” RAS, but also, importantly, they have renal parenchyma which has not been irretrievably damaged by prior ischaemic and hypertensive stresses.
Our patient underwent percutaneous left renal artery angioplasty and stenting. [Q3: C] Currently, stent supported angioplasty has widely replaced plain balloon angioplasty of RAS because of the superior short and long term angiographic results of stenting,25,28–30 especially with far lower rates of re-stenosis seen in atherosclerotic ostial lesions, which might occur because of elastic recoil or plaque resistance. Other benefits include a reduction in renin and angiotensin production30 and larger luminal dilatation. Furthermore, endovascular techniques reduce the operative morbidity and mortality of open surgical repair.31 Technical developments such as drug eluting stents,32 and distal protection devices (e.g., a balloon or filter placed distally during intervention to capture atheromatous and thrombotic debris before it reaches the renal capillary bed), may increase the safety and effectiveness of revascularization. Patients receiving both glycoprotein IIb/IIIa inhibitors and embolic protection devices have less occurrence of platelet-rich emboli in distally placed filters.33 These measures are not widely used, and deterioration in renal function may still continue despite their use.34
Even endovascular revascularization is a procedure which may carry significant risk. Complications may occur in up to 25% of patients,35 most of which are minor, such as groin bruising and haematoma over the percutaneous wound entry site, or temporary deterioration of renal function, presumably due to contrast-induced injury. However, in ASTRAL 6.8% of patients suffered serious complications of revascularization including major renal arterial abnormailities (peudoaneurysm formation, thrombosis and occlusion, renal artery dissection), cholesterol emboliztion and even death. [Q4: D, E]
A range of surgical options are available to treat RAS and these include aortic graft and renal bypass, aorto-renal bypass, aorto-renal endarterectomy and extra-anatomical bypass. At least 70% of patients who undergo surgical repair have concomitant aortic disease, and most clinicians would now recommend surgery for RAS when this is accompanied by more complex aorto-renal disease. The results after surgical revascularization are uncertain because of positive reporting bias and the presence of many relatively small case