Endovascular Interventions

Jose M. Wiley, Cristina Sanina, Peter Faries, Ian Del Conde, George D. Dangas, Prakash Krishnan, Jose M. Wiley, Cristina Sanina, Peter Faries, Ian Del Conde, George D. Dangas, Prakash Krishnan

• Publisher: Wiley-Blackwell
• Year: 2019
• Print ISBN: 9781119283492
• eBook ISBN: 9781119283522
• Edition: 1
• Topic: Medicine
• Subtopic: Cardiology

A practical resource covering both elective and emergency procedures for the practicing vascular and endovascular clinician

This book provides medical professionals (vascular surgeons, interventional cardiologists, interventional radiologists, endovascular neurologists, vascular medicine specialists) with a reference guide to the most common and accepted approach to endovascular management of peripheral vascular disease. It also addresses urgent interventions in the acute setting of the various vascular beds, and covers emerging areas such as stroke intervention and endovascular treatment of pulmonary embolism and vascular trauma.
Edited by a multidisciplinary team, Endovascular Interventions offers in-depth coverage of the field in seven parts: Overview; Supra-Aortic Intervention in High Risk Patients: Innominate, Subclavian, Carotid, Vertebral and Intracranial Interventions; Interventions of the Aorta; Renal and Mesenteric Interventions; Lower Extremity Interventions; Venous Disease; and Vascular Trauma. Each section covers the technical aspects of the procedures as well as the fundamental clinical aspects which are necessary in the evaluation of patients considered for interventions. Chapters feature illustrations, case studies, key learning points, equipment lists, and sample questions and answers which can be used for Board exam practice.

• Practical review of vascular and endovascular medicine covering both elective and emergency procedures
• Illustrated, templated chapters provide rapid answers to questions and include case studies, key learning points, and equipment lists
• Includes sample questions and answers that are handy for Board exam practice
• Edited by multidisciplinary experts

Endovascular Interventions is an excellent review book for all practicing and aspiring vascular and endovascular specialists.

1
Vascular Biology

Cristina Sanina¹, Olga L. Bockeria², Karlo A. Wiley³ and Jonathan E. Feig⁴

¹Department of Internal Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA

²Department of Cardiovascular Surgery, Bakoulev Center for Cardiovascular Surgery, Moscow, Russia

³Cornell University, College of Agriculture and Life Sciences, Ithaca, NY, USA

⁴Johns Hopkins Heart and Vascular Institute, The Johns Hopkins Hospital, Baltimore, MD, USA

Introduction

Like many contemporary sciences, vascular biology has been progressively developing at the junction of many disciplines. New knowledge has been obtained in regard to vessel growth biology, physiology, and genetics as well as physiological and pathophysiological mechanisms underlying endothelial dysfunction and atherogenesis. Based on studies that extend back to the 1920s, regression and stabilization of atherosclerosis in humans have gone from just a dream to something that is achievable. Review of the literature indicates that successful attempts at regression applied robust measures to improve plasma lipoprotein profiles. Examples include extensive lowering of plasma concentrations of atherogenic apolipoprotein B and enhancement of reverse cholesterol transport from atheromata to the liver. Possible mechanisms responsible for lesion shrinkage include decreased retention of atherogenic apolipoprotein B within the arterial wall, efflux of cholesterol and other toxic lipids from plaques, emigration of lesional foam cells out of the arterial wall, and an influx of healthy phagocytes that remove necrotic debris as well as other components of the plaque. Until very recently, with the approval of the PCSK9 inhibitors, the available clinical agents caused less dramatic changes in plasma lipoprotein levels, and thereby failed to stop most cardiovascular events. In addition, although the use of angioplasty and stenting has undoubtedly been beneficial, it does not offer a cure or address the underlying mechanisms of vascular disease.

Vascular Anatomy

Blood vessels are composed of three layers: the inner lining of intima (a monolayer of endothelial cells), the middle layer, the media (a layer or layers of vascular smooth muscle cells), and the outer layer, the adventitia (contains collagen type 1, elastic fibers, myofibroblasts, mesenchymal stem cells, vasa vasorum, and nerves). These three layers are separated with internal and external elastic laminas, a thin layer of connective tissue. Large arteries contain more layers of smooth muscle cells and more elastin, and medium‐sized arteries contain more collagen. The smallest vessels (capillaries) are built from a single layer of endothelial cells with surrounding basal lamina and pericytes. A number of pericytes and their functions differ in respect to the organs in which they are found. Vascular smooth muscle cells and pericytes regulate peripheral vascular resistance, vascular diameter, and direction of blood flow [1].

Endothelium, the Largest Body Organ

The endothelium is a large and complex organ with endocrine, autocrine, and paracrine proprieties that produces nitric oxide (NO), endothelin‐1, prostacyclin‐2, interleukin‐6, vascular endothelial growth factor (VEGF), von Willebrand factor, plasminogen activator, plasminogen activator inhibitor‐1, angiopoietin‐2, adhesion molecules such as P‐selectin, E‐selectin, integrins, and other bioactive molecules. Endothelium controls the recruitment of inflammatory cells and thrombocytes, regulates the coagulation process, extravasation, and vascular tone, and is involved in wound healing through angiogenesis. Endothelial cells cover the entire vasculature in vertebrates with the largest estimated surface amounting to 3000–6000 m². The total weight of endothelium in an adult person is approximately 720 g, of which 600 g is capillaries [2]. Interestingly, endothelial cells not only from arteries and veins but also from different tissues possess diverse tissue‐specific protein expression [3]. NO is a major vasodilator molecule that was discovered by Dr. Furchott in 1980 and named endothelium‐derived relaxing factor. In 1992 NO was identified and in 1998 three US scientists, Robert F. Furchott, Louis J. Ignarro, and Ferid Murad, were awarded the Nobel Prize for NO discovery [4]. NO plays an essential role in vascular smooth muscle cell relaxation, thrombocyte aggregation, endothelial cell turnover, and immune/anti‐inflammatory processes. Endogenous NO is generated from L‐arginine by a family of three calmodulin‐dependent NO synthase (NOS) enzymes that are primarily expressed by three cell types: endothelial cells (eNOS), neurons (nNOS), and immune cells (iNOS) [5]. However, NO can also be released non‐enzymatically from S‐nitrosothiols or nitrate/nitrate. Decreased production or bioavailability of NO and increased expression of endothelin‐1, an endothelium‐derived potent vasoconstrictor, suggest endothelial dysfunction and are associated with hypertension, inflammation, prothrombogenesis, atherogenesis, and cardiovascular events [1]. Inflammation or an increase in proinflammatory circulating molecules such as interleukin‐1 and interleukin‐6, tumor necrosis factor‐α, C‐reactive protein, and neutrophils and macrophages boost C‐reactive protein production by the liver which, in turn, causes eNOS downregulation and increases endothelin‐1 bioavailability, leading to decreased vasodilation, increased shear stress, and vascular atherogenesis. In particular, inflammation upregulates the expression of endothelial cell adhesion molecules that facilitate low‐density lipids (LDLs) and macrophage migration across the vascular endothelium via monocyte chemoattractant protein 1 [6]. Inflammatory cytokines also induce tissue factor and von Willebrand factor synthesis by endothelial cells, initiating coagulation cascade and platelet aggregation. Metalloproteinase ADAMTS‐13, also produced by endothelial cells, stellar liver cells, platelets, and kidney podocytes, cleaves large molecules of von Willebrand factor, but inflammatory conditions decrease ADAMTS‐13 activity, promoting the prothrombotic state. Endothelial cells also provide a rescue mechanism for thrombogenesis by continually producing tissue plasminogen activator, which is cleared by the liver unless fibrin binds to it. Furthermore, inflammatory cytokines promote endothelial cells to produce another tissue plasminogen activator–urokinase‐type to cleave substantial fibrin deposition. Thrombin, a procoagulation protease that converts soluble fibrinogen into insoluble fibrin, in turn activates eNOS leading to NO and prostacyclin‐2 production, causing vasodilatation and platelet aggregation inhibition. In this way endothelium regulates thrombogenesis and thrombolysis [2].

Vasculogenesis, Angiogenesis, and Arteriogenesis

Endothelial cells originate from mesoderm (hemangioblasts), which gives rise to hematopoietic stem cells and endothelial progenitor cells (angioblasts). The vascular network is formed due to three primary processes: vasculogenesis, angiogenesis, and arteriogenesis. The term “vasculogenesis” was defined by Risau in 1997 as the de novo formation of vessels from endothelial progenitor cells, i.e. angioblasts [7]. During vasculogenesis stem cells form primitive primary vascular plexus, i.e. capillaries. Initially, it was considered ...

Table of contents

• Cover
• Table of Contents
• List of Contributors
• 1 Vascular Biology
• 2 Non‐Invasive Testing in Peripheral Arterial Disease
• 3 Carotid and Innominate Artery Stenting for High‐Risk Patients
• 4 Subclavian Artery Stenosis: When and How to Intervene
• 5 Vertebral Artery Occlusive Disease
• 6 Stroke Interventions
• 7 Endovascular Management of Thoracoabdominal Aneurysms
• 8 Abdominal Aortic Aneurysms: Catheter‐Based Interventions
• 9 Aortic Dissection: Urgent Endovascular Treatment
• 10 Management of Acute Aortic Syndrome
• 11 Severe Renal Artery Stenosis: When and How to Intervene
• 12 Mesenteric Ischemia: Chronic and Acute Management
• 13 Catheter‐Based Management of Peripheral AVMs
• 14 Aortoiliac Interventions
• 15 Femoropopliteal Interventions in the Claudicant Patient
• 16 Tibial and Pedal Plantar Interventions in Patients with Critical Limb Ischemia
• 17 The Diagnosis, Evaluation and Contemporary Management of Acute Limb Ischemia
• 18 Pedal Reconstruction in Critical Limb Ischemia
• 19 Access Site Complications
• 20 Acute Deep Vein Thrombosis
• 21 Chronic Venous Disorders
• 22 Endovascular Treatment of Pulmonary Embolism
• 23 Inferior Vena Cava Filters
• 24 Endovascular Treatment for Vascular Trauma
• Index
• End User License Agreement