Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies

Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies Fridon Todua Dudana Gachechiladze

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Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies

Fridon Todua • Dudana Gachechiladze

Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies

Fridon Todua Department of Radiology National Academy of Sciences of Georgia Research Institute of Clinical Medicine I. Javakhishili Tbilisi State University Tbilisi Georgia Editorial Advisor Michael Okujava Department of Radiology Institute of Medical Research Ilia State University Tbilisi Georgia

Dudana Gachechiladze Department of Radiology Programme of Caucasus University Tbilisi Georgia Department of Ultrasound Diagnostics National Medical Academy of Georgia Research Institute of Clinical Medicine Tbilisi Georgia

Department of Neurodiagnostics and Neuroscience Research Institute of Clinical Medicine Tbilisi Georgia

ISBN 978-3-319-91366-7    ISBN 978-3-319-91367-4 (eBook) https://doi.org/10.1007/978-3-319-91367-4 Library of Congress Control Number: 2018945471 © Springer International Publishing AG, part of Springer Nature 2018 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Printed on acid-free paper This Springer imprint is published by the registered company Springer International Publishing AG part of Springer Nature. The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

In Memoriam: Fridon Todua (1944–2017)

Professor Fridon Todua was the founder of the Research Institute of Clinical Medicine, Tbilisi, Georgia—one of the biggest diagnostic and treatment centers not only in Georgia but in the whole region as well. Fridon Todua’s contribution to the development of radiology and oncology in Georgia was tremendous and he was greatly honored throughout the radiological community. He was hugely admired as a leader, researcher, and teacher, and was a great inspiration to many. Fridon Todua was the author of more than 650 scientific works, including 13 monographs. He was the scientific supervisor of more than 85 PhD dissertations. In recognition of his dedication and commitment, he received a number of awards and honors throughout his career and was widely respected for his work and research. He was the recipient of honorary doctorates and memberships from various universities and scientific academies, scientific societies, and scientific associations around the world. He also received many other Georgian and foreign awards, among them the Order of Honor of UC for Contribution to Construction the United Europe, the Russian Federation Order of St. Andrew the First-Called, and the Albert Schweitzer Order.

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Introduction

Cerebral circulatory disorders are a global medical and social problem; about 4.5 million people annually die from stroke, of whom three-quarters are in developing countries. Even in developed countries, stroke has the third highest mortality rate after Coronary heart disease and cancer. In Western developed countries the average mortality rate of stroke varies in the range of 5–100 per 100,000 people per year, which represents 10–12% of the overall mortality. According to different studies (Laitinen-Krispijn and Bijl 2000), the standardized annual mortality of stroke in the 45–85 year age group in Western Europe is 326 per 100,000 people, while in Eastern Europe and some regions of Russia this figure is up to 600 per 100,000 people. It should be noted that in those countries where high-technology diagnostics are widely used for cerebrovascular diseases, the incidence of stroke does not exceed 240–380, while in developing countries in Asia it exceeds 600. Epidemiological statistical analysis shows that the outcome of stoke varies greatly depending on whether modern diagnostic and therapeutic technologies are actively implemented in the management of cerebrovascular diseases. As the proportion of the aged population increases, the incidence of acute vascular accidents, such as stroke, is increased, as is the incidence of chronic cerebrovascular diseases (leukoaraiosis, Binswanger disease, vascular dementia), creating many medical and social problems. Hemorrhage resulting from different diseases of the intracranial vessels (aneurysms, arterio-venous malformations) are some of the most important problems in vascular neurology. It should also be noted that cerebral circulatory disorders are some of the most “expensive” diseases. In developed countries, the overall whole-of-life expenses for one patient with stroke amount to US$55,000–73,000. At the end of the twentieth century, great advances were made in the study of particular cerebrovascular pathologies, as well as in studies of the brain generally, mainly owing to the invention of neuroimaging diagnostics such as computed tomography (CT), magnetic resonance imaging (MRI), and positron-emission tomography, and their widespread implementation in clinical practice. Neuroimaging methods give scientists the opportunity to look into the living human brain and study its structure, blood supply, and functional status, even including subtle molecular and chemical processes. These methods help to reveal vii

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small lesions of several millimeters in size (such as tumors, infarctions, or hemorrhages) and observe their dynamics. The diagnosis (even with the help of up-to-date diagnostic facilities) and the appropriate medical treatment of cerebral circulatory disorders are not possible without exhaustive studies of the causes and mechanisms of these circulatory disorders. Such studies have shown that timely prevention of circulatory risk factors, screening at early stages of the disease, and prompt medical treatment are crucially important. The European Society of Cardiology, the European Society of Atherosclerosis, and the European Society of Arterial Hypertension recommend taking measures for the prevention of cerebral circulation disorders, targeting risk factors such as arterial hypertension, carotid artery damage, cardiac pathologies, hypercholesterolemia, smoking, physical inactivity, and excess weight. Considering that about 75–78% of men and 55–60% of women in the population have at least one of the above risk factors, it is obvious that the problem needs active involvement aimed at the reduction of vascular risk factors. The most frequent cause of cerebral circulatory disorders is atherosclerosis of the extracranial arteries, mainly the carotid arteries. It is particularly worth noting that, according to leading clinical centers, approximately 30–35% of the population has asymptomatic (latent) stenosis of the carotid arteries, which, in addition to certain other factors, may cause carotid system disease, leading to acute cerebrovascular disorders with, further, the necrosis of neuroglial tissues. As extracranial arterial pathologies play an undisputed role in the development of cerebrovascular disorders, it is most important to use simple, non-invasive, safe, and easily reproducible diagnostic methods for these pathologies, thus making it possible to perform effective surgery to prevent atherosclerotic or thromboembolic arterial damage. As well as X-ray contrast angiography, which is widely used, such diagnostic methods include: duplex scanning in color and power Doppler modes, transcranial Doppler sonography, computed angiography, and magnetic resonance angiography; these methods are used in both clinical practice and scientific studies. The above methods have been revolutionary for vascular neurology, allowing investigators to study vascular topography, the lumen, and the vascular walls in vivo, as well as to detect the exact location of pathological lesions, atheromatous plaques, or thrombi, and determine their hemodynamic significance. With the help of modern ultrasound equipment and computed or magnetic resonance angiography, it is possible to diagnose a hemodynamically significant stenosis of the carotid artery with practically 100% accuracy and to plan the optimal tactics for medical treatment. The undisputed advantage of duplex scanning and color Doppler, in comparison with other methods, lies in the ability of these methods to accurately assess the structure and surface of atheromatous plaques. The latest modifications of ultrasound equipment can detect, in 97–98% of cases, potentially embologenic atheromatous plaques. The detection of such plaques is particularly important in modern vascular neurology, given their role in the pathogenesis of local cerebrovascular disorders and multi-infarct dementia. Transcranial Doppler sonography is very important for the detection and assessment of cerebrovascular disorders, allowing investigators to study hemodynamic parameters in the Willis arteries, to assess collateral circulation and reserves, and to detect such features as stenosis, arterial and venous malformations, and aneurysms

Introduction

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in the intracranial vessels. With the help of specific software, it is also possible to monitor microemboli in the Willis arteries and to study cerebral venous hemodynamics during different anomalous occurrences (such as high intracranial pressure, sinus thrombosis, and cerebral thrombophlebitis). Circulatory complications can be avoided through the timely and adequate treatment of the above vascular conditions; such treatment is not possible without efficient diagnostic equipment. Thanks to the new generation of CT and magnetic resonance angiography devices, there have been great advances in the non-invasive diagnosis of various anomalies, pathological conditions, and malformations of the intracranial vessels. These devices help, in practically 100% of cases, to detect cerebral vascular conditions such as saccular and fusiform aneurysms and arterial or venous malformations, and the devices also show their location, topography, contact with surrounding structures, size, shape, and nourishing and draining vessels. Special three-dimensional (3D) reconstruction software shows clear pictures of the vessels. In high-risk patients (those with conditions such as ischemic heart disease, arterial hypertension, and diagnosed stenosis of the carotid arteries), non-invasive investigations are used to detect asymptomatic stenosis, in order to study the structure, hemodynamic importance, and embologenic potential of any atherosclerotic plaque. The world’s leading clinics recommend that targeted ultrasound studies (color Doppler, transcranial Doppler) of the extracranial arteries be done twice per year in high-risk patients. In special cases, screening also includes CT or MRI and magnetic resonance or computed angiography, while in patients with previously diagnosed cerebrovascular diseases, cerebral CT, MRI, or radionuclide perfusion is recommended. Recent global epidemiological studies of cardiovascular conditions clearly show that the real possibility of reducing the spread of vascular neurological diseases lies with the use of diagnostic and treatment facilities for the early detection of cerebrovascular disorders. However, although the above-mentioned modern non-invasive radiological examinations are employed in both the treatment and prevention of transient ischemic attacks and acute stroke, such therapeutic measures cannot be employed for completed strokes or established necrotic lesions following an infarction. Accordingly, non-invasive neurological imaging of cerebrovascular conditions is regarded as valid for conditions such as transient ischemic attacks, but rather, the prevention of risk factors, while clinical and diagnostic assessment of the disease is based on angiography rather than on neuroimaging. Currently, there is no doubt that the most radical therapeutic and preventive measures—such as carotid endarterectomy and endovascular correction of the lumen— for cerebrovascular conditions have developed efficiently as the result of the employment of high-technology neuroimaging and angiography, which allow the assessment of both the structural and functional status of the brain. At the Research Institute of Clinical Medicine (Tbilisi, Georgia), patients with different cerebrovascular and circulatory conditions are examined using the latestgeneration equipment. The equipment used for MRI is Magnetom Avanto and Aera (Siemens) 1.5T and Magnetom Verio and Skyra (Siemens Erlangen, Germany), with a 3.0-T magnetic field.

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The following sequence parameters are used for 3T: T1w-TR 300 ms, TE 15 ms, T2w-TR 6000  ms, TE 117  ms, PDw (Proton-density weighting)-TR 300  ms, TE-15  ms, turbo inversion recovery magnitude (TIRM)-TR 6000  ms, TE 93  ms, fluid-attenuated inversion recovery (FLAIR)-TR 6000 ms, TE 93 ms, T1 1600 ms, GE-TR-863  ms, TE 15  ms, fa (flip angle) 55°, TIRM fat-suppressed-MT-TR 1800 ms, TE 32 ms, T1 110 ms, TIRM fat-suppressed-TR 4000 ms, TE 48 ms, TI 110 ms, multi echo-TR 2400 ms, and TE 26, 58, 90, and 125 ms. Magnetic resonance angiography of the intracranial arteries was performed with time of flight (TOF) sequence fl3d-multiple-trv- TR-21 ms, TE 3.60.4 ms, fa 40°, while for the extracranial arteries, the sequence used was TOF-fl2d-trav-sat-TR-21 ms, TE 3.60 ms, FOV 200 mm, fa 70°, and for venous sinuses, the sequence used was TOF-fl2d-cor-TR-32 ms, TE 14 ms, fa 60°. The following parameters were used for 1.5-T systems: T1se TR-500 ms, TE 8.1, T2tse FOV 230, SE 5(19), TR-4500 ms, TE 101 ms, PD-T2tse TR 2840, TIRM (FLAIR) FOV 230, SE 5(19), TR 9000 ms, TE 111 ms; TIRM fat-suppressed-MT-TR 1800 ms, TE 32 ms, T1 110 ms, TIRM fat-suppressed-TR 4500 ms, TE 48 ms, TI 110 ms. For contrast angiography (with gadolinium) of the extracranial vessels, the following sequence was used: FOV 313, TR 36.9, TE 1.39 ms. For intravenous contrast, we used 20  ml of Magnevist (Bayer Healthcare Pharmaceuticals, Whippany, NJ) 5% solution (1 ml contains 469 mg of gadopentetate dimeglumine). Projection pictures were made according to MIP (Maximum intensity projection) and MPR (Multiplanar reconstruction) algorithms. Cerebral CT and multislice CT angiography of the extra- and intracranial arteries were performed with a multislice tomograph (Aquilion One 640, Toshiba (Otawarashi, Tochigi, Japan)); Siemens tomograph Definition edge 384 sl and a SOMATOM Sensation Cardiac 64 s (Erlangen Germany), with 0.5-, 2-, and 4-mm axial sections. We used 50–100 ml of intravenous Ultravist 370 (Bayer Healthcare Pharmaceuticals, Whippany, NJ) 5% solution (60 ml on average) as contrast. The waiting period for extracranial arteries was 15–18 s. Further reconstruction of images was performed on a special workstation (Vizard; Siemens, Vitrea fX; Toshiba). MIP (Maximum intensity projection), SSD (surface shaded display), VR (Volume rendering), and MPR reconstructions were used across the axial, coronary, and sagittal axes. Ultrasound examination of the extracranial vessels was performed on Toshiba devices Aplio 500 and Aplio i800. Examinations were performed with 5–14 MHz and 7–18 MHz multi-frequency linear transducers. The degree of carotid stenosis was assessed based on ECST (European Carotid Surgery Trial) methodology. Scanning of the intracranial vessels was performed with the Aplio 500 and Aplio i800 devices (Toshiba) at 2–4 MHz frequency. Transcranial emboli were detected with the Nicolett 8080 unit, based on the generally accepted methodology.

Reference Laitinen-Krispijn S, Bijl RV (2000) Mental disorders and employee sickness absence: the NEMESIS study. Netherlands Mental Health Survey and Incidence Study. Soc Psychiatry Psychiatr Epidemiol 35(2):71–77

Contents

Part I Vascular Anatomy and Basic Hemodynamics 1 Anatomy of Cerebral Circulation System ��������������������������������������������    3 References��������������������������������������������������������������������������������������������������   10 2 Basic Principles of Hemodynamics��������������������������������������������������������   11 References��������������������������������������������������������������������������������������������������   20 Part II Basic Principles of Non-invasive Vascular Diagnostics 3 Main Principles of Ultrasound Examination����������������������������������������   23 References��������������������������������������������������������������������������������������������������   31 4 Ultrasound Examination of Extracranial Vessels ��������������������������������   33 References��������������������������������������������������������������������������������������������������   38 5 Technical Aspects of Computer Tomography and CT Angiography ������������������������������������������������������������������������������   39 References��������������������������������������������������������������������������������������������������   44 6 Physical Principles of Magnetic Resonance and Magnetic Resonance Angiography��������������������������������������������������������������������������   47 References��������������������������������������������������������������������������������������������������   52 7 Assessment of CT Angiography and MR Angiography Data��������������   55 References��������������������������������������������������������������������������������������������������   60 Part III Cerebral Ischemia 8 Cerebral Ischemia and Stroke����������������������������������������������������������������   63 References��������������������������������������������������������������������������������������������������   90 9 Capacity of Perfusion- and Diffusion-Weighted MRI (PWI, DWI) and Perfusion CT (PCT) in Revealing of Acute Ischemia������������������������������������������������������������������������������������   95 References��������������������������������������������������������������������������������������������������  104

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Part IV Pathologies of Extracranial Vessels 10 Atherostenosis and Thrombosis of Extracranial Vessels����������������������  109 References��������������������������������������������������������������������������������������������������  134 11 Common Carotid Artery Intima-Media Layer Changes����������������������  137 References��������������������������������������������������������������������������������������������������  141 12 Structural Characteristics of Atherosclerotic Plaque��������������������������  143 References��������������������������������������������������������������������������������������������������  159 13 Surgical and Endovascular Treatment of Extracranial Carotid Stenosis���������������������������������������������������������������������������������������  163 References��������������������������������������������������������������������������������������������������  175 14 Deformation of Extracranial Arteries����������������������������������������������������  179 References��������������������������������������������������������������������������������������������������  187 15 Takayasu’s Arteritis ��������������������������������������������������������������������������������  189 References��������������������������������������������������������������������������������������������������  194 16 Subclavian Steal Effect����������������������������������������������������������������������������  195 References��������������������������������������������������������������������������������������������������  200 17 Dissection of Extracranial Arteries��������������������������������������������������������  201 References��������������������������������������������������������������������������������������������������  207 18 Aneurism and Pseudoaneurism of Extracranial Arteries��������������������  209 References��������������������������������������������������������������������������������������������������  212 19 Congenital Variations of Extracranial Arteries������������������������������������  215 References��������������������������������������������������������������������������������������������������  220 20 Pathological Findings in the Jugular Veins��������������������������������������������  221 References��������������������������������������������������������������������������������������������������  223 Part V Methods of Non-invasive Functional Examination of Cerebrovascular System 21 Detection of Cerebral Microemboli��������������������������������������������������������  227 References��������������������������������������������������������������������������������������������������  229 22 Assessment of Cerebrovascular Reactivity��������������������������������������������  231 References��������������������������������������������������������������������������������������������������  241

Part I Vascular Anatomy and Basic Hemodynamics

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Anatomy of Cerebral Circulation System

Cerebral circulation starts from aortic arch vessels (see the diagram in Fig. 1.1). The first artery coming out of the aortic arch is brachiocephalic trunk (TrB), which then divides into right subclavian and right common carotid arteries (CCA). The other branches are left subclavian and left common carotid arteries. The left CCA originates directly from the aortic arch. The cervical section of both common carotids follows a similar course. Each vessel passes obliquely upward from behind the sternoclavicular joint to the level of the upper border of the thyroid cartilage. In the lower neck, the two common carotid arteries are separated from each other by the trachea. The left CCA is usually longer than the right CCA. Common carotid arteries proceed to the brain and most often at the upper level of thyroid cartilage (at the third or fourth cervical vertebrae) divide into internal carotid arteries (ICA) and external carotid arteries (ECA). The carotid bifurcation (CB) is an anatomically and surgically important landmark as it is involved in a variety of physiological and pathological processes. The height of the carotid bifurcation is classically defined in relation with vertebral levels and is highly variable across literature. Finally, geometry of CB is a determinant of local blood hemodynamic and wall shear stress, commencing or promoting the process of atherogenesis (Uflacker 2007). External carotid artery (ECA) provides approximately 1/3 of the blood flow supplied by common carotid artery; ECA also originates symmetrically on the both side, has a relatively short trunk, and divides into several branches (the superior thyroid artery, the lingual artery, the facial artery, the maxillary artery, the occipital and superficial temporal artery, etc.). The first large branch, superior thyroid artery, is easy detectable on ultrasound examination and can be used for differentiation between ECA and ICA.

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Fridon Todua was deceased at the time of publication.

© Springer International Publishing AG, part of Springer Nature 2018 F. Todua, D. Gachechiladze, Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies, https://doi.org/10.1007/978-3-319-91367-4_1

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Fig. 1.1  Anatomical overview of the extracranial arteries. 1. common carotid artery; 2. external carotid artery; 3. internal carotid artery; 4. superior thyroid artery; 5. lingual artery; 6. facial artery; 7. occipital artery; 8. superficial temporal artery; 9. vertebral artery; 10. thyrocervical trunk; 11. costocervical trunk; 12. descending scapular artery; 13. internal thoracic artery; 14. subclavian artery

At the carotid bifurcation, the CCA widens, and the dilatation continues into the proximal portion of the ICA. This part is called the carotid sinus. Beyond the carotid sinus, the caliber of the ICA is uniform. In this segment the arterial wall has a number of particularities: Medial layer is relatively thin and adventitia is thick, with multiple elastic fibers and baro- and chemoreceptors. The carotid sinus contains baroceptors able to detect acute changes in arterial pressure alongside chemoreceptors able to detect acute changes in arterial oxygen. Those receptors communicate with brainstem and through reflexes regulate homeostasis of these vital parameters (Valdueza et al. 2008).

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Internal carotid artery (ICA) provides 2/3 of the blood flow supplied by CCA. Its diameter is larger than of ECA. The right and left ICAs develop symmetrically and have lateral or dorsolateral position in relation to the ECA. ICA rises to the scull base without branching. The ICA has three main segments: cervical, petrous, and intracranial segments. At the cervical segment, the ICA is almost vertical, from the origin to the carotid canal at the base of the skull. It is closely connected to the jugular vein (JV) and the vagus nerve, which is located between and behind these two vessels, forming a neurovascular bundle. Intrapetrosal part is located in the pyramidal channel of the temporal bone. There is a vertical and a horizontal portion of the petrous segment of the ICA. In this segment it is bordered with the venous plexus. The intracranial portion of the ICA may be divided into three segments: the precavernous segment, the cavernous segment, and the supraclinoid segments. The ICA runs through the carotid canal to the cranial cavity and enters the cavernous sinus, where it forms the curved carotid siphon. The upper part of carotid siphon gives its first branch—ophthalmic artery (OA). After that, the internal carotid artery enters subarachnoid cavity, where it bifurcates into two main branches: middle cerebral artery (MCA) and anterior cerebral artery (ACA). The MCA originates from the division of the ICA. The MCA has the larger caliber among the arteries of the circle of Willis. MCA is slightly curved and runs laterally (M1 segment). At the lateral cerebral fissure, it has 2–5 branches (M2 segment). The anterior cerebral artery (ACA) rises from the anterior wall of the ICA. It runs medially (A1 segments), passing over the optic nerve and chiasm and anteriorly in the cerebral fissure (A2 segment). It is connected by the opposite ACA over the optic chiasm through the anterior communicating artery (AComA). In this segment also starts posterior communicating artery (PComA), which connects carotid and vertebrobasilar arterial systems. Functional particularities of carotid arteries define their histological structure. CCA belongs to so-called elastic-type arteries, which corresponds to its main function—transportation of a larger volume of blood in comparison with the other arterial systems. Elastic artery is a vessel with a large number of collagen and elastin filaments in the tunica media, which gives it the ability to stretch in response to each pulse. Internal carotid artery is a muscular-elastic artery, innervated by a number of cranial, cervical, thoracal, and spinal nerves. Periarterial plexus of internal carotid artery, spreading to intracranial vessels, consists of cervical (mainly superior sympathetic) ganglia (Lasjaunias and Berenstein 1987). The subclavian artery, like a carotid artery, on the right side emerges from the brachiocephalic trunk and on the left side directly from aortic arch. The vertebral artery (VA), in most of cases, originates at the upper posterior aspect of the first segment of the subclavian artery (SA). VA is divided into four main segments, out of which three are extracranial and one intracranial (Fig. 1.2). The first segment, so-called V 1 segment of vertebral artery, starts from the subclavian artery and ends before entering the costotransverse channel. Vertebral artery

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Fig. 1.2  Vertebral arteries anatomy. 1. vertebral artery; 2. thyrocervical trunk; 3. inferior thyroid artery; 4. ascending cervical artery; 5. superior cervical artery; 6. suprascapular artery; 7. internal thoracic artery

enters the costotransverse channel mainly at C-V-VI level or rarely at IV-V vertebral level (V2 segment). Then it proceeds vertically up to the C-II vertebral level and establishes the V 3 segment. The fourth segment (V4) of the VA perforates the dura and runs the cranium (IV segment) anteromedially through the foramen magnum. At the posterior edge of the pons Varolii VA, join the contralateral VA forming the single basilar artery (BA). The BA is approx. 3–4 cm long. Sometimes the course of the BA is tortuous and deviated from the midline. The BA at the anterior edge of the pons Varolii divides into two posterior cerebral arteries (PCA) (Fig. 1.3). The PCA generally receives the supply from the BA and has a communication with the ICA through the posterior communicating artery (PComA). Extracranial part of the vertebral artery is an elastic-type vessel, while its intracranial segment is muscular (distributing) artery. It is innervated by a number of cranial, cervical, and spinal nerves, first two thoracic nerves, and sympathetic cervical plexus. The anterior and posterior circulation systems connect via the unpaired anterior communicating arteries (ACoA) and paired posterior communicating arteries (PComA), to form cerebral arterial system—circle of Willis. The circle of Willis is

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Fig. 1.3  Intracranial arteries and circle of Willis. 1. superior cerebellar artery; 2. basilar artery; 3. pontine branches; 4. vertebral artery; 5. anterior spinal artery; 6. posterior spinal artery; 7. anterior cerebral artery; 8. anterior communicating artery; 9. middle cerebral artery; 10. internal carotid artery; 11. posterior communicating artery; 12. posterior cerebral artery; 13. artery of labyrinth; 14. anterior and posterior cerebellar artery; I–VI cranial nerves

more polygonal than circular. The circle of Willis anatomically connects two carotid systems and also the anterior and posterior circulation systems. The “perfect” Willis’s circle is symmetric, consisting of intracranial parts of ICA, proximal parts of anterior and posterior cerebral arteries, and posterior communicating arteries (Fig. 1.3). Owing to the lack of a valvular system, blood flow through this circle can follow the direction of need. Two parts are connected through the anterior communicating artery in the front part and through the oral segment of the basilar artery in the back part. Functionally, the circle of Willis is an anastomosis between the arterial systems and plays an important role in compensation of hemodynamic changes.

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Analysis of geometrical structures of the Willis’s circle shows that typical (“classical”) anatomy is founded in approximately 30% of the population. The vessels of the circle of Willis vary in caliber and are often maldeveloped or even absent. Cerebral and communicating arteries, anterior and posterior, may be absent, hypoplastic, double, or triple (Riggs and Rupp 1963). Anomalies are mostly presented in the posterior part of the circle of Willis. The most frequent anomaly is absence of posterior communicating artery (6–10% of cases), while aplasia of the anterior communicating artery occurs in 0.5–3% of cases. Posterior trifurcation of internal carotid artery (emersion of posterior cerebral artery from ipsilateral internal carotid artery) occurs in 14–25% of cases, while anterior trifurcation (emersion of both anterior cerebral arteries from a single internal carotid artery) only in 7–16% (Riggs and Rupp 1963; Hendrikse et al. 2005; Kapoor et al. 2008). The intracranial venous circulation, assumed to be 60–70% of the global cerebral blood volume, does have an important role in the equilibrium of cerebral perfusion. Two important differences from the general venous system should be mentioned here. (1) Intracranial venous vessels do not collapse, even if the transmural pressure is zero. (2) There is complete absence of any venous valves up to the level of the internal jugular veins permitting free blood flow in any direction depending on need (Uflacker 2007). Structural units of the cerebral venous system are postcapillary venules, cerebral veins, and venous sinuses. Blood flows from postcapillary network into the intracranial veins. The intracranial veins can be divided into deep and superficial cerebral venous systems (Fig. 1.4). Superficial venous system is draining the blood from the hemispheres. It is supplied with blood from the major part of cerebral cortex and white substance and then provides blood mainly to the sinuses of cortex. The superficial veins over both hemispheres connect to a vascular network which can be classified, according to the flow direction, into ascending and descending veins. The ascending veins take the blood into the superior sagittal sinus (SSS), transverse sinus. The most prominent descending superficial veins are the vein of Labbé, draining into the transverse sinus (TS), and Sylvian vein, predominantly draining into the sphenoparietal sinus (SpPSs) (Fig. 1.4). The deep venous system of the brain is located in the cerebral parenchyma and consists of groups of venous trunks, which collect blood from transparent interseptum, plexuses and walls of lateral ventricles, subcortical nodes, optic thalamus, stem, and cerebellum. Deep system is formed by the internal cerebral veins, the basal veins of Rosenthal (BVR), and the thalamic veins. The site of drainage of this system is the great vein of Galen (VG) and the straight sinus (StS). The BVR usually drain posteriorly into VG. The VG mergers with a number of small profound veins and ten communicate to the StS, which is the main deep collector of venous blood. Superficial and deep venous systems are closely connected both through direct venous anastomoses and anastomoses of venous sinuses. Major part of blood from superficial and deep venous systems (2/3) flows into internal jugular vein through sinuses and 1/3 of this blood into external jugular vein through pericranial anastomoses (Sellar 1995).

1  Anatomy of Cerebral Circulation System

9

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Fig. 1.4  Anatomical overview of the cerebral veins and sinuses. Upper sinus group: 1. superior sagittal sinus; 2. inferior sagittal sinus; 3. straight sinus; 4. confluence of sinuses; 5. transverse sinus; 6. sphenoparietal sinus. Lower sinus group: 7. cavernous sinus; 8. inferior petrosal sinus; 9. sigmoid sinus; 10. superior petrosal sinus. Deep veins: 11. internal cerebral vein; 12. basal vein; 13. great cerebral vein; 14. internal jugular vein; 15. external jugular vein; 16. ophthalmic vein; 17. facial vein

The venous sinuses are the final recipients of the blood. Contrary to other intracranial veins, they cannot change their diameter as they are surrounded by an inflexible dural sheath. They then take the blood via the sigmoid sinus (SiS) to the IJV. Besides the CoS the paired cavernous sinuses (CS) are another major blood collector distributor. It drains blood from the orbit and from the Sylvian veins mainly via the SpPS. From there blood can be drained via the inferior petrosal sinus (IPS) or superior petrosal sinus (SPS) into the IJV. The external jugular vein drains mainly the scalp and face but also some deeper tissues. External jugular vein starts at the level of lower jaw angle, under the ear auricle, and then descends along the lateral surface of musculus sternocleido-mastoideus.

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1  Anatomy of Cerebral Circulation System

The internal jugular vein (JV) drains most of the blood from the skull, brain, and superficial and deep parts of the face and neck. It originates at the jugular foramen at the cranial base, in continuation with the sigmoid sinus. The vein is dilated at the beginning and is called the superior bulb. Behind the sterno-cleido-mastoideal muscle, the jugular vein connects with subclavian vein, and they both create the right and left brachiocephalic veins, the union of which then forms the vena cava superior. The vertebral vein is formed from numerous small tributaries from the internal vertebral plexus, which arise from the vertebral canal above the posterior arch of the atlas. It runs together with the VA through the costotransverse foramina of the two-­ sixth cervical vertebrae and opens in the subclavian vein. Based on a number of large-scale multicenter studies, a consensus was established on the indication to the examination of extra- and intracranial vessels, according to which examination of extracranial arteries is indicated in case of the following conditions: clinical signs of cerebrovascular insufficiency, headache, and high risk of cerebrovascular diseases (smoking, hyperlipidemia, obesity, arterial hypertension, diabetes mellitus, injury of other arterial systems—especially acute coronary syndrome, atherostenosis of lower limb vessels). Examination of intracranial arteries is indicated in case of the following conditions: cerebral circulatory disorders caused by the established stenosis or occlusive processes of extracranial arteries, indirect signs of damage to intracranial arteries, and signs of acute or chronic cerebral ischemia without the known reason; Changes in cerebral parenchyma established by neuroimaging (computer or magnetic resonance tomography). Examination of extra- and intracranial veins is indicated in case of stenosis or occlusive processes in the arterial or venous systems, for the purpose of studying their structure and assessment of permeability and embolic hazard of vessels, in case of deformations, anomalies, arterial and venous aneurisms, arterial and venous malformations, and vasospasm.

References Hendrikse J, Van Raamt AF, Van der Graaf Y et al (2005) Distribution of cerebral blood flow in the circle of Willis. Radiology 235:184–189 Kapoor K, Singh B, Dewan LI (2008) Variations in the configuration of the circle of Willis. Anat Sci Int 83:96–106 Lasjaunias P, Berenstein A (1987) Surgical neuroangiography – 1 functional anatomy of craniofacial arteries. Springer, New York, pp 1–426 Riggs HE, Rupp C (1963) Variation in form of circle of Willis. The relation of the variations to collateral circulation: anatomic analysis. Arch Neurol 8:24–30 Sellar RJ (1995) Imaging blood vessels of the head and neck. J Neurol Neurosurg Psychiatry 59(3):225–237 Uflacker R (2007) Atlas of vascular anatomy: an angiographic approach, 2nd edn. Lippincott Williams & Wilkins, Philadelphia Valdueza J, Schreiber S, Roehl JE, Klingebiel R (2008) Neurosonology and neuroimaging of stroke. Thieme, New York 383pp

2

Basic Principles of Hemodynamics

Just as hydrodynamics describe the motion of fluids, especially “ideal” liquid-water, and the interaction of the fluid with its boundaries, hemodynamics studies flow characteristics of blood and its interaction with the walls of the vessels and different obstacles in their lumen. The underlying principles of fluid mechanics applied to the flow of blood are a complex subject, which is discussed in detail in a number of tests including those by Strakee and Westerhof (1993), Wolf and Fobbe (1995), and Allan et al. (2000). In its journey from the heart to the tissues, the blood passes through vessels of six principal types: elastic arteries, muscular arteries, arterioles, capillaries, venules, and veins. In this system, the arteries show a progressive reduction in diameter as they recede from the heart, from about 25 mm in the aorta to 0.3 mm in some arterioles. The reverse is true for the veins; the diameter is small in the venules and progressively increases as the veins approach the heart. All arteries are comprised of three distinct layers, intima, media, and adventitia, but the proportion and structure of each vary with the size and function of the particular artery. Elastic arteries are aorta and pulmonary artery, as well as proximal segments of magistral arteries; elastic-muscular are large-caliber arteries (carotid, subclavian, pelvic, femoral, and other arteries). Elastic arteries have the thickest walls, containing a high percentage of elastic fibers in all three of their tunics. A big amount of elastic fibers enables them to maximally dilate during the systole and return to the initial condition during the diastole. Their function is to transport blood in permanent flow and amortize systolic pulse wave. An elastic artery is also known as a conducting artery, because the large diameter of the lumen enables it to accept a large volume of blood from the heart and conduct it to smaller branches. Farther from the heart, in relatively low-caliber vessels, where the surge of blood has dampened, the percentage of elastic fibers in an artery’s tunica intima decreases and the amount of smooth muscle in its tunica media increases. The artery at this

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Fridon Todua was deceased at the time of publication.

© Springer International Publishing AG, part of Springer Nature 2018 F. Todua, D. Gachechiladze, Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies, https://doi.org/10.1007/978-3-319-91367-4_2

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point is described as a muscular artery. Their thick tunica media allows muscular arteries to play a leading role in vasoconstriction. In contrast, their decreased quantity of elastic fibers limits their ability to expand. Fortunately, because the blood pressure has eased by the time it reaches these more distant vessels, elasticity has become less important. As it proceeds distally, one structural type of artery gradually transforms into the other. Precapillary vessels (end arteries and arterioles) are of a relatively small diameter and at the same time have walls with a well-developed smooth muscle layer. Arterioles have the same three tunics as the larger vessels, but the thickness of each is greatly diminished. The critical endothelial lining of the tunica intima is intact. The tunica media is restricted to one or two smooth muscle cell layers in thickness. The tunica externa remains but is very thin. Due to their structure, they greatly contribute to the peripheral resistance. Activity of muscle fibers causes changes in the diameter of vessels and, hence, in the traverse section of arteries. Given that hemodynamic resistance is directly dependent upon the diameter of the vessel, the role of these vessels in regulating the volume flow rate and microcirculation mode becomes obvious. Activity of the sphincteric precapillary arterioles determines the number of functioning capillaries and, hence, the size of their metabolic surface. Exchange of gases and other substances occurs in the capillaries between the blood and the surrounding cells and their tissue fluid (interstitial fluid). Flow through capillaries is often described as microcirculation. Capillaries have no traction ability. Their diameter changes passively, following the change of pressure in pre- and postcapillary resistance arteries and sphincters. While diffusion and filtration also take place in venules, the later also belong to metabolic vessels. Additionally, an arteriovenous anastomosis may bypass the capillary bed and lead directly to the venous system. Volumetric vessels include veins. Due to their passive extending capacity, veins have a role of a reservoir. According to the muscle elements in their walls, veins can be of muscle type and tissue type (without muscle elements). Tissue veins are those of the dura mater and pia mater, retina, bones, spleen, and placenta. All these veins are adhered to hard structures of corresponding organs and do not deflate. A venule is an extremely small vein, generally 8–100 μm in diameter. Multiple venules join to form veins. The walls of venules consist of endothelium, a thin middle layer with a few muscle cells and elastic fibers, plus an outer layer of connective tissue fibers that constitute a very thin tunica externa. Venules as well as capillaries are the primary sites of emigration or diapedesis. Veins conduct blood toward the heart. Compared to arteries, veins are thin-­ walled vessels with large and irregular lumens. Because they are low-pressure vessels, larger veins are commonly equipped with valves that promote the unidirectional flow of blood toward the heart and prevent backflow toward the capillaries caused by the inherent low blood pressure in veins as well as the pull of gravity. Unlike veins in the periphery, cerebral veins do not contain valves.

2  Basic Principles of Hemodynamics

13

For the pulsatile pumping action of the heart, blood flow in the arterial system is characterized by alternating phases of acceleration and deceleration. The varying intensities that influence the heart create both volume and pressure changes. The large vessels constitute a reservoir that is sufficiently compliant to store some of pulsatile energy of the heart and allow for a more continuous flow than that created by the heart alone. The magnitude of continuous flow component within the pulsatile flow cycle depends on the peripheral vascular resistance to flow. Flow resistance, especially at the arteries, gives rise to reflections of varying intensity that influence the flow velocity waveforms. According to distal resistance, all the arteries show two basic types of waveform representing pulsatile flow: (1) low-resistance flow arteries (carotid, vertebral, intracranial, renal, hepatic, splenic, genital arteries, truncus coeliacus) and (2) high-­ resistance flow arteries (limb arteries, aorta, superior mesenteric artery). The low-resistance flow type is characteristic of arteries that supply blood to parenchymatous organs and systems. The arteries supplying the brain, kidneys, liver, and spleen exhibit a more continuous flow pattern than demand-oriented vessels that supply the peripheral muscles and skin. The distal resistance in the arterial system of such organs is low in order to maintain a constant perfusion. In low-resistance flow arteries, the following peaks are seen in pulse wave: (1) systolic peak (maximal rate during systole), (2) catacrota (in the beginning left ventricle relaxation), (3) dicrotic wave (at closing of aortal valve), and (4) diastolic peak (in diastolic phase) (Fig. 2.1). In high-resistance flow arteries, the following peaks are distinguished: (1) systolic peak (maximal rate during systole), (2) early diastolic, and (3) late diastolic reversion phase, corresponding to diastole (Fig. 2.2). In normal physiological conditions, laminar blood current is seen in all segments of vascular system, where plasma and cells move in one direction, along the longitudinal axis of the vessel (Fig. 2.3). Flow rate of different liquid layers grows from the wall to the center; the laminar flow has a parabolic distribution of rate, with maximal value in the center. The smaller is the diameter of the vessel, the closer is the central liquid layer to the wall; due to the friction force, the flow slows down (considering the blood viscosity) (Hoskins et al. 1994; Stonebridge et al. 1996; Allan et al. 2000). In some conditions (bifurcation of vessel, stenosis, tortuosity) normal structuring of the current is broken and laminar flow turns into turbulent. Turbulent flow is chaotic and disarranged; blood particles move not only along the longitudinal axis of

dias. Sys.

Fig. 2.1  Low resistance flow profile

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2  Basic Principles of Hemodynamics

Fig. 2.2  High resistance flow profile

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Fig. 2.3  Principles of laminar and turbulent flow

the vessel but in different other directions, even perpendicular to the axis. Due to all this, the stable flow is breached. We often see similar processes in our everyday life. For example, in the narrow places or reaches of the rivers (Fig.  2.4), turbulence presents the same way as in human physiological conditions (ascending aorta, heart, bifurcation or physiological curve of arteries) or pathological conditions (stenosis, pathologic deformation) (Figs. 2.5 and 2.6). Obstacles on the way of the flow (stenosis, deformation, occlusion) cause both local and systemic hemodynamic changes: changes in flow pulse pressure and rate, as well as changes in energetic values (McDonald 1974).

2  Basic Principles of Hemodynamics Fig. 2.4  The pattern of flow of water in the river. Normal, calm flow in the wide segment and the increase of flow and turbulence in the narrow part of river

Fig. 2.5  Flow profiles within a curved vessel

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2  Basic Principles of Hemodynamics

Fig. 2.6 Arterial bifurcation. Flow profile changes

The type and degree of local and systemic hemodynamic abnormalities differ in macro- and microcirculatory circles and depend on several significant factors, such as (1) diameter and length of the stenosed segment, (2) condition of internal surface of the vessel (irregularity), (3) shape and asymmetry of the stenosed segment, (4) stenosed segment area ratio to the intact segment area, (5) gradient of arterial-­ venous pressure, (6) peripheral resistance distally to the stenosis, (7) the heart stroke volume, (8) rheological parameters of blood, (9) availability and degree of collateral compensation, and (10) stiffness permeability of the vascular wall. Apart of the listed factors, shear rate and shear stress are also very important, especially in microcirculatory circle (Zweibei and Knighton 1990). All the phenomena caused by stenosis may be divided into primary, secondary, and tertiary effects. Primary effect is local increase of flow rate (kinetic energy) in the area of stenosis. Secondary effect is change in rate and type of flow, fluctuation of pulse pressure, proximally and distally to the stenosis. Combination of the first and second factors provides for the so-called local hemodynamic shear. Tertiary effect of stenosis is seen in collateral transformations of distal hemodynamics and in changes of responsiveness of the vascular walls (Yonchareon and Young 1979; Khallifa and Giddens 1988). In case of 40% degree arterial stenosis, no local or systemic changes occur. If the degree of stenosis is within the range of 40–65%, primary and secondary factors arise. The higher is the degree of stenosis, the more intense the above effects are. Mean flow velocity decreases proximally to stenosis, and pulse pressure increases; in the direct proximity to the stenosis, the flow becomes turbulent. Flow profile changes from parabolic into linear. Apart of that, part of the flow energy transforms into the heat. The flow becomes much faster in the segment of stenosis, kinetic energy increases, and the flow pressure reduces. Distally to the stenosis, in the turbulent zone, the flow velocity decreases and loses its kinetic energy. In case of moderate stenosis, energy losses are insignificant. This is why, in the post-stenosis segment, both linear and volume parameters improve; tertian effects do not show up (Fig. 2.7).

2  Basic Principles of Hemodynamics

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Fig. 2.7  Schematic representation of flow profile changes in stenosis area

In case of over 60–75% degree of stenosis, both local and systemic effects appear. Local effects are much better expressed than in moderate stenosis. In the segment of critical stenosis, flow pressure and its potential energy tend to zero. Because of increased friction, energy losses grow in the stenosis and post-stenosis segments. According to the Hagen-Poiseuille law, the energy loss of flow is directly proportional to the length of the stenosed segment and inversely proportional to the fourth power of the vessel radius. The flow rate (the flow volume per unit time) is defined according to the Hagen-­ Poiseuille law: I = ( P1 − P 2 ) r π / 8 µ l, where the flow rate I is the flow volume per unit time, P1, P2 is the pressure difference (P) between two ends of the tube, L is the tube length, r is the radius of the tube, and μ is the viscosity. Additional energy losses are caused by acceleration of the flow and turbulence. The severity of energy losses also depends on the shape of stenosis. In case of “sudden” narrowing of the lumen, the losses are much higher than with gradual narrowing. In the poststenotic segment, the lumen is again wider, and the flow divides 4

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2  Basic Principles of Hemodynamics

into slow parietal and fast central layers. In the stenosed segment, parietal particles move slowly because of the low pressure, sometimes in the opposite direction (the flow is split). The negative effect of the increased shear stress and deranged flow causes damages to the endothelium, low-frequency vibration of the wall, and, in some cases, poststenotic dilation. Distally to the stenosis, the flow profile again becomes laminar, and parabolic shape is restored. Despite of this, together with the decrease of flow velocity and flow volume, perfusion pressure also reduces. In case of anastomosis of the damaged vessel with another intact system, the perfusion deficit is compensated through collateral distribution of blood. In the conditions of adequate collateral circulation, the deficit of perfusion distally to stenosis is practically fully compensated. If collateral circulation is insufficient, the deficit is compensated through the dilation of arteries, mainly in the microcirculatory network, in the result of metabolic changes caused by inadequate blood supply (hypercapnia, acidosis). Insufficiency of collateral and functional reserves results in the real perfusion deficit and the resultant clinical symptoms. Assessment criteria of hemodynamical significance of stenosis are still under discussion. The majority of authors believe that hemodynamically significant is such stenosis or occlusion, where perfusion pressure and arterial-venous gradient is reduced distally. The most accurate generally accepted method of assessment of hemodynamic changes is positron-emission tomography (PET), which shows perfusion deficit based on metabolic changes (Valdueza 2008). Veins secure back flow of blood to the heart. Blood runs from capillaries to the larger-caliber veins through venules and then into the heart. In terminal veins and venules, the flow is steady. In relatively wide veins, flow pressure and speed show oscillatory changes, caused by transmission pulsation of the adjacent arteries. In large-caliber veins, changes in the flow are caused by respiratory and heart activity. Phase changes in large-caliber veins are called venous pulse (Wolf and Fobbe 1995; Passariello et al. 2016). Blood flow in veins is secured firstly by the difference of pressure between the small- and large-caliber veins. This difference is relatively small, and this is why a number of factors contribute to the venous outflow: (1) so-called muscular pump, (2) respiratory pump, and (3) heart absorbing activity. Muscular pump acts through compression of skeletal veins in the process of muscle traction. This secures blood flow in one direction (to the heart). Venous valves prevent retrograde flow. Respiratory pump acts with the help of pressure gradient between the thoracic and abdominal cavities in respiratory process. During the inhalation of air, pressure in the thoracic cavity becomes negative and transmural pressure in the vessels increases. Thoracic vessels dilate, pressure falls, and blood is absorbed from the adjacent tissues. Increase of blood flow during inhalation is most expressed in vena cava superior. At the same time, the diaphragm lowers, and pressure in the abdominal cavity increases with the resultant reduction of transmural pressure in abdominal vessels. Gradient between the thoracic and abdominal veins stimulates the blood flow into the thoracic veins, while the backflow to lower limbs is prevented by

2  Basic Principles of Hemodynamics

19

venous valves. During exhalation the vessels act in the opposite way. Respiratory pump activity is best expressed during deep breathing. Heart activity helps absorbing blood from the nearby veins. During the ejection phase, atrioventricular valve moves down and pressure in the right atrium and adjacent magistral veins reduces, causing thus inflow of blood into the heart. In normal conditions blood circulation in venules and terminal veins is constant, because only significant dilation of resistant vessels can enable passing pulse wave to the veins. In larger veins pressure and speed changes may occur in the result of transmission movements of the adjacent arteries. Changes of blood flow in magistral veins are caused by respiration and heart beating. These changes increase as approaching the right atrium. Changes of flow pressure and rate in large-caliber veins are called venous pulse. Its genesis is different from the one of the arterial pulse. It is caused by blood absorbing inflow and outflow during systole and diastole. Curve of the venous pulse is called phlebogram. It shows a number of specific curves (Fig. 2.8). The first positive wave, a-wave, corresponds to contraction of atriums. In short time the second positive c-wave appears, caused by lowering of atrioventricular valve into the right atrium during isovolumetric contraction of ventricles. Then a rapid lowering (s-wave) occurs, which corresponds to the displacement of valves to the apex during the ejection phase. During relaxation of the right ventricle, the atrioventricular valves remain closed and pressure in veins gradually increases. When the valves open and blood runs into the ventricles, pressure falls. After these stages the third positive v-wave appears, followed by incisurad. Together with filling of ventricles, the curve increases to a new a-wave. A

HEP. VEIN VELOCITY TRACING

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Fig. 2.8  Venous pulse (definition is in text)

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ATRIAL SYSTOLE VENTRICULAR DIASTOLE

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2  Basic Principles of Hemodynamics

Venous circulation generally and vascular conditions (insufficiency of valves, thrombosis, extravasal compression) are greatly influenced by myocardial contractile function. Stenosis and occlusive processes in the venous system are usually caused by thrombosis. The primary effect of thrombosis, expressed in local hemodynamic disorders, occurs only in case of full occlusion of the lumen. Partial thrombosis does not cause any significant hemodynamic disorders (no local hemodynamic shear in the venous system), which is explained by low values of flow rate and total energy in the venous system. The secondary effects of thrombosis are expressed in compensatory transformation of collateral system. Blood flow in collateral vessels significantly increases, causing dilation of the lumen and gradual deterioration of the valve with its final insufficiency. Tertiary effects of thrombosis are caused by recanalization. In rechanneled veins the walls are rigid and sclerotic, without valves. Expressed insufficiency of valves causes peripheral stasis, further complicated by changes in the walls of the venous vessels. Unlike arterial system, any occlusion in venous system is hemodynamically significant, because collateral circulation only temporarily corrects hemodynamic disorders. Histological transformation of the walls of collateral veins and changes of the valve system in the course of time cause deterioration of the compensation process and development of chronic venous insufficiency.

References Allan P, Dubbins P, Pozniak M, McDicken WN (2000) Cinical doppler ultrasound. Churchill Livingstone, London 292pp Hoskins PR, Fleming A, Stonebridge P, Allan P, Cameron DC (1994) Scan-plane vector maps and secondary flow motions. Eur J Ultrasound 1:159–169 Khallifa AMA, Giddens DP (1988) Characterization and evolution of poststenotic flow velocity field. Ultrasound Med Biol 14:269–227 McDonald DA (1974) Blood flow in arteries, 2nd edn. Edward Arnold, London Passariello F, Beach K, Francheschi C et al (2016) Basic science of venous hemodynamics. Acta Phlebol 17(2):37–51 Stonebridge P, Hoskins PR, Allan P, Belch JF (1996) Spiral laminar flow in vivo. Clin Sci 91:17–21 Strakee J, Westerhof N (1993) The physics of heart and circulation. Institute of Physiscs, Bristol Valdueza J, Schreiber S, Roehl JE, Klingebiel R (2008) Neurosonology and neuroimaging of stroke. Thieme. 383pp. Wolf KJ, Fobbe F (1995) Color duplex sonography. Principles and clinical application. Thieme, New York 308pp Yonchareon W, Young D (1979) Initiation of turbulence in models of arterial stenoses. J Biomech 12:185–196 Zweibei WJ, Knighton R (1990) Duplex examination of the carotid arteries. Semin Ultrasound CT MR 11(2):97–135

Part II Basic Principles of Non-invasive Vascular Diagnostics

3

Main Principles of Ultrasound Examination

The role of ultrasound examination along with the other up-to-date methods of diagnostics is stably increasing. High-technology diagnostics in angioneurology is impossible without ultrasound examination. Doppler sonography has significant advantages for vascular diagnostics, in comparison with other methods, while it gives possibility to study a vessel of any caliber without inflicting injury to the patient. At the same time, ultrasound studies are limited by the significant variability of the received data, caused by different intrinsic and human factors. It should be considered that like the other methods of radiodiagnostics, the results of study are greatly dependent upon the equipment software, investigator’s professional skills, and study purpose. Recently, diagnostic studies have been divided according to their purposes, by two qualitative levels: first level, detection of the disease and screening, and the second level expert examination. Duplex sonography is a combined method of study, namely, a combination of conventional sonography (visual assessment of vessels) and Doppler sonography. It provides for the study of topography, morphology, and hemodynamics of vessels. Scanning in real-time mode (B-mode) gives information about the anatomy of vessel. Image is received because of the special property of ultrasound to reflect from the tissue with different acoustic resistance. High resistance of the vascular walls gives clearer images than the lumens (blood). In B-mode it is possible to see the picture of the lumen, walls, surrounding tissues, and current morphological changes. It is also possible to receive information about the reasons of circulatory disorders, such as atherosclerosis, embolism, arteritis, extravasal compression of vessels, aneurism, pathological tortuosity, etc. For visual study of vessels, it is necessary to assess the following values:

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Fridon Todua was deceased at the time of publication.

© Springer International Publishing AG, part of Springer Nature 2018 F. Todua, D. Gachechiladze, Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies, https://doi.org/10.1007/978-3-319-91367-4_3

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• • • • • • • •

Permeability (patent, stenosed, occluded) Size (normal, hypoplasia, dilation) Location and direction, deformation, tortuosity, and deviation Type of pulsation (increased, weakened, absent) Pathologic changes in the lumen (atherosclerotic plaque, thrombi, dissection) Structure, size, and spread of plaques and thrombi Structural characteristics of vascular walls (assessment of intima-medial layers) Condition of surrounding tissues (echogenicity, pathologic mass)

B-mode has some disadvantages, namely, occlusion may significantly complicate identification of vessel lumen. It should also be mentioned that a new thrombi cannot be distinguished from lumen by its echogenicity. At the same time, assessment of pulsation is dependent on human factors. Doppler ultrasonography gives information about the physiology of the blood. The method is based on the so-called Doppler effect, when ultrasound signal changes frequency after reflecting moving elements (red blood cells). The Doppler equipment registers changes between emitted and received ultrasound signals. Doppler sonography makes it possible to study moving structures (flowing blood cells), receive graphical images, and analyze quantitative and qualitative parameters of blood flow. Qualitative analysis shows the nature of the blood flow in the vessel. One of the main parameters for the flow investigation is the type of Dopplerographic curve. In low-resistance arteries, Doppler curves present the following peaks: 1 . Systolic peak (corresponds to the maximal flow rate during systole) 2. Catacrota (corresponds to the start of relaxation period) 3. Dicrotic wave (corresponds to the closure of aortal valve) 4. Diastolic peak (corresponds to the diastolic phase) (Fig. 3.1) In highly resistive arteries, the curve presents the following peaks: 1 . Systolic (corresponds to the maximal flow rate during systole) 2. Early diastolic 3. Late diastolic reversion phase (corresponds to diastole) (Fig. 3.2) In normal physiological conditions in all segments of the vascular system, the flow is laminar. It is presumed that in case of such flow, all the blood particles move along the longitudinal axis of the vessel. Parietal blood layer remains still, the second layer slides along it, etc. As a result, the flow distribution profile is parabolic, with maximal flow rate in the center of the lumen. Laminar flow has a small range of flow rates and, consequently, a small range of spectrum parts. Scope of limitations creating the so-called arterial window is also small (McDonald 1974; Hoskins et al. 1994; Stonebridge et al. 1996; Allan et al. 2000). In case of turbulency, the flow is uneven, deranged; the particles move not only along the longitudinal axis but also at certain angles to it, which causes deformation

3  Main Principles of Ultrasound Examination

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Fig. 3.1  Low peripheral flow resistance spectrum—high diastolic forward flow

of the flow rate profile. Turbulency occurs also in physiological conditions, for example, in places of arterial bifurcation or flexion (Khallifa and Giddens 1988; Taylor et al. 1988; Allan et al. 2000). Obstacles on the way (e.g., atherosclerotic plaques) change the type of flow. Hemodynamically important is such vasoconstriction, which causes reduction of blood flow and decrease of perfusion pressure in distal segments, which in turn is the reason of organ ischemia. Turbulence is expressed when the lumen is constricted by >50%. In such conditions the speed of particles differs, and the range of spectral frequencies grows, which is visually expressed in completion of arterial window. In maximal turbulence some currents move in the direction opposite to the main flow, in the result of which negative particles appear in spectrum and are registered below the isoline (Fig. 3.3). Quantitative analysis of the Doppler spectrum is based on the Doppler effect, which was described by Christian Doppler in 1842. According to the Doppler formula, the linear speed of the flow is directly proportional to the so-called Doppler-shift difference in frequency of emitted and received ultrasound signals (White 1982). The relation is expressed in the following formula:

V = ÑFC / 2 F cos a

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3  Main Principles of Ultrasound Examination

Fig. 3.2  High peripheral flow resistance spectrum—peripheral artery pattern

Fig. 3.3  Schematic representation of poststenotic hemodynamic changes

where V is the speed of flow, C the rate of distribution of ultrasound in the environment (in case of blood—1570 cm/s), F the frequency of sent signal, ∇F the Doppler shift, and α the angle between the ultrasound and flow axis.

3  Main Principles of Ultrasound Examination

27

Quantitative (linear) Doppler parameters include: 1. Peak systolic velocity—Vps 2. Maximal end diastolic velocity—Ved 3. Time-averaged maximal velocity—TAMX 4. Time-averaged average flow velocity—TAV 5. Peripheral resistance, or the so-called Pourcelot index—RI 6. Pulsation (Gosling) index—PI 7. Spectral broadening indexes—SBI 8. Relation of systolic and diastolic velocities—S/D 9. Acceleration time—AT 10. Acceleration index—AI Flow volume (amount of blood running through the vessel during certain time) is calculated according to the following formula: Q = VA = V pr 2 where V is linear velocity, A lumen area, and r radius of the vessel. Based on flow continuity principle, the volume flow (flow rate per unit time) in the intact segment of the vessel equals the flow volume rate in the stenosal part of the vessel:

Q1 = Q2



V1A1 = V2 A2



V2 / V1 = A1 / A2

where Q1 and Q2 are the flow volume in the intact and stenosis zones, V1 and V2 the linear velocities in the corresponding segments, and A1 and A2 the lumen areas in the intact and stenosis zones. The detection and assessment of the severity of vascular stenoses with Doppler ultrasound are based on determination of the relative velocity increase or Doppler frequency shift that is produced by the stenosis zone. Relation of linear velocity to the degree of stenosis (V2/V1) is expressed in the diagram (Fig. 3.4). Flow velocities in the zone of stenosis significantly increases. Kinetic energy also increases, while the pressure consequently falls. In case of critical stenosis (>80%), friction causes significant losses of energy; as a result, flow speed tends to zero (Taylor et al. 1988). Apart from velocity/frequency values, it is very important to assess other flow parameters of Doppler spectrum, so-called pulsatility indexes. Such indexes describe the pulsatility of blood flow. In practice, indexes discussed here are used mainly for assessing the peripheral vascular resistance. The most frequently used are Gosling (pulsatility) and Pourcelot (resistance) indexes. Pulsatility index (PI, Gosling index) is calculated according to the following formula (Gosling and King 1974):

PI = ( Vps - Ved ) \ TAMX

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3  Main Principles of Ultrasound Examination

600

500 Blood Flow Volume 400 300

200 100

Blood Flow Velocity

Velocity cm/sec 50%

60% 70%

80% 100%

Percent Diameter Stenosis

Fig. 3.4  Relative increase in flow velocity versus degree of stenosis

The resistance index (RI, Pourcelot index) is calculated according to the following formula (Pourcelot 1974):

RI = ( Vps - Ved ) \ Vps

where Vps is the maximal linear velocity, Ved the end diastolic linear velocity, and TAMX the average velocity during the cardiac cycle. These indexes are especially valuable, as they are independent on the Doppler angle and on several reasons affecting the values of linear velocity. Ultrasound diagnostics of vascular pathologies has significantly improved after invention into clinical practice of duplex scanning mode. This method is a combined ultrasound technique which allows a morphologic and hemodynamic investigation of vessels, to assess vessel patency. It is possible using Doppler ultrasound sample volume under visual control to record a spectral waveform to the vessel section of interest. The flow parameters are studied only in the selected section of interest. Changes in circulation indicate the possible obstacles even when they are not visible (e.g., isoechogenic plaques, thrombi, or artifacts). This method provides for the correction of angle between the lumen and ultrasound beam, which is essential for adequate estimation of the flow rate. Flow rate is assessed with the help of so-called pulse or continuous wave Doppler modes. Latest ultrasound devices are mainly equipped with pulse-Doppler systems (Wolf and Fobbe 1995; Allan et al. 2000). The pulse-Doppler mode is based on the principle, whereby the same piezoelectric element serves both as a transmitter and receiver. The Doppler ultrasound signal is received in the interval between two pulses. By setting a receiving time period

3  Main Principles of Ultrasound Examination

29

through gating, only those ultrasound signals which are reflected from the objects situated at a corresponding depth will be evaluated. This method is particularly important for vascular studies for the advantage to determine the depth of the received echosignal (an assumption is made that ultrasound spread with as average speed of 1540 m/s in soft tissues). Area, where the flow parameters are studied, is called control volume. The main advantage of this method is that it makes possible to study the flow in a strictly limited segment, while its main disadvantage is its inability to study high-speed flows (study of high-speed flows requires corresponding growth of impulse frequency). If the flow rate exceeds a certain limit implied by impulse frequency, this causes aliasing of spectrum. In order to study the flow spectrum, the transducer should be positioned so that the insonation angle is as small as possible. By manually positioning the cursor parallel to the vessel wall, the insonation angle can be measured. The control volume cursor must be placed in the middle of the lumen in the interest zone (e.g., in the pre-stenotic, stenotic, or post-stenotic segment). Angle between the ultrasound beam and longitudinal axis of the vessel must be corrected. Scanning angle must not possibly exceed 60°, as a larger angle may deteriorate the results (Wolf and Fobbe 1995; Bartels 1998; Allan et al. 2000). By continuous wave (CW) Doppler—technically the most simple method—the sound is emitted from a piezoelectric element and received by another piezoelectric element continuously. That’s why the CW Doppler has no depth resolution, i.e., it does not give a possibility to determine the exact location of control flow. Theoretically there is no upper limit to the detectable Doppler frequency. Main advantage of this mode is the possibility to describe both low and high speeds. This method is most efficiently used in echocardiography (Spencer and Reid 1979; Taylor et al. 1988; Carpenter et al. 1995). Recently, the possibilities of duplex scanning have significantly expanded due to the new technologies based on Doppler effect. This applies to color and power Doppler modes. Both of those methods can detect the flow in real-time mode. Color Doppler mode (CFM, color flow mapping; CDV, color Doppler velocity; CFI, color flow imaging; CF, color flow) is composed of gray-scale and a color part. It gives us possibility to simultaneously identify the vessel, detect its anatomic location, assess the lumen and walls (for focal damages) (B-mode), and also estimate the flow parameters in real-time mode (spectral analysis), distribution of rates in the lumen, changes in the direction, and profile of the flow (Mitchell 1990; Wells 1998). Color Doppler provides ordinary gray-scale images in real-time mode. It is used to evaluate structural characteristics of tissue. Color encoding indicates movement within the image field. Signals reflected from the static tissues remain in the gray-­ scale images. Signal reflected from the moving object (RBC) initially has a different velocity, thus creating Doppler shear frequencies (Doppler effect). At any place of Doppler shear, its feature is coded by a specific color. Most ultrasound machines display blood flow in different hues of red and blue. One color represents flow toward the transducer (conventionally coded in red) and the other color flow away from the transducer (conventionally coded in blue).

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3  Main Principles of Ultrasound Examination

Deviation from the average rate is coded in yellow (white) or green, and turbulence is visualized as mosaic mixture of red, blue, green, and yellow. Green is also used as a velocity marker for either individual velocities or a range of blood flow velocities. Coding of flow direction and its rate in different colors simplify the detection of vessels, provide for rapid distinguishing of arteries and veins, and give possibility to assess their location and structure (Fig. 3.5a). In 1993 power Doppler was implemented in medical practice (CDE, color Doppler energy; CPA, color power angio; PD, power Doppler; PDI, power Doppler imaging; UA, ultrasound angio). In comparison with conventional color Doppler, where the relation of Doppler signal frequencies is coded with color signals, power Doppler codes range (energy or power) of signals. Unlike the color Doppler, power Doppler reveals acoustic energy of red blood cells and thus is less dependent upon the speed of RBC or scanning angle. This is why power Doppler gives the possibility to detect a low-speed flow and assess general vascularization of the given area. Power Doppler seems rather efficient in examination of magistral vessels, for distinguishing preocclusive stenosis and occlusion and also in case of nonhomogenous atherosclerotic plaques (Fig. 3.5b). This method helps to accurately reveal the outlines of plaques (irregular surface, niche) (Bluth 1997; Steinke et al. 1997; Valdueza 2008; Naim et al. 2014). a

b

Fig. 3.5  Internal carotid artery stenosis at the origin. (a) Color Doppler mode, (b) power Doppler mode. Flow is reversed distal to the plaque

References

31

References Allan PL, Dubbins PA, Pozniak MA, McDicken WN (2000) Clinical Doppler ultrasound. Churchill Livingstone, London 292pp Bartels E (1998) Color duplex sonography examination of extra-intracranial vessels. Schattauer, Stuttgart Bluth EI (1997) Evaluation and characterisation of carotid plaque. Semin Ultrasound CT MR 18(1):57–65 Carpenter JP, Lexa F, Davis J (1995) Determination of sixty percent or greater carotid artery stenosis by duplex Doppler ultrasonography. J Vasc Surg 22(6):697–703 Gosling RG, King DH (1974) Arterial assessment by Doppler-shift ultrasound. Proc R Soc Med 67:447–449 Hoskins PR, Fleming A, Stonebridge P, Allan P, Cameron DC (1994) Scan-plane vector maps and secondary flow motions. Eur J Ultrasound 1:159–169 Khallifa AMA, Giddens DP (1988) Characterization and evolution of poststenotic flow velocity field. Ultrasound Med Biol 14:269–227 McDonald DA (1974) Blood flow in arteries, 2nd edn. Edward Arnold, London Mitchell DG (1990) Color Doppler imaging: principles, limitation and artifacts. Radiology 177:1–10 Naim C, Douziech M, Therasse É et al (2014) Vulnerable atherosclerotic carotid plaque evaluation by ultrasound, computed tomography angiography, and magnetic resonance imaging: an overview. Can Assoc Radiol J 65(3):275–286 Pourcelot L (1974) Applications cliniques de l’examene Doppler transcutaé. Les Colloques de l’Institut national de la Sante et de la Recherche medicine, vol 34. INSERM, Paris, pp 213–240 Spencer MP, Reid JM (1979) Quantitation of carotid stenosis with continuous wave (CW) Doppler ultrasound. Stroke 10:326–330 Steinke W, Ries S, Artemis N et  al (1997) Power Doppler imaging of carotid artery stenosis. Comparison with color Doppler flow imaging and angiography. Stroke 10:19811–11987 Stonebridge P, Hoskins PR, Allan P, Belch JFF (1996) Spiral laminar flow in  vivo. Clin Sci 91:17–21 Taylor KJW, Burns PN, Wells PNT (1988) Clinical application of Doppler ultrasound. Raven press, New York Valdueza J, Schreiber S, Roehl JE, Klingebiel R (2008) Neurosonology and neuroimaging of stroke. Thieme, Stuttgart 383pp Wells PNT (1998) Ultrasound in vascular pathologies. Eur Radiol 8:849–857 White DN (1982) Johann Christian Doppler and his effect - a brief history. Ultrasound Med Biol 8:583–591 Wolf KJ, Fobbe F (1995) Color duplex sonography. Principles and clinical application. Thieme; 308pp.

4

Ultrasound Examination of Extracranial Vessels

Ultrasound study of extracranial vessels is performed in supine position of the patient. The head should be slightly elevated if desired. The patient should be comfortably positioned with the head resting on the examination bed to avoid neck muscle tension. For better visualization, the neck must be straightened and turned to the opposite direction (Carroll 1996; Bartels 1999; Valdueza et al. 2008). For investigation of neck vessels, linear transducer is used, mainly with operating frequency 7.0–7.5 mHZ. The latest ultrasound equipment implies transducers with frequency range of 5–18 mHZ, which enables to see not only the structure of neck vessels but also relatively profound structures. Carotid Arteries  It is recommended to start examination from the midcervical region of the neck in transverse plane. The CCA can be immediately located. In transverse plane exact position of bifurcation is detected. After that the investigation is proceeded in longitudinal plane. After detection of bifurcation, by slightly angling the transducer medially, the origin of the external carotid artery (ECA) is visualized by angling it laterally the origin of the internal carotid artery (ICA) is displayed. The ICA, ECA, and CCA are carefully traced in longitudinal plane over the entire imageable segment (cephalad to the angle of mandible and caudad to the origin of the CCA). Ultrasound image of ICA (in B-mode) differs from ECA by a larger diameter (especially carotid sinus and bulbus). In the first segment ICA is mainly located laterally, and ECA—medially. Apart from that, the branches of ECA are rather often (50–60%) clearly visible in proximal part (Bartels 1999; Valdueza et  al. 2008). Doppler spectrum parameters are used for final differentiation of internal and external arteries (Fig. 4.1).

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Fridon Todua was deceased at the time of publication.

© Springer International Publishing AG, part of Springer Nature 2018 F. Todua, D. Gachechiladze, Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies, https://doi.org/10.1007/978-3-319-91367-4_4

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Fig. 4.1 Longitudinal image of carotid bifurcation. Color Doppler

Diameter of CCA is in the range of 6.2–7.3 mm. At the same time, the diameter of the left CCA is usually more than of the contralateral one. Normally, the diameter of ICA is within 4.1–5.5 mm, while the dimeter of ECA is within 3.5–5 mm (Lelyuk and Lelyuk 2003). Normal vessel is visualized in gray-scale image as anechogenic tubular structure, free from echogenic fills (plaques, thrombi, etc.); intimal surface is thin and even, without separation. In color mapping mode, the lumen fills completely; flow type is laminar. Arterial walls are smooth, clearly distinguished from lumen. In the area of CCA bifurcation, a moderate physiological turbulence may be detected. The Doppler spectrum waveform of the ICA is characterized by a relatively smooth systolic peak and high diastolic component. Such flow is typical for arteries which supplies cerebral parenchyma, with a low peripheral flow resistance (Fig. 4.2). The flow dynamics of the ICA during a cardiac cycle can be assessed by Color Doppler mode. The color filling of the lumen is clearly visible during systole and diastole due to the high diastolic flow (Middeton et al. 1988; Steinke et al. 1990; Wolf and Fobbe 1995). The ECA is generally located medially to the ICA. Due to the high peripheral resistance in the supply territory (head and facial muscles, scalp), the flow has a relatively low diastolic component in its spectral waveform. In doubtful cases, ECA is detected by the repetitive compressions of branches (temporal or facial arteries), which causes oscillations in the ECA spectrum. Audio signal from ICA is softer and somehow hissy and more distinct in comparison with ECA (Spencer 1979; Bluth et al. 2008). Together with flow rate parameters, resistance index (RI) is another important diagnostic parameter, which in norm is within the range of 0.5–0.75. Increase of RI indicates high resistance—obstacle in the distant segment (Zweibei and Knighton 1990; Carroll 1996; Allan et al. 2000).

4  Ultrasound Examination of Extracranial Vessels

35

a

b

Fig. 4.2  Flow profile in common carotid artery (CCA) (a), internal carotid artery (ICA) (b), external carotid artery (ECA) (c)

36

4  Ultrasound Examination of Extracranial Vessels

c

Fig. 4.2 (continued)

Duplex scanning of vertebral arteries (VA), in comparison with carotid arteries, was for a long time unavailable because of their anatomic peculiarity causing technical difficulties in detecting their location (White 1996; Bartels 1999). VA consists of several segments: V0—origin. V1—from origin to costotransverse gap of the sixth vertebra. V2 (pars transversaria)—segment within the costotransverse channel of the second to sixth vertebras. V3—segment in the atlas region—at the level of the second vertebra, after exit from the transverse process, VA inclines in the lateral posterior direction, proceeds to the transverse process of the Atlanta vertebra, goes through it, and makes a curve. V4—intracranial segment—from great foramen to the connection with contralateral artery.

4  Ultrasound Examination of Extracranial Vessels

37

All segments of VA are available for ultrasound examination; however, V2 segment is the most convenient in terms of location. Implementation of Color Doppler has solved a number of methodological problems and enabled routine examinations of vertebral arteries. Transducer is positioned in the midcervical region, paramedian perpendicularly in the anteroposterior plane. V1 distal and V2 proximal segments are best visualized from this position. Because of acoustic shadow caused from transverse processes of C6-C3 vertebrae, this segment is easily visualized also in B-mode image. Between the traversal processes of cervical vertebrae, the vertebral artery is practically straight. The corresponding vertebral vein usually is located ventrolaterally, parallel to the artery. Turning the probe in the anteroposterior plane caudal to the supraclavicular fossa is possible to visualize the origin and a pretransversal segment V1. For visualization of the VA in the atlas region (V3 segment), the transducer is placed under the mastoid process. Visualization of V1 and V2 is possible both in B-mode and color mapping mode. It is desirable to use both modes for complete investigation. B-mode is used for assessment of morphology of the walls and studying of lumen microstructure, while color mapping mode for studying of its structural particularities (hypoplasia, tortuosity). V1–V3 segments are studied in horizontal position of the patient, when lying, while V4 segment—in the sitting position, with head maximally protruded to the front. It is possible to mix the V0 segment of VA with thyrocervical trunk and V3 segment with occipital artery. VA is located in the medial part, behind the carotid artery. Diameter can be measured both in V1 and V2 segments. Average diameter is 3.5 ± 0.48 mm. However, bigger diameters of up to 5–5.5 mm are not very rare. Reduction of VA diameter up to 3 mm is considered its hypoplasia. Asymmetry of VA diameter is quite frequent, in some cases achieving 200% of its contralateral part (Carroll 1996; White 1996; Bartels 1998). Normal values of diameters, also flow velocities and flow volumes of magistral extracranial arteries, are shown in Table 4.1. Table 4.1  Flow parameters in extracranial arteries in healthy subjects Diameter, Artery mm CCA 5.5 ± 0.3 4.2–6.9 ICA 4.5 ± 0.6 3–6.3 ECA 3.6 ± 0.6 2–6 VA 3.5 ± 0.5 1.9–4.4

Vps, sm/s 72.5 ± 15.8 50–104 61.9 ± 14 32–100 68.2 ± 19.5 37–105 41.3 ± 10.2 20–61

V ed., sm/s 18.2 ± 5.1 9–36 20.4 ± 5.9 9–35 14 ± 4.9 6–27 12.1 ± 3.7 6–27

TAV sm/s 38.9 ± 6.4 15–46 30.6 ± 5.5 14–45 24.8 ± 7.7 12–43 20.3 ± 6.7 6–23

RI 0.74 ± 0.07 0.6–0.87 0.67 ± 0.07 0.5–0.84 0.82 ± 0.06 0.62–0.93 0.7 ± 0.07 0.56–0.86

PI 2.04 ± 0.56 1.1–3.5 1.41 ± 0.5 0.8–2.82 2.36 ± 0.65 1.15–3.95 1.5 ± 0.49 0.6–3.0

Vvol, ml/ min 484 ± 94 348–672 257 ± 56 154–413 191 ± 69.9 64–370 93 ± 33 38–182

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References Allan PL, Dubbins PA, Pozniak MA, McDicken WN (2000) Clinical Doppler ultrasound. Churchill Livingstone, London 292pp Bartels E (1999) Color duplex sonography examination of extra-intracranial vessels. Schattauer, Stuttgart Bluth EI, Benson CB et al (2008) Ultrasonography in vascular diseases. A practical approach to clinical problems, 2nd edn. Thieme, New York Carroll BA (1996) Carotid ultrasound. Neuroimaging Clin N Am 6(4):875–897 Lelyuk VH, Lelyuk SE (2003) Ultrasound angiology. Nastoyashcheie vremia, Moscow, p 336 In Russian Middeton WD, Foley WD, Lowson TL (1988) Color flow Doppler imaging of carotid artery abnormalities. Am J Roentgenol 150:419–425 Spencer MP, Reid JM (1979) Quantitation of carotid stenosis with continuous-wave (C-W) Doppler ultrasound. Stroke. 10(3):326–330 Steinke W, Kloetzsch W, Hennerici M (1990) Carotid artery disease assessed by color Doppler flow imaging: correlation with standard Doppler sonography and angiography. Am J Roentgenol 154:1061–1068 Valdueza J, Schreiber S, Roehl JE, Klingebiel R (2008) Neurosonology and neuroimaging of stroke. Thieme, New York 383pp White DN (1996) Vertebral ultrasonography. In: Zweibei WJ (ed) Introduction to vascular sonography. WB Saunders, Philadelphia Wolf KJ, Fobbe F (1995) Color duplex sonography. Principles and clinical application. Thieme. 308pp. Zweibei WJ, Knighton R (1990) Duplex examination of the carotid arteries. Semin Ultrasound CT MR 11(2):97–135

5

Technical Aspects of Computer Tomography and CT Angiography

In the beginning of the 1970s, invention of computer tomography (CT) by G. Hounsfield was considered the biggest achievement in the history of radiology after the X-ray. This method for the first time gave the possibility to visualize the living brain (Ambrose and Hounsfield 1973). For developing and implementing of the CT method McCormack and Hounsfield were awarded the Nobel Prize. CT was first used for brain investigation. After developing of new generation equipment in 1976–1977, investigation of other organs also became possible. Since then several generations of tomographs have been created, with different numbers of detectors and different power of computer hardware. Broad implementation of CT has become possible only after creation of the third-generation equipment. This equipment was based on X-ray tube and a movable block containing hundreds of detectors. The third-generation CT reduced scanning time up to several seconds, and further developments to hundredth parts of a second. CT has a number of advantages in comparison with the conventional X-ray examination, namely: (1) High sensitivity, enabling to distinguish different organs and tissues according to their density (in the range of about 1–2% and 0.5% in the fourth-generation devices). In classic X-ray examinations, this range is 10–20%. (2) Possibility to examine each layer separately enables us to avoid summation of opacities (3) Possibility to determine size, exact location, and density of each organ, tissue, and pathologic lesion.

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Fridon Todua was deceased at the time of publication.

© Springer International Publishing AG, part of Springer Nature 2018 F. Todua, D. Gachechiladze, Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies, https://doi.org/10.1007/978-3-319-91367-4_5

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5  Technical Aspects of Computer Tomography and CT Angiography

(4) Possibility to study the relationship of a pathological lesion with surrounding structures. (5) Possibility to determine absorption ratio for each tissue and organ. Speed of scanning and receiving of information depends on the construction of tomograph and the method of contrasting. As mentioned above, CT is made from slice to slice, using step-by-step table movement. During examination of one slice, the tomograph table is motionless, while the X-ray tube and detectors make a complete circle. In this process hundreds of views are made, based on which the image is reconstructed. After this the table makes a following step, and the next layer is examined. With standard CT the quality of three-dimensional reconstruction is low (especially for vascular systems). Such systems are less informative for investigation of moving organs, while during dynamic contrast examination, it is possible to contrast only a limited number of slices. Creation of spiral, multislice (spiral, helical, multislice) CT equipment at the end of 1980s was a revolutionary event in medicine. First models of spiral CT (SCT) were created by Siemens and Toshiba. Spiral and multislice CT equipment requires permanent rotation of X-ray tube simultaneously with displacement of table. According to the “X-ray tube-detector” system, these tomographs belong to the fourth generation. After the introduction of helical/spiral CT in 1990 by W. Kalender, this technique was considered an alternative for conventional angiography in selected cases (Kalender and Polacin 1991). In multislice computer tomographs, the X-ray tube moves spirally along the patient’s body. Inside the gantry there is a hole of 50–77 cm diameter, and in the process of scanning, the patient table is moving along this hole (Fig. 5.1). Constant motion of the X-ray tube gave rise to the new technologies of electric energy supply and receiving of information from the detectors. Spiral and multislice CT equipment implies super powerful computer systems with large memory and quick response, which ensures reconstruction of image in short time.

Fig. 5.1  Rotation of the X-ray tube in spiral/ multislice CT

5  Technical Aspects of Computer Tomography and CT Angiography

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Spiral and multislice CT technology is based on the movement of a patient toward the rotation of the X-ray tube in the process of scanning. X-ray beam passes the patient’s body and moves at constant speed spirally around the rotation center and at right angle to the slice; time of scanning corresponds to the time of table movement, which enables to perform scanning 3–4 times faster than with the same class ordinary scanner. In new generation of tomographs, thousands of high-sensibility detectors are used, and the time of scanning spent on one slice reduced first to 1 s, and later, in tomographs of the latest generation, to milliseconds. In spiral or multislice CT study, a very important term is pitch—a step of a spiral expressed in slices. Pitch is the relation of table movement to the thickness of slice during one full rotating circle of the tube. For example, if during the full cycle one slice is scanned, then pitch equals to 1; if two slices are scanned, it equals to 0.5; etc. During spiral and multislice CT, reconstruction is made in an ordinary two-­ dimensional image. But after collection of full information, it is possible to construct the image in different ways. Unlike ordinary conventional tomographs, spiral and multislice tomographs have much better possibilities for three-dimensional reconstruction. Higher-quality three-dimensional images are received with overlapped layers. With the help of spiral/multislice CT, it became possible to increase informative value of studies with intravenous contrast, while it enables to receive series of slices in a short period. Spiral/multislice CT has a number of advantages in comparison with conventional CT: (1) visualization of all anatomic volumes without moving artifacts; (2) better visualization of focal changes in organs moving during respiration; (3) optimal visualization of contrast pole in different phases, which enables clear images of vessels and three-dimensional reconstruction; (4) possibility of retrospective reconstruction at changeable (variable) steps; (5) improved quality of multiplanar reconstruction; (6) reduction of radiation exposure due to broad possibilities of retrospective reconstruction; and (7) reduction of examination time and consequently increase of transmission and improved quality of reconstruction. CT of brain is performed with special equipment in special standard mode. Standard axial slice is parallel to the orbitomeatal line. Thickness of slice is 4–8 mm. Image is received based on the ability of tissues to absorb X-ray beams. Different tissues have different absorbing ratios, which enables to receive image of anatomical structures. Development of CT angiography (CTA) became possible in the result of improvement of spiral and multislice CT. Thin overlapped slices and their further computer processing enabled high-quality three-dimensional images, which is very important for the investigation of vessels. MDCT permit comprehensive high-resolution assessment of cerebrovascular tree starting from the aortic arch up to the superior sagittal sinus (Catallano et al. 2001; Klingebiel et al. 2002). Necessary condition for CT angiography is intravenous injection of contrast agent. For this purpose triiodized or hexaiodized water-soluble contrast media is used. These are iodinated (diatrizoate, metrizoate) or nonionized (iohexol, iopromide, iodixanole) media with iodine concentration of 300–350 mg/mL (60–70%).

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5  Technical Aspects of Computer Tomography and CT Angiography

Recently nonionized media have been broadly used, as they significantly reduce the risk of side effects. Avoiding of side effects is very important, because even the minor side effects (nausea, vomiting, patient movement caused by pain, or feeling of warmth) significantly deteriorate the quality of the received information. CT is performed in three main stages: preparation, selection of protocol, and study and processing of images. Preparation for Study  Study must be performed in fasting condition or after a light breakfast (to avoid adverse reaction to contrast media). All regulations of contrast studies must be observed (history of allergic reactions, concomitant diseases, contraindications, etc.). Patient’s position, considering the area of investigation, is standard. Attention should be paid to avoid disconnection of cannula with automatic injector when the patient changes the position of his/her arm. During angiography of thoracic and abdominal vessels, the patient should be checked for his/her ability to hold breath. CTA is conducted with automatic injector. A single-use plastic cannula is inserted in the peripheral (usually v. cubitalis) vein and connected to the automatic syringe. In order to maintain the speed of 3–5 mL/s, a relatively large diameter of cannula (20G or 18G) should be used. Considering the anatomy of the venous system, it is preferable to make injection in the right arm than in the left one. Quality of contrasting will be higher if a catheter is inserted in a large caliber vein. Selection of CT Angiography Protocol  Study protocol includes selection of tomography parameters and contrast media. Considering the study objective, the operator selects such parameters as thickness of slice (collimating), speed of table displacement (tomography step), spiral step (pitch), size of area under investigation, characteristics of reconstruction matrix and filter (kernel), amperage (mA), type of contrast media, its volume and concentration, time of injection and its speed, and waiting period of scanning. In CT thickness of slice is usually 1–10 mm. In CTA smaller slices are preferable, as this ensures high quality of reconstruction. But in such case, the number of slices and time of examination increase. This is why, for small caliber vessels, the thickness of slice is usually 1.5–3 mm, while for bigger vessels – 5–6 mm. Speed of table displacement is selected within the range of 5–20  mm/s. Reconstruction performed by 25–50% overlapping of slices (e.g., slice 4–5 mm, step  – 1–3  mm) reduces artifacts in three-dimensional and multiplanar reconstructions. During CT angiography (especially with thin and overlapping slices), the load on X-ray tube increases. In most cases, at 150–350 mA amperage in the tube, it is possible to receive a good image with 8–10 mm slices. In such case it is possible to study a 30–40 cm long area. Considering the above, it is obvious that CTA requires powerful X-ray tube and the time of full rotation not exceeding 1 s.

5  Technical Aspects of Computer Tomography and CT Angiography

43

Displacement of table should preferably coincide in time with passing of contrast bolus. In such case contrasting will be more homogenous. Conducting of CTA and processing of images. Usually, after receiving the topogram of the investigated area, native tomograms are made before contrasting. These data give information about the anatomy of the area, type and quality of contrast media, presence of calcinates, and other radiopaque fillings. Before injection of contrast, the circulation time is assessed. Quality of image depends on the interrelation of start times of scanning and injection of contrast. Scanning must be performed when concentration of contrast in the vessel reaches its maximum. For this purpose, a number of average data is used to assess the time of bolus in the zone of interest (calculations are based on the injection speed of 2–3  mL/s and normal hemodynamics). For example, in carotid and vertebral arteries, the time of bolus is within the range of 15–25 s, in intracranial arteries 18–25 s, etc. After determining the time of circulation, bolus time is calculated. Scanning must be completed in the moment bolus passing the zone of interest. This is why, the volume of contrast and injection speed must correspond to the time of scanning. Study of carotid bifurcation with conventional CT started from the 1980s. However this method was not broadly used. After implementation of spiral CTA the situation changed dramatically. In comparison with other methods (ultrasound, MR angiography), the advantage of CTA is obvious, especially in case of stenosis or occlusion. In most cases, the following parameters are used for CTA of carotid arteries: slices of 3/3 mm, pitch = 1, 80–100 mL of nonionized contrast, iodine concentration 300 mg/mL, injection speed 3–5 mL/s, waiting period – 16–20 s. The first slice of spiral is positioned at C7 level, and the last in the skull. So the direction of spiral coincides with the direction of bolus. Time of scanning is 30–60 s. If 3D image is to be received, the data should be reconstructed at a step of 1–2 mm. MIP and SSD methods are most appropriate for 3D images (see the details below). For better quantitative analysis of stenosis seen in 3D image, additional two-dimensional analysis is also necessary. For optimal visualization it is possible to use multiplanar reconstructions (diagonal, sagittal) (Dimmick and Faulder 2009). In terms of investigation of carotid arteries, CT angiography has a number of advantages in comparison with ultrasound and MR angiography. The investigational area is studied fast—in 20–60 s, and the patient has to lie still for a short time (during MRA a patient has to lie motionless for 3–10  min). For investigation of brachiocephalic arteries, we mainly use the latest device Aquilion One 640sl (320 × 0.5 mm) of Toshiba, equipped with a relatively wide range of detectors. The device gives the possibility to study a 16 cm long anatomic area during a single rotation, which is important for investigation of vessels. The high speed of investigation obviously reduces radiation exposure. MRA cannot be performed on patients with metal fillings, implants, pacemakers, etc., while this is not a contraindication with CT angiography. In MRA, turbulence in the area of stenosis may cause misinterpretation of data. This practically never happens with CTA. The only obstacle in this investigation is calcinates. However,

44

5  Technical Aspects of Computer Tomography and CT Angiography

those artifacts do not affect the quality of images as much as with ultrasound (Magarelli et al. 2000; Lell et al. 2007). When comparing CTA with X-ray contrast angiography, it should be noted that CTA enables to avoid complications caused by catheterization of an artery. Axial slices received through CTA enable to study both lumen and walls of the arteries, which is impossible during the X-ray contrast angiography. A certain restriction of CTA is the fact that despite its ability to quicky provide the information, 3D reconstruction and assessment of primary information is quite time-consuming. The most labor-consuming part is editing of images (removal of osteal system). This complicates 3D reconstruction of vertebral arteries. For vertebral arteries MRA is more appropriate. With the help of CTA, noninvasive diagnostics of stenosis and occlusions of intracranial arteries, arterial and venous malformations, and aneurisms of intracranial arteries reached a new level. From this view, efficacy of CTA is no inferior (and sometimes superior) to MRA.  Undoubtful advantage of CTA is better diagnostic efficacy of acute subarachnoidal, intraparenchymal, and intraventricular hemorrhages (Hirai et al. 2001; Anzalone et al. 2005; Barlett et al. 2006; Lell et al. 2007; Wintermark et al. 2008; Saba et al. 2009, 2012). Before injection of contrast, for the purpose of studying anatomic particularities of the brain and revealing of hematomas and calcinates, standard CT is performed. For CTA of intracranial arteries, most frequently the following protocol is used: slice 1/1, 1.5/1.5 or 3/2 mm, 100 mL of nonionized contrast injected at a speed of 3–5 mL/s, waiting period – 25–30 s. Usually 50–60 slices are made in the interest zone, with the center in the area of sella turcica. This enables to visualize internal carotid arteries, basilar arteries, and their branches. In a number of cases, when informational value of CTA is limited, it is possible to perform X-ray contrast angiography at the second stage. Generally, implementation of CTA of extra-intracranial arteries has significantly reduced the necessity of conventional angiography (Lell et al. 2007; Kim et al. 2010; Saba et al. 2012).

References Ambrose J, Hounsfield G (1973) Computerized transverse axial tomography. Br J Radiol 46:148–149 Anzalone N, Scomazzoni F, Castellano R et al (2005) Carotid artery stenosis: intraindividual correlations of 3D time-of-flight MR angiography, contrast-enhanced MR angiography, conventional DSA, and rotational angiography for detection and grading. Radiology 236:204–213 Barlett ES, Walters TD, Symons SP, Fox AJ (2006) Diagnosing carotid stenosis near-occlusion by using CA-angiography. AJNR Am J Neuroradiol 27:632–637 Catallano A, Porelli R et al (2001) Spiral CT-angiography in determination of ICA severe stenosis. Radiology 211(2):76 Dimmick S, Faulder K (2009) Normal variants of the cerebral circulation at multidetector CT angiography. Radiographics 29:1027–1043

References

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Hirai T, Kagori Y et al (2001) Maximal stenosis of extracranial internal carotid artery. Effect of luminal morphology on stenosis measurement by CTA and conventional DSA.  Radiology 221:178–187 Kalender WA, Polacin A (1991) Physical performance characteristics of spiral CT scanning. Med Phys 18:910–915 Kim JJ, Dillon WP, Glastonbury CM et  al (2010) Sixty-four-section multidetector CT angiography of carotid arteries: a systematic analysis of image quality and artifacts. AJNR Am J Neuroradiol 31:91–99 Klingebiel R, Busch M, Bohner G et  al (2002) Multi-slice CT angiography in the evaluation of patients with acute cerebrovascular disease- a promising new diagnostic tool. J Neurol 249:43–49 Lell M, Fellner C, Baum U et al (2007) Evaluation of carotid artery stenosis with multisection CT and MR imaging: influence of imaging modality and postprocessing. AJNR Am J Neuroradiol 28:104–110 Magarelli N, Saarabino T, Simeoni A et al (2000) Carotid stenosis: a comparison between MR angiography and CT angiography. Radiology 218:135 Saba L, Montisci R, Sanfilippo R et al (2009) Multidetector row CT of the brain and carotid artery: a correlative analysis. Clin Radiol 64:767–778 Saba L, Anzidei M, Sanfilippo R et  al (2012) Imaging of the carotid artery. Atherosclerosis 220:294–309 Wintermark M, Jawadi SS, Papp JH et  al (2008) High-resolution CT imaging of carotid artery atherosclerotic plaques. Am J Neuroradiol 29:875–882

6

Physical Principles of Magnetic Resonance and Magnetic Resonance Angiography

In 1950–1960 nuclear magnetic resonance was the most acceptable method of study of configuration of chemical structure of substances and reactive processes. In 1973 Lauterbach performed the first magnetic resonance study. Since 1983, the development of magnetic resonance equipment and its software later gave a possibility to the investigators to receive a high contrast image of 1  mm slice within several seconds. Because of multifactor parameters, information received from MR is different from the one received from X-ray and ultrasound. MR image is based on physical properties of hydrogen atom, while its share in human body is the highest in comparison with other elements. MRI is a map of functional state of hydrogen protons in the investigational area. Pathology is revealed through comparison with the norm. MRI investigation may be performed in any plane without changing of the patient’s position. This significantly improves diagnostics and excludes the patient’s discomfort. Any MR tomograph consists of the following parts: –– Magnet that creates a permanent magnetic field around the patient. –– Gradient coils that create weak variable magnetic field in the central part of the main magnet, which enables choice of interest zone of the investigated object. –– Radio frequency coils; (a) transmitter is used for stimulation in the investigated area; (b) receiver is used for response. For different parts of the body, different receivers are used. –– Computer operates gradient and radio frequency coils, registers changes in signals, and processes and records those changes in order to visually reconstruct them.

✠

Fridon Todua was deceased at the time of publication.

© Springer International Publishing AG, part of Springer Nature 2018 F. Todua, D. Gachechiladze, Noninvasive Radiologic Diagnosis of Extracranial Vascular Pathologies, https://doi.org/10.1007/978-3-319-91367-4_6

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6  Physical Principles of Magnetic Resonance and Magnetic Resonance Angiography

Each magnetic field is characterized by magnetic induction B and is measured in T (Tesla). According to the power of magnetic field, MT tomographs are divided in several groups: Low field – 0.3 10  years prior (Abbott et  al. 1986; Diez-Roux et al. 1995; Lassila et al. 1997; Shah and Cole 2010). We have comprehensively studied the frequency of a number of important vascular risk factors (age, ischemic heart disease, hypercholesterolemia, arterial hypertension, diabetes mellitus, and others) in cases of structural manifestation of cerebral ischemia (infarction, lacunar infarction, subcortical leukoencephalopathy) (Table 8.2). It was proved that dominant risk factor of all ischemic circulatory disorders is arterial hypertension, which is especially frequent in cases of leukoaraiosis and lacunar infarctions. In all ischemic groups, high frequency of hemorheologic cases is also notable (Gachechiladze 2005). At the same time, unlike leukoaraiosis and lacunar infarctions, large, “non-lacunar” infarctions are with high statistical significance associated with atherosclerosis of magistral arteries and ischemic heart disease. Comparative analysis of risk factors gives us the possibility to assume that in the result of damage to small and large Table 8.2  Frequency of main risk factors in discirculatory groups Leukoaraiosis n-54 66.8 15(28%)

Lacunar infarction n-81 61.3 25(30.7%)

Non-lacunar infarction n-65 64.1 42(65%)

Stenosis of internal carotid artery Atherostenosis of peripheral vessels Hypercholesterolemia

31(57%)

42(52%)

59(93%)

7(12.6%)

9(11.1%)

17(22.%)

19(35%)

51(63%)

51(78%)

Arterial hypertension Smoking Diabetes mellitus Hematocrit (>45%) Hyperfibrinogenemia

43(81%) 15(28%) 10(18.5%) 33(61%) 34(63%)

65(80%) 25(31%) 13(16%) 56(69%) 52(64%)

41(63%) 21(33%) 13(20%) 46(71%) 43(67%)

Factor Average age Ischemic heart disease

P p > 0.05 p1-3 3.7 >5

In normal conditions or in case of hemodynamically insignificant stenosis 1.8, this is considered a pathology and has positive correlation with the degree of internal carotid stenosis (Table 10.1). It is assumed that atherostenosis of carotid artery becomes hemodynamically significant (leads to hemoreduction in the distal part of stenosis) only after its degree reaches 50% of the diameter or 70–75% of the cross section. Based on a number of experimental and clinical studies, it was determined that the risk of stroke significantly increases (both in the result of hypoperfusion, i.e., hemodynamic factors, and arterio-arterial mechanism) after the degree of stenosis reaches 75–80% of the diameter or 90% of the cross section (Caroll 1996). From the view of hemodynamic significance (according to different criteria of estimation of the degree of stenosis), internal carotid stenosis is conventionally divided into the following groups: (1) hemodynamically insignificant, 70% narrowing at the origin

Fig. 10.22 Internal carotid artery local severe stenosis. CE MRA. Gad-fl3d-tofMIP; lumen >80% narrowing at the origin

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129

According to some authors, disadvantage of MRA is aggravation of the degree of stenosis in case of insufficient visualization of the lumen, which usually happens with relatively small arteries and stenosis over 70%. Residual lumen in such case is smaller than pixel. Loss of signal in such case can be explained by hemodynamic parameters: turbulence and significant reduction of flow and consequently of contrast (Magarelli et al. 2000; Randoux et al. 2003; Lell et al. 2007; Debrey et al. 2008) Despite improved programs used in new generations of MR scanners, like segmented centric k-space coding, parallel imaging, etc., there is still some need for improvement. In comparison with CTA, resolution in multiplanar reconstruction is worse, which may be the reason of limited fast arterial phase (FP). At the same time, bolus contrast and scanning may be desynchronized, which may cause low-quality contrasting and overloading in the venous phase. MRA (both non-contrast and contrast) is particularly efficient in revealing occlusion of extracranial arteries. In such case, signal from occluded artery disappears, meaning “cutoff,” “amputation” of artery (Fig. 10.23).

Fig. 10.23 Internal carotid artery occlusion. CE MRA. Gad-fl3d-tof-­ MIP; missing left ICA signal

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One of the advantages of MRA, in comparison with CTA, is the better possibility to study vertebral arteries. Due to overlapping of osteal structures, conventional CT and CTA often do not enable to adequately investigate V2 and V3 segments of vertebral artery. MRA does not have this problem. Sensitivity of CTA in diagnosing >70% stenosis of the vertebral artery is approximately 0.68, and specificity 0.93, while the same values of MRA are 0.91 and 0.93, correspondingly (Khan et  al. 2009). In order to assess hemodynamics of atherostenosis of extracranial arteries (location and spread of plaque, degree of stenosis), we have studied 202 patients both with isolated atherosclerosis (AT) and combination of atherosclerosis and arterial hypertension (AT+AH) (Gachechiladze 2005). The study has shown that most commonly, in 125 cases (62%), atherosclerotic plaque was located in bulbus of CCA or I segment of ICA. In 32 cases (16%), the area of stenosis covered medial part of CCA and in 28 cases (13%) medial part of ICA, while in other 18 cases (9%), stenosis had other locations. We also studied the frequency of bilateral stenosis of CCA, and simultaneous stenosis of carotid and vertebral arteries, both in case of isolated atherosclerosis and combination of atherosclerosis and arterial hypertension (Table 10.2). As shown in the above table, simultaneous pathologies of carotid and vertebral arteries prevail in both groups. In case of combination of atherosclerosis and arterial hypertension, bilateral stenosis of carotid arteries is quite common. In order to assess hemodynamic significance of atherostenosis, we studied flow volume rate in case of different degrees of carotid arterial stenosis (Fig. 10.24).

Table 10.2  Spread of atherostenosis of extracranial arteries Type of stenosis Carotid isolated Carotid + vertebral Carotid-unilateral Carotid-bilateral

Atherosclerosis n = 95 47(49%) 48(51%) 55(58%) 40(42%)

Atherosclerosis + Hypertension n = 107 47(44%) 61(57%) 52(49%) 55(51%)

242

214

ml/min

300

Fig. 10.24  Flow volume (ml/min) in case of stenosis of ICA

Total n = 202 94(47%) 109(53%) 107(53%) 95(47%)

140 262

200

Ath+AH

236

100

176

0

Ath

0-50% 50-75%

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131

As shown in the above picture, in case of hemodynamically insignificant stenosis, flow volume rate Q is practically within the normal range (N-278 ± 74 ml/min) and results in 262 ± 46 ml/min in case of isolated atherosclerosis and 242 ± 42 ml/ min in case of combination of atherosclerosis with hypertension. In case of moderate stenosis (50–75%), flow rate is moderately reduced in both groups (15.8%, atherosclerosis, and 24%, atherosclerosis + AH), which does not have significant impact on hemodynamics. At the same time, compensatory increase of flow volume is observed on the contralateral side – 304 ml/min (atherosclerosis) and 288 ml/min (atherosclerosis + AH) in the average. As for critical stenosis, hemodynamics was significantly decreased, as expected, by 42.1% in the group of isolated atherosclerosis and by 47.4% in the AT+AH group. It should also be mentioned that in case of >90% stenosis (11 patients), the flow rate was significantly reduced – 88 ml/min in average (76–106 ml/min), which is 70% less than normal value. In case of critical stenosis, flow rate in contralateral ICA significantly increased (p 50% stenosis. We find it notable that independent factor, lipoprotein(a), increased (5.1 ± 0.61 mmol/l) in patients with hemodynamically significant stenosis. Enhanced lipoprotein(a) level was mainly observed in patients with soft homogenous (Type I) and predominantly soft nonhomogenous (Type II) atherosclerotic plaques. It is also notable that changes in the level of lipoprotein(a) are in correlation with the levels of C-reactive protein, fibrinogen, and blood fibrinolytic activity. Table 10.4  Relation of lipid levels with the degree of stenosis Lipids CHOL mmol/l TRI mmol/l HDL mmol/l LDL(b-lip) mmol/l Apo-A mg/dl Apo-b mg/dl Lip (a) Atherogenic index

Stenosis 50% N-136 6.18 ± 0.52 1.82 ± 0.21 1.01 ± 0.16 4.18 ± 0.82 98.6 ± 8.6 174.6 ± 6.8 5.1 ± 0.61 4.72 ± 0.45

P >0.05 >0.05 0.05 >0.05 >0.05 >0.05 >0.05

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133

Our goal was to study the natural dynamics of atherosclerotic plaque and assess the impact of various risk factors on this process. For this purpose, we studied 72 patients (29 women and 43 men) with different degrees of carotid stenosis. The age of patients varied between 44 and 76  years (mean age, 64.3 ± 8.4 years). In 28 cases (39%), initial examinations revealed 50% stenosis. Based on the above, annual risk of stroke resulted in 2.02%. During the observation period, three fatal cases occurred. Hence, in patients with >50% stenosis, annual risk of death, in the result of stroke or other vascular reasons, resulted in 4.04% (2.02%, stroke, and 2.02%, other vascular reasons). Repeated ultrasound examination showed that in the majority of patients (41 patients, 57%), the size of plaques practically did not change; in 3 patients (4.6%), plaques regressed, while in 28 patients (39%), plaques showed progression. At the initial stage of examination, average degree of stenosis in the investigated group resulted in 56%. At the last stage, it reached 68% (12% progression). Assessment of progression in the degree of stenosis showed that progression of 160 mmHg, progression of stenosis is significantly higher than in normotensive patients – 13.8% and 11.3% correspondingly (p  0.9 mm has been reconfirmed as a marker of asymptomatic organ damage, although it has been proven that in middle-aged and elderly patients, the threshold values indicating high cardiovascular risk are higher (Mancia et al. 2014). It is established that change of IMT occurs earlier in response to atherogenic factors than clinical manifestation. This is why IMT monitoring with high-efficacy ultrasound equipment enabling simple visualization is used to study efficacy of different antiatherogenic and antihypertensive drugs (Crouse 1995; Terry et al. 1996; Bonithon-Kopp et al. 1996a, b; Taute et al. 2000; Zanchetti et al. 2009). On gray-scale image, arterial wall is visualized in three layers, which due to different echogenicity are presented with two hypoechogenic parallel lines (tunica intima and tunica adventitia), divided by hypo-anechogenic space (tunica media). Internal echogenic line represents the lumen-intima surface and external line— media-adventitia surface. The “double-line pattern” of the arterial wall represent intima-media complex (Fig. 11.1). Quantitative study of intima-media layer of the carotid artery, with high-resolution ultrasound equipment, was first performed by Pignioli et al. (1986). IMT (average and maximal) is determined with the help of accepted methodology in the back wall of CCA, 1 cm proximally to bifurcation, in three different locations. Typically, normal common carotid IMT at age 10 is approximately 0.4–0.5  mm, while from the fifth decade of life onward, this progresses to 0.7–0.8 mm or more (Renton et al. 1992; Salonen and Salonen 1992).

endothelium internal elastic lamina media external elastic lamina adventitia

Fig. 11.1  View of arterial wall in cross section. Electronic microscopy

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11  Common Carotid Artery Intima-Media Layer Changes

IMT exceeding 1 mm is considered abnormal. Modern ultrasound technique for vascular studies is equipped with special program for automatic measurement of intima-media thickness—auto-IMT (Fig. 11.2). Atherosclerotic and angiopathic processes cause not only increase of IMT but also deterioration of its structure and calcific insertions (Fig. 11.3). There is a view that people with atherosclerotic risk factors (dyslipidemia, arterial hypertension, diabetes mellitus, hereditary factors, etc.) must be annually checked for IMT. On the basis of a number studies, measurements of IMT at the carotid bulb and at the ICA are more useful than CCA-IMT, both for risk classification and risk prediction, likely because intimal thickening and plaques form at the bulb and at the ICA (Tasheem and Lee 2014). In the recent years, MR tomographs with powerful magnetic field (1.5T, 3T) have been used for examination of intima-media layer. According to some authors, informative value of MRI in assessing the structure of vascular wall varies within 82–93% (Cai et al. 2002; Duivenvoorden et al. 2009). In order to assess the dynamics of intima-media layer, we studied 114 patients within the 43–75 age range, out of which 65 patients (57%) had arterial hypertension and 59 (52%) dyslipidemia. Interval before the repeated ultrasound examination varied between 10 and 28 months (18 months in average). Fig. 11.2 Common carotid artery intact intima-medial layer. B-mode, longitudinal image

Fig. 11.3  Thickening of intima-medial layer. B-mode, longitudinal image

References

141

Ultrasound examinations have shown that in the majority of cases, 97 (85%), IMT was progressing. In the other 17 cases (15%), it remained unchanged. At the initial stage of study, average IMT was 1.07 ± 0.12 mm. Average growth during the study period resulted in 0.12 ± 0.07 mm, which corresponds to the data on IMT progression. It should be noted that progression was most expressed in patients with arterial hypertension, rather than in those with isolated hypercholesterolemia, 0.34 and 0.28 mm correspondingly. As it was expected, progression of IMT was subject to combination of several risk factors: if in case of isolated hypercholesterolemia, IMT increased by 0.28 mm, in case of combined hypercholesterolemia and AH, it increased by 0.38 mm, while in case of third additional risk factor of smoking, the growth resulted in 0.46 mm (p 50%) nonhomogenous plaque. Longitudinal plane. Gray-scale mode

Fig. 12.6 Type IV. Uniformly echogenic homogenous or calcified. Longitudinal plane. Gray-­scale mode

recommend to monitor their dynamics or to perform endarterectomy (Van Damme and Vivario 1993; Eliaziw et al. 1994; European Carotid Plaque Study Group 1995). However, these classifications showed a rather weak inter-investigator reliability. An alternative approach to objectifying the plaque’s structural composition is to quantify its echogenicity by computer-assisted image analysis. There are several possibilities for analyzing images, such as gray-scale median (GSM), pixel distribution analysis (PDA), and virtual histology (VH). Gray-scale median (GSM) analysis quantifies plaque echodensity seen on B-mode ultrasonography. With the use of Adobe Photoshop, ultrasound images can be standardized and the GSM value calculated, categorizing lesions into echolucent plaques and echogenic plaques. The technique involved standardization of B-mode images and adjustment with the signals from blood (normalized GSM 0) and GSM 195 for adventitia. According to gray-scale median score, several types of plaques are identified: Type I. Uniformly echolucent (black) 25 occupy 15–50% of the plaque area.

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12  Structural Characteristics of Atherosclerotic Plaque

Fig. 12.7 Type V. Unclassified, heavy calcification causing acoustic shadowing and poor image quality. Longitudinal plane. Color Doppler mode

Type III. Mainly echogenic: pixels with gray-scale values >25 occupy 50–85% of the plaque area. Type IV/V. Uniformly echogenic: pixels with gray-scale values >25 occupy >85% of the plaque area (Nicolaides et al. 2005). Assessment of plaque surface and detection of possible ulceration is very important in clinical practice. Classification of surface was offered by Polak et al. (1992). According to this classification, a surface may be assessed as: 1. 2. 3. 4.

Smooth (Fig. 12.8) Moderately irregular (excavation does not exceed 0.4 mm) (Fig. 12.9) Highly irregular (excavation exceeds 0.4 mm) (Fig. 12.10) Ulcerated (excavation at least 2 mm in depth and 2 mm in length) (Fig. 12.11)

Modern high-level scanners are equipped with additional resolution and optimization programs, which significantly improve the quality of images and reduce “noise” and number of artifacts, which is very important in assessment of atherosclerotic plaque structure. Contrast-enhanced ultrasound (CE-US) examination has been lately used for the assessment of plaque structure, mainly neovasculogenesis. Microbubbles of contrast media clearly show any heterogeneity and intra-plaque microvascularization. The degree of neovascularization established through CE-US fully corresponds to the newly created vessels revealed by histologic tests. It was also established that intra-plaque neovascularization lesions more frequently occur in symptomatic patients (both cerebral and cardiac ischemia (Xiong et al. 2009; Staub et al. 2011).

12  Structural Characteristics of Atherosclerotic Plaque Fig. 12.8 Smooth surface plaque. Longitudinal plane. Gray-scale mode

Fig. 12.9  Plaque with the mild surface irregularity. Longitudinal plane. Gray-scale mode. Excavation of plaque surface doesn’t exceed 1.4 mm

Fig. 12.10 Irregular surface plaque. Longitudinal plane. Gray-scale mode. Excavation of plaque surface >1.4 mm

151

152

a

12  Structural Characteristics of Atherosclerotic Plaque

b

Fig. 12.11  Ulcerated surface plaques. (a) Transverse plane. (b) Longitudinal plane. Gray-scale mode. On the plaque surface, concavities in 2.4–2.7 mm in depth are defined

Very often A-type perflutren microspheres (Optison, GE Healthcare) and lipid perflutren microspheres (Definity; Bristol-Myers Squibb Medical Imaging) are used in studies. A-type perflutren microspheres and lipid perflutren microspheres are solved in proportion of 3 and 1.5 mL in 7 and 8.5 mL of saline correspondingly (final volume 0.10  mL). Contrast is injected in peripheral vein as a 2  mL bolus. Contrast reaches carotid artery in 10–30 s from injection. Since 2010, several pilot studies have been conducted, where the structure of plaques was assessed with the help of ultrasound elastography. Ultrasound elastography (UEG) is a relatively new method of assessing mechanical properties of tissues, providing additional information about their structure. UEG is a map of deformations of a biologic tissue in response to a mechanical stress. UEG function in three steps: application of a stress/force on the tissue, measurement of tissue displacement/strain in response to the applied stress, and estimation of tissue elasticity/rigidity. For the same applied stress, rigid tissues will have smaller displacements than soft tissues. According to the recent studies, features of vulnerable plaques in UEG typically consist of a high local strain rate and spatially nonuniform strain rate distributions; in contrast, stable plaques typically are associated with low local strain rate and relatively uniform strain rate distributions (Garrard and Ramnarine 2014). Multislice CTA is one of the most efficient methods of assessing atherosclerotic plaques. One of its advantages in comparison with MRA is that patients have to lie motionless and withhold gulping for a relatively short time—from 40  s to 1  min. Various plan 3D reconstructions enable to differentiate arterial lumen and calcificates, as well as ulcerated plaque surface (Figs.  12.12 and 12.13). According to different data, efficacy of CTA in detecting plaque calcification tends to 97%. A number of authors (Randux et al. 2001; Wintermark et al. 2008) believe that irregularity and especially ulceration of surface are better visualized on CT angiogram than with the help of conventional digital subtraction or MR angiography (Fig. 12.14). Method of axial reconstruction used in modern CT scanners (receiving of high-­ resolution images of axial arterial sections along the virtual axis of arterial lumen) is one of the most highly informative methods of assessing atherosclerotic plaques. In case of making high-resolution images of perfused (contrasted) arterial lumen, it

12  Structural Characteristics of Atherosclerotic Plaque

153

Fig. 12.12 MDCTA MIP image showing a severe carotid stenosis at the origin. Heavy calcinated, irregular surface plaque

is possible to assess the condition of lumen and study the structure, components, and surface of plaques. Currently both MDCT and MRI studies imply morphological assessment criteria, according to which there are four conditions of lumen: circular, ellipse, multilobar, and wave-shaped. It is established that local symptoms mostly occur in case of multilobar (36%) and wave-shaped (10%) sections (Hokari et al. 2011). Classification of plaque into fatty (120 HU) also showed good interobserver agreements and sensitivities of 85%, 89%, and 100%, respectively (Saba et al. 2009, 2012; Das et al. 2009). The major advantages of MDCTA lie in its availability, rapidity, ability to measure absolute tissue density, and ability to identify and quantify calcifications with great accuracy. The role of MDCTA in plaque component characterization shows promise but still lacks specificity to identify lipid core and IPH. Beam-hardening artifacts associated with calcification alter Hounsfield values and contribute to inaccurate plaque characterization. In our institute, the latest generation of CT scanners, Siemens Definition Edge 384sl, Sensation Cardiac 64sl, and Toshiba Aquilion ONE 640, is equipped with

154

12  Structural Characteristics of Atherosclerotic Plaque

Fig. 12.13  Severe carotid stenosis. MDCT- MPR reconstruction. Reformatted images show nonhomogenous calcified plaque. Corresponding axial image at the site of maximal stenosis demonstrates surface irregularity

Fig. 12.14  Internal carotid artery stenosis. MDCT. VRT, MPR reconstruction. Massive calcified plaque at the origin of the ICA. Reformatted axial images allow assessment of plaque composition

12  Structural Characteristics of Atherosclerotic Plaque

155

modern modifications of axial reconstruction programs, one of the most highly informative methods of assessing the structure of atherosclerotic plaques. This method enables within several seconds to estimate the condition of lumen, structure components, and surface of plaque and assess embologenicity (Figs. 12.15 and 12.16). Together with ultrasound examination, due to vessel wall and flow-dependent images, MRA enables high-resolution investigation to identify arterial lumen.

Fig. 12.15  Internal carotid artery severe stenosis. MDCT. MPR reconstruction. Nonhomogenous circular plaque at the origin of the ICA. Reformatted axial images allow assessment of stenosis severity and plaque composition

Fig. 12.16  Severe carotid stenosis. MDCT-curved MPR reconstruction. Reformatted images show nonhomogenous calcified plaque. Corresponding axial image at the site of maximal stenosis demonstrates surface irregularity

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12  Structural Characteristics of Atherosclerotic Plaque

Compared with other imaging techniques, multicontrast MRI (T1, T2, proton density, 3D TOF) has very good sensitivity and specificity to identify and measure plaque components. Multicontrast MRI can identify and characterize plaque components such as lipid-rich necrotic core, fibrous cap thickness, IPH, and calcifications. Main plaque components—lipids, cholesterol crystals, and triglycerides—have short T2 signals. At the same time, MIP and FLAIR modes enable to estimate the plaque structure and identify ulcerated surface. MR characteristics of five main plaque components (calcification, fibrous tissue, fibrous tissue with extracellular fat, fat, thrombus) are based on different intensities of signal on T2-weighted (echo-time 50  ms), partially T2-weighted (echo-time 30 s), diffusive-weighted images (Fig. 12.17). For the purpose of assessment of atherosclerotic plaques with the help of high-­ power (>1.5 T) MRI equipment, the following criteria are accepted: Type I, inactive and thick; Type II, inactive and thin; and Type III, rupture. Inactive and thick capsule is visualized on TOF angiogram as a thick dark homogenous line distinguishing the lumen; smooth surface is seen on T1- and T2-weighted images. In case of inactive thin capsule, dark borderline is not visible on TOF angiogram, while the surface on T1-, interim-, and T2-weighted images is smooth. In case of damaged capsule (rupture), nonhomogenous dark borderline may be visible or not visible. Nonhomogenous uneven lumen is visualized on T1-, interim-, and T2-weighted images. Multicontrast MRI (T1, T2, proton density, 3D TOF) had 81% sensitivity and 90% specificity for identifying a thin or ruptured cap. Fibrous cap thickness on T1-weighted (T1W) imaging both pre- and postgadolinium injection also has a good correlation with histology. IPH was accurately identified by multicontrast MRI as a hyperintense signal on T1W tse (turbo spin echo) images with 93% sensitivity and 96% specificity and on T1W 3D gradient echo images (direct thrombus MRI) with 84% sensitivity and specificity

a

b

c

Fig. 12.17  Nonhomogenous carotid plaque. MR axial images. Calcifications correspond to the  area of hypointensity on T1, TOF, and T2 sequences. The fibrous cap can be seen on TOF (hypointesive signal band between the smooth lumen boundary)

12  Structural Characteristics of Atherosclerotic Plaque

157

(Randoux 2003, Mitsumori et al. 2003; Cai et al. 2005; Cappendijk et al. 2005; Patterson et al. 2009). For calcified plaques T2-tirm-tra-dark-fl, T1-TFE proton density (PD) program is preferable, while for other plaque components (fibrous cover, lipid insertions, thrombotic masses), T1-TFE (segmented gradient echo), T2, proton density (PD), and time of flow (TOF) programs are more informative (Yuan et  al. 2001; Saam et al. 2006, Debrey et al. 2008; Patterson et al. 2009) . Some authors advise to use combination of two out of the above three programs: T1-turbo-SE, T2-turbo-SE, and interim-weighted turbo-SE.  Such combinations enable to differentiate four main components of atherosclerotic plaque—fibrous part, lipids, calcification, and hemorrhage (Fig. 12.18). Sensitivity and specificity of MRI in differentiation of all plaque components vary in the range of 95–100%; however specificity in identifying thrombus is approximately 84% (Fayad and Fuster 2000; Yuan et al. 2001). For identification of unstable components of plaque, 3D TOF, “light blood,” and T1 double inversion-­restoration (DIR) SE images are used. Their sensitivity reaches 81–83%, and specificity 90–92% (Hatsukami et al. 2000; Yuan et al. 2001; Esposito et al. 2007; Ota et al. 2010). AHA introduced modified plaque classification for MDCTA (Wintermark et al. 2008) and MRI (Cai et al. 2005) MDCTA description Lesion type  I–II Thin plaque with no calcification  III Plaque with small lipid cores and no calcification  IV–V Plaque with a large lipid core, covered by a fibrous cap, possible small calcifications  VI Ulcerations and/or wide hemorrhage and/or thrombosis  VII Plaque with a lipid core or fibrotic tissue, with large calcifications  VIII Plaque with fibrous tissue, no lipid core, possible calcifications High-resolution MRI description Lesion type  I–II Near-normal wall thickness, no calcification  III Diffuse intimal thickening or small eccentric plaque with no calcification  IV–V Plaque with a lipid or necrotic core, surrounded by fibrous tissue with possible calcification  VI Complex plaque with possible surface defect, hemorrhage or thrombus  VII Calcified plaque  VIII Fibrotic plaque without lipid core and with possible small calcifications

Our goal was to establish structural echo-semiotics of atherosclerotic plaques and study the relation of plaque structure and the type of hemodynamics. For this purpose, we studied 202 patients with atherostenosis of carotid arteries. Relation of plaque structure with clinical signs was studied in 187 patients with ischemic cerebrovascular disorders (from circulatory disorders to ischemic stroke) (Table 12.1). For assessment of plaque structure, we used modified classification of Geroulakos et al. (1993), according to which atherosclerotic plaques were classified as follows:

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12  Structural Characteristics of Atherosclerotic Plaque

Fig. 12.18 Nonhomogenous atherosclerotic plaque. (a) Severe carotid stenosis on MRA- Gad-fl-2D-tof-MIP. (b) Transverse plane. T2se. High intensity on T2 se indicates regions of intra-plaque hemorrhage

Table 12.1  Structure of atherosclerotic plaque by different types of circulatory disorders Type of plaque I II III IV V

Initial disorder n-16 1 (6%) 4 (25%) 3 (19%) 5 (31%) 3 (19%)

Discirculatory encephalopathy n-66 6 (9%) 14 (21%) 17 (26%) 19 (29%) 10 (15%)

Transitory ischemia n-52 9 (17%) 14 (27%) 15 (29%) 9 (17%) 5 (10%)

Stroke n-53 7 (14%) 15 (28%) 18 (34%) 10 (20%) 3 (6%)

Total n-187 23 (12%) 47 (25%) 53 (28%) 43 (23%) 21 (11%)

Type I, 23 patients; Type II, 47 patients; Type III, 53 patients; Type IV, 43 patients; and Type V, 21 patients. Homogenous plaque has regular signal produced by fibrous tissue. Heterogeneous/ nonhomogenous plaque has mixed signal and may contain anechogenic zones corresponding to intra-plaque hemorrhage. As per the above table, majority of patients had Type III, mainly hyperechogenic nonhomogenous plaques, which may be explained by the contingent of patients (age, accompanying arterial hypertension, natural evolution of plaques).

References

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Uneven surface or ulceration was revealed in 80 cases (43%). This was most frequent in nonhomogenous—Type II (35–76%) and III (19–35%) plaques. It is notable that uneven plaque surface was established with 41 (79%) patients with transitory ischemia and 28 (55%) patients with ischemic stroke, while only 8 (12%) patients with DE and 2 (12%) patients with initial circulatory disorders had uneven plaque surface, which confirms the importance of embologenic plaques in pathogenesis of local ischemia. We have found a certain correlation between the size (length) of atherosclerotic plaque and its echo structure. Extended (>1.5 cm) plaques were mainly (62%) of nonhomogenous structure (Types II and III). At the same time, while conditionally “asymptomatic” patients with initial circulatory disorders and discirculatory encephalopathy had mainly extended isohypoechogenic homogenous plaques of Type I (52%), “symptomatic” patients with TIA and stroke had mainly extended plaques of Type III. Apart from clearly embologenic plaques of Types II and III, isoechogenic (Type I) plaques are also notable. Such plaques were detected in 19 (10%) patients, out of which in 9 (47%) cases plaques were associated with local ischemia (5-TIA, 4-stroke), thus indicating their potential embologenity. As already mentioned, atherosclerotic plaque contains various components (lipids, cholesterol derivates, fibrous elements, calcium insertions, etc.). Their concentration ensures stability of plaque and determines its structural type. Different plaques respond to external factors in different ways. We have assessed the dynamics of plaques with different echo structure. According to the type of structure, we found 21 “soft” homogenous (hypoechogenic) plaques, 21 hard (fibrous or calcific) homogenous plaques, and 38 nonhomogenous plaques. The study showed that hard plaques were relatively stable—only 3 (14%) of such plaques progressed in time, while 4 (13%) of soft plaques and more than a half—31 (55%) of nonhomogenous plaques showed progression. At the same time, the degree of progression in hard plaques was significantly lower than in soft and nonhomogenous plaques, 8.8%, 11.2%, and 14.6% correspondingly (p