The Carotid and Supra-Aortic Trunks: Diagnosis, Angioplasty and Stenting

By Michel Henry, Edward B. Diethrich and Antonios Polydorou

Carotid Angioplasty and Stenting (CAS) is a new approach to treat a carotid stenosis.  This new book provides interventional cardiologists, both as beginners or fully experienced, with a reference on all aspects of angioplasty and stenting of the carotid and supra-aortic trunks.

Focusing on both the entire range of angioplasty and stenting treatment options for the surgeon treating patients on the operating table, and the range of radiological techniques used for the cardiologist to diagnose carotid artery stenosis (CAS) and associated conditions, this important book describes the best indications, the different techniques, the results, and also the limitations of CAS based on randomized studies and particularly the last published data (CREST study).

Suitable for both novice and experienced interventionalists, it also addresses diagnosis of a carotid stenosis and complications from CAS and how to manage them.

• Language: English
• Publisher: Wiley
• Release date: Feb 25, 2011
• ISBN: 9781444329827

Book preview

Part 1: Epidemiology, Anatomy and Imaging

1

Epidemiology and pathophysiology of carotid artery disease

Kosmas I. Paraskevas,¹ Nikolaos Bessias,¹ Dimitri P. Mikhailidis²

¹Red Cross Hospital, Athens, Greece

²Royal Free Hospital Campus, University College London, London, UK

Carotid artery disease can be the cause of cerebrovascular symptoms, namely transient ischemic attacks (TIAs), amaurosis fugax, and stroke. This chapter considers the epidemiology and pathophysiology of carotid artery disease.

Epidemiology

According to the most recent World Health Organization (WHO) report,¹ cerebrovascular disease (stroke) is the second leading cause of death worldwide after ischemic heart disease. In 2004, stroke was responsible for 9.7% (n = 5 700 000) of deaths worldwide. A further analysis by national income, showed that whereas stroke was the fifth leading cause of death in low-income countries, accounting for 1 500 000 deaths in 2004 (5.6% of total deaths), it was the second leading cause of death in high-income countries, accounting for 800 000 deaths (9.3% of total deaths) and the leading cause of death in middle-income countries, accounting for 3 500 000 deaths in 2004 (14.2% of total deaths).¹ Optimistic and pessimistic scenarios for the projected deaths due to stroke worldwide for the years 2008, 2015, and 2030 as calculated by the WHO are given in Table 1.1.

Table 1.1 Optimistic and pessimistic scenarios for projected deaths due to stroke for the years 2008, 2015, and 2030.²

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Approximately 9 000 000 episodes of first-ever stroke occurred worldwide in 2004.² A separate analysis by region showed 700 000 first-ever strokes in Africa, 900 000 in North and South America, 400 000 in the Eastern Mediterranean, 2 000 000 in Europe, 1 800 000 in South-East Asia, and 3 300 000 in the Western Pacific.²

Stroke is the third leading cause of death in the US after ischemic heart disease and cancer.³ Among adults older than 20 years, the estimated prevalence of stroke in 2005 was 5 800 000 (approximately 2 400 000 males and 3 400 000 females). Each year about 780 000 people experience a new or recurrent stroke. About 600 000 of these are first attacks and 180 000 are recurrent episodes. On average, every 40 s someone in the US has a stroke.³ Of all strokes in the US population, 87% are ischemic, 10% are intracerebral hemorrhage, and 3% are subarachnoid hemorrhage.³

Male stroke incidence rates are greater than female rates at younger ages but not at older ages. The male-to-female incidence ratio was 1.25 for 55–64 years; 1.50 for 65–74 years; 1.07 for 75–84 years; and 0.76 for over 85 years. Blacks have almost twice the risk of first-ever stroke compared with whites. The age-adjusted stroke incidence rates at 45–84 years are 6.6 and 4.9 per 1000 population in black males and females, and 3.6 and 2.3 in white males and females, respectively.³

Stroke accounted for 1 in every 16 deaths in the US in 2004.³ Stroke mortality for that year was 150 074 (58 800 males; 91 274 females). Stroke total mention mortality (includes deaths where the given cause was listed anywhere on the death certificate or was selected as the underlying cause, whether primary or secondary) in 2004 was approximately 253 000.

Apart from being a leading cause of death, stroke is also a major cause of moderate/severe disability. According to the data provided by the WHO, in 2004 there were 30 700 000 stroke survivors worldwide: 1 600 000 in Africa, 4 800 000 in North and South America, 9 600 000 in Europe, 4 500 000 in South-East Asia, and 9 100 000 in the Western Pacific.² In terms of disease burden as measured using disability-adjusted life years (DALYs), where 1 DALY represents the loss of the equivalent of 1 year of full health, in 2004 and for all ages, stroke was the sixth leading cause of burden of disease, being responsible for 46 600 000 DALYs worldwide.⁴ This ranking is deceiving because it is the average from both low- and high-income countries. If we consider low-income countries alone, stroke does not appear in the top 10 causes of disease; instead conditions such as malaria and tuberculosis dominate.⁵ Thus, for medium- and high-income countries, stroke is in fact even higher in the ranking; it is the third leading cause of disease burden, being responsible for 27 500 000 and 4 800 000 DALYs, respectively.⁴ Optimistic and Pessimistic scenarios for the projected DALYs due to stroke worldwide for the years 2008, 2015, and 2030 as calculated by the WHO are shown in Table 1.2.

Table 1.2 Optimistic and pessimistic scenarios for projected disability-adjusted life years (DALYs) due to stroke for the years 2008, 2015, and 2030.²

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Pathophysiology

Atherosclerosis is the primary pathologic entity responsible for the development of carotid artery disease, accounting for approximately 90% of lesions in the Western world. The remaining 10% are caused by a variety of diseases (Table 1.3).⁶

Table 1.3 Other causes of carotid artery disease.

Atheromatous lesions characteristically occur at branches or arterial bifurcations. The most common site is at the bifurcation of the common carotid artery, particularly the carotid bulb. The predilection of the carotid bifurcation for atheromatous plaques relates to arterial geometry, flow velocity profiles, flow streamline patterns, and wall shear stress.⁷

The initial lesion of atherosclerosis is the fatty streak.⁸,⁹ The formation of fatty streaks arises from a focal increase in the content of lipoproteins within the intima. These lipoproteins undergo chemical modifications, namely lipoprotein oxidation and non-enzymatic glycation.⁸,⁹ After the accumulation of extracellular lipid, recruitment of leukocytes (monocytes and lymphocytes) occurs.¹⁰ Low-density lipoprotein (LDL) particles augment the expression of leukocyte adhesion molecules and also promote the chemotaxis of leukocytes through induction of cytokine release from vascular wall cells, such as interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α).⁹ The monocytes differentiate into macrophages and begin to ingest the lipoprotein particles by receptor-mediated endocytosis, thus transforming into lipid-laden foam cells.¹¹ Some lipid-laden foam cells may die as a result of programmed cell death (apoptosis). This death of mononuclear phagocytes results in formation of the lipid-rich center, often called the necrotic core, of more complicated atherosclerotic plaques.⁹ Cytokines and growth factors [such as transforming growth factor-β (TGF-β)] elicited by modified lipoproteins, vascular wall cells, and infiltrating leukocytes can modulate function of arterial smooth muscle cells. These molecules stimulate the migration of smooth muscle cells from the tunica media into the intima.⁹ The smooth muscle cells synthesize the bulk of the extracellular matrix of the complex atherosclerotic lesion. In addition to locally produced mediators, atherogenic signals, related to blood coagulation and thrombosis, contribute to the evolution of atheroma.⁹,¹² Fatty streak formation begins under a morphologically intact endothelium.¹² In advanced fatty streaks, however, microscopic breaches in endothelial integrity occur.¹² Microthrombi rich in platelets form at such sites due to exposure of the highly thrombogenic extracellular matrix of basement membrane.¹² Platelet adhesion to the exposed matrix is the initial step in thrombus formation.¹²

The atherosclerotic plaque evolves with time. A complex balance between entry and removal of lipoproteins, accumulating leukocytes, cell proliferation and cell death, extracellular matrix production, and accumulation of calcium (calcification of the plaque) contribute to plaque evolution and lesion formation.⁹ With time, the atherosclerotic plaque increases in size, causing stenosis of the vascular lumen. The increasing stenosis of the vessel lumen has an adverse effect on blood flow and may give rise to an auscultated bruit. Whether detection of a carotid bruit during the general physical examination should be considered an alarming sign or an accidental finding has been extensively debated.¹³,¹⁴ Carotid bruits predict cardiovascular events and probably deserve further investigation.¹³,¹⁴ In addition, carotid bruits are associated with vascular risk factors (e.g., smoking, hypercholesterolemia, hypertension, diabetes mellitus).¹³,¹⁴

As the atherosclerotic plaque increases in size, a number of additional events take place that explain many of the clinical manifestations of atherosclerosis. With time, the microthrombi on the endothelium give rise to larger thrombi.¹² These further occlude the lumen, restricting blood supply to the tissues. Additionally, large plaques have a propensity to rupture.⁹,¹²,¹⁵ Plaques that have proved vulnerable to rupture tend to have thin fibrous caps, relatively large lipid cores, and a high content of macrophages. As a result of plaque instability and plaque rupture, the thrombi formed on the surface of the plaque are released into the circulation (emboli), giving rise to acute ischemic events (i.e., stroke).⁹,¹²,¹⁵ Following such an atheromatous discharge, an open cavity remains within the central portion of the lesion, a so-called carotid ulcer. Carotid ulcers are the nidus for platelet aggregation and further thrombus formation and, thus, the source of further atherosclerotic emboli (secondary arterial emboli).⁹,¹²,¹⁵

Carotid plaque echolucency, as assessed by ultrasonography, also defines which plaque is high risk for atheroembolic events.¹⁶–¹⁸ Plaque echolucency is associated with increased lipid content and macrophage density (and sometimes hemorrhage).¹⁶–¹⁸ On the other hand, fibrous tissue and calcification dominate echodense plaques.¹⁶–¹⁸ Echolucent carotid plaques are associated with a higher risk for future ischemic stroke episodes,¹⁶–¹⁸ as well as coronary events.¹⁹ These plaques are also associated with elevated levels of triglyceride-rich lipoproteins and reduced levels of high-density lipoprotein (HDL) cholesterol.¹⁷ Risk factor intervention may be more beneficial in patients with echolucent than in those with echodense plaques.¹⁶–¹⁸

Several risk factors have been associated with an increased risk for the development of carotid atherosclerosis and carotid artery disease. These include smoking,¹⁸,²⁰–²³ hypertension,¹⁸,²⁰–²³ hyperlipidemia,¹⁸,²³,²⁴ and diabetes mellitus.¹⁸,²⁴,²⁵ Modification of these risk factors (i.e. smoking cessation, tight blood pressure, blood glucose, and lipid control) is associated with a considerable vascular risk reduction.¹⁸,²⁰–²⁵

Is Reversal of Carotid Atherosclerosis Possible?

Since carotid atherosclerosis is a progressive disease, measures to delay (or even reverse) its progression are of crucial importance. Early studies reported an association between LDL and carotid intima–media thickness (IMT).²⁶,²⁷ As a result several studies have evaluated the effect of lowering LDL (e.g. with statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) on carotid IMT progression rates [i.e. the Asymptomatic Carotid Artery Progression Study (ACAPS),²⁸ the Kuopio Atherosclerosis Prevention Study (KAPS),²⁹ the Monitored Atherosclerosis Regression Study (MARS),³⁰ the Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) study,³¹ the Regression Growth Evaluation Statin Study (REGRESS),³² etc.). The vast majority of these trials demonstrated a significant regression of carotid IMT after statin therapy.

Two meta-analyses³³,³⁴ have reported an overall decrease in IMT following statin treatment. The first, which included over 90 000 participants in statin trials, showed that there was a strong correlation between LDL lowering and carotid IMT reduction (r = 0.65; P = .004).³³ Each 10% reduction in LDL cholesterol concentration was estimated to reduce carotid IMT by 0.73% per year (95% CI = 0.27–1.19).³³ The other meta-analysis, which included 10 trials and a total of 3443 individuals, showed that statin therapy significantly reduced the rate of carotid atherosclerosis progression.³⁴ The total weighted mean difference of carotid IMT progression between patients receiving statins versus placebo was −22.35% (95% CI = –18.14–26.56%; P < .00001).³⁴

In a review of the literature, our group showed that routine statin treatment in patients with carotid artery disease not only favorably modulates carotid IMT progression, but also reduces the risk of stroke and combined cardiovascular events.³⁵ Routine statin use, however, is not cost-effective in asymptomatic patients with a 10-year Framingham risk score of less than 10% and evidence of subclinical carotid atherosclerosis.³⁶

Conclusions

Carotid artery disease is a leading cause of death and moderate/severe disability worldwide. Its manifestations (TIAs and stroke) are not only associated with increased hospital costs, but are also an important psychosocial and economic burden (as expressed in DALYs) for all countries, irrespective of whether they are low, moderate or high income. It is therefore crucial to decrease its prevalence and prevent the occurrence of the projected scenarios shown in Tables 1.1 and 1.2.

References

1. World Health Organization. The global burden of disease: 2004 update. Part 2: Causes of death. Available at: http://www.who.int/healthinfo/global_burden_disease/GBD_report_2004update_part2.pdf

2. World Health Organization. Health statistics and health information systems. Projections of mortality and burden of disease, 2002–2030. Available at: http://www.who.int/healthinfo/global_burden_disease/projections/en/index.html

3. World Health Organization. The global burden of disease: 2004 update. Part 3: Disease incidence, prevalence and disability. Available at: http://www.who.int/healthinfo/global_burden_disease/GBD_report_2004update_part3.pdf

4. American Heart Association/American Stroke Association. Heart Disease and Stroke Statistics: 2008 Update at-a-glance. Available at: http://www.americanheart.org/downloadable/heart/1200078608862HS_Stats%202008.final.pdf

5. World Health Organization. The global burden of disease: 2004 update, Part 4: Burden of disease: DALYs. Available at: http://www.who.int/healthinfo/global_burden_disease/GBD_report_2004update_part3.pdf

6. Moore WS. Fundamental consideration in cerebrovascular disease. In: Rutherford RB, ed. Vascular Surgery, 6th edn. New York: Elsevier Inc., 2005, pp: 1879–1896.

7. Zarins CK, Giddens DP, Bharadvaj BK, Sottiurai VS, Mabon RF, Glagov S. Carotid bifurcation atherosclerosis. Quantitative correlation of plaque localization with flow velocity profiles and wall shear stress. Circ Res 1983;53:502–514.

8. Staprans I, Pan XM, Rapp JH, Feingold KR. The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis. Mol Nutr Food Res 2005;49:1075–1082.

9. Cullen P, Rauterberg J, Lorkowski S. The pathogenesis of atherosclerosis. Handb Exp Pharmacol 2005;170:3–70.

10. Libby P, Aikawa M, Jain MK. Vascular endothelium and atherosclerosis. Handb Exp Pharmacol 2006;176:285–306.

11. Shashkin P, Dragulev B, Ley K. Macrophage differentiation to foam cells. Curr Pharm Des 2005;11:3061–3072.

12. Gawaz M, Langer H, May AE. Platelets in inflammation and atherogenesis. J Clin Invest 2005;115:3378–3384.

13. Paraskevas KI, Hamilton G, Mikhailidis DP. Clinical significance of carotid bruits: an innocent finding or a useful warning sign? Neurol Res 2008;30:523–530.

14. Pickett CA, Jackson JL, Hemann BA, Atwood JE. Carotid bruits as a prognostic indicator of cardiovascular death and myocardial infarction: a meta-analysis. Lancet 2008;371:1587–1594.

15. Liapis CD, Paraskevas KI. Do carotid surface irregularities correlate with the development of cerebrovascular symptoms? An analysis of the supporting studies, the opposing studies and the possible pathomechanism. Vascular 2006;14:88–92.

16. Daskalopoulou SS, Daskalopoulos ME, Theocharis S, et al. Metallothionein expression in the high-risk carotid atherosclerotic plaque. Curr Med Res Opin 2007;23:659–670.

17. Nordestgaard BG, Gronholdt ML, Sillesen H. Echolucent rupture-prone plaques. Curr Opin Lipidol 2003;14:505–512.

18. Paraskevas KI, Mikhailidis DP, Liapis CD. Internal carotid artery occlusion: association with atherosclerotic disease in other arterial beds and vascular risk factors. Angiology 2007;58:329–335.

19. Honda O, Sugitama S, Kugiyama K, et al. Echolucent carotid plaques predict future coronary events in patients with coronary artery disease. J Am Coll Cardiol 2004;43:1177–1184.

20. Homer D, Ingall TJ, Baker HL Jr, O’Fallon WM, Kottke BA, Whisnant JP. Serum lipids and lipoproteins are less powerful predictors of extracranial carotid artery atherosclerosis than are cigarette smoking and hypertension. Mayo Clin Proc 1991;66:259–267.

21. Sutton-Tyrrell K, Alcorn HG, Wolfson SK Jr, Kelsey SF, Kuller LH. Predictors of carotid stenosis in older adults with and without isolated systolic hypertension. Stroke 1993;24:355–361.

22. Malatino LS, Benedetto FA, Mallamaci F, et al. Smoking, blood pressure and serum albumin are major determinants of carotid atherosclerosis in dialysis patients. CREED investigators: Cardiovascular risk extended evaluation in dialysis patients. J Nephrol 1999;12:256–260.

23. Lim YJ, Kim YW, Choe YH, Ki CS, Park SK. Risk factor analysis for development of asymptomatic carotid stenosis in Koreans. J Korean Med Sci 2006;21:15–19.

24. Cheng KS, Mikhailidis DP, Hamilton G, Seifalian AM. A review of the carotid and femoral intima-media thickness as an indicator of the presence of peripheral vascular disease and cardiovascular risk factors. Cardiovasc Res 2002;54:528–538.

25. Inzitari D, Eliasziw M, Gates P, et al. The causes and risk of stroke in patients with asymptomatic internal- carotid-artery stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 2000;342:1693–1700.

26. Salonen R, Seppanen K, Rauramaa R, Salonen JT. Prevalence of carotid atherosclerosis and serum cholesterol levels in Eastern Finland. Arteriosclerosis 1988;8:788–792.

27. Rubens J, Espeland MA, Ryu J, et al. Individual variation in susceptibility to extracranial carotid atherosclerosis. Arteriosclerosis 1988;8:387–397.

28. Furberg CD, Adams HP, Applegate WB, et al. Effect of lovastatin on early carotid atherosclerosis and cardiovascular events. Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group. Circulation 1994;90:1679–1687.

29. Salonen R, Nyyssonen K, Porkkala E, et al. Kuopio Atherosclerosis Prevention Study (KAPS). A population-based primary preventive trial of the effect of LDL lowering on atherosclerotic progression in carotid and femoral arteries. Circulation 1995;92:1758–1764.

30. Hodis HN, Mack WJ, LaBree L, et al. Reduction in carotid arterial wall thickness using lovastatin and dietary therapy: a randomized controlled clinical trial. Ann Intern Med 1996;124:548–560.

31. MacMahon S, Sharpe N, Gamble G, et al. Effects of lowering average or below-average cholesterol levels on the progression of carotid atherosclerosis: results of the LIPID Atherosclerosis Substudy. LIPID Trial Research Group. Circulation 1998;97:1784–1790.

32. de Groot E, Jukema JW, Montauban van Swijndregt AD, et al. B-mode ultrasound assessment of pravastatin treatment effect on carotid and femoral artery walls and its correlations with coronary arteriographic findings: a report of the Regression Growth Evaluation Statin Study (REGRESS). J Am Coll Cardiol 1998;31:1561–1567.

33. Amarenco P, Labreuche J, Lavallee P, Touboul PJ. Statins in stroke prevention and carotid atherosclerosis: systematic review and up-to-date meta-analysis. Stroke 2004;35:2902–2909.

34. Kang S, Wu Y, Li X. Effects of statin therapy on the progression of carotid atherosclerosis: a systematic review and meta-analysis. Atherosclerosis 2004;177:433–442.

35. Paraskevas KI, Hamilton G, Mikhailidis DP. Statins: an essential component in the management of carotid artery disease. J Vasc Surg 2007;46:373–386.

36. Paraskevas KI, Wierzbicki AS, Mikhailidis DP. METEOR: aiming at the stars for asymptomatic carotid artery atherosclerosis? Int J Clin Pract 2007;61:1242–1246.

2

Neuroanatomy

Michael H. Wholey,¹ Fadi El-Merhi²

¹University of Texas Health Science Center of San Antonio, San Antonio, TX, USA

²American University of Beirut Medical Center, Beirut, Lebanon

Introduction

Knowledge of the major arteries in the head and neck are important for any physician involved in the diagnosis and treatment of vascular neurologic diseases such as atherosclerosis. The neurovascular anatomy is not difficult to master and with new imaging modalities such as computed tomography angiography (CTA) and magnetic resonance angiography (MRA) and improved resolution of standard angiographic systems, visualizing the more complex variants is becoming more common.

The simplest divisions for the neurovascular anatomy include the arteries in the cervical and cranial regions. The cervical region includes the great vessels that arise from the aortic arch as they course through the neck. The cranial circulation is divided into the anterior circulation, including the anterior and middle cerebral arteries and their branches, and the posterior circulation comprising the posterior cerebral and the basilar artery with its cerebellar branches.

Cervical Neurovascular Anatomy

The aortic arch is usually composed of three major branches, including the innominate or brachiocepahlic artery, which then divides into the right common carotid and right subclavian arteries (Figure 2.1). The right vertebral artery arises from the right subclavian artery. The second branch is the left common carotid artery (CCA) and the third is the left subclavian artery, which then provides the left vertebral artery. Bovine arch is a very common variation (20–30% of aortic arches in our series) in which the left common artery arises off the innominate artery (Figure 2.2). Another fairly common variation is the left vertebral artery arising off the aortic arch between the left common carotid and the left subclavian arteries (Figure 2.3). The third variation that we have seen occasionally is an anomalous take-off of the right subclavian artery (Figure 2.4).

Figure 2.1 Standard aortic arch with the take-off of the great vessels. Left anterior oblique projection with the pigtail catheter placed before the take-off of the innominate artery.

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Figure 2.2 Angiographic image of bovine arch anatomy in which the left common carotid and innominate artery share the same trunk.

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Figure 2.3 Three-dimensional CTA image of the aortic arch with the left vertebral artery arising directly off the aorta.

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Figure 2.4 Anomalous take-off of the right subclavian artery off the aortic arch. It courses between the esophagus and the spine, and resumes its course along the right shoulder and arm.

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The cervical portion of the carotid arteries includes the CCA and its branches of the internal and external carotids. This bifurcation commonly occurs approximately at the c3 vertebral artery level. The external carotid is divided into major branches consisting of the superior thyroid, lingual, fascial, and internal maxillary arteries (Figure 2.5).

Figure 2.5 Lateral cervical carotid angiogram showing the carotid bifurcation and the major branches of the internal and external carotids.

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The carotid lesions in the three different patients shown in Figure 2.6 illustrate the varying appearances of cervical carotid lesions, each carrying a different level of risk for distal embolization. The low Hounsfield units of the soft plaque are suggestive of vulnerable plaque, but this has not been proven and more work needs to be performed in this area. In our series of CTA patients who later underwent carotid artery stenting, areas of potential embolic burden showed other features of ulceration, admixture of calcium, and dystrophic plaque burden.¹ Further research is needed to classify high carotid lesions.

Figure 2.6 Three patients showing the varying appearances of cervical carotid lesions.(A) Mild calcified plaque guarding the origin of the internal carotid artery (ICA) followed by a high-grade focal soft tissue plaque. (B) Dystrophic high-grade lesion of the proximal ICA composed of a core of soft tissue plaque partially covered by a calcified exterior: calcified plaque obstructing the external carotid artery. (C) Long lesion of the proximal ICA with ulceration and composed primarily of soft tissue plaque. This image reveals the extent of the plaque into the common carotid artery.

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The internal carotid continues on into the skull base and then emerges to form the circle of Willis (Figure 2.7). The major segments of the internal carotid artery (ICA) are commonly referred to as the cervical, petrous, cavernous, and supraclinoid. Another more detailed system is as follows:

C1: Cervical segment, identical to the commonly used cervical portion

C2: Petrous segment

C3: Lacerum segment; C2 and C3 comprise the commonly used petrous portion

C4: Cavernous segment, almost identical to the commonly used cavernous portion

C5: Clinoid segment; not identified in some earlier classifications, and lies between the commonly used cavernous portion and cerebral or supraclinoid portion

C6: Ophthalmic or supraclinoid segment

C7: Communicating or terminal segment; C6 and C7 together comprise the commonly used cerebral or supraclinoid portion.

Figure 2.7 Lateral view of the distal internal carotid artery in the petrous cavernous segment: C1, cervical segment; C2, petrous segment; C3, lacerum segment; C4, cavernous segment; C5, clinoid segment.

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The posterior circulation of the brain has a major component arising from the vertebral arteries. The two vertebral arteries customarily arise from the subclavian arteries (extraosseous or V1; Figure 2.8). They enter the vertebral column at the C7 vertebral body and course superiorly (foraminal or V2). They exit at approximately C3, forming the extraspinal (V3) and then the intradural (V4) as they merge to form the basilar artery. Before merging, the vertebral artery has a key branch, the posterior inferior cerebellar artery (PICA), which provides flow to the lower brainstem. The basilar artery then continues on and provides the posterior circulation to key vessels, including the anterior inferior cerebellar artery (AICA) and superior cerebellar artery (Figures 2.9 and 2.10).

Figure 2.8 Oblique view of the vertebral arteries.

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Figure 2.9 Angiography and CT coronal images of the vertebral artery.

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Figure 2.10 Posterior circulation is revealed by angiography with cerebral coronal views.

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Cranial Neurovascular Anatomy

The major arteries supplying the brain, paired internal carotid and vertebral arteries, form a unique anastomosis, the circle of Willis, named after Dr Thomas Willis who was the first to accurately describe it and its physiologic significance in 1664.² Even then, he surmised its importance in two clinical circumstances: incidental detection of occlusion of major arteries in asymptomatic cases; and when surgical occlusion of a major vessel in considered.² (Figures 2.11–2.14).

Figure 2.11 Axial view of the complete Circle of Willis using CTA MPR images. MCA, middle cerebral artery; PCA, posterior cerebral artery; ACom, anterior communicating artery; ACA, anterior cerebral artery; PCom, posterior communicating artery.

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Figure 2.12 Three-dimensional CTA image of the circle of Willis. MCA, middle cerebral artery; PCA, posterior cerebral artery; ACom, anterior communicating artery; ACA, anterior cerebral artery; PCom, posterior communicating artery.

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Figure 2.13 CTA coronal image of a complete circle of Willis revealing the anterior and middle cerebral arteries with a patent anterior communicating artery.

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Figure 2.14 MRA image of the intracranial image revealing the distal right internal carotid artery and the anterior and middle cerebral arteries.

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With the advent of carotid stenting and with devices that temporarily occlude flow to the cerebral circulation, there is renewed interest in the circle of Willis. These new carotid embolic protection devices arrest flow in the distal common carotid and external carotid arteries while intervention is performed on the cervical ICA. They have been very helpful in reducing major neurologic events associated with stenting, but there is an intolerance in 5–23% of patients.³–⁵

The literature has described variations in the components of the circle of Willis. We reviewed the circle of Willis in our series of 212 patients, many of whom went on to receive carotid stents.⁶ Our results were similar to other published results in which the circle of Willis was found to be complete in only 18–41%.⁷,⁸ Other reported variations include hypoplasia of one or both posterior communicating arteries (PCOMs) (34%, which was less than our 47%)⁷,⁸ and a hypoplastic/absent A1 segment of the anterior cerebral artery (ACA) (17%, compared to our 11%).⁷,⁸ Primitive or fetal posterior cerebral artery (PCA) was found in 14% of our series compared to 15% in other series.⁹,¹⁰

Several publications haveaddressed the relationship between the circle of Willis and its variations and propensity for stroke, particularly in the presence of fetal PCA. In a fetal-type PCA a larger area is dependent on the ICA as leptomeningeal vessels cannot develop between the anterior and posterior circulation.¹⁰,¹¹ The tentorium prevents cerebellar vessels from connecting to the PCA territory.¹¹,¹² Therefore, patients with a fetal PCA could be more prone to developing vascular insufficiency.¹⁰ Whether patients with the fetal PCA anomaly have a higher risk of ischemic stroke in the territory of the PCA is not known.¹¹,¹²

The PCAs are paired, branching off the top of the basilar artery and curving posterosuperiorly around the midbrain. The PCAs supply parts of the midbrain, subthalamic nucleus, basal nucleus, thalamus, mesial inferior temporal lobe, and occipital and occipitoparietal cortices. In addition, the PCAs, via the posterior communicating arteries, may become important sources of collateral circulation for the middle cerebral artery (MCA) territory.

The ICA provides flow to the anterior cerebral circulation consisting of the ACA and MCA. The ACA supplies most of the medial surface of the cerebral cortex (anterior three-fourths), frontal pole (via cortical branches), and anterior portions of the corpus callosum. Perforating branches (including the recurrent artery of Heubner and medial lenticulostriate arteries) supply the anterior limb of the internal capsule, inferior portions of the head of the caudate, and anterior globus pallidum.

The MCA can be classified into four parts:¹³

M1: The first part of the MCA is the sphenoidal segment, also known as the horizontal segment. The M1 segment perforates the brain with numerous anterolateral central (lateral lenticulostriate) arteries, which irrigate the basal ganglia.

M2: The insular segment, also known as the Sylvian segment, which may bifurcate or sometimes trifurcate into trunks in this segment, which then extend into branches that terminate towards the cortex.

M3: The opercular segments extend laterally exteriorly from the insula towards the cortex.

M4: These finer terminal or cortical segments irrigate the cortex. They begin exterior to the Sylvian fissure and then extent distally away from the cortex.

The MCA is the largest branch of the internal carotid. It supplies a portion of the frontal lobe and lateral surface of the temporal and parietal lobes, including the primary motor and sensory areas of the face, throat, hand, and arm, and in the dominant hemisphere, the areas for speech (Figure 2.15).

Figure 2.15 (A) Coronal view and (B) lateral view of a cerebral angiogram showing anterior (ACA) and middle cerebral arteries (MCA) and their branches. PCA, posterior cerebral artery.

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The venous anatomy for the cerebral circulation mirrors much of its arterial counterpart. There are several centrally located veins that return the flow via the internal jugular vein (Figure 2.16).

Figure 2.16 (A) Coronal view and (B) lateral view of the late-phase angiogram showing the venous anatomy.

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Conclusions

It is essential that interventionalists understand the anatomy of the cervical and carotid circulation. It is straightforward and the basic anatomy can be applied for diagnostic and interventional purposes. Interventionalists must become as familiar with CTA and MRA as they are with conventional diagnostic angiography. The role of these new modalities is changing our approach to diagnosing atherosclerotic disease.

References

1. Wholey MH. Role of CTA in predicting complicated CAS cases. Presented at MEET 2008, Cannes, France.

2. Rana PVS. Dr. Thomas Willis and his circle of Willis in the brain. Nepal J Neurosci 2005;2:77–79.

3. Whitlow PL, Lylyk P, Londero H, et al. Carotid artery stenting protected with an emboli containment system. Stroke 2002;33:1308–1314.

4. Faries PL, DeRubertis B, Trocciola S, Karwowski J, Kent KC, Chaer RA. Ischemic preconditioning during the use of the PercuSurge occlusion balloon for carotid angioplasty and stenting. Vascular 2008;16:1–9.

5. Hendrikse J, van Raamt AF, van der Graaf Y, Mali WP, van der Grond J. Distribution of cerebral blood flow in the circle of Willis. Radiology 2005;235:184–189.

6. Wholey MH, Wu A, Nowak I, Wu W. CTA and the circle of Willis. Endovasc Today 2009:1–7.

7. Bates M, Parodi J. Proximal balloon catheter occluding system: The Parodi Anti-Emboli System. In: Al-Mubarak N, Roubin GS, Iyer SS, et al., eds. Carotid Artery Stenting: Current Practice and Techniques. Philadelphia: Lippincott Williams & Wilkins, 2004, pp. 201–210.

8. Riggs HE, Rupp C. Variations in form of circle of Willis. Arch Neurol 1963;8:8–14.

9. Krabbe-Hartkamp MM, van der Grond J, de Leeuw FE, et al. Circle of Willis: morphologic variation on three-dimensional time-of-flight MR angiograms. Radiology 1998;207:103–111.

10. Alpers BJ, Berry RG, Paddison RM. Anatomical studies of the circle of Willis in normal brain. AMA Arch Neurol Psychiatry 1959;81:409–418.

11. Chuang YM, Liu CY, Pan PJ, et al. Posterior communicating artery hypoplasia as a risk factor for acute ischemic stroke in the absence of carotid artery occlusion. J Clin Neurosci 2008;15:1376–1381.

12. Cloft H. Intracranial atherosclerosis: a few good images? AJNR Am J Neuroradiol 2005;26:989–990.

13. Krayenbühl H, Ya x15F_Minion-Regular_8n_000100 argil MG, Huber P, Bosse G. Cerebral Angiography. New York: Thieme, 1982, pp. 105–123.

3

Value of computed tomography and magnetic resonance imaging

Allan W. Reid, Giles H. Roditi

Glasgow Royal Infirmary, Glasgow, UK

Introduction

Stroke is the second leading cause of death, accounting for 5.7 million deaths per year worldwide.¹ In the diagnosis and prevention of stroke, computed tomography (CT) and magnetic resonance imaging (MRI) play critically important roles.

The development of CT owes much to the success of the British pop group The Beatles! In 1972, (Sir) Godfrey Hounsfield developed the then revolutionary scanner supported jointly by the United Kingdom Department of Health and Social Security and EMI, the music recording company, financially buoyant following the phenomenal success of their recording artists, The Beatles.² The first clinical CT image produced on the EMI scanner using X-rays was of the brain and its surrounding cerebrospinal fluid (CSF) spaces. The information was gathered axially on fluorescent detectors and displayed in the transverse plane. The initial CT scans had a very large pixel size with wide slice thickness leading to very chunky images. Advances in technology over the four decades since, mean that slice thickness and pixel size are now so small that the voxels are isometric. As a result, the image, although still axially acquired, can be reformatted in any plane to the same high resolution.

The pioneering work on MRI was carried out by Peter Mansfield of Nottingham, UK and Paul Lauterbur of New York, USA, and would later win them the Nobel Prize for Physiology or Medicine in 2003. In clinical use since the early 1980s, MRI uses magnetic fields and radiofrequency pulses to image and map the water content of the body and so produce very elegant images of the brain. Because MRI does not rely on a rotating gantry (unlike CT) and has no moving parts, it can directly scan in any plane. Its ability to detect small shifts in tissue water content makes it very sensitive to early damage in stroke disease.

Recent advances in computer-based technology have enabled fast acquisition and processing of large amounts of digital data, which is essential to capturing dynamic information , and as a result both CT and MRI can provide high-quality arteriographic images following peripheral intravenous contrast injection. CT and MR angiography (CTA and MRA) of the supra-aortic great vessels are now mainstay investigations in the planning of treatment for carotid artery disease.

With the advent of CT positron emission tomography (CT-PET), functional imaging has begun to play a role in predicting the stability of progressive vascular disease and the need for and risks of intervention.

This chapter sets out the current clinical state of CT- and MR-based techniques in use to assess and diagnose patients with suspected supra-aortic great vessel disease, and to plan and follow-up endovascular therapy.

Imaging the End Organ

The first imaging investigation undergone by a patient with symptoms suggestive of carotid artery disease is a CT scan of the end organ, namely the brain. In stroke, scanning should be carried out immediately on acute presentation to differentiate hemorrhage from ischemia and to exclude other potential causes of the symptoms, namely brain tumors.³,⁴ The positive diagnosis of an ischemic stroke, and identification of its size and location can help guide further investigation, aid management, and predict outcome.

CT is widely available, rapid, and easy to use in acutely ill patients. A plain unenhanced CT of the brain is a highly sensitive technique for acute hemorrhage (Figure 3.1). However, it is often normal in the first few hours after an ischemic stroke, beginning to delineate after 6 h, which is of course beyond the current licensing window for thrombolysis. After this early period, CT will usually very clearly show the location of an acute ischemic event and distinguish between anterior, middle, and posterior cerebral arterial territories (Figure 3.2). Occasionally the causal vessel, usually the middle cerebral artery (Figure 3.3), can be visualized filled with slightly hyperdense thrombus against the relatively lower density of the brain and surrounding CSF in the cisterns. CT is less able to show small infarcts in the posterior fossa, for which MRI is the preferred imaging method. The accuracy of CT begins to fall a week after the acute event and discrimination between hemorrhage and ischemia is increasingly difficult as blood products begin to resorb.⁵,⁶

Figure 3.1 (A) Large intracranial hematoma, with layering of blood products causing a fluid level. There is breakthrough into the subarachnoid space with blood filling the lateral ventricles and extensive midline shift. (B) Small right intracerebral hemorrhage typical of a lenticulostriate hypertensive bleed in the transverse and (C) coronal planes.

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Figure 3.2 Large ischemic infarct causing low attenuation on CT throughout the anterior two-thirds of the middle cerebral artery’s territory in the left cerebral hemisphere and compression of the anterior horn of the lateral ventricle.

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Figure 3.3 Middle cerebral artery sign in a patient with a clinically extended established stroke. (A) Right middle cerebral artery is hyperdense, indicating contained thrombus (arrows). (B) Established, posteriorly-sited middle cerebral artery territory infarct (arrow), with acute extension of the infarct into the rest of the middle cerebral territory, anteriorly. As a result, there is alteration in the gray–white matter differentiation and local mass effect, compressing the anterior horn of the right lateral ventricle.

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In the acute 3–6 h window after onset of symptoms, CT perfusion can be used to accurately delineate ischemic tissue, and importantly the ischemic penumbra where potentially recoverable tissue is located. CT perfusion can be performed on any standard helical CT scanner, immediately following an unenhanced scan. The cerebral blood flow is evaluated dynamically after the injection of iodinated contrast agent. Ischemic regions show reduced flow with delayed time-to-peak and prolonged transit times compared to normal brain. CT perfusion maps can be rapidly produced on appropriate workstations⁷ to show the extent of the acute stroke before it is detectable on an unenhanced scan (Figure 3.4). In the acute situation, this information is rapidly acquired, produced, and interpreted, and is an accurate technique with good interobserver agreement for both the identification of intravascular thrombus and for the size of the penumbra.⁸

Figure 3.4 Value of CT perfusion imaging. (A) Unenhanced CT scan showing no change following a clinical acute infarct. There is no hemorrhage. (B) Dynamic arterial enhancement as part of the perfusion study begins to demonstrate an unenhanced, right middle cerebral territory infarct. (C) Cerebral blood flow map and (D) mean transit time map for the same slice, showing a marked reduction in blood flow and time to enhance in the infarcted territory and its surrounding, potentially recoverable, penumbra.

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The practicalities of MRI make it less suited to the acute emergency situation and have limited its widespread use. MRI is contraindicated in patients with pacemakers, certain cardiac valve prostheses, cerebral aneurysm clips, cochlear implants, and pregnancy during the first trimester due to the risk of deafness in the unborn child. Similarly, patients who are critically ill or confused may be unable to lie in the magnet safely for the required and significant length of time. In all, up to 20% of acutely ill stroke patients may be unsuitable for MRI.⁹

For the majority who are able to undergo MRI, gradient-echo sequences will show hemorrhage (Figure 3.5) with similar accuracy to CT in the acute setting.¹⁰ Diffusion-weighted MR imaging (DWI) sequences will show ischemia (Figure 3.6) with much greater sensitivity than CT, especially during the first 3 h. DWI is a technique now widely available in which the signal from the brain reflects the capacity of water molecules to diffuse normally. In acute stroke the cytotoxic edema with cellular swelling causes restriction of water movement and increased signal; experimentally this has been shown to occur within 10 min of onset of ischemia. In perfusion-weighted imaging (PWI), which is not as widely available, the cerebral blood flow is evaluated dynamically after the injection of contrast agent; ischemic regions show reduced flow with delayed time-to-peak and prolonged transit times compared to normal brain. The combination of DWI and PWI is a potentially valuable tool in immediate stroke care since it may allow accurate delineation of the infarct core (irreversible damage represented by diffusion abnormality due to cytotoxic edema) and the potentially salvageable ischemic penumbra (the surrounding perfusion deficit around the core). However, the availability of this type of imaging remains limited as it is still currently a research tool. Another form of MRI that is widely available and useful in stroke evaluation is susceptibility-weighted imaging (SWI) where a gradient-echo sequence is used that is sensitive to magnetic field inhomogeneity, such as that produced by hemosiderin. This is particularly sensitive for detecting hemorrhage and is able to pick up cerebral microbleeds that CT does not show, e.g. in amyloid angiopathy. A stroke imaging brain protocol would thus include standard morphologic imaging of the brain, DWI, and SWI. If time is of the essence, then DWI is the most important sequence; it will not show hemorrhage as well as specific SWI sequences, but performed as an echoplanar technique it is sensitive to magnetic field inhomogeneity and can depict significant hemorrhage.

Figure 3.5 Intracranial hemorrhage on gradient-echo MRI, the ferromagnetic blood products causing a dense signal artifact in the right frontoparietal region.

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Figure 3.6 Greater sensitivity of MRI. (A) A normal CT scan in a patient presenting acutely with stroke. (B) A FLAIR MRI sequence, a short time later, shows high signal in a right middle cerebral infarct. (C) DWI sequence in the same patient shows more extensive cytotoxic edema than on the FLAIR sequence. DWI is more sensitive at picking up early damage – within 10 min of the infarct.

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In a prospective analysis of 356 patients, of whom 217 had a final diagnosis of acute stroke, Chalela et al.¹⁰ showed that although both CT and MRI had high specificity, MRI with DWI had an 83% sensitivity for all acute causes of stroke, while CT had a much lower 27% sensitivity for all acute stroke and only 16% for acute ischemic stroke. Potentially DWI can detect lesions within minutes of the onset of ischemia.¹¹

MRI using DWI and gradient-echo sequences is recommended in patients presenting with acute stroke who are not severely ill, especially if the lesion is thought to lie in the posterior fossa or neurologic deficit is limited or unusual (such as brainstem syndromes). MRI is also recommended in patients with late presentation when CT is less able to differentiate the cause.¹² Patients with transient ischemic attack (TIA) – a cerebral event lasting less than 24 h – also undergo mandatory brain imaging to assess the presence and extent of damage. CT is usually the first-line investigation due to its widespread availability and accuracy. In true TIA, brain imaging should be normal but it is still useful to exclude mimics, e.g. meningioma and other tumors. Arteriovenous malformations, too, can mimic TIA due to epileptiform phenomena. Small lacunar infarcts indicate established embolic damage, often to be found in the basal ganglia. These may be single or multiple and so contribute to the diagnosis of a multi-infarct state.

In the assessment of patients for consideration of carotid intervention following a TIA, CT scanning will suffice in the majority for whom the diagnosis of carotid territory TIA is clear cut. However, if the CT scan is normal but the clinical scenario is inconclusive, then MRI with DWI should be performed as demonstration of diffusion abnormality may be helpful.

The effect of carotid intervention can be demonstrated by CT or MRI brain perfusion scanning, assessing the brain uptake of contrast with time. This can detect variations in brain perfusion before and after carotid stent placement in severe stenosis with a significant normalization of the blood flow parameters in the brain supplied by the stented vessel.¹³

The complications of carotid intervention can also be established by brain imaging. Fairman et al.¹⁴ described 4.8% of patients experiencing a stroke after carotid stenting – over half of which were post procedure, predischarge. Of the remainder, almost a quarter occurred during the procedure and a fifth following discharge.

Imaging the Causal Lesion and Planning the Intervention

CTA and MRA of the extracranial circulation are second-line investigations where the initial diagnostic modality for disease around the carotid arterial bifurcation,⁴ Doppler ultrasound, is abnormal.⁴,¹⁵,¹⁶ Ultrasound is a guide to the presence of significant disease and hence to an indication for interventional treatment. However, there is increasing evidence that imaging techniques which provide an angiographic-style image, such as CTA and MRA, have better reproducibility, lower interobserver variation, and higher accuracy in assessing/quantifying carotid disease than ultrasound.¹⁷

When the decision of intention to treat by active intervention is made, usually based by the results of clinical findings and Doppler ultrasound, most specialists confirm the severity of carotid artery disease with MRA or multislice CTA. This will accurately grade the disease and assess the whole carotid system for tandem lesions, tortuosity, anatomic variation and aortic or origin disease. The latter three are particularly important in the assessment of suitability for catheter-based intervention. Both MRA and CTA are non-invasive and so provide a safer and less invasive complementary study than catheter angiography, which can have complication rates as high as 4%.¹⁸ Currently the literature on accuracy of CTA for supra-aortic vasculature is limited compared to contrast-enhanced (CE)-MRA for which there is good meta-analysis evidence of high accuracy. Hence, because CTA also adds ionizing radiation and high volume nephrotoxic contrast to the work-up, CE-MRA should be the imaging method of choice when Doppler ultrasound demonstrates significant carotid stenosis. CTA should be reserved for patients in whom MRA is contraindicated (see below) or cannot be performed, such as those who experience claustrophobia.

Thus, unless contraindicated, every carotid bifurcation lesion being considered for intervention should undergo CE-MRA, which has a better discriminatory power than Doppler ultrasound for 70–99% stenosis.¹⁹ CE-MRA involves the intravenous injection of a gadolinium-based contrast agent that is imaged during its first pass through the arterial system, before venous return in the jugular system contaminates the image. Accurate timing is required as venous return occurs in less than 8 s following arterial enhancement. The application of parallel imaging, which dramatically reduces the acquisition time (and/or increases the acquired spatial resolution)²⁰ and sophisticated k-space sampling techniques, including time-resolved sequences, have allowed high-definition images of the supra-aortic great vessels while still maintaining the required rapid imaging. The image is recorded on a three-dimensional (3D) gradient-echo sequence in a coronally acquired block of data which must then be interrogated and reformatted on a workstation. With CE-MRA there is intrinsically low signal from surrounding tissue compared to the intensely high signal of the CE vessel lumen, hence little post-processing of the images is required. Bone and calcification are ignored due to their very low water content, so unlike for CT, do not cause problems with overlap of the vessels under examination.

Such an MRA examination enables the entire carotid and subclavian system to be visualized from the aortic arch up to the circle of Willis, and out to the axillary arteries within a single breathhold (Figure 3.7). Anatomic variation of the aortic arch occurs in up to 25% of cases, usually minor.²¹ The rarer, disadvantageous variations, usually the left common carotid artery (CCA) arising as the first branch of the brachiocephalic together with brachiocephalic or carotid artery origin stenosis, can affect catheter access and so influence the choice of endovascular intervention versus surgery.

Figure 3.7 (A) MRA of the aortic arch up to the circle of Willis. There is a conventional anatomy and an 80% stenosis of the left internal carotid artery (ICA) with a deep ulcer crater. (B) Restricted MIP of the same volume dataset demonstrating the left ICA, free of overlapping vessels.

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The interpretation of the dataset is critical to accurate results. Most MRA examinations of the supra-aortic great vessels are acquired as a coronal block of data that includes the carotid, vertebral, and subclavian arteries. These should be viewed slice by slice in the plane of acquisition to build up a true image of the degree of narrowing. Reformatting into an axial or sagittal plane is also helpful in quantifying the stenosis. However, these reformats all show the vessel piecemeal and the most common summary view of the supra-aortic arterial territory on MRA is the maximum intensity projection (MIP). This summates the brightest points in the block of data and so builds the information on each individual slice into a composite image of the whole arterial tree. Because it employs a threshold (which can be arbitrarily set) to select the brightest points for summation, thick-slab MIP may over- or under-estimate the true degree of stenosis. Against that, it produces images that are crucial to the understanding of the anatomy as well as the location and complexity of the stenosis. Careful use of these reformats, detailed analysis of the slice-by-slice source images, and thin-slab sliding MIP lead to very accurate results. In a recent comparison with conventional digital subtraction arteriography Timaran et al.²² have shown CE-MRA to have an 87% sensitivity and 100% specificity for both detection of aortic arch anatomic type and stenosis greater than 80%; a 75% sensitivity and 98% specificity for ulcerated plaque; and a 100% sensitivity and 100% specificity for determining suitability for carotid artery stenting. Overall, the diagnostic accuracy of CE-MRA is highest in the assessment of 70–99% stenosis, with a sensitivity and specificity of 95%.¹⁷

CE-MRA gives exquisite anatomic information about the vessels and their disease, but no information about flow unless time-resolved sequences are available. Information about flow and its direction can be obtained from time-of-flight MRA. This was the first MRA technique to be described and does not employ contrast agents. In the supra-aortic territory it can show flow voids in post-stenotic turbulence, as well as reversal of flow in the external carotid artery in tight CCA stenosis or in the vertebral artery in a subclavian steal situation (Figure 3.8). A third technique, phase-contrast MRA, has recently been developed further to trace the flow of individual virtual particles of blood within the vessel along measured 3D velocity vector fields.²³,²⁴ This new advance, vector tracking, color codes the resulting 3D pathway of each virtual particle of blood according to velocity. This allows the exquisite demonstration of normal laminar flow inside the aorta and with present technology its major branches, and therefore any abnormal flow pattern or turbulence. Currently in evaluation, this technique will provide a powerful research tool to non-invasively assess the degree to which return to a normal flow pattern has followed endovascular treatment, which is especially important in assessing the technical success or otherwise of new devices.

Figure 3.8 (A) CE-MRA thin MIP of a tight right subclavian stenosis. Both vertebral arteries fill but there is no information regarding their direction of flow. (B) Time-of-flight axial MRA showing flow towards the head. The carotid arteries and the left vertebral artery show signal indicating flow in that direction. There is no signal from the right vertebral artery. (C) Time-of-flight axial MRA showing flow away from the head. The veins of the neck show signal as does the right vertebral artery (circle), indicating that its flow direction is reversed to provide collateral flow because of the promimal subclavian stenosis.

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Modern MRI scanners are able to produce high-definition black blood images of the carotid arterial wall, as if empty of blood. When electrocardiograph gated, this gives very precise detail of the vessel wall and intima and can be used to study dissection along with CE techniques (Figure 3.9). Black blood imaging also gives exquisite detail of atheromatous plaque and allows direct measurement of the ensuing stenosis, usually at right angles to the direction of flow. The demonstration of intraplaque hemorrhage on MRI can predict particulate embolization during carotid endarterectomy.²⁵ Advances in MR resolution, particularly with surface coils, take this to a new level and plaque can now be characterized into its constituent tissue types. The relative signal intensity of carotid plaque is different for fibrous cap, fibrosis, calcification, myxomatous tissue, lipid core, and intraplaque hemorrhage. This paves the way for virtual histology MRI. If the overall relative signal intensity is measured in T1-weighted images for the whole carotid plaque, soft plaque can be diagnosed with a 79.4% sensitivity and 84.4% specificity.²⁶ Symptomatic lesions have been shown to have a higher incidence of ruptured fibrous caps, hemorrhage or thrombus, necrotic lipid cores, and complex type VI American Heart Association (AHA) lesions compared to asymptomatic ones.²⁷ Macrophages will take up ultra-small superparamagnetic particles of iron oxide (USPIO) administered intravenously. These USPIO agents can be imaged 24 h after injection by MRI, giving an indication of macrophage activity in plaque, an important factor in destabilization.²⁸ Although these techniques demonstrate the technical possibilities and future direction of carotid MRI, they remain in ongoing evaluation in major centers. The mainstay of current MR investigation remains the demonstration of stenosis on CE-MRA.

Figure 3.9 Aortic root repair complicated by dissection which traveled up the common carotid artery (CCA) in a symptomatic patient. (A) Black blood image of the aortic arch showing the intimal dissection flap. (B) CE-MRA showing the dissection continuing up the brachiocephalic into the right CCA.

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However, MRA is not suitable for every patient (see above for contraindications). Metal implants such as stents pose their own problems (see above).

If MRA is contraindicated, CTA is an accurate, alternative method to identify, locate, and quantify the stenosis (Figure 3.10). Like MRA, it will also confirm the anatomy of the supra-aortic great vessels and any origin or tandem lesion which may influence the decision to treat and demonstrate the carotid artery from the arch of the aorta to the circle of Willis. CTA has high sensitivity and specificity when compared to conventional digital subtraction arteriography.²⁹ Because supra-aortic CTA produces a 3D dataset, comprising some 600–800 slices, it is essential to interrogate this interactively at a workstation. Meticulous technique is required to use the full range of digital reformats to display accurately the degree of a 3D stenosis in a 3D imaging acquisition on a 2D workstation monitor. As a result, the interpretation of CTA can be operator dependent. Vessel tortuosity, overlapping bone, and calcification all pose additional problems. There are four reformats routinely available, which are of clinical use in interpreting the CT dataset:

Figure 3.10 CTA with sagittal restricted MIP of the carotid bifurcation showing an irregular, ulcerated plaque causing 90% narrowing. Early venous filling of the internal jugular vein is shown behind the carotid artery.

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1. The multiplanar reformat (MPR) is the simplest, displaying the information as a single voxel layer in any plane – axial, coronal, sagittal, or oblique – free from overlap. However, it reconstructs in a linear fashion and because the carotid is often tortuous, the stenosis appears to vary according to plane. The MPR should be scrolled through the vessel to build up an image of the stenosis in the operator’s mind.

2. Alternatively, a curved planar reformat (CPR) will reconstruct the dataset along the central axis of the vessel, straightening out the artery and negating any tortuosity. A longitudinal section of the artery is therefore included in one image. This will exquisitely demonstrate the narrowing so long as CPR is carried out in at least two planes – usually coronal and sagittal. However, surrounding information is badly distorted as the reconstruction is aligned to the long axis of the vessel. This technique used to be very labor intensive, requiring manual tracing of the tortuous vessel axis. Seeding techniques have been developed which carry out this task automatically (Figure 3.11) and rapidly so long as there is a continuous column of contrast medium within the vessel, i.e. no occlusion.

Figure 3.11 CTA of the carotid bifurcation with automated curved planar and transverse reformats, produced by simply seeding the vessel on the workstation, in order to show the two-dimensional narrowing in the three mutual planes.

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3. The MIP on the other hand summates the brightest points – usually contrast medium and calcium – in a volume of tissue containing the vessel. However, a very focal yet eccentric stenosis may be partially concealed by the contrast medium either side of the tightest point. Overlapping vessel branches and large calcified plaque can also obscure the stenosis.

4. Volume-rendered reformats show the column of contrast medium as a 3D structure, as if a resin cast of the vessel lumen with the arterial wall removed. Because it uses an arbitrary threshold technique to choose which density of volume to display, voxels at the margin of the lumen (where density of contrast medium is less) may not be included in the display. As a result, great care has to be taken to avoid overestimating stenosis. Because of the limitations of interrogating a 3D display on a 2D computer screen, this technique tends to be used more to understand tortuous anatomy, especially congenital variants (Figure 3.12). It is therefore very useful in planning the safe approach to catheter-based interventions.

Figure 3.12 CT volume rendered three-dimensional reformat showing aberrant anatomy in a right-sided aortic arch: the left common carotid artery arises as the first branch, the right carotid followed by the right subclavian, and on the descending portion, the left subclavian artery.

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Interobserver agreement is greater for the MIP reformat in carotid CTA with a sensitivity of 91.1% compared to 87.8% for MPR.³⁰ A 93.9% sensitivity and 98.7% specificity is claimed for the detection of carotid plaque ulceration with multidetector CTA using MIP, MPR, and volume-rendered reformats; the latter images proved the most accurate.³¹

Plaque calcification can be particularly challenging for CTA as blooming artifact exaggerates plaque extent, obscuring the lumen of the vessel. Depending upon the attained contrast medium density within the vessel, calcification can be very difficult to separate from the contrast medium column to visualize the true stenosis. In such cases, the axial plane is often the most useful, imaging the cross-sectional narrowing, surrounded not overlapped by the calcium (Figure 3.13). Unlike CE-MRA where the surrounding tissues are suppressed to show just the luminal contrast medium, CTA clearly shows the tissues adjacent to the contrast medium column. As a result, the vessel wall, surrounding structures, and contained thrombus can be readily seen (Figure 3.14). Plaque can also be visualized as a filling defect between the vessel wall and the contrast medium column, especially as the latter penetrates the atheroma when ulceration is present (Figure 3.15).

Figure 3.13 Limitation of CTA at a calcified bifurcation. (A) MIP showing the summated calcification obscuring the contrast-enhanced lumen. (B) Transverse section through the carotid bifurcation shows calcium is causing 70% narrowing of the internal carotid artery, posteriorly, with relatively minor involvement of the external carotid artery, anteriorly.

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Figure 3.14 Coronal MPR of a CTA showing occlusion of the prevertebral portion of the left subclavian artery.

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Figure 3.15 Oblique sagittal CTA showing 80% stenosis of the internal carotid artery with deep ulceration into the atheromatous plaque.

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