Clinical and angiographic manifestations inpatients without previous diagnosis of Takayasu´s arteritis

Here some cases are presented to illustrate the radiological findings by DSA and Doppler US from this study. Figure 1 shows the case of a woman with cerebrovascular disease in the young (right facial hemiparesis). MRI showed hyperintense left frontotemporal with lenticular involvement and vascular luxury in the T1 sequence with gadolinium corroborating stroke, color Doppler study at the origin of the common carotid artery shows circumferential homogeneous myointimal thickening and with color the vessel is seen partly perfused with a turbulent flow. In the left common carotid the thickening is occlusive. The DSA showed effect on supra-aortic trunks in the early arterial phase, and diameter decrease is observed at the origin of the right common carotid artery, occlusion of the left common carotid artery, and the vertebral artery on the same side, with subclavian steal demonstrated in the late arterial phase and through the posterior communicating artery it is retrogradely opacified, giving irrigation to the left upper extremity. This case was considered as TA type I. Figure 2 shows the case of a woman with vertebrobasilar manifestations and cerebral stroke. In the DSA occlusion of the supra-arterial vessels stands out, there is only flow through the right vertebral artery. This case was classified as TA type I.  

Figure 1 A) Arterial phase DSA shows left common carotid and subclavian artery occlusion, black arrow. B) Late phase with left subclavian steal, white arrow. C) Color and gray scale Doppler show heterogeneous color and occlusion by left homogeneous circumference carotid thickening. D) MRI of TI with left frontotemporal luxury vascularity gadolinium E) MRI in flair sequence with frontotemporal hyperintensity and nuclear lenticular involvement

Figure 2 A) Arterial phase showing only right vertebral permeability. B) Doppler color with increased vertebral diameter and homogeneous flow. C) Late arterial phase DSA vertebral-carotid communication, short arrow. D) Doppler power showing collaterality arriving at bifurcation (head of arrow)

Figure 3 shows a woman with symptoms of hypertension. The DSA has normal supra-aortic vessels and infrarenal aortic stenosis with right renal exclusion and critical stenosis of the left renal artery. This patient corresponded to TA type IV.

Figure 3 A and B) Thoracic aortogram and supra-aortal trunks showing normal trajectory and morphology. C) Aortogram showing aortic infrarenal stenosis with right renal exclusion (black arrow) and critical stenosis of left renal artery (white arrow).

Figure 4 refers to a patient with neurological manifestations and secondary hypertension. The DSA shows stenosis of supra-aortic vessels, and occlusion of the right renal artery. This case was classified as TA type V.

Figure 4 A) DSA shows involvement of common carotid, subclavian arteries. Dotted arrows. B) Right common carotid artery selectivity, showing long thinning with short pre-bifurcation stenosis, long arrow. C) Abdominal aorta with right renal artery occlusion, black bordered arrow. D) Selection of left subclavian with proximal tertiary stenosis, curved arrow. E and F) Carotid color Doppler, showing diffuse and homogenous thickening of intima-media with significant diameter deduction with turbulence. G) Right kidney reduced in size with relation with medullar cortex lost. H) Color Doppler showing flow in aorta with reduced flow towards right renal artery with aliasing, white arrow.

Discussion

In the study, the main manifestations for which DSA was done were CVD in the young, RVH, and arterial insufficiency of the upper extremities. The most common type of TA was type I, V which explains the manifestations of CVD and RVH, respectively.

TA is a systemic granulomatous vasculitis whose clinical manifestations are: the result of stenosis, occlusion, and dilatation of the large vessels that affect this illness.¹¹ The manifestations that guide the diagnosis of this vasculitis are decreased or absent pulses, which was present in 100% of patients when they were intentionally looked for, and vascular murmurs in 70%. Other clinical manifestations of our patients were neurological, with stroke in the young in 40%. They were also: headache, dizziness, and visual disturbances, as has been reported previously.¹²

Another reason for study in our patients was RVH (30%), explained by renal stenosis. Secondary hypertension of renovascular origin as consequence of TA has been reported in up to 60% of cases and must be identified in a timely manner because it can lead to kidney failure. RVH is generally resistant to medical therapy and often requires angioplasty or surgical bypass.¹³ One manifestation of interest was the subclavian steal, which is characterized by stenosis proximal to the subclavian artery leading to retrograde flow of the vertebral artery on the same side, which acts as a collateral flow. The subclavian steal may be asymptomatic because the Willis polygon produces enough collateral circulation; however, in symptomatic cases, patients report involved extremity and cerebral ischemia as in one of our cases.^14-16

Vascular imaging studies - such as arteriography- make it possible to identify the vascular anatomy, but not inflammation of the vessel wall.11 Imaging studies such as DSA allow one to identify the distribution of the affected vessels and greatly facilitate the diagnosis of patients with suspected TA.¹⁷ DSA is the gold standard for detecting and classifying the type of vascular lesion (permeability of vessels, areas of stenosis, occlusions, and aneurysmal dilation). With suspicion of TA, complete angiography is recommended to classify and provide medical treatment and/or alternative surgical treatment if necessary.

Color Doppler ultrasound is a noninvasive test that can show wall thickening of affected arteries in early stages and can rule out atheromatous disease. It is increasingly used for diagnosis and monitoring of large-vessel vasculitis. Carotid, vertebral, and subclavian vessels can be studied by CDU. It is a useful study in the prestenotic phase of TA and is complementary to studies with DSA, because it can identify changes in the heart, renal artery, and subclavian stenosis, among others. It can also identify inflammation of the wall of the ascending aorta, valvular regurgitation, pericardial effusion, and more.¹⁸ In our study, CDU was complementary to the findings observed by DSA study. 

In this paper, DSA was a great help to establish the definitive diagnosis of TA and its correct classification. According to Numano’s classification, in our patients TA type I followed by V and IV were the most frequent. These types of TA have also been reported in other populations.^19-21 The clinical and angiographic manifestations observed in our patients are similar to those reported in other countries.^19-27

In our study, the diagnosis of referral in the first place was stroke in the young with involvement of the supra-aortic trunks, followed by RVH, as in the case of two of the patients who were not suspected of Takayasu’s arteritis, one with normal supra-aortic trunks and involvement of the abdominal and renal aorta, and the second case with involvement of supra-aortic trunks, abdominal and both renal aortas. Splenorenal anastomosis was done to the left renal stenosis.

The study showed experience with TA in one hospital for one year, suggesting that is a common vasculitis in Mexico. Our patients were female and had severe manifestations of TA such as CVD and RVH, so the study protocol in these patients should include not only selective arteriography, but a total arteriography to identify other changes at other arterial levels. Moreover, it is important to do physical examination with complete assessment of the pulses, and to investigate history of claudication of extremities, headache, eye lesions, arthralgia and/or arthritis, and skin conditions such as erythema nodosum.

Our work has limitations such as being a cross-sectional study with duration of one year, in which a small sample of patients was found in whom TA was intentionally looked for.

In conclusion, the main clinical manifestations were vascular (absent and/or decreased pulses), followed by stroke and renovascular hypertension.

References

1. Numano F, Okawara M, Inomata H, Kobayashi Y. Takayasu´s arteritis. Lancet 2000; 356:1023-5.
2. Aluquin VP, Albano SA, Chan F, Sandborg C, Pitlick PT, Magnetic Resonance imaging in the diagnosis and follow up of Takayasu´s arteritis in children. Ann rheum Dis 2002;61:526-9.
3. Sheikhzadeh A, Tettenborn I, Noohi F, Efterkhazadeh M, Schnabel A. Oclusive thromboaortopathy Takayasu disease: clinical and angiographic features and a brief review of literature . Angiology 2002;53:29 40.
4. Johnston SL, Lock RJ, Gompels MM, Tayakayu arteritis: J Clin Pathol 2002; 55:481-6.
5. Soto ME, Espinola N, Flores-Suarez LF, Reyes PA.Takayasu arteritis: clinical features in 110 Mexican Mestizo patients and cardiovascular impact on survival and prognosis. Clin Exp Rheumatol. 2008; 26(3 Suppl 49):S9-15.
6. Hall S, Barr W, Lie JT, Stanson AW, Kazmier FJ, Hunder GG. Takayasu arteritis: a study of 32 North American patients. Medicine (Baltimore) 1985;64:89-99.
7. Kerr G. Takayasu´s arteritis. Curr Opin Rheumatol 1994;6:32-8.
8. Sharma BK, Jain S. Suri, Numano F. Diagnostic criteria for Takayasu arteritis. Int J Cardiol 1996;54 (suppl): S141-S7.
9. Hata A, Noda M, Moriwaki R, Numano F. Angiographic findings of Takayasu arteritis: new classification . Int J. Cadiol 1996;54 (suppl):S155-S163.
10. Arend WP, Michel BA, Bloch DA, Hunder GG,Calabrese LH, Edworthy SM, et al. The AmericanCollege of Rheumatology 1990 criteria for theclassification of Takayasu arteritis. Arthritis Rheum.1990;33:1129-34.
11. Chatterjee S, Flamm SD, Tan CD, Rodriguez ER. Clinical diagnosis and management of large vessel vasculitis: Takayasu arteritis. Curr Cardiol Rep. 2014;16:499.
12. Li-xin Z1, Jun N, Shan G, Bin P, Li-ying C. Neurological manifestations of Takayasu arteritis. Chin Med Sci J. 2011;26:227-30.
13. Chaudhry MA, Latif F . Takayasu’s arteritis and its role in causing renal artery stenosis. Am J Med Sci. 2013;346:314-8.
14. Hashimoto A, Iwazu Y, Ando Y, Inoue M, Saito O, Asakura S, Muto S, Yagisawa T, Kusano E. Difficult hemodialysis induction due to subclavian steal syndrome in a patient with Takayasu’s arteritis.Nihon Jinzo Gakkai Shi. 2011;53:1034-40.
15. Lusic I1, Maskovic J, Jankovic S, Cambj-Sapunar L, Hozo I.Endoluminal stenting for subclavian artery stenosis in Takayasu’s arteritis. Cerebrovasc Dis. 2000;10(1):73-5.
16. Di Renzo M1, Pasqui AL, Pieragalli D, De Franco V, Bracco S, Venturi C, Bruni F, Puccetti L, Verzuri MS, Auteri A.Takayasu’s arteritis: case report of a patient with recurrent subclavian steal syndrome. Heart Vessels. 2004;19:94-7.
17. Schmidt WA. Imaging in vasculitis. Best Pract Res Clin Rheumatol. 2013;27:107-18.
18. Schmidt WA. Role of ultrasound in the understanding and management of vasculitis.Ther Adv Musculoskelet Dis. 2014;6:39-47.
19. Park MC, Lee SW, Chung NS, Lee SK. Clinical characteristic and outcomes of Takayasu, analysis of 108 patients. Scand J Rheumatol. 2005;34:284-92.
20. Schmidt J, Kermani TA, Bacani AK, Crowson CS, Cooper LT, Matteson EL, Warrington KJ.Diagnostic features, treatment, and outcomes of Takayasu arteritis in a US cohort of 126 patients.Mayo Clin Proc. 2013;88:822-30.
21. Nooshin D, Neda P, Shahdokht S, Ali J.Ten-year Investigation of Clinical, Laboratory and Radiologic Manifestations and Complications in Patients with Takayasu’s Arteritis in Three University Hospitals. Malays J Med Sci. 2013;20:44-50.
22. Bicakcigil M, Aksu K, Kamali S, Ozbalkan Z, Ates A, Karadag O, et al. Takayasu in Turkey. Rheumatology. 2009;27:859-64
23. Kechaou M, Frigui M, Ben Hmida M, Bahloul Z. Takayasu arteritis in Southern Tunisia a study of 29 patients. Presse Med. 2009;38:1410-4.
24. Suwanwela N, Piyachon C. Takayasu in Thailand, clinical and imaging. Features Int J Cardiol. 1996; 54(Suppl):S117-34.
25. Arnaud L, Haroche J, Limal N, Toledano D, Gambotti L, Costedoat Chalumeau N, et al. Takayasu arteritis in France, a single-center retrospective study of 82 cases. Medicine (Baltimore). 2010;89:1-7.
26. Moriwaki R Noda M, Yakijama M, Sharma BK, Numano F. Clinical manifestations of Takaya arteritis in India and Japan: new classification of angiographic findings. Angiology 1997;48:369-79.
27. Ghannouchi JN, Khalifa M, Rezgui A, Alaoua A, Ben JE, Braham A, et al. Takayasu disease in Central Tunisia, 27 cases. J Mal Vase. 2010;35:4-11.

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