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Year : 2016  |  Volume : 13  |  Issue : 1  |  Page : 82-85

Balloon aortoplasty for management of arterial hypertension in Takayasu arteritis: Case report and review

Department of Interventional Cardiology, R.G. Kar Medical College and Hospital, Kolkata, West Bengal, India

Date of Web Publication13-Jan-2016

Correspondence Address:
Viral Tandel
Department of Interventional Cardiology, R.G. Kar Medical College and Hospital, 1, Khudiram Bose Sarani, Kolkata - 700 004, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0189-7969.173853

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The clinical course of Takayasu arteritis varies from nonspecific constitutional symptoms such as fever, malaise, rashes, loss of appetite, dizziness, and so on during the acute phase to those resulting from arterial stenosis and ischemia in chronic phase. We report a case of a young female presenting with resistant hypertension and lower limb claudication. The diagnosis was confirmed by multiple detector computed tomography-renal angiogram, which showed narrowing of abdominal aorta just above celiac trunk along with wall thickening. The lady was treated with balloon aortoplasty following which the claudication symptoms were subsided and blood pressure was normalized.

Keywords: Arterial hypertension, balloon aortoplasty, Takayasu arteritis

How to cite this article:
Majumder B, Tandel V, Das R, Venkatraman D. Balloon aortoplasty for management of arterial hypertension in Takayasu arteritis: Case report and review. Nig J Cardiol 2016;13:82-5

How to cite this URL:
Majumder B, Tandel V, Das R, Venkatraman D. Balloon aortoplasty for management of arterial hypertension in Takayasu arteritis: Case report and review. Nig J Cardiol [serial online] 2016 [cited 2021 Jun 20];13:82-5. Available from: https://www.nigjcardiol.org/text.asp?2016/13/1/82/173853

  Introduction Top

Takayasu arteritis (TA), a granulomatous pan arteritis, affects the aorta and its major branches, typically before 40 years of age. The disease predominates in women, with a male to female ratio of 10:1. Being a rare disorder and heterogeneous nature of its manifestations, the disease is often diagnosed late. Clinical suspicion and appropriate imaging modality are crucial for the diagnosis. While the exact etiology of TA remains unknown, various treatment modalities such as steroid during the active phase to balloon aortoplasty with or without stenting and surgical repair are being used. In our case, it was the balloon aortoplasty which proved beneficial for the patient.

  Case Report Top

A 21 years female patient was referred to our hospital for the management of resistant hypertension. She was on tablet metoprolol XL 100 mg/day, tablet amlodipine 10 mg/day, and tablet torsemide 2.5 mg/day. Detailed history revealed her of being suffering from lower limb claudication. There was no history of upper limb claudication, dizziness, transient blackouts, chest pain, or palpitation. Family history was nonsignificant.

On examination, she had BMI of 19 kg/m 2, pulse rate of 74/min, blood pressure in right upper limb was 194/112 mm of Hg, in left upper limb 190/112 mm of Hg, in right lower limb 118/92 mm of Hg, and in left lower limb 116/92 mm of Hg. Jugular venous pressure was normal with normal waveforms. Heart sounds were normal, and no murmur was audible over the precordium. A bruit was present in the epigastric region. No bruit was audible over the carotids.

Laboratory findings showed an erythrocyte sedimentation rate and C-reactive protein in the normal range, hemoglobin level was 12 g%, and serum creatinine was 0.9 mg/dl with no dyslipidemia. Electrocardiogram showed left ventricular hypertrophy. Echocardiography revealed concentric left ventricular hypertrophy with normal size and function of both right and left ventricle, valves, and pericardium was normal, ascending and aortic arch showed no narrowing or turbulence.

Renal artery Doppler examination was normal. Multiple detector computed tomography-renal angiogram showed no abnormalities of the renal artery, however, there was gross narrowing of aorta about 2.3 cm above the celiac trunk [Figure 1]. Other branches of the aorta were normal. The cortical and medullary nephrogram were normal on both sides.
Figure 1: Multiple detector computed tomography showing significant narrowing of abdominal aorta above renal arteries

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The diagnosis of TA was made in this patient based on the American College of Rheumatology criteria 1990[1] and Sharma et al. modified Ishikawa's criteria for TA.[2]

A close differential diagnosis for TA is atherosclerosis. Typically the patients with atherosclerosis are more than 40 years of age, usually having other risk factors such as smoking, hypertension, diabetes, and dyslipidemia. They may present earlier in life as seen with familial dyslipidemia. Angiogram typically reveals abrupt narrowing with lesions confined to vessel origin and carotid bifurcation.

The patient was treated with balloon aortoplasty procedure through right femoral artery route [Figure 2] and [Figure 3]. The pressure gradient across the narrowing was 94 mm of Hg. The lesion was dilated with a noncompliant aortoplasty balloon of size 36 mm × 16 mm at 20 atmospheric pressure. Postprocedure, the pressure gradient across the site was reduced to 36 mm of Hg.
Figure 2: Fluoroscopic image during balloon aortoplasty. Black arrows demonstrate the discrete stenotic lesion causing indentation of the balloon. White arrows demonstrating dilatation of stenotic segment at full dilatation of balloon

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Figure 3: Intra-arterial aortogram showing significant improvement in aortic diameter postprocedure

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The patient was discharged in a stable condition, and blood pressure returned to normal within a week with no symptoms of lower limb claudication.

  Discussion Top

TA is an idiopathic large vessel vasculitis affecting aorta and its branches. Women are ten times more affected than males with a median age of 25 years. TA has been best known to affect the Asians, especially the Japanese population with the incidence of 1 in every 3000 autopsies having the feature of TA.

The exact etiology of this disease is not known, and several etiologic factors have been proposed, including spirochetes, Mycobacterium tuberculosis, streptococci, circulating antibodies due to an autoimmune process, and genetic aspects. There are some differences in the sites affected by inflammatory process among different ethnic groups. Japanese patients with TA have a higher incidence of aortic arch involvement, whereas, in patients from Korea, India, and the Western countries, the abdominal aorta and renal arteries are most frequently affected. However, all patterns of vascular changes have been detected in every country.[3]

The clinical course of the disease is divided into an early active inflammatory phase and late chronic phase. The active phase lasts for weeks to months and may have a remitting and relapsing course. It is characterized by systemic disease with symptoms of fever, general malaise, night sweats, loss of appetite, weight loss, headaches, dizziness, arthralgia, skin rashes, etc. The late chronic phase is the result of arterial stenosis and/or occlusion resulting in ischemia of organs. Its clinical manifestations are varied and related to the location of arterial lesions.

In TA, arterial stenosis occurs 3 to 4 times more frequent than an aneurysm. Claudication is the most common symptom and bruit, elevated blood pressure, and pulse asymmetry are the most common findings. Aneurysm is frequently seen in aortic root where it can lead to valvular regurgitation.

Hypertension in TA is thought to be the result of three mechanisms: (a) Mechanical, in which hypertension proximal to narrowed aorta (atypical coarctation) is due to high resistance to cardiac output imposed by narrowing.[4] (b) Neural, in which hypertension proximal to narrowed aorta results from aortic arch baroreceptors readjustment and this allows to ensure adequate blood supply to organs distal to narrowed aorta.[5] Moreover, (c) hormonal, in which hypertension is caused by renal hypoperfusion due to stenotic lesions of one or both renal arteries or aorta alone.[1],[2] A decrease in elasticity of arterial walls observed in TA may also contribute to the elevation of the blood pressure.[6] In our patient, systolic arterial hypertension seemed to result from narrowing of the thoracic aorta, renal ischemia, and probably aortic arch baroreceptors hyposensitivity.

There is no specific test for TA. The diagnosis is based on clinical features in conjugation with vascular imaging abnormalities. While the intra-arterial angiography still remains the standard for diagnosis and evaluation of TA, it has been largely replaced by computed tomography angiography or magnetic resonance angiography. These techniques, in addition to visualizing the arterial lumen, may provide valuable information about inflammation in the arterial wall and periarterial structures. This might facilitate the diagnosis of TA at an early stage, in which arterial wall thickening is present, and the lumen diameter is preserved.

Treatment is based on the use of immunosuppressants such as prednisone. However as many as 40% of the patients relapses on tapering the steroid therapy. Alternative therapies such as azathioprine, cyclophosphamide, mycophenolate mofetil, and tacrolimus hydrate are also used, especially for corticosteroid-resistant disease. Hypertension should be treated aggressively often with the multidrug regimen, but physicians should be warned against ACE inhibitors until renal artery stenosis has been excluded.

In the presence of symptomatic stenotic or occlusive lesions, endovascular revascularization procedures such as bypass grafts, patch angioplasty, endarterectomy, percutaneous transluminal angioplasty (PTA), or stent placement should be taken into consideration. These procedures should be undertaken with great care and be reserved for specific indications. Both surgical and endovascular treatments become risky and achieve poorer outcomes if they are undertaken during a period of inflammatory activity.

Because of multifocal involvement and dense transmural fibrosis, surgical reconstructive procedures are difficult and are associated with significant morbidity, mortality, and postoperative complications. Percutaneous transfemoral balloon angioplasty (PTA) has emerged as an effective, less invasive, and safer technique in this debilitating disease. Intermediate and long-term follow-up results of dilatation of lesions of the aorta by balloon angioplasty are excellent.[7] The procedure is highly effective for discrete stenotic lesion and much less effective for long segment, ectatic, or calcified lesions. However, because the stenosis is rigid and noncompliant, higher balloon inflation pressure is required to stretch and split the thick and more rigid fibrous tissue compared with atherosclerotic aortic stenosis.

Restenosis develops in 15–20% of the cases. To prevent marked restenosis, stenting is currently added, especially for long-segment lesions. Consequently, at present, it appears reasonable to attempt less invasive percutaneous balloon aortoplasty with/without stenting for stenotic/occlusive lesions of the aorta in TA.

In our case, the lesion was discrete and hence, we decided to go for balloon angioplasty without stenting. The balloon was inflated at high pressure so that the thick and rigid fibrous wall tissue could be stretched and the adequate result obtained. Since the active phase reactants were not elevated, immunosuppression therapy was not prescribed to our patient.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Arend WP, Michel BA, Bloch DA, Hunder GG, Calabrese LH, Edworthy SM, et al. The American college of rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum 1990;33:1129-34.  Back to cited text no. 1
Sharma BK, Jain S, Suri S, Numano F. Diagnostic criteria for Takayasu arteritis. Int J Cardiol 1996;54:S141-7.  Back to cited text no. 2
Ogino H, Matsuda H, Minatoya K, Sasaki H, Tanaka H, Matsumura Y, et al. Overview of late outcome of medical and surgical treatment for Takayasu arteritis. Circulation 2008;118:2738-47.  Back to cited text no. 3
Fadouach S, Abid-Allah M, Mehadji BA, Tahiri A, Chraibi N. Hypertension and Takayasu disease. Report of 8 cases. Ann Cardiol Angeiol (Paris) 1998;47:155-9.  Back to cited text no. 4
Hamida BM, Maazoun F, Marzouk S, Frigui M, Bouattour F, Chaabouni Y, et al. Hypertension in Takayasu disease. J Hypertens 2010;28:15-72.  Back to cited text no. 5
Ng WF, Fantin F, Ng C, Dockery F, Schiff R, Davies KA, et al. Takayasu's arteritis: A cause of prolonged arterial stiffness. Rheumatology (Oxford) 2006;45:741-5.  Back to cited text no. 6
Tyagi S, Singh S, Mukhopadhyay S, Kaul UA. Self-and balloon-expandable stent implantation for severe native coarctation of aorta in adults. Am Heart J 2003;146:920-8.  Back to cited text no. 7


  [Figure 1], [Figure 2], [Figure 3]


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