Takayasu aortoarteritis is a rare, chronic granulomatous panarteritis with significant morbidity amongst young patients. Current challenges include a lack of awareness about the condition, delays in diagnosis due to its varied presentation, and suboptimal methods for assessing disease activity. The development of noninvasive imaging including magnetic resonance angiography and positron emission tomography is aiding earlier diagnosis. Early initiation of immunosuppressive treatment is crucial to control active inflammation and minimize arterial injury. Recent studies investigating biological agents such as tumour necrosis factor-α antagonists are encouraging. Surgical revascularization should only be undertaken following careful consideration, as restenosis is common. The indications for considering intervention include uncontrolled hypertension due to renal artery stenosis, severe symptomatic coronary artery or cerebrovascular disease, severe aortic regurgitation, stenotic or occlusive lesions resulting in critical limb ischemia, and aneurysms at risk of rupture. In these cases, the risk benefit ratio for intervention is good. Open surgery, at present, has better outcomes compared to endovascular techniques. However, technological advances in endovascular treatment are continually improving. Controlling disease activity prior to and following revascularization is key to preventing complications. A multidisciplinary approach to the diagnosis and management of Takayasu arteritis is essential to achieve satisfactory patient outcomes. 1. Introduction Takayasu aortoarteritis (TA) is a rare, chronic large-vessel granulomatous panarteritis of unknown aetiology, affecting the aorta and its major branches. The disease typically presents at less than 40 years of age. The aorta can be affected along its length and all branches can be involved, in addition to the pulmonary and coronary arteries. The most commonly affected branches are the subclavian artery and the common carotid artery. Histopathology reveals adventitial thickening, focal leukocytic infiltration of the tunica media, and intimal hyperplasia [1]. Arterial inflammation leads to stenotic or occlusive arterial lesions, predisposing to symptomatic end-organ ischemia. Less commonly, more acute inflammation leads to medial degeneration in the arterial wall resulting in aneurysmal dilatation [2]. Although the pattern of disease varies geographically, stenotic lesions found in >90% of patients predominate, whereas aneurysms are only reported in approximately 25% [3]. TA is associated with considerable
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