The most serious consequence of TAA is aortic dissection or aortic rupture, which present as tearing, chest pain, and hypotension, respectively. A large-sized aneurysm can impinge upon the adjacent anatomical structures and exert a local mass effect including hoarseness, from left recurrent laryngeal nerve stretching stridor, from tracheal or bronchial compression cough, dyspnea, and recurrent pneumonitis, from lung compression dysphagia, from oesophageal compression and plethora and edema, from the compression of the superior vena cava. Vague chest discomfort, neck, and jaw pain may occur with aneurysms involving the arch. Aneurysms are typically discovered incidentally on imaging ordered for other indications. The majority of patients with an aortic arch aneurysm are asymptomatic or directly presents with life-threatening complications. Independent risk factors for both atherosclerosis and aneurysm, including hypertension and smoking, exert a direct effect on the vasculature, adding to the multifactorial pathophysiology of aneurysm formation. Along with the mechanical weakening, atherosclerosis may also induce aneurysm formation by degenerative ischemic changes, through the obstruction of the vasa vasorum. This matrix remodeling promotes the expansion of the vessel in an attempt to normalize diameter and hemodynamic forces. Also, the narrowing of the arterial lumen by an atherosclerotic thrombus triggers a compensatory process in the media in responseВ to the shear stress on the wall. The resultant medial degeneration leads to the weakening of the aortic wall, which in turn results in aortic dilatation and aneurysm formation.ДЄs most of the cases of an isolated aortic arch aneurysm are seen in relation to underlying atherosclerosis, lab findings suggest that inflammatory cells present within the atheroma accelerate the breakdown of matrix protein by the release of the inflammatory mediators. Endothelium, smooth muscle cells, and inflammatory cells infiltrating the media and adventitia act as the source for these proteases. Major theories on the development of aneurysm have surfaced from in-vitro studies that emphasize the role of the breakdown of extracellular matrix proteins by proteolytic enzymesВ such as elastase, collagenase, plasmin, and matrix metalloproteinases (MMPs). The literature on the pathophysiology of aortic aneurysm is continuously evolving and reflects an interplay of protein degeneration, thrombosis, hemodynamic stress, and inflammatory cytokines contributed by genetic triggers and developmental risk factors.

The upward convexity of the aortic arch stems out the following three main branches: The distal portion of the aortic arch lies to the left of the trachea, transverses downwards, and terminatesВ adjacent to the lower border of T4, where it continues as theВ descending aorta. It represents the continuation of the ascending thoracic aorta, whichВ begins at the level of the upper border of the second sternocostal jointВ of the right side courses posteriorly, superiorly, and to the left. The aortic arch is derived from the left branch of the fourth pharyngeal arch during embryonic development.

Aortic arch aneurysms include any thoracic aneurysm that involves the brachiocephalic vessels. ДЄ true aneurysm is defined as a pathological dilation of a segment of a blood vessel involving all three layers of the vessel wall (tunica intima, media, and adventitia) and having at least a 50% increase in diameter compared with the expected normal diameter of the artery. Aneurysms of the aortic arch are commonly found in association with aneurysms of the adjacent ascending or descending aorta.В The trueВ incidence and natural course are still relatively unknown however, aneurysms involving the arch pose a significant challenge pertaining to surgical management and can be complicated by neurological injury and life-threatening cardiovascular events. An isolated aortic arch aneurysm is an uncommon disease entity and often remains clinically silent, given its indolent growth pattern.

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