Coronary aneurysms are typically defined as sections of a coronary artery where the diameter is more than 1.5 times that of an adjacent normal segment. In rare circumstances, these aneurysms can become exceedingly large, leading to the classification of giant coronary artery aneurysms. Despite their occurrence, there is no clear consensus on the precise definition of giant coronary artery aneurysms, and their etiology remains somewhat ambiguous. Numerous potential causes have been suggested, with atherosclerosis being the most prevalent in adults, accounting for up to 50% of cases. In pediatric populations, Kawasaki disease and Takayasu arteritis are the primary causes. Although often discovered incidentally, coronary artery aneurysms can lead to severe complications. These complications include local thrombosis, distal embolization, rupture, and vasospasm, which can result in ischemia, heart failure, and arrhythmias. The optimal approach to medical, interventional, or surgical management of these aneurysms is still under debate and requires further clarification. This literature review aims to consolidate current knowledge regarding coronary artery aneurysms' pathophysiology, emphasizing their definition, causes, complications, and treatment strategies. Recent research has begun to explore the molecular mechanisms involved in the formation and progression of coronary artery aneurysms. Various molecules, such as matrix metalloproteinases (MMPs), inflammatory cytokines, and growth factors, play crucial roles in the degradation of the extracellular matrix and the remodeling of vascular walls. Elevated levels of MMPs, particularly MMP-9, have been associated with the weakening of the arterial wall, contributing to aneurysm development. Inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukins (IL-1β and IL-6) have been implicated in promoting inflammatory responses that further degrade vascular integrity. Additionally, growth factors such as vascular endothelial growth factor (VEGF) may influence angiogenesis and vascular remodeling processes. Understanding these molecular pathways is essential for developing targeted therapies aimed at preventing the progression of coronary artery aneurysms and improving patient outcomes.

Coronary artery aneurysm (CAA) is a clinical entity defined by a focal enlargement of the coronary artery exceeding the 1.5-fold diameter of the adjacent normal segment. Atherosclerosis is the main cause in adults and Kawasaki disease in children. CAA is a silent progressive disorder incidentally detected by coronary angiography, but it may end with fatal complications such as rupture, compression of adjacent cardiopulmonary structures, thrombus formation and distal embolization. The pathophysiological mechanisms are not well understood. Atherosclerosis, proteolytic imbalance and inflammatory reaction are involved in aneurysmal formation. Data from previously published studies are scarce and controversial, thereby the management of CAA is individualized depending on clinical presentation, CAA characteristics, patient profile and physician experience. Multiple therapeutic approaches including medical treatment, covered stent angioplasty, coil insertion and surgery were described. Herein, we provide an up-to-date systematic review on the pathophysiology, complications and management of CAA.