Coronary artery aneurysm is defined as focal dilatation of the coronary artery — when the diameter exceeds 1.5 times the normal segment it is termed an aneurysm, while dilatations not exceeding 1.5 times are called ectasia. Prevalence is 1.5-5% in coronary angiography series. Two main etiological groups exist: atherosclerosis (50-70%) is the most common cause in adults, while Kawasaki disease is the predominant etiology in children (the most common cause of acquired heart disease in childhood in developed countries). Other causes include: connective tissue disorders (Marfan, Ehlers-Danlos), vasculitis (polyarteritis nodosa, Takayasu), trauma, post-percutaneous coronary intervention (iatrogenic), and infective (mycotic) aneurysm. Complications: intraluminal thrombus formation and distal embolization (myocardial infarction), rupture (rare but fatal — hemopericardium and tamponade), and progressive enlargement with compression-related symptoms. CT angiography (CTA) is the gold standard for diagnosis — demonstrating luminal width, wall thickness, thrombus presence, and relationship to surrounding structures with superior spatial resolution.
Age Range
1-75
Peak Age
50
Gender
Equal
Prevalence
Uncommon
Coronary artery aneurysm develops from structural weakening of the arterial wall, with different mechanisms depending on etiology. In atherosclerotic aneurysms: chronic inflammation within atheromatous plaque destroys the elastic lamina and medial smooth muscle layer through matrix metalloproteinases (MMP-2, MMP-9) — wall thinning and focal enlargement occur. The tunica media beneath the lipid-core plaque is damaged and the vessel wall cannot resist pressure and dilates. On CTA, this appears as calcified atherosclerotic plaque + luminal widening. In Kawasaki disease: vasculitis-induced acute coronary arteritis destroys the internal elastic lamina and medial smooth muscle through neutrophil and macrophage infiltration — aneurysm forms in the acute phase. Granulation tissue leads to wall thickening, and fibrosis leads to chronic remodeling. Giant aneurysms (>8 mm) predispose to intraluminal stasis and thrombus formation. On CTA, calcified wall + thrombus + luminal widening is pathognomonic for Kawasaki sequelae. Thrombus pathophysiology: Virchow's triad (stasis + endothelial damage + hypercoagulability) is activated within the aneurysm — flow slows in the enlarged lumen (stasis), damaged endothelium triggers the coagulation cascade, and thrombus grows from the wall to narrow the lumen or embolizes to cause distal myocardial infarction. On CTA, thrombus appears as a low-density filling defect within the lumen — the density difference between opaque contrast and thrombus is directly proportional to iodine concentration.
Focal dilatation of the coronary artery (diameter ≥1.5 times normal segment) together with the presence of low-density mural thrombus within the lumen on coronary CTA is the most characteristic imaging finding of coronary artery aneurysm. This finding has both diagnostic (aneurysm presence and size) and prognostic (thromboembolic complication risk) significance. CTA evaluates aneurysm location, size, morphology (fusiform vs saccular), wall structure (calcification, thickening), thrombus presence, and distal coronary bed status in a single examination — its advantage over conventional angiography is showing not only the lumen but also the wall and perivascular structures.
On coronary CT angiography (CTA), coronary artery aneurysm appears as focal luminal widening in the affected segment — diameter is ≥1.5 times the normal proximal segment. It may show fusiform (spindle-shaped, >50% circumferential involvement) or saccular (sac-shaped, <50% circumferential involvement) morphology. LAD and RCA are the most commonly affected arteries (70-80%). CTA evaluates aneurysm size (length × width), location, number, wall thickness, calcification, and thrombus presence in a single examination. ECG-gated acquisition and bolus-tracking provide optimal opacification. Multiplanar and curved-planar reformatting demonstrates the aneurysm's relationship to the entire coronary tree.
Report Sentence
On coronary CTA, a fusiform/saccular aneurysm measuring ___ mm in diameter is seen in the proximal/mid ___ (LAD/RCA/CX) (normal segment diameter: ___ mm, ratio: ___×); intraluminal thrombus is observed/not observed.
On non-contrast CT (calcium scoring protocol), dense coronary calcification and widened artery silhouette may be seen at the aneurysm site. In atherosclerotic aneurysms, calcified plaques are prominent — Agatston score is high. In Kawasaki sequelae, calcified aneurysm wall and intimal thickening are characteristic. In giant aneurysms (>20 mm), the widened artery may be misinterpreted as a mediastinal mass — attention to this pitfall is needed on pre-contrast CT. Calcification of mural thrombus suggests chronic thrombus. Non-contrast CT can also detect acute complications such as hemopericardium (high-density pericardial fluid >25 HU).
Report Sentence
On non-contrast CT, widened silhouette and dense wall calcification are seen in the ___ coronary artery, consistent with coronary artery aneurysm.
On delayed phase CT, intramural thrombus within the aneurysm appears as a low-density filling defect between the opacified contrast-filled lumen and the wall. Thrombus may be in two forms: mural (wall-adherent, crescent-shaped or coating along the wall) or occlusive (completely occluding the lumen). Acute thrombus is at soft tissue density (30-60 HU), chronic organized thrombus may be lower density and calcified. The delayed phase is important for differentiating acute thrombus from slow flow — slow flow opacifies on delayed phase while true thrombus remains low-density. CTA also evaluates the distal coronary bed — thromboembolic occlusion or stenoses determine myocardial infarction risk.
Report Sentence
On CTA, mural thrombus measuring ___ mm in thickness is seen in the aneurysm lumen, with residual patent lumen of ___ mm; thromboembolic occlusion in the distal coronary bed is not observed/is observed.
On cardiac MRI cine SSFP sequences, coronary artery aneurysm appears as bright blood signal in the dilated coronary lumen. Large aneurysms (>10 mm) can be directly detected on axial cine images — targeted coronary MRA is needed for smaller aneurysms. Cine images show the flow pattern within the aneurysm: laminar flow produces homogeneous bright signal, turbulent flow produces signal loss ('flow void'). Mural thrombus may be seen as a low-signal area at the lumen margin but sensitivity is lower compared to CTA. MRI's advantage: myocardial perfusion and viability assessment can be performed simultaneously — myocardial damage related to the aneurysm (infarction, ischemia) is detected with LGE and stress perfusion.
Report Sentence
On cardiac MRI cine sequences, dilated lumen and bright flow signal is seen in the ___ coronary artery, consistent with an aneurysm measuring ___ mm in diameter.
On LGE sequences, thromboembolic myocardial infarction related to coronary artery aneurysm can be detected — subendocardial or transmural late gadolinium enhancement (bright signal) is seen in the myocardial territory supplied by the affected coronary artery. This finding is clinically critical because: 1) it proves that thromboembolic complication of the aneurysm has occurred, 2) it evaluates myocardial viability (transmural scar = non-viable, subendocardial scar = partially viable), 3) it strengthens anticoagulant therapy indication. Absence of LGE indicates preserved myocardium and is prognostically favorable. Simultaneous stress perfusion MRI assessment can detect active ischemia related to the aneurysm.
Report Sentence
On LGE sequences, subendocardial/transmural late gadolinium enhancement is observed in the myocardial territory supplied by the ___ coronary artery aneurysm, consistent with chronic myocardial infarction; myocardial viability is ___ (below/above 50% transmural).
On transthoracic echocardiography (TTE), large coronary artery aneurysms (especially proximal LAD and RCA) can be directly visualized — seen as dilated coronary artery lumen from parasternal short axis or subcostal views. Doppler evaluates flow pattern within the aneurysm: turbulent flow produces mosaic Doppler signal. In Kawasaki disease, echocardiography is the primary modality for follow-up — provides repeated radiation-free monitoring in children. Echocardiography also evaluates complications: pericardial effusion (rupture suspicion), regional wall motion abnormalities (ischemia/infarction), and ventricular function. Transesophageal echocardiography (TEE) provides better spatial resolution but is invasive.
Report Sentence
On echocardiography, aneurysmal dilatation measuring ___ mm in diameter is seen in the ___ coronary artery, showing turbulent/laminar flow pattern on Doppler.
Criteria
Most common cause in adults. Develops on background of diffuse coronary atherosclerosis. Results from medial smooth muscle destruction and elastic lamina loss. Usually fusiform morphology. RCA is most commonly affected artery.
Distinct Features
CTA shows calcified atherosclerotic plaque with widened lumen. Accompanying coronary stenoses are common. Advanced age (>50), male predominant, cardiovascular risk factors. Antiplatelet + statin therapy is primary management.
Criteria
Develops after Kawasaki disease in childhood (predominantly under 5 years). Aneurysm forms as a result of acute coronary vasculitis. Giant aneurysms (>8 mm or Z-score >10) carry highest complication risk. Bilateral proximal involvement (LAD + RCA) is characteristic.
Distinct Features
CTA shows calcified aneurysm wall + stenosis/occlusion (chronic remodeling). Risk of acute coronary syndrome at young age. IVIG therapy reduces aneurysm risk from 25% to 4% in acute phase. Long-term anticoagulant/antiplatelet therapy (giant aneurysms). Annual CTA or MRA follow-up recommended.
Criteria
Develops on background of infective endocarditis or septicemia. Vessel wall destruction from bacterial arteritis. Saccular morphology more common — localized vessel wall destruction. High risk of rapid enlargement and rupture. Rare but fatal.
Distinct Features
CTA shows perivascular inflammation (fat stranding), saccular aneurysm, rapid size increase (serial imaging). Positive blood culture + endocarditis findings support diagnosis. Urgent antibiotic therapy + surgery (excision or bypass) may be required. Rupture risk much higher than other types.
Criteria
Develops on background of Marfan syndrome, Ehlers-Danlos (especially type IV), Loeys-Dietz syndrome. Generalized structural weakness of arterial wall (elastin/collagen mutations). Multiple aneurysms in different vascular beds may accompany (aortic aneurysm, cerebral aneurysm).
Distinct Features
CTA shows smooth-walled fusiform dilatations, atherosclerosis minimal or absent. Detection of coronary aneurysm at young age (<40) should suggest connective tissue disorder. Genetic counseling and screening of entire vascular bed recommended. Tissue fragility in surgical approach requires critical attention.
Distinguishing Feature
Coronary artery fistula shows dilated coronary artery lumen but accompanies fistula tract with abnormal drainage (pulmonary artery, right atrium, or coronary sinus). In aneurysm, no abnormal drainage exists — focal dilatation and thrombus are seen. Tracing the fistula tract on CTA shows the drainage site.
Distinguishing Feature
In coronary artery dissection, intimomedial flap and true/false lumen distinction is seen (double lumen). In aneurysm, no intimomedial flap exists — single widened lumen is seen. Dissection usually presents with acute chest pain and in spontaneous coronary dissection (SCAD) is common in young women in the peripartum period.
Distinguishing Feature
In pseudoaneurysm, all layers of the arterial wall (intima + media + adventitia) have ruptured — the enhancing collection is in the extravascular space surrounded by perivascular hematoma and connected to the artery via a neck (narrow passage). In true aneurysm, all layers of the arterial wall are intact (even if attenuated). On CTA, narrow neck + perivascular hematoma is pathognomonic for pseudoaneurysm.
Urgency
routineManagement
medicalBiopsy
Not NeededFollow-up
6-monthCoronary artery aneurysm management is determined by etiology, size, thrombus presence, and complications. Medical therapy is the primary approach: antiplatelet therapy (aspirin ± clopidogrel) in all patients, anticoagulant therapy (warfarin or DOAC) indicated in giant aneurysms (>8 mm) and thrombus presence. In Kawasaki sequelae, long-term (usually lifelong) antithrombotic therapy is required. In atherosclerotic etiology, statin and cardiovascular risk factor management are added. Surgical indications: symptomatic thrombosis/embolism (acute coronary syndrome), progressive enlargement, rupture or rupture risk (giant saccular aneurysm), and recurrent thromboembolic events despite medical therapy — bypass surgery (aneurysm excision + graft) or percutaneous treatment (covered stent) may be performed. Follow-up: size monitoring with CTA or MRA at 6-12 month intervals, ventricular function assessment with echocardiography. In Kawasaki patients, Z-score monitoring and continuation of cardiological follow-up during transition to adulthood is critical.
Coronary artery aneurysms carry risks of rupture, thrombosis, and distal embolization. Giant aneurysms (>8 mm) are particularly dangerous. Atherosclerotic aneurysms require anticoagulation and antiplatelet therapy, while Kawasaki disease requires IVIG + aspirin + long-term follow-up. CT angiography is the gold standard for diagnosis and follow-up. Surgery (ligation, grafting, resection) is indicated for large symptomatic or complicated aneurysms. Kawasaki-associated aneurysms may regress in childhood but require lifelong cardiovascular risk monitoring.