Multi‐Modality Imaging Evaluation and Optimal Management of Complex Coronary Artery Aneurysms

ABSTRACT

Coronary artery aneurysms (CAA) present variably and require multimodal imaging—catheterization, CTCA, stress echocardiography among others—for diagnosis. Management, individualized per patient, includes medical, percutaneous, or surgical approaches. A successful surgical case showed improved cardiac function and symptoms, highlighting the vital role of advanced imaging in guiding treatment.

1. Introduction

Coronary artery aneurysms can be prevalent in 0.3%–5.3percentage of the population3, with mean age of 65.5 years and male‐predominance in ~78.5% [1]. Coronary artery aneurysm is a rare entity, defined as the enlargement of a coronary artery segment to 50% of the distal reference diameter [2]. The main etiologies and risk factors for CAA include congenial atherosclerotic coronary artery disease, vasculitis and connective tissue diseases (e.g., Kawasaki and Marfan syndrome), intracoronary procedural injury, postinfectious etiologies [1, 3]. It has several clinical presentations from an incidental finding to chest pain and acute coronary syndrome, to occasional rupture and cardiac tamponade. Management of CAA remains controversial with paucity of studies which are observational as well as guidelines [3].

2. Case History/Examination

A 58‐year‐old man with history of hypertension, chronic obstructive pulmonary disease, presented to the emergency department with progressively worsening shortness of breath, with associated dizziness and abdominal discomfort for three days. The patient had hypoxia with an oxygen saturation of 89% while receiving 10 L/min oxygen, tachypnea and expiratory wheeze on physical examination, with normal blood pressure, heart rate and heart sounds.

3. Methods (Differential Diagnosis, Investigations and Treatment)

Chest X‐ray showed pulmonary edema and laboratory tests showed elevated creatinine of 3.42 mg/dL. He was initially managed for acute kidney injury and acute hypoxic respiratory failure, secondary to COPD exacerbation. Overnight, he developed chest pain and worsening dyspnea, with electrocardiogram showing ST segment elevation of 2 mm in V4‐V6 with ST depression in II, IIII, aVF (as shown in Figure 1). was intubated for airway protection as he had become unresponsive while on non‐invasive ventilation. He was transferred to our facility after the diagnosis of ST elevation myocardial infarction (STEMI) with heart failure and high‐sensitivity troponin levels peaking at 1715 ng/L over X hours and N‐terminus pro‐ brain natriuretic peptide of 57,634 pg/mL.

FIGURE 1.

Patient's electrocardiogram showing 2 mm ST elevation in V4, V5 and V6, and ST depression in inferior leads (II, III and AVF), concerning lateral myocardial injury in this patient's clinical context.

He underwent acute cardiac catheterization at our hospital revealing aneurysmal left anterior descending (LAD, proximal) with filling defect consistent with thrombus in the mid segment, right coronary artery (RCA, proximal to mid) and ectasia of the left circumflex (LCX) arteries, with significant LAD and RCA stenoses. Images from the patient's coronary angiography, with findings of ectatic and aneurysmal vessels and filling defects, are shown in Figure 2A,B. Hemodynamic study was consistent with post‐capillary pulmonary hypertension (wedge pressure mean 29 mmHg, pulmonary artery pressures 67/38 (mean 45) mmHg, cardiac index 4.0 L/min). Transthoracic echocardiography showed moderately impaired left ventricular ejection fraction (LVEF) of 30% with LAD territory akinesis, severely impaired right ventricle, no significant valvular abnormalities or pericardial effusion. For viability evaluation, cardiac magnetic resonance (CMR) showed a moderate ischemic cardiomyopathy with LVEF 33%, subendocardial ischemic scar of the apex, anterior and anteroseptal walls of the LAD territory, moderate right ventricle impairment and subendocardial late gadolinium enhancement in the LAD territory, as seen in CMR images in Figure 2C,D. To better depict coronary anatomy, computed tomography coronary angiography (CTCA) showed LAD aneurysm up to 2.4 cm in the mid segment with thrombosed sacs, RCA aneurysm up to 9 mm proximally and moderate scattered and mixed coronary atherosclerotic changes with moderate stenoses of the LAD and RCA, as shown in preoperative CCTA images in Figure 3A,D. For etiology assessment, vascular medicine was consulted with impression of most likely from atherosclerotic disease, given no history of Kawasaki disease or other vasculitis. His preoperative medications were ticagrelor 180 mg, aspirin 325 mg, furosemide 40 mg, carvedilol 12.5 mg tablet, valsartan 80 mg.

FIGURE 2.

Coronary angiography images (A–B): Ectatic and dominant right coronary artery (yellow arrow) with aneurysmal proximal and mid segments. No significant stenoses were seen. Left main was short and ectatic, bifurcating into left anterior descending (LAD) and left circumflex (LCx) coronary artery. Proximal LAD was aneurysmal (green arrow). Hazy filling defects seen in mid‐distal LAD, likely thrombus. LCx was ectatic. Cardiac Magnetic Resonance Imaging (C–D): Short axis delayed post contrast images depicting subtle subendocardial (< 25%) delayed gadolinium enhancement along LAD territory (blue arrowhead). All segments were viable. Aneurysmal proximal LAD is redemonstrated (green arrow).

FIGURE 3.

Coronary Computed Tomography Angiography images. Pre‐operative (A–D): Ectatic right coronary artery (A and B, yellow arrow) with aneurysmal proximal and mid segments. Short segment, ectatic left main (B, black asterisk), bifurcating into left anterior descending (LAD) and left circumflex (LCx) coronary artery. Proximal LAD was aneurysmal (C and D, green arrow). Post‐operative (E–H): Aortocoronary venous graft to right coronary artery (E and F, orange arrow). Status post repair for aneurysmal proximal LAD (G and H, blue arrow), interposed with a vein graft (G, white asterisk).

4. Conclusions and Results (Outcome and Follow up)

After completion of a multidisciplinary assessment based on the patient's clinical presentation and complex anatomical findings on angiography and CCTA of several aneurysmal segments, thrombi and atherosclerotic changes, a decision was made to proceed with coronary artery bypass graft surgery. The LAD coronary aneurysm was opened and interposed with the vein graft and all clots were removed from within the aneurysm. Small septal branches less than 1 mm diameter were ligated. Three diagonal branches were reconstructed in an end‐to‐end and side‐to‐side fashion with a separate vein graft attached to the LAD graft. The RCA was also grafted with a vein graft. The patient had an uncomplicated postoperative course. Postoperative echocardiogram showed improvement of biventricular systolic function to low‐normal, including LVEF 50% and repeat CTCA showed patent native coronary and vein grafts. Post operative CCTA images are shown in Figure 3E,H. On discharge, his medical therapy included aspirin 81 mg daily, atorvastatin 20 mg, furosemide 20 mg, metoprolol succinate 50 mg, prasugrel 10 mg. At six‐week follow‐up, the patient's symptoms improved and he was engaged in cardiac rehabilitation. 14 months later, the patient had a hospitalization with COPD exacerbation, during which he was found to have mild hypervolemia and received a brief duration of diuresis inpatient.

5. Discussion

⁴¹Coronary artery ectasia and CAA have been used interchangeably but contemporary literature have standardized classifications as follows: CAA indicates enlargement of coronary vessel 1.5 times adjacent segments, while ectasias are more diffuse and not quite reaching this threshold [4]. Morphologically, if the transverse diameter is larger than the longitudinal, the aneurysm is saccular, and if vice versa, fusiform [3]. About 0.05% of the cases can have large or giant aneurysms at than 2.0 cm in size [1], which our patient had and are rarely present in multiple vessels [5]. Most affected vessels with CAA are in descending aorta RCA, LAD, left main and LCX [6]. In a systematic review, the most common etiology of CAA was found to be Kawasaki (43.3%) followed by atherosclerotic disease (16.4%), which our patient had [6]. A common presentation is incidental finding in up to 5% of patients on CT or coronary angiography (2). However, symptomatic presentations include chest pain, acute coronary syndrome, fistula formation, compression of adjacent structures (e.g., SVC syndrome or mediastinal mass), congestive heart failure, or rarely rupture causing hemopericardium and cardiac tamponade [3]. In patients with CAA studied in a multicenter registry study on patients undergoing cardiac catheterization, the majority (61.5%) of the CAA patients presented with ACS, including 20.3% with STEMI [1]. The patient in our case presented with ACS leading to cardiac systolic dysfunction and elevated filling pressures. His comorbidities, particularly COPD, further complicated the clinical course with respiratory distress and the need for mechanical ventilation. Patients with COPD may also have associated disproportionate precapillary hypertension, not evident in this case.

Coronary artery aneurysms are detected with multiple modalities that facilitate in assessing the anatomy of the aneurysms, specifically frequency and extension, distribution, maximal diameter, and associated possible thrombi. Coronary angiography provides extensive information regarding anatomy; however, it comes with its risks especially in younger patients and limitations in determining milder lesions and differentiating between a true and pseudo aneurysm. However, incorporating it with intravascular ultrasound (IVUS) has become the gold standard. IVUS provides critical information regarding the structural and functional anatomy of aneurysms [7].

There is also an emerging role of noninvasive coronary angiography in the detection and understanding of coronary aneurysms. CT coronary angiography, although it involves the exposure to radiation and contrast, can provide specific complex details of the anatomy of coronary aneurysms [8]. Other noninvasive modalities include echocardiography [9], assessing internal vessel diameters, presence of possible thrombus and location of the aneurysms. This tool can be particularly utilized in long‐term follow‐up in adulthood after detection of aneurysms in general with Kawasaki disease [7].

Coronary MR angiography is another useful imaging modality. However, it is not as sensitive as CTCA [10], which may not always be available and may need additional studies. Nevertheless, it can be utilized when other noninvasive modalities may be contraindicated and for subsequent follow up [11]. In patients with systolic dysfunction and myocardial infarction, MRI can be used to assess necrotic damage and viability, further guiding management.

In summary, multi‐modality imaging is crucial to diagnose and guide management strategies for patients with CAA, with each modality having unique features while having its own limitations. Coronary angiography, while being invasive, can give valuable delineation of intravascular anatomy when IVUS is added. Thrombi that may be missed in angiography can be detected in CCTA, a sensitive, noninvasive tool, which may still not visualize distal segments. MRA and echocardiography may not be able to provide accurate and detailed information; however, they can be utilized well for follow up, whilst providing more cardiac findings, with stress echocardiography being particularly useful for detecting ischemia in high‐risk patients with Kawasaki disease [12].

Treatment of CAA consists of medical, percutaneous and surgical options. In terms of medical management, patients should have aggressive risk factor management, given the large implication with atherosclerotic disease, including indicated therapy for concomitant coronary artery disease, hyperlipidemia, etc. Use of dual antiplatelet has been hypothesized to be a potential strategy, as well as anticoagulation given the phenomenon of slow flow from the aneurysms [13, 14], however, it has not been supported by trials [3, 15]. Similarly, a potential role of angiotensin‐converting enzyme has also been suggested with the inhibition of TGF‐B and statins suggested with the inhibition of metallic proteinase; however, not proven with long‐term randomized data [16]. Notably, nitrates should be avoided given exacerbation of myocardial ischemia that was seen in a study [17].

Patients who have undergone cardiac catheterization closure or surgical repair for coronary artery aneurysm should be encouraged to adhere to antiplatelet therapy and, in some cases, anticoagulation, along with close follow‐up with a cardiologist [15]. Medical management, although optimizing risk factors, potentially improving coronary flow, for larger aneurysms, based on their anatomy, or those causing symptoms (angina or ACS), interventional procedures may be necessary. Percutaneous coronary intervention (PCI) with stent placement or embolization may be considered to exclude the aneurysm and restore normal blood flow. Coil embolization or covered stent placement may be used to occlude the aneurysm and prevent further expansion [18]. Surgical treatment options for coronary artery aneurysms (CAA) may involve various approaches, including aneurysm ligation, resection, or marsupialization with interposition graft. However, the prevailing surgical technique often entails opening the CAA, suturing its incoming and outgoing vessels and if required, performing bypass grafting to restore normal blood flow [16, 18]. Whether surgical or percutaneous revascularization, management of coronary artery aneurysms can be technically challenging. These are highly individualized plans based on a patient's presentations and morphology of the aneurysm. Proposed algorithms for management of coronary artery aneurysms have been seen in the literature [3, 16]. In patients that are asymptomatic and have minimal risk of complications, medical management and risk factor modification can be attempted. A large aneurysm, percutaneous or surgical options can be pursued. In patients with ACS, especially STEMI, PCI is recommended to restore TIMI III flow. In patients with stable angina, if the culprit aneurysm is PCI and amenable, PCI techniques can be tried and if not successful, surgical excision and CABG can be pursued [3].

Coronary artery aneurysms can have a wide range of morphological phenotypes, etiologies, severity and clinical presentation. Anatomical delineation is necessary with a combination of coronary catheterization, CTCA and MR angiography and the first two are preferred to assess atherosclerosis and thrombotic burden and functional and viability assessment including CMR, stress echocardiography and/or nuclear imaging may be considered to guide intervention. Management involves medical therapies, percutaneous interventions and surgical and care should be individualized based on the patient's presentations and individual needs. We showed a case of a patient, in which, utilization of novel imaging techniques and extensive multidisciplinary expert opinions led to successful CAA surgical management together with medical therapy led to improvement of cardiac function and symptoms.

Author Contributions

Aro Daniela Arockiam: conceptualization, writing – original draft, writing – review and editing. Sharmeen Sorathia: writing – original draft, writing – review and editing. Rishabh Khurana: visualization. Ankit Agrawal: writing – review and editing. Elio Haroun: writing – review and editing. Alexandra Hall: validation, writing – review and editing. Christine Jellis: validation. Shinya Unai: validation. Tom Kai Ming Wang: supervision, validation, writing – review and editing.

Funding

The authors have nothing to report.

Arockiam A. D., Sorathia S., Khurana R., et al., “Multi‐Modality Imaging Evaluation and Optimal Management of Complex Coronary Artery Aneurysms,” Clinical Case Reports 14, no. 2 (2026): e72091, 10.1002/ccr3.72091.

Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.