Coronary Artery Aneurysms

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CHAPTER 36 Coronary Artery Aneurysms

Jon C. George, Mariana Meyers, Robert C. Gilkeson

DEFINITION

Coronary artery aneurysm (CAA) is defined as a dilation more than 1.5 times the diameter of adjacent normal segments.¹ It was first described by Morgagni in 1781²^,³; the first case report was published by Bougon in 1812,¹^,⁴ and the first documented case with angiography was published by Munker in 1958.⁵^,⁶ Before the advent of coronary angiography, CAAs were detected primarily at postmortem examination; however, most cases today are incidental findings on angiography.

PREVALENCE AND EPIDEMIOLOGY

The reported incidence of CAAs ranges from 0.2% to 4.9% among patients undergoing evaluation for coronary disease.¹^,⁵ They occur predominantly in men at a ratio of almost 3 : 1.⁴ CAAs are predominantly caused by atherosclerosis (52%). They may be single or multiple, may be focal or diffuse, and can involve various segments of the coronary circulation. They most commonly involve the right coronary artery (Fig. 36-1) followed by the left anterior descending (Fig. 36-2) and the left circumflex (Fig. 36-3) arteries.⁴

FIGURE 36-1 A 67-year-old patient with a right coronary artery (RCA) aneurysm presented for preoperative CT angiography evaluation. A, Coronal volume rendered image shows large calcified RCA aneurysm (arrow). B, Oblique sagittal maximum intensity projection better defines the full extent of the aneurysmal dilation (arrow) of the RCA. C, Conventional catheter angiography confirms aneurysmal dilation of the RCA (arrow).

FIGURE 36-2 A and B, Coronary CT angiography shows focal aneurysm (arrows) of the left anterior descending coronary artery. A, Axial image. B, Coronal oblique volume rendered image.

FIGURE 36-3 An 86-year-old woman with shortness of breath. A, Coronary CT angiography shows contrast collection at the level of the mitral annulus (arrow) consistent with aneurysm of the left circumflex coronary artery. B, Oblique maximum intensity projection CT angiography defines aneurysmal dilation of diffusely diseased circumflex artery (arrow).

Atherosclerotic aneurysms of the left main coronary artery are rare, but have been reported.⁷ Other important etiologies include congenital (17%), mycotic-embolic (11%), dissecting (11%), syphilitic (4%), and unclassified (5%).⁴ Although most cases worldwide are secondary to atherosclerosis, systemic inflammatory diseases such as Takayasu arteritis (Fig. 36-4) and the mucocutaneous lymph node syndromes of Kawasaki disease (Fig. 36-5) account for many cases in East Asia.⁸ Modern interventional techniques have also resulted in iatrogenic causes of CAAs. In the current era of percutaneous intervention, CAAs can be seen secondary to balloon angioplasty or stent deployment.⁹ The increasing use of coronary artery bypass grafting techniques has resulted in numerous reports of saphenous vein graft aneurysms (Fig. 36-6), although they remain uncommon.

FIGURE 36-4 A 21-year-old woman with history of Takayasu disease. Axial oblique maximum intensity projection from coronary CT angiography shows aneurysmal dilation of left main coronary artery (arrow).

FIGURE 36-5 An 8-month-old infant with Kawasaki disease. A, Axial maximum intensity projection CT angiography shows aneurysmal dilation of the right coronary artery (arrow). B, Sagittal oblique maximum intensity projection CT angiography confirms aneurysmal right coronary artery (arrow).

FIGURE 36-6 A 76-year-old man presented for postoperative CT angiography assessment of coronary artery bypass graft patency. A, Axial oblique maximum intensity projection image shows a fusiform contrast collection (arrow) adjacent to the ascending aorta. B, Coronal volume rendered image confirms proximal pseudoaneurysm of a saphenous vein graft (arrow).

Although CAAs may be found at any age, atherosclerotic subtypes are predominant later in life, whereas congenital (Figs. 36-7 and 36-8), mycotic-embolic, and dissecting types are found in younger age groups. Multiple CAAs in childhood and adolescence are usually late complications of Kawasaki disease (Fig. 36-9).¹⁰

FIGURE 36-7 A 17-year-old patient with Down syndrome and uncorrected endocardial cushion defect. Axial maximum intensity projection CT shows diffuse coronary artery ectasia of the left coronary artery (arrows).

FIGURE 36-8 A 9-year-old child with congenital aortic stenosis. Axial maximum intensity projection CT shows fusiform dilation of the proximal left main coronary artery (arrow).

FIGURE 36-9 A 3-year-old patient with Kawasaki disease. A, Axial maximum intensity projection CT shows aneurysmal dilation of left anterior descending coronary artery (arrow). B, Catheter angiography confirms large LAD aneurysm (arrow).

CAAs are associated with systemic syndromes of hyperlipidemia and hypertension, but a correlation between aneurysm size and cardiac risk factors has not been proven.⁸^,¹¹ They have been shown to be more prevalent in patients with aortic aneurysms, which is corroborated by studies showing increased diameter indices of iliac arteries in patients with known CAA (Fig. 36-10).¹²

FIGURE 36-10 A 50-year-old man with a history of dissecting aortic aneurysm and phenotypic features of Marfan syndrome. A, Axial oblique maximum intensity projection CT angiography shows diffuse aneurysmal dilation of the coronary arteries (arrows). B, Coronal volume rendered CT angiography image of the aneurysmal right coronary artery (arrow).

ETIOLOGY AND PATHOPHYSIOLOGY

CAA is likely a variant of obstructive coronary artery disease in most cases; however, its pathogenesis has not been fully elucidated. Systemic hypertension, inflammatory stimuli such as tobacco or increased inflammatory response in the vessel wall, hyperhomocysteinemia, and chronic Epstein-Barr virus infection are implicated as etiologic factors. Genetic predisposition or gene disruption, interference with normal cross-linking of collagen, and activation of matrix metalloproteinases are all possible factors implicated in the weakening of the vessel wall in aneurysmal disease.⁸

MANIFESTATIONS OF DISEASE

Clinical Presentation

Presentations of CAAs are almost always suggestive of coronary ischemia requiring further ischemic evaluations, which generally detect the anomaly.³ Because CAAs are usually associated with obstructive atherosclerotic coronary disease, the clinical course depends on the severity of the associated stenosis,³ and can culminate in myocardial infarction or sudden death complicated by thrombus formation, distal embolization, shunt formation, or rupture.⁸ Exercise-induced angina pectoris or myocardial infarction may occur without significant coronary artery stenosis, however, and is usually attributed to distal microembolization of thrombus or microcirculatory dysfunction reflected by depressed coronary flow reserve in these patients.⁸^,¹³ The natural history and prognosis of this entity are unknown; however, observational studies have documented development of myocardial infarction with angiographically documented occlusion of the involved aneurysmal vessel.³^,⁵

CAAs complicated by rupture or fistula formation (into a cardiac chamber) may create a continuous murmur on auscultation. The standard of reference for the diagnosis of CAAs is via a percutaneous approach with coronary angiography, which provides information about the size, shape, location, and number of aneurysms.⁸ Evaluation and serial follow-up may require other diagnostic methods. Intravascular ultrasound further allows for distinguishing true and false aneurysms.⁸

Cardiac CT angiography enables a noninvasive alternative for initial diagnosis and follow-up. Its tomographic capabilities enable improved visualization of extraluminal pathology and important surrounding extravascular anatomy.¹⁶ In suspected aneurysmal disease, standard cardiac CT angiography protocols are performed. Prospective ECG gating or retrospective ECG gating can be performed with dose modulation using 120 kV and 800 mAs (effective). An intravenous contrast agent is administered: 75 to 100 mL of 350 to 375 mg I/mL contrast agent, followed by 30 mL of saline. Studies are typically performed with an automated bolus tracking technique with the region of interest placed in the ascending aorta or with a timing bolus. Studies performed with retrospective gating are reconstructed at 10% intervals of the cardiac cycle. Although standard multiplanar reconstructions are performed for diagnosis, volume rendered reconstruction techniques can be helpful in preoperative planning.

DIFFERENTIAL DIAGNOSIS

Important differential diagnoses in the evaluation CAAs include benign and malignant mediastinal masses. CAAs may mimic cardiac/pericardial masses on standard CT acquisitions. CAAs need to be distinguished from focal aneurysms or pseudoaneurysms of the aorta and the sinuses of Valsalva. The imaging advances of retrospective ECG gating and three-dimensional reconstruction enable confident differentiation of CAAs from ventricular aneurysms.

TREATMENT OPTIONS

Medical

The management of CAAs can be medical, percutaneous, or surgical. If the patient is asymptomatic, and medical therapy is chosen, the regimen should include antiplatelet therapy with or without anticoagulation to prevent thromboembolic complications.³^,¹⁶ Risk factor modification with statins and antihypertensives may be beneficial in slowing the progression of atherosclerotic aneurysmal disease, but this has not been established.

Surgical/Interventional

Surgery is generally advised for large aneurysms associated with significant coronary stenosis, which includes ligation and bypass of the aneurysm.¹⁷ Percutaneous approaches are increasingly being reported for moderate-sized aneurysms with associated coronary stenosis via polytetrafluoroethylene-covered balloon-expandable¹⁸ or self-expandable stents.¹⁹ Even complicated aneurysms with fistulization, when appropriate, can be addressed percutaneously with coil embolization (Fig. 36-11).²⁰