Aortic plaques can be visualized, characterized, and quantified by a variety of imaging modalities including transesophageal echocardiography (TEE), computed tomography (CT), and magnetic resonance imaging (MRI) [14]. TEE, predominantly two dimensional (2D), is typically the first-line imaging technique for the detection and measurement of aortic plaque (Fig. 27.2) [1]. The association between clinical embolization and advanced aortic atherosclerotic plaque visualized on TEE was first reported in 1990 [10]. Further studies later confirmed that aortic plaque detected by TEE represents a potential source for systemic emboli [15–17]. Noncalcified complex atheromas in the ascending aorta and aortic arch correlated with a higher risk where a plaque thickness ≥4 mm measured on TEE emerged as a clinically important predictor of increased vascular embolic events [17–19]. These embolic events could have represented both arterial thromboembolism and atheroembolism. However, additional case reports with biopsy-proven CES found an association with complex aortic atheromas visualized on TEE, thereby strengthening not only the role of the aortic plaque in CES but also the role of TEE in detecting these plaques [20]. Real-time three-dimensional (3D) TEE is a newer imaging technique that may provide additional morphological detail of the plaque and could have an increasing clinical role in the future [21].

CT and MRI are additional imaging techniques that can be considered for detection and characterization of aortic plaque that may provide a less invasive and more comprehensive evaluation of aortic atherosclerosis relative to 2D and 3D TEE (Figs. 27.3 and 27.4) [22–24]. For imaging of the major branches of the thoracic aorta, CT and MRI are superior to TEE as TEE has a blind spot around the origin of the brachiocephalic artery due to interposition of the air-filled bronchi between the esophagus and the artery. In addition, the abdominal aorta is incompletely visualized on TEE as it is limited to the proximal abdominal aorta between the diaphragm and origin of the superior mesenteric artery. Therefore, for complete visualization of the aorta-iliac-femoral arterial system, CT or MRI is preferred .

Conventional arteriography has a low sensitivity for aortic plaque detection and often fails to detect plaques that are identified on other imaging modalities. In addition, arteriography is invasive and could lead to mechanical disruption of an aortic plaque and subsequent arterial cholesterol embolization or thromboembolism and, therefore, should generally be avoided [25].

Spontaneous rupture of an aortic plaque shares similar mechanistic features to plaque rupture in other arterial beds. Plaque composition rather than plaque size is thought to play the principal role in plaque vulnerability. More vulnerable plaques often have larger lipid cores and thinning of fibrotic caps mediated by a complex interaction between inflammatory and extracellular matrix cells. Therefore, inflammation may play a critical role in altering plaque composition and thus increasing a plaque’s vulnerability to spontaneous rupture [26].

The rate of spontaneous aortic plaque rupture in the general population has been extrapolated from older pathoanatomic series that were published in the era before the widespread use of intra-arterial cannulation for diagnostic and therapeutic purposes; this estimated rate ranged from <1 to 3.4 % [5, 27, 28]. However, the incidence of spontaneous plaque rupture leading to CES remains low even among higher-risk populations. One antemortem retrospective study of 519 patients with complex aortic plaque diagnosed by TEE found CES to occur at a rate of 1 % over a 3-year follow-up. For comparison, this CES rate is significantly lower than the 20 % rate of arterial thromboembolism observed in the same cohort [29].

Traumatic aortic plaque rupture can occur following intra-arterial manipulation during catheterization or cardiovascular surgery. Although cholesterol embolization has been reported in association with cardiac catheterization, it is considered a rare complication. The reported incidence of clinically apparent CES after cardiac catheterization is <2 % [30–32]. The data remains inconclusive regarding whether or not radial access versus femoral access results in a lower incidence of this complication [30, 33]. CES, particularly cerebral atheroembolism, has been a major concern following transcatheter aortic valve replacement (TAVR) with early registries reporting an incidence of 2.4–4 %. However, the incidence seems to be declining with the use of smaller catheters and more stringent patient selection criteria. The routine use of intra-arterial embolic protection devices may lead to an even further decline in embolization events [34].

CES in association with cardiovascular surgery is also rare. Risk is directly correlated with extent and severity of atherosclerosis in the ascending aorta. CES has been reported more frequently in association with coronary revascularization than valvular operations [35]. Off-pump cardiovascular surgeries may lead to less embolic events compared to the use of cardiopulmonary bypass techniques [36]. CES has also been a rare complication associated with carotid endarterectomy, carotid stenting, and abdominal aorta procedures including endovascular aneurysm repair (EVAR) [37–39].

The incidence of intra-plaque hemorrhage and an associated increase in plaque rupture leading to CES as a consequence of thrombolytic or anticoagulation therapy remains controversial. Case reports have suggested that CES can develop subsequent to thrombolytic therapy given for the acute management of various conditions including myocardial infarction and deep venous thrombosis. Although a small prospective trial of post-myocardial infarction patients treated with or without thrombolytic therapy failed to demonstrate a relationship [40], there still exists a controversy [41]. Similarly, case reports have suggested that anticoagulation is also associated with an increase in CES and that discontinuation of therapy can lead to clinical improvement [42, 43].

In addition to warfarin, the novel anticoagulants have also been suggested to play a role in development of CES [44]. However, it is difficult to determine if this is a causal relationship or merely an association. At this time, no randomized trials have specifically evaluated anticoagulation as an independent risk factor for development of CES. There is limited literature to support that the use of anticoagulation in patients with concurrent CES is safe and feasible among patients with a separate indication for anticoagulation [45]. Therefore, per current evidence, the causal relationship between cholesterol embolization and the use of anticoagulation and/or thrombolytic therapy can neither be proven nor refuted. Based on this unresolved controversy, routine use of anticoagulation among patients with CES is not generally recommended. However, use of anticoagulation in CES appears reasonable in patients with a separate indication for anticoagulation including atrial fibrillation, left ventricular thrombus, or mechanical prosthetic valve [1].