TTE allows assessment of the aortic root and the proximal ascending aorta but cannot adequately image aortic arch plaques [67, 68]. However, echocardiographic evaluation of the aorta is a routine part of the standard echocardiographic examination. Although TTE is not the technique of choice for overall assessment of the aorta, it is useful for the diagnosis and follow-up of some segments of the aorta. TTE is one of the techniques most used to measure proximal aortic segments in clinical practice [69, 70]. The long-axis view affords the best opportunity for measuring aortic root diameters by taking advantage of the superior axial image resolution. Of paramount importance for evaluation of the thoracic aorta is the suprasternal view (Figs. 1.1 and 1.2). This view primarily depicts the aortic arch and the three major supra-aortic vessels (innominate, left carotid, and left subclavian arteries), with variable lengths of the descending and, to a lesser degree, ascending aorta. Although this view may be obstructed, particularly in patients with emphysema or short, wide necks, it should be systematically sought if aortic disease is evaluated. From this window, aortic coarctation can be visualised and functionally evaluated by continuous-wave Doppler; a persistent ductus arteriosus may also be identifiable by colour Doppler. Dilatation and aneurysm, plaque, calcification, thrombus, or dissection membranes are detectable if image quality is sufficient. A systematic comparison of harmonic TTE and TEE made to detect aortic plaques and thrombi revealed high sensitivity for the detection of aortic arch atheromas protruding ≥4 mm into the lumen [2]. However, the entire thoracic descending aorta is not well visualised by TTE.

TEE allows us not only to assess plaque mobility, ulceration, and composition [71], but also to obtain detailed information on the anatomic relationship between the plaque location and the origin of the large arterial branches [12, 25, 32, 72–76].

Beside the possibility of structural damage, other limitations associated with this diagnostic technique include the need for conscious sedation and patient cooperation for swallowing the probe, both quite difficult in patients with stroke [71]. In addition, due to the shadow associated with the tracheal air column near the origin of the innominate artery, which masks a portion of the ascending aorta when monoplanar and biplanar probes are used, an estimated 2 % of plaques are missed [77]. The use of multiplanar probes may reduce this problem [78] (Fig. 1.3).

The presence of detectable atherosclerotic plaques in the aorta indicates the presence of atherosclerotic disease and is a possible source of embolism [12]. Aortic atheromas are characterised by irregular intimal thickening of at least 2 mm, with increased echogenicity. They often have superimposed mobile components, mainly thrombi. The morphology of atheromatous plaques is dynamic, with frequent formation and resolution of mobile components [45]. TEE is the imaging modality of choice for diagnosing aortic atheromas. It provides higher-resolution images than TTE and has good inter-observer reproducibility [79]. The prevalence of aortic atheromas on TEE varies depending on the population studied. In a community-based TEE study [80], aortic atheromas were present in 51 % of the population over 45 years, being complex in 7.6 %. Atheroma prevalence increased with age, smoking, and pulse pressure. TEE characterises the plaque by assessing plaque thickness, ulceration, calcification and superimposed mobile thrombi, thereby determining the embolic potential of each plaque. The advantages of TEE over other non-invasive modalities include its ability to assess the mobility of plaque in real time. The French Aortic Plaque in Stroke group showed that increasing plaque thickness of ≥4 mm is associated with a significantly increased embolic risk [39]. They used TEE to characterise aortic arch plaque thickness in 331 patients older than 60 years with stroke. Increasing plaque thickness was associated with an increased risk of embolic events. The odds ratio for aortic arch plaque <1 mm and stroke was 1.0. The odds ratio was 3.9 for plaque between 1 and 3.9 mm thick and 13.8 for plaques >4 mm thick. The presence of mobile lesions (thrombi) superimposed on aortic atheromas has been recognized to imply a high embolic risk. Other characteristics of the lesions seen on TEE, such as ulceration ≥2 mm in aortic plaques and no calcified plaques, were also associated with a higher risk of stroke [81]. Thus, atherosclerotic plaques are defined as complex in the presence of protruding atheromas of 4 mm in thickness, mobile debris, or the presence of plaque ulceration, and defined as simple if the plaques lack these morphological features (Fig. 1.4).

A grading system for severity of atherosclerosis in the thoracic aorta has been proposed by Montgomery. Grade I = normal or minimal intimal thickening; Grade II: extensive intimal thickening; Grade III = atheroma <5 mm; Grade IV = atheroma ≥5 mm; Grade V = mobile lesion (Fig. 1.5).

Two recent community-based studies found no association between aortic atheromas and future stroke [59, 80]. An alternative explanation is that atheromatous plaque is merely a marker for diffuse atherosclerosis that predisposes patients to systemic embolism by other cardiovascular mechanisms. The embolic potential of atherosclerotic aortic lesions during invasive procedures or during open-heart surgery is well established [82, 83]. Some studies have shown the risk of stroke or peripheral embolism after cardiac catheterization or intra-aortic balloon pump placement in patients with severe aortic atherosclerosis diagnosed by TEE [82]. A strong association between aortic stenosis and aortic atherosclerosis has recently been established [84]. The presence of plaques in the aorta of patients with aortic stenosis has important implications since these patients often undergo invasive diagnostic and therapeutic procedures that can dislodge particularly thick plaques and the attached thrombotic material. Large mobile aortic thrombi are possible causes of systemic emboli and appear to be a complication of atherosclerosis. TEE is the best technique for diagnosing and monitoring the evolution of these large thrombi [85]. Figure 1.6 shows a three-dimensional image of large complex plaques in the thoracic aorta of a patient undergoing TAVI for severe aortic stenosis.

In epiaortic imaging, the transducer is placed directly over the aortic arch in a surgical setting. Although it allows us to image aortic arch plaque the information derived is usually used to select operative techniques in order to reduce the risk of perioperative strokes [86, 87].

MR may be used for detection and measurement of aortic arch plaque [77, 88] and to monitor aortic plaque progression and regression [86]. Contrast MR is also used to identify morphological features such as calcification, thrombus, fibrocellular tissue and lipids which may be useful to detect plaque stability.

Contrast MR angiography may underestimate the plaque thickness and its use may be limited in obese or claustrophobic patients as well as in subjects who have metallic implants.

Multidetector CT has been demonstrated to be an accurate and powerful tool for detecting atheroma in extra- and intracranial vessels. CT is the test of choice for detecting vascular calcification and can reliably detect and measure protruding aortic plaques [77, 89]. CT identifies more plaques throughout the aortic arch and around the origins of the major cerebral arteries in particular compared to TEE (Fig. 1.7). These may represent potential embolic sources of acute ischaemic stroke. Better plaque detection may have an impact on the best available secondary prevention regimen in individual patients if proximal embolic sources are suspected. MDCT allows evaluation of the whole arterial vasculature. In addition, MDCT has the ability to visualize the vessel wall and to give a quantitative measurement of calcified and noncalcified plaque.

However, CT may underestimate the amount of non-calcified plaque and mobile thrombus that presumably is at high risk for embolisation [77]. In conjunction with positron emission tomography, it can be used to localise fluorodeoxyglucose uptake by the plaque, identifying active plaques and plaques prone to rupture (unstable) [90], but its clinical utility has yet to be established.

Concerning specifically pre-operative (cardiac surgery) evaluation, preoperative CT scans in patients at high risk may help identify aortic areas at risk before entering the operating room, lead to more thorough screening in the operating room, and result in a more aggressive strategy to avoid calcified areas.

The occurrence of microembolic signals, as detected by transcranial Doppler (TCD) ultrasonography, can be a marker of severe aortic atherosclerosis, and monitoring these signals should enable the application of appropriate surgical methods to coronary artery bypass patients who are at higher risk of stroke [91]. Asymptomatic cerebral embolic signals (ES) may be associated with severe (≥4 mm) aortic arch atherosclerosis but not with aortic arch atherosclerosis <4 mm or no aortic arch atherosclerosis [92].

The need for contrast injection and radiation as well as the risk of iatrogenic complications due to the invasive nature of the procedure make this technique rarely used to assess aortic plaques [93].

There are no published and conclusive randomised trials to guide the therapy of aortic embolism. So, only strategies for general atherosclerosis management are usually recommended.

Beside nonspecific risk modification (e.g. smoking cessation), strategies include medical, surgical, and interventional therapy.

In acute aortic thromboembolism, interventional approaches may be used to treat end–organ ischaemia (e.g. percutaneous intervention to restore the flow of a cerebral artery occluded by a thromboembolus). Covered stents, endarterectomy and even arterial bypass surgery have been used in a small number of patients with aortic embolism with limited success. Some authors suggest that mural aortic thrombi can be successfully treated with a definitive surgical procedure in selected patients, with low mortality and morbidity [57]. Despite this, at the moment there is no convincing evidence to recommend either endarterectomy or aortic stenting for stroke prevention in patients with thoracic aortic plaques [8]. Indeed, although a handful of case reports on aortic arch endarterectomy in patients with thromboembolism originating from aortic arch atheroma have reported successful results, this procedure seems to be associated with a relatively high rate of perioperative stroke and mortality (34.9 % with endarterectomy versus 11.6 % without endarterectomy), especially when performed to limit stroke during cardiac surgical procedures requiring cardiopulmonary bypass (coronary bypass surgery and valve surgery) [14]. Even if covered stents may offer the potential advantage of shielding severely diseased aortic segments to prevent further embolisation, peri–procedural embolisation may occur during diagnosis or interventional endovascular manipulations. Endovascular stenting for treatment of aortic embolism has largely been limited to abdominal aortic and infrainguinal forms of the disease [134].

Randomised blinded controlled trials are therefore needed to test currently available treatment options, both medical and surgical, to prevent embolic vascular events.

No data exist in this filed. Large fix aortic plaques are a very common finding particularly in old patients with conventional and non conventional atherosclerotic risk factor and are associated in several cases to stratified thrombi. As previously underlined plaque thickness of ≥4 mm is associated with a significantly increased embolic risk. Therefore an aggressive treatment with anticoagulant plus statins may be reasonably advocated even though data on this topic are lacking.