Atrial Fibrillation (AF ) is the most common arrhythmia and affects about 1 % of the US population [5]. The lifetime incidence of atrial fibrillation is about 26 % for men and 23 % for women [6]. The prevalence of AF in a population increases with age, a correlation with the increased incidence of acute occlusive disease in our aging population.

Thromboembolic events, both central and peripheral, are increased and contribute to the high morbidity and mortality with atrial fibrillation. The most common destination of emboli from atrial fibrillation is the cerebral circulatory system leading to strokes and transient ischemic attacks. Although the incidence of peripheral embolism from AF is lower as compared to cerebral vasculature, about 30–80 % of patients with peripheral thromboembolic phenomenon have AF [7]. This makes AF one of the most significant risk factors in embolic peripheral ischemia. More specifically, the annual incidence of acute limb ischemia in AF is 0.4 % (lethality 16 %) [8]. Symptoms can vary depending on the degree of arterial luminal obstruction and extent of collateral flow caused by preexisting peripheral arterial disease.

Most thrombi associated with AF are formed in left atrial appendage. Echocardiography is an important diagnostic tool, with transesophageal echocardiography (TEE) significantly increasing the sensitivity of the detection of left atrial appendage thrombus (Fig. 12.1). Newer imaging technologies such as magnetic resonance imaging (MRI) or computerized tomography can also be utilized but are used less frequently in clinical practice.

The risk of thromboembolism varies widely across the population of patients with AF, according to the presence or absence of clinical risk factors. The rate of ischemic stroke or peripheral embolization (without antithrombotic therapy) also increases as the number of risk factors increase. This trend is the basis of the two major risk prediction models used in clinical practice to determine the need for anticoagulation—CHADS₂ score and more recently CHA₂DS₂-VASc score [9, 10]. Anticoagulation decreases the risk of thromboembolism (Tables 12.1, 12.2, and 12.3). The current American Heart Association guidelines recommend anticoagulation for patients with CHA₂DS₂-VASc score ≥2 [11].

Warfarin has been well established to reduce the risk of stroke or embolism in patients with atrial fibrillation, however requires regular blood level monitoring. Recently, new oral anticoagulants have been approved that do not require rigorous blood level monitoring of warfarin. These include dabigatran, apixaban, and rivaroxaban [11]. The major trials studying these novel oral anticoagulants did not separately analyze for peripheral embolism in their primary outcome. However, the overall rate of the combined primary outcome (i.e., stroke plus peripheral thromboembolism) has shown to be either non-inferior or significantly lower as compared to warfarin [12–14].

Furthermore, new devices to ligate, resect, or occlude the left atrial appendage, the most common location to form a thrombus, are under investigation. The Watchman device, manufactured by Boston Scientific, has shown superiority in primary outcome of stroke, cardiovascular death, and systemic embolism over warfarin [15]. In December 2013, Food and Drug Administration (FDA) advisors voted 13-1 that the benefits associated with the Boston Scientific Watchman device outweighed the risks in AF patients. The FDA approved the device in 2015.

Sluggish flow of the intracavitary blood in the ventricles predisposes to thrombus formation. As such, ventricular mural thrombus is most commonly associated with myocardial infarctions (MI), ventricular aneurysms, and dilated cardiomyopathies among other systemic diseases that affect the heart (e.g., amyloidosis, Chagas disease, systemic lupus erythematosus, carcinoid heart disease). Myocardial infarction can cause wall motion abnormality and/or systolic dysfunction, hence causing the sluggish flow. The likelihood of developing a left ventricular (LV) thrombus after an acute MI varies with infarct location and size. A large anterior myocardial infarction with anteroapical aneurysm formation has the highest rates of LV thrombus development, compared to other areas of infarction. Earlier studies, prior to the percutaneous coronary intervention (PCI) era, had reported the rates of up to 46 % in anterior MI [16–18]; however, more recent studies with PCI report an incidence of about 4 % [19]. Most LV mural thrombi develop within the first two weeks after MI [16, 20].

In the pre-thrombolytic era, the risk of embolization from a left ventricular thrombus has been reported to be anywhere from 10 to 20 % in patients not on anticoagulation [21–23]. Embolization from cardiomyopathies seems to occur more often than thrombus within an aneurysm, likely secondary to the thrombus surface exposure to the LV cavity [24]. The incidence of systemic embolization of mural thrombus for left ventricular aneurysms, myocardial infarctions , and congestive cardiomyopathy are 0–36, 0–24, 11 %, respectively [25].

A number of diagnostic modalities can be used to diagnose ventricular mural thrombus. The most widely used modality in clinical practice is echocardiography (Fig. 12.2). Certain echocardiographic characteristics can predict the risk of embolization; the two most important ones associated with higher risk are thrombus mobility and protrusion into the left ventricular cavity [20–26]. Other diagnostic studies include angiography, radionuclide scintigraphy, indium II-labeled platelets, and computed tomography (CT). Once diagnosed, the recommended treatment is anticoagulation with warfarin or heparin products for at least three months.

Endocarditis, whether acute or subacute, can be a source of emboli causing central nervous system injury, arteritis, and end-organ ischemia. Nearly 50 % of patients will develop an embolic event and often involve the coronary vessels, spleen, kidneys, brain, and extremities [27, 28]. The incidence of critical limb ischemia, however, is not very well defined. The risk of embolization is correlated with the size of the vegetation, location, and organism involved. Some studies have shown significantly greater rates of embolization with vegetation size >10 mm. This risk seems to be highest when mitral valve is involved [28–30]. Infective endocarditis (IE) caused by Staphylococcus or fungal organisms appears to carry a higher risk of embolization independent of the vegetation size [29].

Modified Duke’s criterion is utilized to evaluate the patient with infective endocarditis (Table 12.4). The emphasis is given to the two more important diagnostic tests, the blood cultures and echocardiography. Echocardiography is fundamental in diagnosing endocarditis. The echocardiographic features included in the major classification of the Modified Duke’s criteria are the evidence of an oscillating intracardiac mass or vegetation, an annular abscess, a prosthetic valve partial dehiscence, and a new valvular regurgitation [28].

Echocardiography should be done on all cases suspicious of infective endocarditis. In patients whom the clinical suspicion is low, and where it is likely to obtain good images, a transthoracic echocardiogram (TTE) is reasonable. On the other hand, if there are poor echocardiographic windows (e.g., in obese patients or patients with severe lung disease) or if there is high clinical suspicion of IE or its complications (prosthetic valve, staphylococcal bacteremia, or new atrioventricular block), then transesophageal echocardiogram should be performed first. This is because in these cases a negative TTE will not definitely rule out IE or its potential complications (Fig. 12.3).