 Introduction/Background Noncerebral systemic arterial embolism is an important cause of patient morbidity and mortality [1]. Arterial emboli can originate from a variety of cardiac and noncardiac sources. Cardiac sources include thrombus within the left atrium and left ventricle, valvular disease such as endocarditis, and cardiac neoplasms. Noncardiac sources of arterial embolism include thrombus and atherosclerosis within the aorta and peripheral arteries. Intracardiac thrombus has been thoroughly described in the cardiology and neurology literature with several factors that predispose its formation and the potential for arterial embolization. For example, atrial fibrillation has been shown to be a significant risk factor for atrial thrombogenesis [2,3]. Complex left atrial appendage morphology also confers increased likelihood of thrombus development [4]. Myocardial infarction often results in focal hypokinesis or akinesis of the left ventricular myocardium, which predisposes to thrombus formation [5,6]. Aortic and mitral valve endocarditis as well as valvular neoplasms are other potential sources for arterial embolism detectable with imaging [7,8]. Aortic thrombi tend to be associated with aortic pathology including dissection, aneurysm, or ulcerative lesions [9,10]. Thrombus formation can also occur in the aorta secondary to hypercoagulable states such as malignancy, trauma, postoperative states, hormonal therapy, and inherited hypercoagulable disorders [1,11,12]. When a cardiac or noncardiac embolic source dislodges, the resulting embolus can occlude a variety of peripheral and visceral arteries causing ischemia [1,9,11,12]. Characteristic locations for noncerebral arterial occlusion include the upper extremities, abdominal viscera, and lower extremities [1,9,11]. Ischemia in these regions can progress to tissue infarction resulting in limb amputation, bowel resection, or nephrectomy.
Workup of Noncerebral Systemic Arterial Embolic Source.  Introduction/Background Noncerebral systemic arterial embolism is an important cause of patient morbidity and mortality [1]. Arterial emboli can originate from a variety of cardiac and noncardiac sources. Cardiac sources include thrombus within the left atrium and left ventricle, valvular disease such as endocarditis, and cardiac neoplasms. Noncardiac sources of arterial embolism include thrombus and atherosclerosis within the aorta and peripheral arteries. Intracardiac thrombus has been thoroughly described in the cardiology and neurology literature with several factors that predispose its formation and the potential for arterial embolization. For example, atrial fibrillation has been shown to be a significant risk factor for atrial thrombogenesis [2,3]. Complex left atrial appendage morphology also confers increased likelihood of thrombus development [4]. Myocardial infarction often results in focal hypokinesis or akinesis of the left ventricular myocardium, which predisposes to thrombus formation [5,6]. Aortic and mitral valve endocarditis as well as valvular neoplasms are other potential sources for arterial embolism detectable with imaging [7,8]. Aortic thrombi tend to be associated with aortic pathology including dissection, aneurysm, or ulcerative lesions [9,10]. Thrombus formation can also occur in the aorta secondary to hypercoagulable states such as malignancy, trauma, postoperative states, hormonal therapy, and inherited hypercoagulable disorders [1,11,12]. When a cardiac or noncardiac embolic source dislodges, the resulting embolus can occlude a variety of peripheral and visceral arteries causing ischemia [1,9,11,12]. Characteristic locations for noncerebral arterial occlusion include the upper extremities, abdominal viscera, and lower extremities [1,9,11]. Ischemia in these regions can progress to tissue infarction resulting in limb amputation, bowel resection, or nephrectomy.