Embolism from the heart or the thoracic aorta often leads to clinically significant morbidity and mortality due to transient ischemic attack, stroke or occlusion of peripheral arteries. Transthoracic and transesophageal echocardiography are the key diagnostic modalities for evaluation, diagnosis, and management of stroke, systemic and pulmonary embolism. This document provides comprehensive American Society of Echocardiography guidelines on the use of echocardiography for evaluation of cardiac sources of embolism. It describes general mechanisms of stroke and systemic embolism; the specific role of cardiac and aortic sources in stroke, and systemic and pulmonary embolism; the role of echocardiography in evaluation, diagnosis, and management of cardiac and aortic sources of emboli including the incremental value of contrast and 3D echocardiography; and a brief description of alternative imaging techniques and their role in the evaluation of cardiac sources of emboli. Specific guidelines are provided for each category of embolic sources including the left atrium and left atrial appendage, left ventricle, heart valves, cardiac tumors, and thoracic aorta. In addition, there are recommendation regarding pulmonary embolism, and embolism related to cardiovascular surgery and percutaneous procedures. The guidelines also include a dedicated section on cardiac sources of embolism in pediatric populations.

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In this article we describe an approach to dextrocardia in adult patients and illustrate the imaging manifestations of the most common underlying disorders.

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DL-alpha-Difluoromethylornithine is an enzyme-activated inhibitor of ornithine decarboxylase and an antagonist of polyamine metabolism that has been successful in clinical trials against West African sleeping sickness caused by Trypanosoma brucei gambiense. Its potential for use against the more virulent East African form of the disease, caused by T. brucei rhodesiense, is not certain. We examined 14 East African clinical isolates from the Kenya Trypanosomiasis Research Institute strain bank plus 2 established isolates for susceptibility to DL-alpha-difluoromethylornithine and to standard trypanocides. Seven of 16 strains were partially or totally refractory to DL-alpha-difluoromethylornithine in our test system. Four strains were also refractory to arsenical drugs, and five were refractory to diamidines. The results indicate that other novel agents or combinations of established agents may be needed for chemotherapy of East African disease.

CES (also referred to as cholesterol crystal embolization, atheromatous embolization or atheroembolism) occurs when cholesterol crystals and other contents of an atherosclerotic plaque embolize from a large proximal artery to smaller distal arteries, causing ischemic end-organ damage. Clinical manifestations of CES include constitutional symptoms (fever, anorexia, weight loss, fatigue and myalgias), signs of systemic inflammation (anemia, thrombocytopenia leukocytosis, high erythrocyte sedimentation rate, elevated levels of C-reactive protein, hypocomplementemia), hypereosinophilia, eosinophiluria, acute onset of diffuse neurologic deficit, amaurosis fugax, acute renal failure, gut ischemia, livedo reticularis and blue-toe syndrome. CES may occur spontaneously or after an arterial procedure. There is no specific laboratory test for CES. Retinal exam demonstrating Hollenhorst plaques supports the diagnosis of CES. Biopsy of target organs (usually skin, skeletal muscles or kidneys) is the only means of confirming the diagnosis of CES. Treatment consists of supportive care and general management of atherosclerosis and arterial ischemia.

Cholesterol emboli syndrome is a relatively rare, but potentially devastating, manifestation of atherosclerotic disease. Cholesterol emboli syndrome is characterized by waves of arterio-arterial embolization of cholesterol crystals and atheroma debris from atherosclerotic plaques in the aorta or its large branches to small or medium caliber arteries (100-200 μm in diameter) that frequently occur after invasive arterial procedures. End-organ damage is due to mechanical occlusion and inflammatory response in the destination arteries. Clinical manifestations may include renal failure, blue toe syndrome, global neurologic deficits and a variety of gastrointestinal, ocular and constitutional signs and symptoms. There is no specific therapy for cholesterol emboli syndrome. Supportive measures include modifications of risk factors, use of statins and antiplatelet agents, avoidance of anticoagulation and thrombolytic agents, and utilization of surgical and endovascular techniques to exclude sources of cholesterol emboli.