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Pericardial diseases constitute pathologic processes that involve the pericardium, the pericardial sac and its contents, and the thoracic structures surrounding the heart. Cardiovascular perturbations associated with pericardial disease range from the asymptomatic electrocardiographic findings in uremic pericarditis to catastrophic circulatory collapse observed in the setting of acute hemorrhagic pericardial tamponade. The clinical features of pericardial diseases may resemble right-side failure, notably right ventricular (RV) failure and tricuspid insufficiency, but can also present as left-side failure manifesting as shortness of breath, reduced exercise tolerance, and multiorgan hypoperfusion. However, clinical management of pericardial pathology may differ significantly from that of ventricular dysfunction or valvular heart disease. As a consequence, timely diagnosis and initiation of appropriate medical or surgical therapy is imperative. This chapter deals specifically with the clinical utility of transesophageal echocardiography (TEE) in the evaluation, diagnosis, and characterization of pericardial disease including constrictive pericarditis and cardiac tamponade.

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The pericardium consists of three layers: a fibrous layer that blends with the adventitia of the great vessels and systemic and pulmonary venous inflows, a parietal layer lining the inner surface of the fibrous pericardium, and a visceral layer lining the epicardium.1 The visceral component is made up of a single layer of mesothelial cells, is attached to the surface of the heart and epicardial fat, and regulates the production of pericardial fluid (normally 5 to 30 mL may be seen in the pericardial space).2 This layer also reflects back on itself to line the outer fibrous layer forming the parietal pericardium.1 The latter is composed of collagen fibers meshed with elastic fibers that allow considerable flexibility of the pericardium during childhood and early adult years, although this elasticity is lost with advancing age. The pericardial space conforms to the shape of the heart, and extends superiorly for a short distance along the great vessels to form a small pocket posteriorly, known as the transverse sinus. Similarly, the oblique sinus is formed by an extension of the pericardium posterior to the left atrium between the pulmonary veins. The function of the pericardium includes protection of the heart from the spread of infection or malignancy from surrounding structures, reduction of friction between the heart and the adjacent tissues, control of hydrostatic forces on the heart, prevention of acute chamber dilatation, and maintenance of diastolic coupling between the ventricles.2

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Despite its ability to isolate the heart from direct extension of infectious and noninfectious pathogens, pericardial inflammation occurs in nearly 5% of the population according to autopsy findings, but is clinically detected in fewer than 0.1% of hospital admissions.3 The causes of pericarditis are numerous: idiopathic, infectious (viral, tuberculosis, acute bacterial, fungal, toxoplasmosis, or amebiasis), acute myocardial infarction, uremia, neoplastic disease, radiation, autoimmune (acute rheumatic fever, systemic lupus erythematosus, or rheumatoid arthritis), sarcoidosis, amyloidosis, drugs (hydralazine, procainamide, phenytoin, or penicillin), trauma, postcardiotomy for cardiac surgery, dissecting aortic aneurysm, myxedema, and chylopericardium.4 Most cases tend to be idiopathic or viral in ...

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