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The pericardium serves many important but subtle functions. It limits distension and facilitates interaction of the cardiac chambers, influences ventricular filling, prevents excessive torsion and displacement of the heart, minimizes friction with surrounding structures, prevents the spread of infection from contiguous structures, and equalizes gravitational, hydrostatic, and inertial forces over the surface of the heart. The pericardium also has immunologic, vasomotor, fibrinolytic, and metabolic activities. Therapeutically, the pericardial space can be used for drug delivery.
The pericardium is affected by virtually every category of disease ( Box 68.1 ), including idiopathic, infectious, neoplastic, immune/inflammatory, metabolic, iatrogenic, traumatic, and congenital.
Idiopathic
Infectious: Bacterial, viral, mycobacterial, fungal, protozoal, HIV associated
Neoplastic
Metastatic: (Breast, lung, melanoma, lymphoma, leukemia), primary (mesothelioma, fibrosarcoma)
Immune/inflammatory: Connective tissue disease, arteritis, acute myocardial infarction, post–pericardial injury syndrome
Metabolic: Nephrogenic, myxedema, amyloidosis, aortic dissection
Iatrogenic: Drugs, radiation therapy, device/instrumentation, cardiac resuscitation
Traumatic: Blunt, penetrating, surgical
Congenital: Pericardial cysts, congenital absence of pericardium, mulibrey nanism
Acute pericarditis is a syndrome of pericardial inflammation characterized by typical chest pain (sharp, retrosternal pleuritic pain that radiates to the trapezius ridge, often aggravated by lying down and relieved by sitting up), a pathognomonic pericardial friction rub (characterized as superficial, scratchy, crunchy , and evanescent), and specific electrocardiographic changes (diffuse ST-T wave changes [ Fig. 68.1 ] with characteristic evolutionary changes and PR segment depression). These manifestations vary in terms of presentation (chest pain >85%–90%, pericardial friction rub ≤33%, electrocardiogram [ECG] changes 60%). The 2015 European Society of Cardiology (ESC) guidelines suggest that at least two of the four of the following criteria are needed to establish the diagnosis: pericardial pain, pericardial rub, ECG changes, and pericardial effusion. Additional supporting findings include elevation in inflammatory markers (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], white blood cell [WBC]) and evidence of pericardial inflammation by computed tomography (CT) or magnetic resonance imaging (MRI).
Causes of pericarditis include infectious (viral, bacterial, fungal, mycobacterial, human immunodeficiency virus [HIV] associated), neoplastic (usually metastatic from lung or breast; melanoma, lymphoma, or acute leukemia), myocardial infarction, injury (postpericardiotomy, traumatic), radiation, metabolic (myxedema, uremia), and connective tissue disease. In the developed world, the most common etiology is viral, whereas tuberculosis is the most frequent cause in developing countries.
Hospitalization is warranted for high-risk patients with an initial episode of acute pericarditis in order to determine a cause and to observe for the development of cardiac tamponade; close, early follow-up is critically important for the remainder of patients not hospitalized. Features indicative of high-risk pericarditis include fever greater than 38°C, subacute onset, an immunosuppressed state, trauma, oral anticoagulant therapy, myopericarditis, a moderate or large pericardial effusion, cardiac tamponade, and failure of initial outpatient medical therapy
Acute pericarditis usually responds to oral nonsteroidal anti-inflammatory agents (NSAIDs), such as aspirin (650 mg every 3–4 hours) or ibuprofen (600–800 mg every 6 hours). Colchicine (1 mg/day) may be used to supplement the NSAIDs as it may reduce symptoms and decrease the rate of recurrences. Chest pain is usually alleviated in 1 to 2 days, and the friction rub and ST-segment elevation resolve shortly thereafter. Most mild cases of idiopathic and viral pericarditis are adequately treated within a week or two of treatment, but the duration of therapy is variable and patients should be treated until inflammation or an effusion, if present, has resolved. The intensity of therapy is dictated by the distress of the patient, and narcotics may be required for severe pain. Corticosteroids should be avoided unless there is a specific indication (such as connective tissue disease or uremic pericarditis) because they enhance viral multiplication and may result in recurrences when the dosage is tapered. Strenuous exercise should be avoided until there is no longer evidence of active disease.
Based on the colchicine for acute pericarditis (COPE) trial, the ESC guidelines recommend a weight-adjusted colchicine dose of 0.5 mg once daily for patients less than 70 kg or 0.5 mg BID for those 70 kg or more for at least 3 months to improve response to medical therapy and prevent recurrences.
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