Nejm 2004;351;2195; Lancet 2004;363:717; Jama 2003;289:1150

Cause: Multiple; idiopathic most common in young adults, but causes include

Infections: Coxsackie A or B virus, echovirus, adenovirus, mumps virus, infectious mononucleosis, varicella, hepatitis B, HIV, tuberculosis, pneumococcus, staphylococcus, streptococcus, gram-negative septicemia, Neisseria meningitidis, Neisseria gonorrhoea; histoplasmosis, coccidioidomycosis, candida, blastomycosis, toxoplasmosis, amebiasis, mycoplasma, nocardia, actinomycosis, echinococcosis, Lyme disease

Acute MI

Uremia

Radiation injury

Autoimmune disorders: SLE, rheumatoid arthritis, seleroderma, mixed connective tissue disease, Wegener’s granulomatosis, polyarteritis nodosa, acute rheumatic fever

Inflammatory disorders: sarcoidosis, amyloidosis, inflammatory bowel disease, Whipple’s disease, temporal arteritis, Behcet’s syndrome

Drugs: hydralazine, procainamide, phenytoin, isoniazid, phenylbutazone, dantrolene, doxorubicin, methysergide, penicillin

Neoplasm

Trauma

Dressler’s syndrome; postpericardiotomy syndrome

Dissecting aortic aneurysm

Hypothyroidism

The cause in 9 out of 10 cases is either viral or unknown (Am J Cardiol 1995;75:378).

Epidem: Purulent pericarditis is most often seen as a complication of lung infection with staphylococcus, pneumococcus, or streptococcus. It may also be a life-threatening complication of infective endocarditis.

Histoplasmosis is the most common cause of fungal pericarditis. Coccidioidomycosis pericarditis is seen in the U.S. Southwest and San Joaquin Valley.

Although 60% of dialysispts will develop pericardial effusion, clinical pericarditis is seen in < 20% of dialysispts.

Breast and lung cancer, leukemia, Hodgkin’s disease, and non-Hodgkin’s lymphoma account for 80% of malignant pericarditis. Ovarian and gi malignancy, multiple myeloma, and melanoma are also associated with pericarditis.

12-48% ofpts with SLE develop pericarditis (Mayo Clin Proc 1999;74:275), but it is frequently not clinically apparent and tamponade occurs in < 10% ofpts. Approximately 25% ofpts with RA develop pericarditis.

2-25% ofpts with lupus-like syndrome from hydralzine or procainamide are reported to develop pericarditis.

10-40% of cardiac surgerypts develop postpericardiotomy syndrome 1-8 wk after the procedure.

Up to 1/3 ofpts with myxedema develop pericardial effusion.

Pathophys: Inflammation can involve a superficial layer of myocardium. Fibrin deposits are particularly dense in tuberculous pericarditis, and virtually all untreatedpts subsequently develop constrictive pericarditis.

Very large pericardial effusions can develop rapidly in histoplasmosis pericarditis.

Primary pericardial tumors are rare and are most frequently mesotheliomas.

Sx: Chest pain may be pleuritic, and may improve with sitting up and worsen when lying supine. Dyspnea is possible.

Bacterial pericarditis presents as acute illness with fever, chills, night sweats, and dyspnea.

Si: Pericardial friction rub may be evanescent. It is best heard at LLSB with the pt leaning forward. 85% ofpts will have rub in course of the disease.

Crs: Idiopathic pericarditis is usually self-limited. Pain improves with rx in 1 wk and EKG findings resolve in 2-4 wk; < 20% ofpts will have a recurrence within 6 mon.

Cmplc: Large pericardial effusion; constrictive pericarditis; up to 15% ofpts with acute pericarditis will develop cardiac tamponade (Am J Cardiol 1985;56:623)

Lab: EKG: Sinus tachycardia; ST elevation (concave upward) in multiple leads, followed in hr/d by resolution of ST elevation; T-wave flattening followed by T-wave inversion. If the ratio of ST elevation (in mm)/T-wave inversion amplitude (in mm) in lead V6 > 0.24, acute pericarditis is likely (Circ 1982;65:1004).

Echocardiogram can demonstrate pericardial effusion but manypts with acute pericarditis will not have significant effusion.

Elevated ESR, leukocytosis, and mild elevation of CK-MB are observed. Plasma troponin I level is elevated in 35-50% ofpts (J Am Coll Cardiol 2003;42:2144).

Tbc skin test, BUN, and creatinine tests are appropriate for allpts. Depending on the differential dx, ANA, rheumatoid factor, TSH, HIV test, blood cultures, and heterophile antibody may also be indicated.

Pericardial fluid analysis: Cell count, glucose, protein, LDH, bacterial culture, and cytology. Exudates are characterized by specific gravity > 1.015, fluid total protein > 3.0 g/dL, fluid/serum protein ratio > 0.5, fluid LDH ratio > 0.6, fluid/serum glucose ratio < 1.0. Cytologic study had a sensitivity of 92% and a specificity of 100% for malignant effusion (Chest 1997;111:1213). Cell cytology is diagnostic in 85% ofpts with malignant pericarditis.

X-ray: CXR may be normal or show globular heart. 25% ofpts will have pleural effusion.

Rx: ASA 2-4 gm po qd, ibuprofen 1600-3200 mg po qd, indomethacin 75-225 mg po qd for control of pain. If no response, give steroids (eg, prednisone 60-80 mg/d). Steroids may increase the risk of later recurrence.

Close observation for signs of developing tamponade and restriction of activity are required.

Warfarin should be avoided. If anticoagulation is mandatory, switch to iv heparin.

Diagnostic pericardiocentesis is reserved forpts with suspected purulent pericarditis or malignancy.

Colchicine 0.6 mg po bid may be a useful adjunct in prevention of recurrent idiopathic pericarditis (Circ 1998;97:2183).

Large idiopathic chronic pericardial effusion is usually well tolerated for long periods but tamponade can develop unexpectedly. Pericardiectomy should be considered whenever a large effusion recurs after pericardiocentesis (Nejm 1999;341:2054).

Cause: Fibrin deposition during acute pericarditis leads to fusion and thickening of visceral and parietal pericardium, resulting in chronic restriction of diastolic filling of heart

Epidem: TB was formerly the most common cause, but it now accounts for < 15% of cases in industrialized countries. Most cases are of unknown cause. Mediastinal radiation, post-surgical pericarditis, chronic renal failure, collagen vascular disease, and metastatic malignancy also are possible causes (Am Hrt J 1987;113:354).

Pathophys: Heavily fibrosed and calcified pericardium produces elevation and equilibration of diastolic pressures in all 4 cardiac chambers. Early diastolic filling of ventricles is relatively unimpaired, but filling comes to an abrupt halt for the remainder of diastole due to restriction by the pericardium.

Sx: Dyspepsia, anorexia; dyspnea, orthopnea; fatigue, weight loss, muscle wasting; chest pain

Si: Elevated jugular pulse with Kussmaul’s sign (inspiratory increase in systolic jugular venous pressure—can be difficult to assess at bedside); diastolic pericardial knock (usually earlier and higher pitched than S₃ gallop); normal/diminished arterial pulses; pulsus paradoxicus is uncommon; pleural effusion; hepatomegaly, edema, ascites