Idiopathic Pericarditis

The cause of acute pericarditis is often difficult to establish, and idiopathic pericarditis remains the most common diagnosis.

Viral Pericarditis

Coxsackievirus B virus and echovirus are the most common viruses, and a fourfold increase in antiviral titers is required for the diagnosis. Patients often experience a prodrome of an upper respiratory tract infection. The prognosis of viral pericarditis is good, the course is usually self-limited, and patients may be treated on an outpatient basis.

Purulent Pericarditis

Before the antibiotic era, pneumonia was the prime cause of purulent pericarditis. Currently, causes include thoracic surgery, chemotherapy, immunosuppression, and hemodialysis. Presentation is usually acute with high fevers, chills, night sweats, and dyspnea, but the classic findings of chest pain or friction rub are rare. Cardiac tamponade is common (42% to 77% of patients in select series), and mortality is high.

If purulent pericarditis is suspected, hospital admission with immediate pericardiocentesis and intravenous broad-spectrum antibiotics is mandatory, followed by early surgical drainage. Findings on pericardial fluid analysis include a high protein level (>6 g/dL), low glucose level (<35 mg/dL), and very high leukocyte count (6,000-240,000/mm³).⁵

Tuberculous Pericarditis

Tuberculous pericarditis occurs in 1% to 2% of cases of pulmonary tuberculosis. Immunocompromised or human immunodeficiency virus (HIV)-positive patients are at increased risk.⁶ Nonspecific symptoms such as dyspnea, fever, chills, and night sweats develop slowly, and a friction rub or chest pain is often absent. The ECG is usually unrevealing, but the chest radiograph may be most useful when findings of pulmonary tuberculosis are present (Figs. 2 and 3). A patient with suspected or diagnosed pericardial tuberculosis should be hospitalized, and antituberculous therapy (e.g., rifampin, isoniazid, streptomycin, ethambutol) started promptly.

Figure 2 Extensive pericardial calcifications on chest radiograph (posteroanterior projection).

Extensive pulmonary infiltrates caused by tuberculosis can be noted (also see Fig. 3).

Figure 3 Extensive pericardial calcifications on chest radiograph (lateral projection).

These were caused by tuberculosis (also see Fig. 2).

Analysis of the pericardial fluid shows high specific gravity, very high protein level (often >6 g/dL), and predominantly lymphocytic cells. A pericardial biopsy with acid-fast bacilli polymerase chain reaction testing is recommended for all patients with suspected tuberculous pericarditis. However, a normal pericardial biopsy does not exclude the diagnosis.

Uremic and Dialysis-Associated Pericarditis

Uremic pericarditis occurs in 6% to 10% of patients with advanced renal failure before hemodialysis is initiated; blood urea nitrogen levels usually exceed 60 mg/dL. The typical ST-segment elevation on the ECG usually is absent. A large hemorrhagic effusion caused by impaired platelet function is common, although tamponade is rare. Dialysis-associated pericarditis is caused by fluid overload, and the fluid is usually serous. With both forms, initiation or intensification of hemodialysis is indicated, usually leading to improvement in 1 to 2 weeks.^7,8

Pericarditis following Myocardial Infarction

Post-MI pericarditis is a common complication (25%-40% of patients with MI) and occurs early, within 3 to 10 days after the MI. Its development correlates with the extent of necrosis, is more common with anterior than inferior infarcts, and is associated with a higher 1-year mortality rate and incidence of congestive heart failure.⁹

The diagnosis of post-MI pericarditis requires symptoms or a new pericardial friction rub; a pericardial effusion alone is nonspecific. In addition to the typical ST elevation seen with acute pericarditis that may be difficult to differentiate from the actual MI in this setting, findings on the ECG are persistently positive T waves more than 2 days after MI or normalization of previously inverted T waves.¹⁰

Malignancy

Pericarditis associated with malignancy is caused mostly by metastatic disease. Pericarditis is common in metastasized bronchogenic or breast carcinoma, Hodgkin’s disease, and lymphoma (Fig. 4); it is rare in primary mesothelioma and angiosarcoma. Diagnosis is based on analysis of pericardial fluid cytology, which has a sensitivity ranging from 70% to 90% and a specificity of 95% to 100%.¹

Figure 4 Metastatic infiltration of the pericardial space.

The primary tumor was a lymphoma.

Radiation Pericarditis

Recent or remote mediastinal radiation can cause pericarditis at any time from weeks to months after the exposure.

Traumatic Pericarditis

Sharp or blunt trauma (Figs. 5 to 7) and even a minimally invasive procedure such as cardiac diagnostic or interventional catheterization has been associated with pericardial irritation.

Figure 5 Hemorrhagic pericarditis.

The patient underwent chest compressions during resuscitative efforts.

Figure 6 Hemopericardium.

Figure 7 Hemopericardium after blunt chest trauma.

Electrocardiography

The ECG in acute pericarditis has four consecutive stages (Table 1). Stage 1, characterized by diffuse ST elevation, is the most useful stage for the diagnosis of acute pericarditis (Fig. 8). The distinction between pericarditis and acute MI is difficult at times, but there are several clues (Table 2).¹² Troponin levels may be elevated in up to 50% of patients with pericarditis but in the absence of myocarditis, the prognosis remains unchanged.¹³

Table 1 Stages of Acute Pericarditis by Electrocardiography

Figure 8 Stage 1 of acute pericarditis.

There are diffuse concave ST elevation and PR elevation in the aV_R and V₁ leads.

Table 2 Electrocardiographic Differentiation of Acute Pericarditis and Myocardial Infarction

Chest Radiography

The chest radiograph may be entirely normal unless there is a pericardial effusion causing cardiomegaly (Fig. 9) or there are changes caused by an underlying disease.

Figure 9 Chest radiograph of cardiomegaly.

This patient had a very large pericardial effusion.

Echocardiography

An episode of acute pericarditis that responds well to therapy may be followed clinically. Indications for echocardiography are symptoms persisting for longer than 1 to 2 weeks, the presence of hemodynamic abnormalities, clinical suspicion of a large or increasing pericardial effusion, or recent cardiac surgery.

Medical Management

Treatment of the underlying disease is the mainstay of therapy.¹⁴ Nonsteroidal anti-inflammatory drugs (NSAIDs) can be used for pain relief; agents such as indomethacin and aspirin have similar efficacy.¹⁵ Ibuprofen may be started at a dose of 400 mg every 8 hours and increased for symptom relief.¹⁵ Ketorolac tromethamine may be used as a parenteral agent for relief of symptoms.¹⁶ NSAIDs are contraindicated in the early period (<7-10 days) after MI (can predispose to cardiac rupture), and aspirin should be used instead.

If pericarditis recurs (20%-30% of patients) or response to NSAIDs is poor, prednisone may be started at high doses and then tapered over 3 weeks. Use of steroids in acute pericarditis can promote a recurrence.¹⁷ As with NSAIDs, steroids should be avoided in post-MI pericarditis because there is an increased incidence of myocardial wall rupture.

Colchicine may be effective for persistent or refractory cases of Dressler’s syndrome and idiopathic pericarditis.^18,19 The COPE (Colchicine for Acute Pericarditis) trial found that colchicine in addition to aspirin reduces the recurrence of pericarditis from 32.3% to 10.7%.²⁰ If they are not mandatory, anticoagulants should be avoided during the acute phase of pericarditis to reduce the risks of bleeding and tamponade.