Etiology
Pericarditis is caused by many different conditions. The etiological classification of pericardial diseases comprises infectious pericarditis, pericarditis in autoimmune diseases, postmyocardial infarction syndrome, and auto-reactive (chronic) pericarditis.
11 There has been a sharp decline in infectious pericarditis in the last few years, except in immunocompromised individuals, such as those with acquired immunodeficiency syndrome (AIDS).
12
Viruses associated with pericarditis include influenza, coxsackie A or B, varicella, mumps, hepatitis B, mononucleosis, and human immunodeficiency virus (HIV).
7 Idiopathic pericarditis is thought often to be the result of viral pericarditis where the virus is never identified. Bacterial infections, such as tuberculosis, are rare in the United States, but have surged in incidence in regions of the world where HIV and AIDS are epidemic. Other bacteria that cause pericarditis include
Staphylococcus, Pneumococcus, and
Streptococcus species.
Aspergillosis and
histoplasmosis are among the fungal infections that can cause pericarditis.
Frequently, the patient’s history indicates that a viral infection preceded the pericarditis. Sometimes the pericarditis itself is the first presenting symptom of a systemic disease, such as systemic lupus erythematosus or malignancy. In viral pericarditis, the pericardial fluid is most commonly serous, of low volume, and resolves spontaneously.
9 Exudative, hemorrhagic, and leukocyte-filled large effusions may be associated with neoplastic, tuberculous, and purulent pericarditis.
6
Assessment Findings
The onset of symptoms can be acute, as is commonly seen in viral pericarditis, or insidious, as seen in uremic pericarditis. Acute
viral pericarditis is nearly always preceded by a recent respiratory, gastrointestinal, or “flu-like” illness. A prodrome of fever, malaise, and myalgia is common in acute pericarditis, although older patients may not exhibit fever.
1
A major symptom of pericarditis is chest pain that is retrosternal or left precordial, radiating to the trapezius ridge and varying with posture. The pain is transmitted through the phrenic nerves, and usually occurs on the left side. Shoulder pain should be distinguished from trapezius ridge pain by having the patient physically point to the specific site of pain. Frequently the chest pain caused by pericarditis induces shallow tachypnea as patients attempt to splint their chest movement.
2 The pain is generally worse when lying supine and is relieved by sitting.
A pericardial friction rub is pathognomonic for pericarditis, but is frequently not present, may come and go, and can vary in quality and intensity. Auscultation for a pericardial friction rub is accomplished with the diaphragm of the stethoscope at the left middle to lower sternal border during both inspiration and expiration, while the patient changes positions.
2 Often best heard at end expiration while the patient is leaning forward, the sound is classically a rasping or creaking with a triple cadence, but can also be bi- or monophasic.
1
A diagnosis of acute pericarditis is made if the patient has a pericardial friction rub or chest pain, and widespread ST segment elevation on electrocardiography.
10 It is important to differentiate pericarditis from myocardial infarction (MI) and pulmonary embolism.
Table 30-1 describes the different features from these three conditions.
10
The pericardium itself does not produce electrical activity. The electrocardiogram (ECG) changes seen in pericarditis are a result of superficial inflammation of the myocardium underneath the pericardium. The ECG of a patient with pericarditis may be normal, atypically abnormal with nonspecific changes, or have a fourstage sequence that is diagnostic.
Figure 30-1 shows the electrocardiographic manifestations of pericarditis.
In stage I, there are ST segment deviations, primarily due to inflammation on the ventricular surfaces. PR segment deviations are also usually present. Stage I is virtually pathognomonic of acute pericarditis when it involves all or almost all leads with early ST junction elevations that produce an appearance of T waves “jacked-up” on the QRS interval, but that is otherwise normal.
2 The ST segment is always depressed in aVR.
4
In early stage II, the ST segments return to baseline, and PR segments may now be depressed. In late stage II, the T waves flatten and then invert. In stage III, the ECG is characteristic of diffuse myocardial injury. In stage IV, the ECG evolves back to the prepericarditis state.
2 Stage IV may last days or months.
4
The changes seen in the ECG of a patient with pericarditis can occur over hours, particularly from stages I to II, or can take place over days or weeks, most often as stage III evolves to stage IV. Because of more prompt recognition and treatment of pericarditis, not all stages may be exhibited.
4 The ST elevation seen in pericarditis is usually distinguished from that of acute MI by the absence of Q waves, upward ST segments, and the absence of associated T wave inversion.
13 In research examining the cause of ST segment abnormalities in emergency department
chest pain patients, pericarditis was found in 1% of the study population.
14
Evaluation of laboratory results almost always reveals an elevated erythrocyte sedimentation rate. Leukocytosis is present early but, depending on etiology, may give way to lymphocytosis. Serum cardiac enzymes are frequently normal unless the myocardium is involved, and then they give some indication as to the degree of involvement. In a study on viral or idiopathic pericarditis, troponin I elevation was frequently observed (32% of cases) and associated with young age, male gender, ST segment elevation, and pericardial effusion at presentation.
15 It is uncertain if elevated troponin I levels have any prognostic value.
15
In some parts of the world, such as South Africa, tuberculosis is a major health problem, and can be complicated by tuberculosis
pericarditis. The need for early diagnosis has led to emphasis on biochemical tests such as the pericardial adenosine deaminase test, and the use of interferon as an indicator of pericardial disease due to tuberculosis.
16
Echocardiography is critical to assess the pericardium in pericardial disease. Computed tomography (CT) and magnetic resonance imaging (MRI) allow examination of the entire chest, so abnormalities that might be related to the pericardial findings can be assessed.
Medical Management
The goal of treatment in acute pericarditis is to relieve pain and prevent complications.
9 Treatment of the underlying cause is also a priority. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment. Ibuprofen is preferred by many clinicians due to its rare side effects, favorable impact on coronary flow, and large dose range.
2 Depending on the severity and response, 300 to 800 mg every 6 to 8 hours may be initially required, and is best continued until the effusion is resolved, which may be days or weeks.
11 Aspirin (325 to 650 mg four times a day) is also commonly used to treat pericarditis.
3 Gastrointestinal protection during NSAID therapy is important.
3,
11,
17 Colchicine (0.5 or 6 mg b.i.d.) added to an NSAID or as monotherapy also appears to be effective in initial episodes, and to prevent recurrences.
11,
12 Systemic corticosteroid therapy is recommended only in connective tissue diseases, autoreactive or uremic pericarditis.
3,
11 Intrapericardial corticosteroids have been effective and do not cause systemic side effects.
11
Pericarditis due to bacterial infections such as tuberculosis is treated by directing treatment to the cause. The mainstay of treatment of tuberculosis pericarditis in Africa is the 6-month course of antituberculosis drugs recommended by the World Health Organization.
18 Pericardiocentesis is recommended in all patients suspected of tuberculosis to facilitate diagnosis.
19
Constrictive Pericarditis.
Constrictive pericarditis results from a scarred, and often thickened and calcified pericardium that limits diastolic ventricular filling.
20 Tuberculosis is responsible for most cases of constrictive pericarditis in Africa and Asia.
21 Other causes of constrictive pericarditis are idiopathic, postradiation, and postsurgical.
22,
23
The often thickened, adherent pericardium restricts ventricular filling and limits chamber expansion and maximal diastolic volumes. End-diastolic pressures in all heart chambers are typically elevated and equalized. During classic constriction, Kussmaul’s sign, inspiratory jugular venous distention, replaces the normal inspiratory venous “collapse” that reflects a normal inspiratory decrease of 3 to 7 mm Hg in right atrial pressure. This sign is a hallmark of constrictive pericarditis.
2 Patients present with signs of heart failure, although pulmonary edema is usually not a feature.
3,
24
A calcified pericardium is often visible on chest x-ray film.
25,
26 CT, MRI, and echocardiography are tools also used to diagnose constrictive pericarditis.
3 CT allows detection of calcification that occurs in restrictive pericarditis.
5 Many abnormal findings can be seen on the echocardiogram that indicate constrictive pericarditis, such as premature opening of the pulmonic valve and rapid posterior motion of the left ventricular posterior wall in early diastole, with little or no posterior motion during the rest of diastole. However, these findings are not specific for constrictive pericarditis and can be caused by other conditions, such as restrictive cardiomyopathy (RCM).
27,
28
Pericardiectomy, surgical removal of the pericardium, is the treatment for symptomatic constrictive pericarditis.
24 The procedure may be either a total or a partial pericardiectomy. In a recent study, total pericardiectomy was associated with lower perioperative and late mortality, as well as a better hemodynamic condition for the patient.
22 Idiopathic etiology was associated with better outcomes in two studies.
22,
24
Recurrent Pericarditis.
Recurrent pericarditis is a complication of acute pericarditis. Recurrence is diagnosed by recurrent pain and one or more of the following signs: fever, pericardial friction rub, ECG changes, effusion on echocardiography, and elevation of white blood count, C-reactive protein level, or the erythrocyte sedimentation rate.
17 The rate of recurrence is reported to vary from 15% to 50%. It is considered an autoimmune phenomenon.
17 Imazio et al.
17,
29 found an increased risk of recurrence if corticosteroids were used during treatment of the first episode of pericarditis. Risk factors for recurrence in another study were identified as female gender, previous use of corticosteroids, and previous recurrent pericarditis.
30 Use of colchicine along with NSAIDs during a first episode of pericarditis has been found to decrease recurrence.
29
Approximately 20% of pericarditis patients have a recurrence within months, or rarely, within years.
31 In a systematic review spanning 40 years of literature on patients with idiopathic recurrent pericarditis, the complication rate of pericardial tamponade was 3.5%, and no patients developed constrictive pericarditis.
32
Pericarditis Associated With MI
Early Acute Post-MI Pericarditis.
In the immediate period after MI, an early pericardial syndrome may develop and then resolve over a period of approximately 1 week. Pericardial involvement is correlated to infarct size.
33 The ECG shows a typical pattern of pericarditis and is helpful in differentiating between pericardial and ischemic pain. Pericardial friction rubs may be heard. As in all pericarditis, rubs are virtually 100% specific, but sensitivity depends on frequency of auscultation, because they tend to come and go over hours.
12 The course is usually benign, and treatment consists of aspirin or other NSAIDs. Treatment of MI with thrombolysis and mechanical revascularization appear to have reduced the incidence of this form of pericarditis by at least 50%.
33
Dressler’s Syndrome.
Dressler’s syndrome of chest pain, pleurisy, pericarditis with friction rub, severe malaise, moderate fever, and leukocytosis occurs 3 weeks to several months post-MI. The underlying pathologic process is unknown, but it is thought to reflect a late autoimmune reaction mediated by antibodies to circulating antigens.
34 In contrast to early post-MI pericarditis, inflammation is diffuse and not localized to the myocardial injury site.
33