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Acute pericarditis, a diffuse inflammation of the pericardial sac and superficial myocardium, has a number of underlying causes. These include infection (primarily viral), immunologic disorders, uremia, trauma, malignancy, cardiac ischemia and acute myocardial infarction (1). However, most pericardial diseases are caused by a limited number of relatively common processes that are generally easy to identify (2,3). The repercussions of these different etiologies can be classified into three basic types of clinical manifestations (2, 3, 4).

· The first type corresponds to symptoms derived from pericardial inflammation that essentially present as pericardial pain and fever.

· The second to symptoms due to pericardial effusion which, in its most severe form, may lead to cardiac tamponade.

· The third to symptoms due to thickening, retraction, and calcification of the pericardium, indicative of constrictive pericarditis (4).

In clinical practice using a traditional diagnostic approach, idiopathic and viral acute pericarditis is found in 80–90% of cases in immunocompetent patients from developed countries (5). The incidence of pericarditis in postmortem ranges from 1-6%, while it is diagnosed antemortem in only 0.1% of hospitalized patients and in 5% of patients seen in EDs with chest pain without myocardial infarction The possible sequelae of pericarditis include cardiac tamponade, recurrent pericarditis and pericardial constriction (6).


Acute pericarditis is inflammation of the pericardium that either occurs as an isolated process or with concurrent  myocarditis.

Constrictive pericarditis is characterized by compromised cardiac function caused by a thickened, rigid, and fibrous  pericardium secondary to acute pericarditis.



1. Most commonly viral

2. Bacterial  (tuberculosis, seen especially in constrictive pericarditis)

3. Fungal

4. Toxoplasmosis

· Myocardial infarction: pericarditis may occur either within  1–3 days as an immediate reaction (i.e., post- infarction   fibrinous pericarditis), or weeks to months following an acute myocardial infarction (Dressler syndrome).

· Postoperative (post- pericardiotomy syndrome): blunt or sharp trauma to the pericardium

· Collagen vascular disease: systemic lupus erythematosus,  rheumatoid arthritis

· Other causes: renal failure (uremia), tumors (Hodgkin lymphoma), radiation.

More than half of patients with pericarditis will present complaining of chest pain that may radiate to the back, neck or shoulders (7). The main pathognomonic sign of acute pericarditis is pericardial friction rub, detected by auscultation in approximately 60% to 85% of the cases. Such a finding allows definitive diagnosis of acute pericarditis, but diagnosis cannot be discarded in its absence. Friction rub is a scratchy superficial sound that is heard most strongly in the mesocardium and the lower left parasternal edge and that varies in strength with respiratory movements. It is normally louder when breathing in. Typically, friction rub has three components (presystolic caused by atrial contraction, systolic caused by ventricular contraction, and diastolic associated with the phase of rapid ventricular filling in the protodiastole) (8).

A pericardial friction rub is best heard at the lower sternal border or apex when the patient is sitting forward on his or her hands and knees. Other findings on physical exam may include fever (may reach 104◦F/40◦C) (9), cardiac dysrhythmias (e.g., premature atrial and ventricular contractions), tachypnea and dyspnea. Individuals with associated cardiac tamponade may show jugular venous distension, tachycardia, hypotension or pulsus paradoxus (9).

Markers of inflammation, such as white blood cell count, erythrocyte sedimentation rate, and serum C-reactive protein concentration, are usually elevated; however (10), these tests provide little information about the underlying cause of pericarditis and so are of limited use in devising a strategy for further management. It has been suggested that many patients with idiopathic acute pericarditis have an underlying viral infection; however, viral cultures and antibody titers have not proven to be clinically useful and the diagnosis of viral acute pericarditis does not alter management (11). Given the frequency of auto-immune disease as the underlying cause of acute pericarditis, routine serologic testing for antinuclear antibody and rheumatoid factor is of low yield and should be ordered only if the clinical presentation is suggestive of these diseases (12). The magnitude of the elevation in the serum troponin concentration appears to correlate with the magnitude of the ST- segment elevation, and the concentration usually returns to normal within one to two weeks after diagnosis (4, 12). An elevated troponin does not predict an adverse outcome, although a prolonged elevation (lasting longer than two weeks) suggests myocarditis, which has a worse prognosis (4, 5).

The 12-lead ECG in patients with acute pericarditis classically shows widespread upward concave ST-segment elevation and PR-segment depression (4). In addition, lead aVR on the ECG can demonstrate ST-segment depression and PR-segment elevation (2). The ECG abnormalities evolve through four classic stages (13). Stage I is characterized by ST-segment elevation, prominent T waves and PR- segment depression. Stage II is characterized by a normalization of the initial abnormalities, namely resolution of the ST-segment elevation. Stage III involves T wave inversion, usually in the same distribution where ST-segment elevation was encountered. Finally, Stage IV is a normalization of all changes with a return to the baseline ECG. Persistent ST-segment elevation and pathologic Q waves are not encountered in patients with pericarditis – these ECG findings should suggest another etiology (13).

The diagnostic test of choice for large effusions, cardiac tamponade and constrictive pericarditis is two- dimensional Doppler echocardiography. This imaging modality can demonstrate moderate or large effusions. In cardiac tamponade, Doppler examination may show the characteristic swinging motion of the heart that gives rise to electrical alternans on the ECG. Doppler studies are helpful in differentiating pericarditis from restrictive cardiomyopathy (14).

The signs and symptoms of pericarditis may be confused with ST-segment elevation myocardial infarction during the first few hours after onset. Nevertheless (4), certain features will generally allow correct differential diagnosis. Dissecting aortic aneurysm is rarely mistaken for pericarditis when the case history is recorded correctly because, unlike pericarditis, the onset of pain is sharp, very intense, and located in the back rather than the precordial region. It should be remembered, however, that an aortic aneurysm may hemorrhage into the pericardial sac, leading to cardiac tamponade (11, 14).

Most patients with idiopathic pericarditis can be managed conservatively, with a nonsteroidal anti-inflammatory drug (NSAID) such as indomethacin, ibuprofen or aspirin. These agents are believed to be equally effective (14). Colchicine (administered at a dose of 0.6 mg twice daily) appears to be effective alone or in combination with ibuprofen in treating acute pericarditis, although it has not been tested in randomized trials; it is preferred in patients who have recurrent pericarditis (4, 5). Patients who do not respond to an NSAID may need a short course of prednisone (5–10 mg per day for one to two weeks) (14).

When the identified etiology of acute pericarditis is not viral or idiopathic, management should be directed toward treating the underlying cause. Patients with no high-risk features can be managed as outpatients. Medical management for viral or idiopathic acute pericarditis has been centered on three major agents—NSAIDs, colchicine, and corticosteroids. The management and prognosis of patients with myopericarditis are similar to those of patients with acute pericarditis. Rarely, patients do not respond to this therapy or show evidence of recurrent pericarditis; these patients require a prolonged corticosteroid course (i.e.,several months).

Key Teaching Points:

· Pain from pericarditis typically worsens on inspiration and improves while sitting up and leaning forward.

· The 12-lead ECG in acute pericarditis classically shows widespread upward concave ST-segment elevation, PR segment depression and PR-segment elevation in lead aVR.

· Plasma troponin levels are elevated in 35–50% of patients with pericarditis, a finding thought to be caused by epicardial inflammation rather than myocyte necrosis.

· The most common physical finding in patients with pericarditis is a pericardial friction rub, which occurs in approximately 50–85% of cases.

Conflicts of interests None stated by the authors

Financing None stated by the authors.


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Lizzeth Karina Ordóñez Pérez 1

María Virginia Pinzón Fernández 2

Luisa Fernanda Zúñiga-Cerón 3

Jhan Sebastián Saavedra-Torres 4

       1- Doctor, Universidad del Cauca, Faculty of Health Sciences, Department of Internal Medicine, Health Research Group (GIS) - Popayán - Colombia.

2- Bacteriology, Esp. Education, Master's Degree in Public Health, PhD candidate in Medical Anthropology, Full Professor at Universidad del Cauca.

3- Student of medicine – Universidad Nacional de Colombia, Faculty of Medicine, Laboratory of the Field Corporation (DLC), Health Research Group

(GIS) - Popayán - Colombia.

4 -Student of medicine - Universidad del Cauca, Faculty of Health Sciences, Department of Internal Medicine, Corporación del Laboratorio al Campo

(DLC), Health Research Group (GIS) - Popayán - Colombia.