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Drugs & Diseases > Cardiology

ACUTE PERICARDITIS

Updated: Apr 02, 2019
* Author: Sean Spangler, MD; Chief Editor: Terrence X O'Brien, MD, MS, FACC
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Sections
Acute Pericarditis

* Sections Acute Pericarditis
* Overview

* Practice Essentials
* Background
* Anatomy
* Pathophysiology
* Etiology
* Epidemiology
* Prognosis
* Show All
* Presentation

* History
* Physical Examination
* Show All
* DDx
* Workup

* Approach Considerations
* Routine Laboratory Studies
* Chest Radiography
* Echocardiography
* Computed Tomography Scanning
* Magnetic Resonance Imaging
* Electrocardiography
* Pericardiocentesis
* Pericardial Fluid Analysis
* Other Procedures
* Show All
* Treatment

* Approach Considerations
* Prehospital Care
* Emergency Department Care
* Treatment of Specific Types of Pericarditis
* Pericardiectomy and Other Surgical Procedures
* Complications
* Consultations and Long-Term Monitoring
* Diet and Activity
* Show All
* Medication

* Medication Summary
* Nonsteroidal anti-inflammatory drugs
* Anti-inflammatory agents
* Salicylates
* Corticosteroids
* Show All
* Questions & Answers
* Media Gallery
* References

Overview

PRACTICE ESSENTIALS

Acute pericarditis is an inflammation of the pericardium characterized by
pericarditic chest pain, pericardial friction rub, and serial
electrocardiographic (ECG) changes (eg, new widespread ST-elevation or PR
depression; new/worsening pericardial effusion). [1, 2, 3, 4] The first and last
stages of ECG changes are seen in the images below.

Stage 1 electrocardiograph changes in a patient with acute pericarditis.
View Media Gallery

Stage 4 electrocardiograph changes in the same patient as in the previous image,
taken approximately 3 months after acute pericardial illness. The patient
remained symptom free despite continued T-wave inversion.
View Media Gallery

SIGNS AND SYMPTOMS

Chest pain is the cardinal symptom of pericarditis, usually precordial or
retrosternal with referral to the trapezius ridge, neck, left shoulder, or arm.
Common associated signs and symptoms include low-grade intermittent fever,
dyspnea/tachypnea (a frequent complaint and may be severe, with myocarditis,
pericarditis, and cardiac tamponade), cough, and dysphagia. In tuberculous
pericarditis, fever, night sweats, and weight loss are commonly noted (80%).

Specific causes of pericarditis include the following:

* Idiopathic causes

* Infectious conditions, such as viral, bacterial, and tuberculous infections

* Inflammatory disorders, such as RA, SLE, scleroderma, and rheumatic fever

* Metabolic disorders, such as renal failure and hypothyroidism

* Cardiovascular disorders, such as acute MI, Dressler syndrome, and aortic
dissection

* Miscellaneous causes, such as iatrogenic, neoplasms, drugs, irradiation,
sarcoidosis, cardiovascular procedures, and trauma

See Presentation for more detail.

DIAGNOSIS

Initial evaluation includes a clinical history and physical examination, ECG,
echocardiography, chest radiography, and lab studies.

ECG can be diagnostic in acute pericarditis and typically shows diffuse ST
elevation. The ratio of the amplitude of ST segment to the amplitude of the T
wave in leads I, V4, V5, and V6 on electrocardiogram can be used to
differentiate acute pericarditis (AP) from early repolarization (ER) and early
repolarization of left ventricular hypertrophy (ERLVH), according to a recent
study. When ST elevation was present in lead I, the ST/T ratio had the best
predictive value for discriminating between AP, ER and ERLVH. The study involved
25 patients with AP, 27 with ER, and 28 with ERLVH. [5]

Echocardiography is indicated if pericardial effusion is suspected on clinical
or radiographic grounds, the illness lasts longer than 1 week, or myocarditis or
purulent pericarditis is suspected.

A chest radiograph is helpful to exclude pulmonary conditions that may be
responsible for or are associated with the cause of pericarditis (ie, cancer,
infection, SLE, sarcoidosis, etc). It is not helpful for evaluating the presence
of pericardial fluid, as patients with small effusions (less than a few hundred
milliliters) may present with a normal cardiac silhouette; it is only helpful
for diagnosing fluid in patients with effusions larger than 250 mL.

Laboratory tests may include CBC; serum electrolyte, blood urea nitrogen (BUN),
and creatinine levels; erythrocyte sedimentation rate (ESR) and C-reactive
protein (CRP) levels; and cardiac biomarker measurements, lactate dehydrogenase
(LDH), and serum glutamic-oxaloacetic transaminase (SGOT; AST) levels. Serum
titers for suspected infectious etiologies and testing for tuberculosis exposure
(ie, PPD or interferon-gamma release assays) may be helpful.

See Workup for more detail.

MANAGEMENT

Treatment for specific causes of pericarditis is directed according to the
underlying cause. For patients with idiopathic or viral pericarditis, therapy is
directed at symptom relief.

Pharmacologic treatment

Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstays of
therapy. NSAID agents have a similar efficacy, with relief of chest pain in
about 85-90% of patients within days of treatment. A full-dose NSAID should be
used, and treatment should last 7-14 days.

Colchicine, alone or in combination with aspirin or an NSAID, can be considered
as first-line therapy as an adjunct for patients with acute pericarditis,
particularly to prevent recurrences. [3, 4]

Corticosteroids should not be used for initial treatment of pericarditis unless
it is indicated for the underlying disease, the patient’s condition has no
response to NSAIDs or colchicine, or both agents are contraindicated.

Surgical treatment

Surgical procedures for pericarditis include pericardiectomy,
pericardiocentesis, pericardial window placement, and pericardiotomy.

Pericardiectomy is the most effective surgical procedure for managing large
effusions, because it has the lowest associated risk of recurrent effusions.
This procedure is used for constrictive pericarditis, effusive pericarditis, or
recurrent pericarditis, steroid dependence, and/or intolerance to other medical
management.

Patients with effusions larger than 250 mL, effusions in which size increases
despite intensive dialysis for 10-14 days, or effusions with evidence of
tamponade are candidates for pericardiocentesis.

Pericardial window placement is used for effusive pericarditis therapy. In
critically ill patients, a balloon catheter may be used to create a pericardial
window, in which only 9 cm2 or less of pericardium is resected.

Consider subxiphoid pericardiotomy for large effusions that do not resolve. This
procedure may be performed under local anesthesia and has a lower risk of
complications than pericardiectomy.

See Treatment and Medication for more detail.

Next: Background

BACKGROUND

Acute pericarditis is an inflammation of the pericardium characterized by
pericarditic chest pain, pericardial friction rub, and serial
electrocardiographic (ECG changes (eg, new widespread ST-elevation or PR
depression; new/worsening pericardial effusion). [1, 2, 3] {ref4 Pericarditis
and cardiac tamponade involve the potential space surrounding the heart or
pericardium; pericarditis is one cause of fluid accumulation in this potential
space, and cardiac tamponade is the hemodynamic result of fluid accumulation.

For more information, see the Medscape Drugs and Diseases articles Constrictive
Pericarditis, Effusive-Constrictive-Pericarditis, Pediatric Infective
Pericarditis, and Imaging in Constrictive Pericarditis.

For patient education information, see the Cholesterol Center and Heart Health
Center, as well as Pericarditis, Heart Attack, and Chest Pain.

Previous
Next: Background

ANATOMY

The pericardium (pericardial complex) serves as a protective barrier from the
spread of infection or inflammation from adjacent structures. It is composed of
the parietal pericardium (an outer fibrous layer) and the visceral pericardium
(an inner serous membrane made of a single layer of mesothelial cells). The
fibrous pericardium is a flask-shaped, tough outer sac with attachments to the
diaphragm, sternum, and costal cartilage. The visceral pericardium is thin,
adjacent to the surface of the heart, and attached to the epicardial fat; it
reflects back on itself to form the parietal pericardium.

The pericardium normally contains as much as 20-50 mL of an ultrafiltrate of
plasma. Approximately 90-120 mL of additional pericardial fluid can accumulate
rapidly in the pericardium without an increase in pressure. The capacity of the
atria and ventricles to fill is mechanically compromised with further fluid
accumulation, which can result in marked increases in pericardial pressure,
eliciting reduced stroke volume, decreased cardiac output, and hypotension
(cardiac tamponade physiology). The rapidity of fluid accumulation influences
the hemodynamic effect. With slow accumulation of fluid, the pericardium has
time to stretch and accommodate the fluid increase so that hemodynamic
compromise does not ensue. Drainage of the pericardium occurs via the thoracic
duct and the right lymphatic duct into the right pleural space.

Previous
Next: Background

PATHOPHYSIOLOGY

Pericardial physiology includes three main functions. First, through its
mechanical function, the pericardium promotes cardiac efficiency by limiting
acute cardiac dilation, maintaining ventricular compliance with preservation of
the Starling curve, and distributing hydrostatic forces. The pericardium also
creates a closed chamber with subatmospheric pressure that aids atrial filling
and lowers transmural cardiac pressures. Second, through its membranous
function, the pericardium shields the heart by reducing external friction and
acting as a barrier against extension of infection and malignancy. Third,
through its ligamentous function, the pericardium anatomically fixes the heart.

In most cases of acute pericarditis, the pericardium is acutely inflamed and has
an infiltration of polymorphonuclear (PMN) leukocytes and pericardial
vascularization. Often, the pericardium manifests a fibrinous reaction with
exudates and adhesions. The pericardium may develop a serous or hemorrhagic
effusion. A granulomatous pericarditis occurs with tuberculosis, fungal
infections, rheumatoid arthritis (RA), and sarcoidosis. In recurrent
pericarditis, the innate immune system appears to play a role in its
pathogenesis. [6, 7]

Uremic pericarditis is thought to result from inflammation of the visceral and
parietal layers of the pericardium by metabolic toxins that accumulate in the
body owing to kidney failure. Other factors may be involved, however, because
pericarditis also may occur in patients with chronic renal failure who are
already receiving dialysis therapy.

Previous
Next: Background

ETIOLOGY

The underlying cause of pericarditis may be infectious or noninfectious. [1] In
developed nations, although pericarditis is predominantly referred to as
idiopathic, the most frequent causes are autoreactive/lymphocytic, malignant,
and infectious. [6]

A retrospective study (2004-2014) that evaluated the etiology of acute
pericarditis in 32 children found that the most common cause was infectious
(34%), followed by inflammatory disorders (28%). [8] Staphylococcus aureus was
the responsible agent in four of five cases of purulent pericarditis; all five
patients also had concurrent infection of the soft tissue, bone, lung, or other.
Other infectious agents included Histoplasma capsulatum, Mycoplasma pneumoniae,
influenza A, and Enterovirus. [8]

This section will first briefly discuss acute pericarditis, chronic
pericarditis, and cardiac tamponade; then, several specific entities that cause
pericarditis will be briefly reviewed.

ACUTE PERICARDITIS

Serous pericarditis is usually caused by noninfectious inflammation such as
occurs in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).
Fibrous adhesions rarely occur.

Fibrous and serofibrinous pericarditis represent the same basic process and are
the most frequent type of pericarditis. Common causes include acute myocardial
infarction (MI), postinfarction (including Dressler syndrome), uremia,
radiation, RA, SLE, and trauma. Severe infections may also cause a fibrinous
reaction, as does routine cardiac surgery.

Purulent or suppurative pericarditis due to causative organisms may arise from
direct extension, hematogenous seeding, lymphatic extension, or by direct
introduction during cardiotomy. Immunosuppression facilitates this condition.
Clinical features include fever, chills, and spiking temperatures. Constrictive
pericarditis is a serious potential complication.

Hemorrhagic pericarditis involves blood mixed with a fibrinous or suppurative
effusion, and it is most commonly caused by tuberculosis or direct neoplastic
invasion. This condition can also occur in severe bacterial infections or in
patients with a bleeding diathesis. Hemorrhagic pericarditis is common after
cardiac surgery or trauma and may cause tamponade. The clinical significance is
similar to suppurative pericarditis.

Until proven otherwise, caseation within the pericardial sac is tuberculous in
origin. Untreated, caseous pericarditis is the most common antecedent to chronic
constrictive pericarditis of a fibrocalcific nature.

CHRONIC PERICARDITIS

Adhesive mediastinopericarditis is a reaction that usually follows suppurative
or caseous pericarditis, cardiac surgery, or irradiation. This condition is
rarely caused by a simple fibrinous exudate. The pericardial potential space is
obliterated, and adhesion of the external surface of the parietal layer to
surrounding structures occurs. Clinically, systolic contraction of the ribcage
and diaphragm and pulsus paradoxus may be observed. The increased workload may
cause massive cardiac hypertrophy and dilatation, which can mimic an idiopathic
cardiomyopathy.

Constrictive pericarditis is usually caused by suppurative, caseous, or
hemorrhagic pericarditis. The heart may become encased in a 0.5-cm–thick to
1-cm–thick layer of scar or calcification (concretio cordis), resembling a
plaster mold. Contrary to clinical findings in adhesive mediastinopericarditis,
the heart cannot become hypertrophic or dilate because of insufficient space.

Imazio et al suggest that constrictive pericarditis is a rare complication of
viral or idiopathic acute pericarditis (< 0.5%). However, it appears to be
comparatively frequent for specific etiologies, especially bacterial. [9]

CARDIAC TAMPONADE

Tamponade is more common in patients with malignant pericarditis. Effusions
caused by tumors often progress to tamponade, eliciting bleeding in the
pericardium. Blood accumulates more rapidly than a transudate or exudate and
more commonly causes tamponade.

Identification of any pericardial fluid in the setting of penetrating injury to
the thorax or upper abdomen requires aggressive resuscitation; penetrating
cardiac injuries may occur, with hemopericardium as the most common feature. In
acute massive hemopericardium, the time is insufficient for defibrination to
occur. The hemopericardium organizes and may partially clot, resulting in a
pericardial hematoma. The hematoma may appear echogenic instead of echo free.

Potential sources of iatrogenic cardiac perforation include central line
placement, pacemaker insertion, cardiac catheterization, sternal bone marrow
biopsies, and pericardiocentesis. The right atrium is the most common site of
perforation from catheter placement. Perforation, as well as direct catheter
infusion of fluids, can cause tamponade. In fact, a tamponade delay of hours to
days has occurred secondary to catheter misplacement.

In one case report, tamponade was described as the first manifestation of
dermatopolymyositis. [10]

Specific causes of pericarditis include the following and are briefly reviewed
below:

* Idiopathic causes

* Infectious conditions, such as viral, bacterial, and tuberculous infections

* Inflammatory disorders, such as RA, SLE, scleroderma, and rheumatic fever

* Metabolic disorders, such as renal failure, hypothyroidism, and
hypercholesterolemia

* Cardiovascular disorders, such as acute MI, Dressler syndrome, and aortic
dissection

* Miscellaneous causes, such as iatrogenic, neoplasms, drugs, irradiation,
sarcoidosis, cardiovascular procedures, and trauma

IDIOPATHIC CAUSES

Between 26% and 86% of cases of acute pericarditis are idiopathic in nature.
[11] No clinical features distinguish idiopathic cases from viral pericarditis.
It is likely that most idiopathic cases are undiagnosed viral infections.
Seasonal peaks occur in spring and fall.

More recently, there has been evidence that the innate immune system and
autoinflammation contribute to acute and recurrent pericarditis. [6, 7]

Chronic idiopathic pericarditis is defined as a pericardial effusion that
persists more than 3 months without any apparent etiology. Pericardiocentesis
alone results in resolution of large effusions; however, recurrence is common.

VIRAL INFECTION

Viral infection is the most common cause of acute pericarditis and accounts for
1-10% of cases. The disease is usually a short self-limited disease that lasts
1-3 weeks and can occur as seasonal epidemics, especially coxsackievirus B and
influenza.

Causative viruses include coxsackievirus B, [12] echovirus, adenoviruses,
influenza A and B viruses, enterovirus, mumps virus, Epstein-Barr virus, human
immunodeficiency virus (HIV), herpes simplex virus (HSV) type 1,
varicella-zoster virus (VZV), measles virus, parainfluenza virus (PIV) type 2,
and respiratory syncytial virus (RSV), cytomegalovirus (CMV), and hepatitis
viruses A, B, and C (HAV, HBV, HCV, respectively).

Patients may have associated myocarditis. Pericardial involvement is frequent in
persons with HIV, but is usually an asymptomatic pericardial effusion of small
volume. Individuals with advanced HIV infection develop pericardial involvement
more frequently, with one study noting right atrial diastolic compression in 5%
of cases involving advanced HIV infection. [13] Symptomatic pericarditis occurs
in less than 1% of cases involving HIV, and its etiology can include the usual
causes, opportunistic infection, Kaposi sarcoma, and HIV.

BACTERIAL INFECTION

Bacterial infections accounts for 1-8% of pericarditis cases and result from
direct pulmonary extension, hematogenous spread, myocardial abscess or
endocarditis, penetrating injury to chest wall from either trauma or surgery, or
a subdiaphragmatic suppurative lesion. Purulent pericarditis may result from
previous aseptic pericarditis, and a high percentage of patients develop
constrictive pericarditis.

Organisms that have been isolated include gram-positive species such as
Streptococcus pneumoniae and other Streptococcus species and Staphylococcus.
[14] Isolated gram-negative species include Proteus, Escherichia coli,
Pseudomonas, Klebsiella, Salmonella, Shigella, Neisseria meningitidis, and
Haemophilus influenzae.

Less common organisms include Legionella, Nocardia, Actinobacillus, Rickettsia,
Borrelia burgdorferi (Lyme borreliosis), Listeria, Leptospira, Chlamydophila
psittaci, and Treponema pallidum (syphilis).

Anaerobes have also been isolated in 40% of patients in reviews of the pediatric
population.

Previously, Pneumococcus was the predominant organism. However, in the
antibiotic era, staphylococcal and gram-negative species have become more
common. Most cases are now associated with thoracic surgery, renal disease, and
immunosuppression.

TUBERCULOUS INFECTION

Tuberculosis accounts for 4% of cases and should be considered in all instances
of pericarditis without a rapid course, especially in high-risk groups, such as
elderly patients in nursing homes and those with acquired immunodeficiency
syndrome (AIDS). [15] Approximately 50% of affected patients develop
constrictive pericarditis. On rare occasion, acute purulent pericarditis is
caused by coinfection with Mycobacterium tuberculosis and S aureus, and this may
be the first manifestation of infection with human immunodeficiency virus (HIV).
[16]

FUNGAL AND PARASITIC INFECTION

Fungal organisms that may cause acute pericarditis include Histoplasma,
Blastomyces, Coccidioides, Aspergillus, and Candida. Parasitic organisms include
Entamoeba, Echinococcus, and Toxoplasma.

UREMIA

The putative toxins suggested to precipitate uremic pericarditis when they
accumulate are poorly characterized, but they may include urea, creatinine,
methylguanidine, guanidinoacetate, parathyroid hormone, beta2-microglobulin,
uric acid, and others. More than one toxin apparently may be involved, although
considerable controversy surrounds this point.

The precise pathogenetic changes induced by these toxins when causing uremic
pericarditis have not been elucidated, although a rough correlation with the
degree and the duration of azotemia exists; the blood urea nitrogen (BUN) level
is usually greater than 60 mg/dL (22 mmol/L). Uremic pericarditis may be
associated with hemorrhagic or serous effusion, although considerable overlap
exists. Hemorrhagic effusions are more common and result in part from
uremia-induced platelet dysfunction.

Some authors distinguish between 2 types of pericarditis in patients with renal
failure. One type is uremic pericarditis, which occurs in patients with uremia
who have never received dialysis. The other type is dialysis-associated
pericarditis, which occurs in patients who are already receiving dialysis. In
the latter case, inadequate dialysis may usually be implicated, because
aggressive dialysis often leads to resolution. Other causes of
dialysis-associated pericarditis may include volume overload
and bacterial or viral infections.

In an observational study that employed data from 88 maintenance hemodialysis
patients, investigators found that intensive dialysis is the most effective
treatment for dialysis-associated pericarditis in patients on dialysis who have
diabetes and those who do not. [17] Following the intensification of
hemodialysis, pericarditis improved in 85.1% of patients with diabetes and in
82.9% of those without diabetes. Among patients with diabetes, 85.1% survived
without recurrence of pericarditis, 4.3% survived but did suffer recurrence, and
10.6% died, with similar outcomes recorded in the group without diabetes (87.8%,
4.9%, and 7.3%, respectively). [17]

RHEUMATOID ARTHRITIS

Pericarditis occurs predominantly in males with severely destructive and nodular
RA. The pericardial involvement is usually clinically silent, with the diagnosis
made in only 2% of adults and 6% of juveniles with RA. Rarely, pericarditis
precedes the onset of RA. Autopsy studies show a pericarditis prevalence of
11-50%.

SYSTEMIC LUPUS ERYTHEMATOSUS, SCLERODERMA, SARCOIDOSIS

Clinically evident pericarditis has been reported in 25% of patients with SLE
and usually occurs in lupus flare-ups, but it may be the presenting
manifestation. Autopsy series reveal pericardial involvement in 62% of lupus
patients.

Pericarditis is recognized in 5-10% of patients with scleroderma, with a 70%
autopsy prevalence. Pericardial effusions occur in 40% of patients with
scleroderma and can be due to scleroderma, myocardial failure (restrictive
cardiomyopathy), and renal failure. Restrictive cardiomyopathy and pericardial
constriction can coexist. Usually, pulmonary hypertension, right heart failure,
and systolic dysfunction occur.

Sarcoidosis may result in pericarditis, but this condition rarely causes cardiac
tamponade or constrictive pericarditis

RHEUMATIC FEVER

Pericarditis in those with rheumatic fever occurs more commonly in lower
socioeconomic groups and in children, often accompanying endocarditis and
myocarditis, with a worse prognosis. Consider rheumatic fever as an etiology in
any child with pericarditis. However, this disease is not a demonstrated cause
of constrictive pericarditis.

In adults, pericarditis may not occur with myocardial or valvular involvement,
and it is associated with a better prognosis. The pericarditis usually appears
7-10 days after the onset of fever and arthritis. Often, stage 1
electrocardiographic (ECG) findings are absent (see Electrocardiography).

OTHER INFLAMMATORY CONDITIONS

The following conditions may also cause acute pericarditis:

* Sjögren syndrome

* Mixed connective-tissue disease

* Reiter syndrome

* Ankylosing spondylitis

* Inflammatory bowel disease

* Wegener granulomatosis

* Vasculitis (eg, giant cell arteritis, polyarteritis)

* Polymyositis

* Behçet syndrome

* Whipple disease

* Familial Mediterranean fever

* Serum sickness

RENAL FAILURE

Richard Bright described uremic pericarditis in 1836. Since that classic
description, this common complication of chronic renal failure has evolved from
an ominous event heralding the terminal stages of disease to an event that, with
early management, is likely to have a good outcome. Furthermore, advances in
dialysis technology with early and timely management of chronic renal failure
have dramatically reduced the prevalence of uremic pericarditis. Uremic
pericarditis has a prevalence of 6-10% in patients with acute or chronic renal
failure, and it continues to be associated with significant morbidity and
occasional mortality.

Renal failure accounts for approximately 12% of cases of pericarditis. In the
predialysis era, pericarditis developed in 35-50% of patients with uremia who
had chronic renal failure and less commonly in those with acute renal failure.
Death often followed in several weeks. With dialysis, the pericarditis incidence
rate is less than 10%; however, this condition occurs after the onset of
dialysis in 8-12% of cases.

Asymptomatic pericardial effusions can occur in 36-62% of patients with uremia
who require dialysis; these effusions are often small to moderate in size and
can occur secondary to volume overload. Pericardial effusions can lead to
significant hemodynamic complications during routine dialysis. Moreover, the
presence of a large pericardial effusion that persists for longer than 10 days
after intensive dialysis has a high likelihood of causing tamponade.

HYPOTHYROIDISM

Hypothyroidism accounts for as many as 4% of pericarditis cases. In fact,
myocardial involvement is common, and pericardial involvement usually occurs
with severe hypothyroidism. Patients may develop large pericardial effusions,
but they rarely develop tamponade.

CHOLESTEROL PERICARDITIS

Cholesterol pericarditis, also called gold-paint pericarditis, is a complication
of a chronic pericardial effusion exacerbated by cholesterol crystals. It
usually presents with large effusions that are not hemodynamically important,
and development of constriction is rare. Granulomatous pericarditis has been
implicated in some cases.

MYOCARDIAL INFARCTION

After a transmural infarction, a fibrinous pericardial exudate appears within 24
hours, begins to organize at 4-8 days, and completes organization at 4 weeks.
[18, 19] Pericardial pain occurs less frequently than the friction rub, which is
often detected on the second or third day after an acute MI but may be heard
within 24 hours and as late as 10 days.

Before thrombolytic therapy, infarct-associated pericarditis ranges from 7% to
23% of cases. At autopsy in one study, almost all patients were noted to have
localized fibrinous pericarditis overlying the area of infarction. With
thrombolytic therapy and direct infarct angioplasty, the incidence of
post–MI-associated pericarditis has decreased to 5-8%.

Overall, pericardial involvement indicates a larger infarction, greater
incidence of left ventricular dysfunction, and greater mortality. The
pericarditis usually heals without consequence; effusions may occur, but they
rarely lead to tamponade.

DRESSLER SYNDROME

Dressler syndrome is now considered rare. When pericarditis associated with
Dressler syndrome does occur, it is usually observed 2-3 weeks after a
myocardial infarction. Initially, the syndrome was described in as many as 4% of
patients following and acute MI. Later studies suggested a much lower incidence.
Dressler syndrome is rarely described with pulmonary embolism.

This syndrome may be a unique autoimmune-mediated phenomenon to myocardial
antigens, or it may merely be an unrecognized post–MI pericarditis. Patients may
develop pulmonary infiltrates and large pericardial effusions.

Because of the risk of hemorrhagic pericarditis, anticoagulant therapy should be
stopped in patients with Dressler syndrome.

AORTIC DISSECTION AND TAKOTSUBO CARDIOMYOPATHY

Aortic dissection accounts for 1% of cases of acute pericarditis, especially for
cases with hemorrhage into the pericardium.

Takotsubo cardiomyopathy is a transient cardiac syndrome that involves left
ventricular apical akinesis and mimics acute coronary syndrome.

NEOPLASM

Malignancy account for 5-17% of pericarditis cases; in patients presenting with
acute pericarditis or pericardial effusion, 4-7% have an unsuspected malignancy.
Primary neoplasm of the heart and pericardium is rare; most cases of
neoplasm-related pericarditis are a result of metastatic disease. Autopsy
studies have noted that approximately 10% of patients with cancer develop
cardiac involvement, and it is often clinically silent. The neoplastic cells
reach the pericardium through the bloodstream, through the lymphatic system, or
via local growth.

Neoplastic disease, particularly advanced disease, is the most frequent cause of
tamponade in the hospital. Occasionally, the tumor encases the heart and causes
constrictive pericarditis rather than tamponade.

Pericardial mesothelioma and angiosarcoma are lethal malignancies with
aggressive local spread that respond poorly to treatment. Infants and children
can present with a teratoma in the pericardial space. These can often be
successfully removed.

Lung cancer, including adenocarcinoma and squamous and small cell carcinoma,
accounts for approximately 33% of cases; breast cancer accounts for 25%;
leukemia and lymphoma, including Hodgkin and non-Hodgkin, account for 15% of
cases; and malignant melanoma represents another 5%. Almost all other
malignancies, except primary brain, comprise the rest of the cases. Kaposi
sarcoma has also become a more prominent cause of neoplastic disease with the
AIDS epidemic.

DRUGS

Some medications, including penicillin and cromolyn sodium, induce pericarditis
through a hypersensitivity reaction. The anthracycline antineoplastic agents,
such as doxorubicin and cyclophosphamide, have direct cardiac toxicity and can
cause acute pericarditis and myocarditis.

Pericarditis can also develop from a drug-induced lupus syndrome caused by
medications including procainamide, hydralazine, methyldopa, isoniazid,
mesalazine, and reserpine. Methysergide causes constrictive pericarditis through
mediastinal fibrosis. Dantrolene, phenytoin, and minoxidil produce pericarditis
through an unknown mechanism.

Smallpox vaccination infrequently leads to myocarditis. In a review of a large
vaccination program in the US military, approximately 12 per 100,000 vaccinated
troops developed myopericarditis within 14 days of vaccination. [20, 21] Whether
this was due to a direct viral cytopathic effect or an immune-mediated
phenomenon is unclear.

IRRADIATION

Pericardial disease is the most common cardiac toxicity from radiation therapy.
Others are coronary artery disease, conduction disturbance, and myocardial and
valvular disease. [22] A high incidence of such toxicity occurs with high doses,
especially those greater than 4000 rad.

Radiation pericarditis can present as acute pericarditis, with or without
effusion; chronic constrictive pericarditis; or effusive-constrictive
pericarditis.

INVASIVE CARDIAC PROCEDURES

Electrophysiologic studies, radiofrequency ablation, pacemaker implantation, and
percutaneous coronary intervention are among several invasive cardiac procedures
that can cause pericarditis.

Postpericardiotomy syndrome is similar to Dressler syndrome, except that
postpericardiotomy syndrome occurs after cardiac surgery. Several series note an
incidence rate of 10-40%; approximately 1% of patients with postpericardiotomy
syndrome develop tamponade.

Pericardial effusions can occur in the absence of typical features of
postpericardiotomy syndrome. In one study, 56% developed pericardial effusions
early after cardiac surgery, without correlation to pericarditis or tamponade.
The effusions were more common after heavy postoperative bleeding.

TRAUMA

Approximately 1% of cases of acute pericarditis are caused by trauma, such as
penetrating and nonpenetrating cardiac trauma. Also consider esophageal rupture
or perforation and pancreatitis.

Previous
Next: Background

EPIDEMIOLOGY

Epidemiologic data on the incidence of acute pericarditis are lacking, likely
because this condition is frequently inapparent clinically, despite its presence
in numerous disorders. However, it appears to be the most common form of
pericardial disease and a relatively common cause of chest pain. [1]

Lorell noted a diagnosis of acute pericarditis in approximately 1 per 1000
hospital admissions. [23] In addition, acute pericarditis comprises 1% of
emergency room visits in patients with ST-segment elevation. [24] In fact, the
reported incidence of acute pericardial tamponade is approximately 2% of
penetrating trauma; however, this condition is rarely seen in blunt chest
trauma.

Uremic pericarditis may occur in 6-10% of patients with advanced renal failure
before initiation of dialysis. When patients with large effusions are studied,
uremia may account for up to 20% of cases in some series. The widespread
availability of dialysis has reduced the incidence of uremic pericarditis.

Malignant disease is the most common cause of pericardial effusion with
tamponade in developed countries; However, tuberculosis should be considered in
endemic areas.

Acute pericarditis is more common in men than in women. However, although this
condition is more common in adults than in children, adolescents are more
commonly affected than young adults. Nonetheless, Merce et al found no
difference in etiology, clinical course, and prognosis between elderly and
younger patients with moderate and large pericardial effusions. [25]

Previous
Next: Background

PROGNOSIS

The prognosis in individuals with pericarditis depends on the etiology of this
condition, as well as the presence of a pericardial effusion and/or tamponade.
Idiopathic and viral etiologies usually have a self-limited course, without any
risk of evolution toward constrictive pericarditis. [26, 27] Most post–MI cases
have a benign course; however, pericarditis is associated with larger infarcts,
and therefore, overall long-term mortality may be increased.

Poor prognostic factors include the following features at presentation [1, 3, 4]
:

* Temperature above 100.4ºF (38ºC)

* Subacute disease course

* Presence of a large pericardial effusion or tamponade

* Unsuccessful therapy with aspirin or nonsteroidal anti-inflammatory agents
after at least 1 week of therapy

Minor predictors of poor prognosis include the following [3, 4] :

* Myopericarditis

* Immunosuppression

* Trauma

* Oral anticoagulation therapy

Factors associated with the development of complicated pericarditis include the
following [28] :

* Early administration of high-dose corticosteroids

* Lack of colchicine treatment

* Elevated levels of high-sensitivity C-reactive protein

Patients with scleroderma or children with rheumatic fever and pericarditis have
a poor prognosis, and purulent, tuberculous, and neoplastic pericardial
involvement have more complicated courses with worse outcomes. Purulent
pericarditis is associated with a mortality rate nearing 100% for untreated
persons and a mortality rate of 12-40% for treated patients. The mortality rate
in tuberculous pericarditis approaches 50%.

Uremic pericarditis continues to be associated with significant morbidity and
occasional mortality. Of patients with uremic pericarditis, 3-5% may develop
hemorrhagic pericarditis.

For penetrating injuries, the prognosis depends heavily on the rapid
identification of tamponade. Mortality may occur in 3-5% of cases resulting from
cardiac tamponade or arrhythmias. Favorable factors include minor perforations,
isolated right ventricular wounds, systolic blood pressure more than 50 mm Hg,
and the presence of tamponade.

Clinical Presentation

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Media Gallery

* Stage 1 electrocardiograph changes in a patient with acute pericarditis.

* Stage 4 electrocardiograph changes in the same patient as in the previous
image, taken approximately 3 months after acute pericardial illness. The
patient remained symptom free despite continued T-wave inversion.

* Chest radiographs revealing markedly enlarged cardiac silhouette and
normal-appearing lung parenchyma in prepericardiocentesis (A) and
postpericardiocentesis (B). Courtesy of Zhi Zhou, MD.

* Recording of aortic pressure showing pulsus paradoxus. During inspiration,
systolic pressure declines 20 mm Hg. Courtesy of Zhi Zhou, MD.

* This ultrasonogram demonstrates a normal subcostal 4-chamber view of the
heart. The pericardium is brightly reflective (echogenic or white in
appearance). LA = left atrium; LV = left ventricle; RA = right atrium; RV =
right ventricle. Part B courtesy of Wikimedia Commons/Patrick J Lynch and C
Carl Jaffe.

* H&E stain, medium power magnification showing a rheumatoid nodule in
rheumatoid pericarditis, composed of histiocytes and scattered multinucleated
giant cells (lower right) surrounding necroinflammatory debris (upper left).

* Pap stain, high power magnification of adenocarcinoma metastatic to the
pericardium on pericardiocentesis with the red arrow showing a normal
mesothelial cell and the black arrowhead showing adenocarcinoma.

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CONTRIBUTOR INFORMATION AND DISCLOSURES

Author

Sean Spangler, MD Cardiologist, William Beaumont Army Medical Center

Sean Spangler, MD is a member of the following medical societies: American
College of Cardiology, American College of Physicians