Acute Pericarditis - Clinical Presentation and Diagnosis - UpToDate

23/2/24, 14:11 Acute pericarditis: Clinical presentation and diagnosis - UpToDate
Official reprint from UpToDate®

www.uptodate.com © 2024 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
Acute pericarditis: Clinical presentation and diagnosis

AUTHOR: Massimo Imazio, MD, FESC, FHFA
SECTION EDITOR: Martin M LeWinter, MD
DEPUTY EDITOR: Susan B Yeon, MD, JD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2024.

This topic last updated: Feb 14, 2023.
INTRODUCTION
The pericardium is a fibroelastic sac made up of visceral and parietal layers separated by a
(potential) space, the pericardial cavity. In healthy individuals, the pericardial cavity contains
15 to 50 mL of an ultrafiltrate of plasma.
Diseases of the pericardium present clinically in one of several ways:
● Acute and recurrent pericarditis

● Pericardial effusion without major hemodynamic compromise
● Cardiac tamponade
● Constrictive pericarditis
● Effusive-constrictive pericarditis
Acute pericarditis refers to inflammation of the pericardial sac. The term myopericarditis, or
perimyocarditis, is used for cases of acute pericarditis that also demonstrate features
consistent with myocardial inflammation. (See 'Diagnosis' below.)
The clinical presentation and diagnostic evaluation for acute pericarditis will be reviewed
here. The etiology of pericarditis, treatment and prognosis of acute pericarditis, and other
pericardial disease processes are discussed separately. (See "Etiology of pericardial disease"
and "Acute pericarditis: Treatment and prognosis" and "Recurrent pericarditis" and
"Myopericarditis" and "Cardiac tamponade" and "Constrictive pericarditis: Diagnostic
evaluation" and "Pericardial effusion: Approach to diagnosis".)
https://www-uptodate-com.bibliotecavirtual.udla.edu.ec/contents/acute-pericarditis-clinical-presentation-and-diagnosis/print?search=pericarditis… 1/37
EPIDEMIOLOGY
Acute pericarditis is the most common disorder involving the pericardium. Epidemiologic
studies are largely lacking, and the exact incidence and prevalence of acute pericarditis are
unknown. However, acute pericarditis is recorded in approximately 0.1 to 0.2 percent of
hospitalized patients and 5 percent of patients admitted to the emergency department for
nonischemic chest pain [1,2].
● In an observational study from an urban area in northern Italy, the incidence of acute
pericarditis was 27.7 cases per 100,000 persons per year [3].
● In an observational study from Finland that included 670,409 cardiovascular admissions

to 29 hospitals across the country over a 9.5-year period, the standardized incidence
rate for pericarditis requiring hospitalization was 3.3 cases per 100,000 person-years
[1].
Acute pericarditis is a common disorder in several clinical settings, where it may be either the
first manifestation of an underlying systemic disease or represent an isolated process. In
developed countries, most cases of acute pericarditis are considered of possible or
confirmed viral origin, although the exact etiology of most cases remains undetermined
following a traditional diagnostic approach [2]. (See "Etiology of pericardial disease".)
Patients with human immunodeficiency virus (HIV) infection treated with antiretroviral
therapy who develop acute pericarditis have an etiologic spectrum very similar to non-HIV-
infected patients. However, HIV infection itself, along with tuberculosis, persist as major
causes of acute pericarditis in developing countries or in patients without access to
antiretroviral therapy. (See "Cardiac and vascular disease in patients with HIV", section on
'Pericardial disease'.)
CLINICAL FEATURES
Acute pericarditis can present with a variety of nonspecific signs and symptoms, depending
on the underlying etiology. The major clinical manifestations of acute pericarditis include
[2,4]:
● Chest pain – Typically sharp and pleuritic, improved by sitting up and leaning forward.
(See 'Chest pain' below.)
● Pericardial friction rub – A superficial scratchy or squeaking sound best heard with
the diaphragm of the stethoscope over the left sternal border. (See 'Pericardial friction
rub' below.)
● Electrocardiogram (ECG) changes – New widespread ST elevation and PR depression.

(See 'Electrocardiogram' below.)
● Pericardial effusion – A pericardial effusion is a common feature of pericarditis but is

not required for diagnosis. (See 'Echocardiogram' below.)
Patients with an infectious etiology may present with signs and symptoms of systemic
infection such as fever and leukocytosis. Viral etiologies in particular may be preceded by
"flu-like" respiratory or gastrointestinal symptoms. Patients with a known autoimmune
disorder or malignancy may present with signs or symptoms specific to their underlying
disorder.
Chest pain — The vast majority of patients with acute pericarditis present with chest pain
(>95 percent of cases) [5]. The chest pain of pericarditis must always be distinguished from
other common and/or life-threatening causes of chest pain ( table 1) such as myocardial
ischemia, pulmonary embolism, aortic dissection, gastroesophageal reflux disease, and
musculoskeletal pain. (See "Evaluation of the adult with chest pain in the emergency
department" and "Outpatient evaluation of the adult with chest pain".)
Chest pain that results from acute pericarditis is typically fairly sudden in onset and occurs
over the anterior chest. Unlike pain due to myocardial ischemia, chest pain due to
pericarditis is most often sharp and pleuritic in nature, with exacerbation by inspiration or
coughing [2]. One of the most distinctive features is the tendency for a decrease in intensity
when the patient sits up and leans forward. This position (seated, leaning forward) tends to
reduce pressure on the parietal pericardium, particularly with inspiration, and may also allow
for splinting of the diaphragm. Radiation of chest pain to the trapezius ridge has also been
considered to be fairly specific for pericarditis. In some patients, dull, oppressive pain may
occur; in such cases, it is more difficult to distinguish pericarditis from other causes of chest
pain.
Chest pain is likely to be present in cases of acute pericarditis caused by infection, but may
be minimal or absent in patients with uremic pericarditis or pericarditis associated with a
rheumatologic disorder (although in some patients, pleuritic chest pain and pericarditis can
be the initial presentation of systemic lupus erythematosus). (See "Pericardial involvement in
systemic autoimmune diseases".)
Pericardial friction rub — The presence of a pericardial friction rub on physical examination
is highly specific for acute pericarditis ( movie 1). Classically, pericardial friction rubs are
triphasic, with a superficial scratchy or squeaking quality. Pericardial friction rubs are often
intermittent, with an intensity that tends to wax and wane, and are best heard using the
diaphragm of the stethoscope. (See "Auscultation of heart sounds", section on 'Pericardial
friction rub and other adventitious sounds'.)
Pericardial friction rubs, which occur during maximal movement of the heart within its
pericardial sac, are said to be generated by friction between the two inflamed layers of the
pericardium. However, this commonly offered explanation for its mechanism may be an
oversimplification, as patients with a pericardial effusion may also have an audible friction
rub.
The classic pericardial friction rub consists of three phases, corresponding to movement of
the heart during atrial systole, ventricular systole, and the rapid filling phase of early
ventricular diastole. Patients in atrial fibrillation lack atrial systole, and therefore will have a
two-phase rub. Additionally, for uncertain reasons, some rubs are present only during one
(one component) or two phases (two components) of the cardiac cycle [6]. In a review of
auscultation and phonocardiography in 100 patients with a pericardial rub, the rub was
triphasic in 52 percent of patients, biphasic in 33 percent, and monophasic in 15 percent [6].
Pericardial rubs may be localized or widespread, but are usually loudest over the left sternal
border [6]. The intensity of the rub frequently increases after application of firm pressure
with the diaphragm, during suspended respiration, and with the patient leaning forward or
resting on elbows and knees ( picture 1). This last maneuver is designed to increase
contact between visceral and parietal pericardium, but is seldom used in practice since it is
cumbersome for the patient.
Friction rubs tend to vary in intensity and can come and go over a period of hours; therefore,
the sensitivity for detection of a rub is variable and depends in large part on the frequency of
auscultation. Pericardial rubs may be easier to hear in patients without a pericardial effusion,
but this finding is not universal and is not well documented. In a report of 100 patients with
acute pericarditis, a pericardial rub was present in 34 of 40 (85 percent) without an effusion
[7]. This prevalence is considerably higher than the 35 percent incidence of friction rubs
reported in another series [5].
Breath-holds during auscultation permit distinction of a pericardial friction rub from a

pleuropericardial or pleural rub. A pleuropericardial rub results from friction between the
inflamed pleura and the parietal pericardium, while a pleural rub is the result of friction
between the inflamed visceral and parietal pleura. As such, pleuropericardial and pleural
rubs can be heard only during the inspiratory phase of respiration. (See "Auscultation of
heart sounds", section on 'Pericardial friction rub and other adventitious sounds'.)
Electrocardiogram — The ECG in acute pericarditis may evolve through as many as four
stages with highly variable temporal evolution of ECG changes. The four typical stages of
ECG changes ( figure 1) in patients with acute pericarditis include:
Typical ECG findings
● Stage 1, seen in the first hours to days, is characterized by widespread ST elevation

(typically concave up) with reciprocal ST depression in leads aVR and V1
( waveform 1). There is also frequently an atrial current of injury, reflected by
elevation of the PR segment in lead aVR and depression of the PR segment in other
limb leads and in the left chest leads, primarily V5 and V6. Thus, the PR and ST
segments typically change in opposite directions. PR segment deviation, which is highly
specific, though less sensitive, is frequently overlooked.
The TP segment is recommended as the baseline for comparison when measuring both
PR and ST segment changes in acute pericarditis.
● Stage 2, typically seen in the first week, is characterized by normalization of the ST and
PR segments.
● Stage 3 is characterized by the development of diffuse T-wave inversions, generally

after the ST segments have become isoelectric. It is typically seen in the subacute
phase, and its duration is not well documented and likely highly variable.
● Stage 4 is represented by normalization of the ECG. It can occur directly from stage 1 in
self-limited cases or with prompt response to medical therapy.
Atypical ECG findings — Pericarditis does not always result in the typical ECG changes
described above. In many patients, the ECG returns to normal without going through the
above stages if the disease responds well to treatment or spontaneously resolves. Moreover,
some patients have no subepicardial inflammation, and the ECG remains normal, as
discussed below.
Atypical ECG changes are seen in up to 40 percent of patients with acute pericarditis [5].
Additionally, localized ST elevation and T-wave inversion occur before ST-segment
normalization in a minority of patients with acute pericarditis without myocardial
involvement. These changes can simulate ECG changes seen in patients with an acute
coronary syndrome. (See 'Differentiation from acute myocardial infarction' below and "ECG
tutorial: Myocardial ischemia and infarction" and "ECG tutorial: ST and T wave changes".)
Changes in the ECG in patients with acute pericarditis signify inflammation of the
epicardium, since the parietal pericardium itself is electrically inert. However, some causes of
pericarditis do not result in significant inflammation of the epicardium and, as such, may not
alter the ECG. An illustration of this is uremic pericarditis, in which there is prominent fibrin
deposition but little or no epicardial inflammation. As a result, the ECG often shows none of
the changes associated with pericarditis [8].
The temporal evolution of ECG changes with acute pericarditis is highly variable from one
patient to another. Treatment can accelerate or alter ECG progression. The duration of the
ECG changes in pericarditis also depends upon its cause and the extent of associated
myocardial damage [9].
Arrhythmias — Sustained arrhythmias are uncommon in acute pericarditis, except in the

postthoracotomy setting. This was illustrated in a review of 100 consecutive patients in which
only seven arrhythmias were identified; all were atrial and all occurred in patients with
underlying heart disease [10]. In a separate report comparing patients with myopericarditis
and uncomplicated acute pericarditis, cardiac arrhythmias were more commonly present in
patients with myopericarditis (odds ratio 17.6, 95% CI 5.7-54.1) [3]. Thus, the presence of
atrial or ventricular arrhythmias is suggestive of concomitant myocarditis or an unrelated
cardiac disease.
Differentiation from acute myocardial infarction — While both acute pericarditis and
acute myocardial infarction (MI) can present with chest pain and elevations in cardiac
biomarkers, the ECG changes in acute pericarditis differ from those in acute ST-elevation MI
(STEMI) in several ways ( table 2) [11]. These distinctions assume that the pericarditis does
not occur during or soon after an acute MI. (See "Electrocardiogram in the diagnosis of
myocardial ischemia and infarction" and "Pericardial complications of myocardial infarction"
and "ECG tutorial: ST and T wave changes" and "ECG tutorial: Myocardial ischemia and
infarction".)
● Morphology – The ST-segment elevation in acute pericarditis begins at the J point,

which represents the junction between the end of the QRS complex (termination of
depolarization) and the beginning of the ST segment (onset of ventricular
repolarization), rarely exceeds 5 mm, and usually retains its normal concavity
( waveform 1). Although similar patterns can occur with STEMI (where ST-segment
elevation also begins at the J point), the typical finding in a STEMI patient is convex
(dome-shaped) ST elevation (a pattern not characteristic of acute pericarditis) that may
be more than 5 mm in height ( waveform 2).
● Distribution – ST-segment elevations in STEMI are characteristically limited to

anatomical groupings of leads that correspond to the localized vascular area of the
infarct (anteroseptal and anterior leads V1 to V4; lateral leads I, aVL, V5, and V6; inferior
leads II, III, and aVF) ( waveform 2). The pericardium envelops the heart, and,
therefore, the ST changes are more generalized and typically present in most leads
( waveform 1).
● Reciprocal changes – Acute STEMI is often associated with reciprocal ST-segment

changes, which are not seen with pericarditis, except in leads aVR and V1.
● Concurrent ST and T-wave changes – ST-segment elevation and T-wave inversions do

not generally occur simultaneously in pericarditis, while they commonly coexist in acute
STEMI ( waveform 2). Furthermore, the evolution of repolarization abnormalities

often takes place more slowly and more asynchronously among affected leads in
pericarditis than in STEMI.
● PR segment – PR elevation in aVR with PR depression in other leads due to a

concomitant atrial current of injury is frequently seen in acute pericarditis but rarely
seen in acute STEMI.
● Other – Hyperacute T waves ( waveform 3), new pathologic Q waves, and QT

prolongation are all rare in patients with acute pericarditis but are common in acute MI.
Differentiation from early repolarization variant — The early repolarization variant ECG
pattern may be present in as many as 20 percent of healthy young adults and is often
confused with acute pericarditis [12]. Early repolarization variant is characterized by ST
elevation of the J point at the beginning of the ST segment. As a result, there is elevation of
the ST segment itself, which maintains its normal configuration ( waveform 4). In early
repolarization variant, ST elevation is most often present in the anterior and lateral chest
leads (V3 to V6), although other leads can be involved. (See "Early repolarization".)
The following ECG features can be helpful in distinguishing acute pericarditis from early
repolarization variant:
● ST elevations occur in both the limb and precordial leads in most cases of acute
pericarditis (47 of 48 in one study), whereas approximately one-half of subjects with
early repolarization variant have no ST deviations in the limb leads [13].
● PR deviation and evolution of the ST and T changes strongly favor pericarditis, as

neither is seen in early repolarization variant.
● A ratio of ST elevation to T-wave amplitude in lead V6 greater than 0.24 favors the
presence of acute pericarditis, as suggested by a small study [14]).
Patients with chronic kidney disease — Two forms of pericarditis have been described
among patients with advanced chronic kidney disease: "uremic pericarditis," which generally
refers to pericarditis beginning before dialysis or within eight weeks of dialysis initiation; and
"dialysis-associated pericarditis," which refers to pericarditis typically arising any time after
eight weeks of dialysis initiation. The clinical features of pericarditis in chronic kidney disease
can have similarities to those observed with other causes, although classic ECG findings are
less commonly seen in these patients.
● Uremic pericarditis results from inflammation of the visceral and parietal membranes
of the pericardial sac. While the cause is uncertain, uremic toxins have been implicated
due to the rapid resolution of symptoms that typically follows initiation of dialysis. With
the exception of systemic immune disorders (such as lupus erythematosus or

scleroderma), there is no relationship between uremic pericarditis and the underlying
cause of kidney disease.
● Dialysis-associated pericarditis may have a more complex pathogenesis since it is less

responsive to increasing the frequency or intensity of dialysis. Pericardial fluid among
patients with dialysis-associated pericarditis is often serosanguinous due to heparin
administration during dialysis and presence of uremic platelet dysfunction. It is also
more likely to be associated with hemodynamic instability [15]. The cause is not known,
but repetitive anticoagulation, viral infection, and disordered calcium and phosphorous
balance with hyperparathyroidism have been postulated to play a role in some patients.
DIAGNOSTIC EVALUATION
Our approach to diagnostic testing — For a patient who presents with suspected acute
pericarditis, we recommend the following evaluation, which is in general agreement with the
recommendations of various professional societies [16,17]:
● History and physical examination – This evaluation should consider disorders that are
known to involve the pericardium, such as prior malignancy, autoimmune disorders,
uremia, recent MI, and prior cardiac surgery. The examination should pay particular
attention to auscultation for a pericardial friction rub and the signs associated with
cardiac tamponade.
● Initial testing in all suspected cases:
• An ECG. (See 'Electrocardiogram' above.)
• Chest radiography. (See 'Chest radiograph' below.)
• Complete blood count, troponin level, erythrocyte sedimentation rate, and serum C-
reactive protein level. (See 'Cardiac biomarkers' below and 'Signs of inflammation'
below.)
• Echocardiography, with urgent echocardiography if cardiac tamponade is suspected.

Even a small effusion can be helpful in confirming the diagnosis of pericarditis,
although the absence of an effusion does not exclude the diagnosis [16]. In addition,
echocardiography can be particularly helpful if purulent pericarditis is suspected, if
there is concern about myocarditis, or if there is radiographic evidence of
cardiomegaly, particularly if this is a new finding. (See 'Echocardiogram' below.)
● Selected additional testing – Follow-up testing should be performed on a case-by-case

basis and may include:
• Blood cultures if fever higher than 38°C (100.4°F), signs of sepsis, or a documented,
concomitant bacterial infection (eg, pneumonia).
• Viral studies (eg, culture, polymerase chain reaction, viral serology, etc) are not
routinely obtained (with the exception of serology for HIV and hepatitis C virus),
since the yield is low and management is not altered for most patients [18].
• Antinuclear antibody (ANA) titer in selected cases (eg, young women, especially
those in whom the history suggests a rheumatologic disorder). Rarely, acute
pericarditis is the initial presentation of systemic lupus erythematosus (SLE). It is
important to recognize that a positive ANA is a nonspecific test. A rheumatology
consult should be sought in patients with pericarditis in whom a diagnosis of SLE is
being entertained. (See "Non-coronary cardiac manifestations of systemic lupus
erythematosus in adults".)
• Tuberculin skin test or an interferon-gamma release assay if not recently performed.

The interferon-gamma release assay is most helpful in immunocompromised or
HIV-positive patients and in regions where tuberculosis is endemic. However, the
choice of testing varies by country and by level of suspicion. (See "Tuberculosis
infection (latent tuberculosis) in adults: Approach to diagnosis (screening)", section
on 'Diagnostic approach'.)
• Multimodality imaging is an integral part of modern management for pericarditis

and pericardial diseases. Among multimodality imaging tests, echocardiography is
recommended for all patients, followed by cardiovascular magnetic resonance (CMR)
imaging with administration of gadolinium or computed tomography (CT) imaging
for selected patients (eg, nondiagnostic echocardiography, concerns about
constrictive pericarditis, complicated course, suspicion of specific etiology, etc)
[16,19].
• Pericardiocentesis should be performed for therapeutic purposes in patients with

cardiac tamponade, and should be considered for diagnostic purposes in patients
suspected of having a malignant or bacterial etiology, or in patients with a
symptomatic effusion refractory to medical therapy. (See "Pericardial effusion:
Approach to diagnosis".)
Echocardiogram — Echocardiography is often normal in patients with the clinical

syndrome of acute pericarditis unless there is an associated pericardial effusion. While the
finding of a pericardial effusion in a patient with known or suspected pericarditis supports
the diagnosis, the absence of a pericardial effusion or other echocardiographic abnormalities
does not exclude it.
Large and/or hemodynamically significant pericardial effusions are rare as the initial
presentation of acute pericarditis. In one series of 300 consecutive patients with acute
pericarditis, pericardial effusion was present in 180 patients (60 percent). In most cases the
effusion was small or moderate in size (79 and 10 percent, respectively) without
hemodynamic consequences. Cardiac tamponade was present in only 5 percent of patients
[5]. (See "Echocardiographic evaluation of the pericardium" and "Pericardial effusion:
Chest radiograph — Chest radiography is typically normal in patients with acute

pericarditis. Although patients with a substantial pericardial effusion may exhibit an enlarged
cardiac silhouette with clear lung fields ( image 1), this finding is uncommon in acute
pericarditis since at least 200 mL of pericardial fluid must accumulate before the cardiac
silhouette enlarges [2,20]. However, acute pericarditis should be considered in the evaluation
of a patient with new and otherwise unexplained cardiomegaly.
Cardiac biomarkers — Acute pericarditis may be associated with increases in serum

biomarkers of myocardial injury such as cardiac troponin I or T. In one series of 118
consecutive cases with idiopathic acute pericarditis, an elevated level of cardiac troponin I
was detected in 38 patients (32 percent) [19]. Such patients should be considered to have
myopericarditis.
Signs of inflammation — Since pericarditis is an inflammatory disease, laboratory signs of

inflammation are common in patients with acute pericarditis. These include elevations in the
white blood cell count, erythrocyte sedimentation rate, and serum C-reactive protein
concentration. While elevation in these markers supports the diagnosis, they are neither
sensitive nor specific for acute pericarditis. Additionally, in the hyperacute phase of
pericarditis, these markers may remain normal, and increased levels may be found only on
follow-up. However, markers of inflammation play a role in determining the optimal duration
and approach to tapering of therapy. (See "Acute pericarditis: Treatment and prognosis".)
CMR and/or CT — Both CT and CMR can help to evaluate the thickness of the pericardium.
CMR imaging is generally the preferred examination to depict the presence and intensity of
pericardial and myocardial inflammation. CT is the preferred examination to study
pericardial calcifications and concomitant pleuropulmonary diseases.
CMR provides useful assessment of pericardial inflammation ( image 2) since the inflamed
pericardium is bright and thickened on T2-weighted imaging (edema) and enhanced after
contrast injection (late gadolinium enhancement). Concomitant myocarditis may also be
depicted simultaneously during CMR. Evidence of pericardial inflammation by CT/CMR is a
supportive finding for the diagnosis of pericarditis in doubtful cases (eg, atypical
presentation, chest pain without C-reactive protein elevation or other objective evidence of
disease) [21].
CT may be useful to confirm the diagnosis and to evaluate concomitant pleuropulmonary

diseases and lymphadenopathies, thus suggesting a possible etiology of pericarditis (ie,
tuberculosis, lung cancer) [16]. Noncalcified pericardial thickening with pericardial effusion is
suggestive of acute pericarditis. Moreover, with the administration of iodinated contrast
media, enhancement of the thickened visceral and parietal surfaces of the pericardial sac
confirms the presence of active inflammation. CT attenuation values can help in the
differentiation of exudative fluid (20 to 60 Hounsfield units), as found with purulent
pericarditis, and simple transudative fluid (<10 Hounsfield units).
In selected cases, 18F-fluorodeoxyglucose (FDG) positron emission tomography/CT may be

helpful in identifying pericardial FDG uptake ("ring of fire") suggestive of inflammation or
malignancy [18,22]. FDG uptakes are higher with tuberculous or malignant pericardial
disease compared with idiopathic pericarditis [23].
Pericardiocentesis and pericardial biopsy — Studies in patients with acute pericarditis

have reported a low yield for diagnostic pericardiocentesis and pericardial biopsy; however,
some authors have advocated for a more extensive use of these techniques for diagnostic
purposes. The majority of patients with uncomplicated acute pericarditis do not require
invasive pericardial procedures. However, some high-risk patients may require
pericardiocentesis for both therapeutic and diagnostic purposes ( table 3). In addition,
while pericardial biopsy is not required to make the diagnosis of acute pericarditis, it may
rarely be necessary in an attempt to diagnose a specific etiology.
● Pericardiocentesis — In patients with a pericardial effusion, pericardiocentesis or

surgical drainage can serve both diagnostic and therapeutic purposes. Among patients
with acute pericarditis, decisions regarding drainage of a pericardial effusion are based
on its echocardiographic characteristics (eg, size and composition) and clinical
significance (eg, causing hemodynamic compromise).
• Patients with symptomatic effusions and evidence of cardiac tamponade should

undergo prompt pericardial drainage. (See "Cardiac tamponade".)
• When a significant pericardial effusion is present, a diagnostic pericardiocentesis is

indicated if a specific etiology is highly suspected and diagnosis cannot be reached
by other means. The investigation is especially indicated when a neoplastic or
bacterial etiology is suspected and a definite diagnosis can only be made by
identification of the etiologic agent in the pericardial fluid. Fluid samples should be
sent for cytology, tumor markers, Gram stain, bacterial cultures, and, if tuberculosis
is suspected, polymerase chain reaction testing, adenosine deaminase, or gamma
interferon levels. (See "Pericardial effusion: Approach to diagnosis" and "Pericardial
disease associated with cancer: Clinical presentation and diagnosis".)
• Pericardiocentesis may also be performed for diagnostic and/or therapeutic

purposes for large effusions refractory to medical treatment [24].
• Effusions that are small to moderate in size and do not cause hemodynamic
compromise (ie, cardiac tamponade) generally do not require drainage, unless a
sample of the effusion is necessary for diagnostic purposes. Moreover,
pericardiocentesis performed percutaneously has a significantly higher complication
rate if the effusion is not large.
A detailed discussion regarding the performance of pericardiocentesis and the

treatment of pericardial effusions is presented separately. (See "Pericardial effusion:
● Pericardial biopsy — Pericardial biopsy is generally performed as a part of a

therapeutic procedure (surgical drainage) in patients with recurrent pericardial
effusions and cardiac tamponade after prior pericardiocentesis (therapeutic biopsy),
and as a diagnostic procedure in patients with an illness lasting more than three weeks
despite treatment without a definite diagnosis. Technical advances in instrumentation
with introduction of pericardioscopy, and in contemporary virology and molecular
biology, have improved the diagnostic value of epicardial/pericardial biopsy. The
diagnostic yield of pericardial biopsy is typically higher in patients with pericardial
effusion with or without pericarditis than in those who present with apparent acute
pericarditis without effusion. Polymerase chain reaction techniques may represent a
useful adjunct to conventional laboratory studies in the investigation of pericardial
samples, allowing the rapid identification of microorganisms otherwise not easily found
[24,25]. Tissue samples should be sent for cytology, tumor markers, Gram stain,
bacterial cultures, and, if tuberculosis is suspected, polymerase chain reaction testing.
(See "Pericardial effusion: Approach to diagnosis", section on 'Pericardial fluid analysis
and biopsy'.)
DIAGNOSIS
Acute pericarditis — Acute pericarditis is diagnosed by the presence of at least two of the
following criteria ( table 4) [2]:
● Typical chest pain (sharp and pleuritic, improved by sitting up and leaning forward).
● Pericardial friction rub (a superficial scratchy or squeaking sound best heard with the
diaphragm of the stethoscope over the left sternal border) ( movie 1).
● Characteristic changes on the ECG (typically widespread ST-segment elevation)

( waveform 1).
● New or worsening pericardial effusion.
These diagnostic criteria are consistent with the 2015 European Society of Cardiology
guidelines on pericardial diseases [18]. In atypical presentations, additional supporting
findings include the evidence of systemic inflammation (eg, elevation of C-reactive protein)
or pericardial inflammation on an imaging technique such as pericardial contrast-
enhancement on computed tomography or pericardial edema and late gadolinium
enhancement on cardiac magnetic resonance imaging [4,18]. (See 'CMR and/or CT' above.)
The diagnosis of acute pericarditis is usually suspected based on a history of characteristic

pleuritic chest pain, and confirmed if a pericardial friction rub is present. Pericarditis should
also be suspected in a patient with persistent fever and either a pericardial effusion or new
unexplained cardiomegaly [4].
Myopericarditis or perimyocarditis — The term myopericarditis, or perimyocarditis, is used

for cases of acute pericarditis that also demonstrate features consistent with myocardial
inflammation. Because the same viruses that are responsible for acute pericarditis can also
cause myocarditis, it is not uncommon to find some degree of myocardial involvement in
patients with acute pericarditis. The terms "myopericarditis" and "perimyocarditis" are
sometimes used interchangeably or they can be used to indicate the dominant site of
involvement. Cases that involve the myocardium in which pericarditis is predominant (with
normal ventricular function) are reported as myopericarditis; alternatively, the term
perimyocarditis is sometimes used when myocardial involvement is most prominent
(particularly if ventricular function is reduced). However, in clinical practice, myopericarditis is
more common and this term is often used in both senses [26,27]. (See "Myopericarditis".)
ASSESSMENT OF RISK AND NEED FOR HOSPITALIZATION
High-risk patients with acute pericarditis should be admitted to the hospital in order to
initiate appropriate therapy and expedite a thorough initial evaluation. Patients with high-
risk features are at increased risk of short-term complications and have a higher likelihood of
a specific disease etiology [5,28]. Conversely, patients with uncomplicated (ie, low-risk) acute
pericarditis can usually be evaluated and sent home, with outpatient follow-up to assess the
efficacy of treatment and complete the diagnostic evaluation [5,28].
Features of acute pericarditis associated with a higher risk or potential need for
hospitalization include [5,28]:
● Fever (>38°C [100.4°F]).
● Subacute course over days to weeks (without acute onset of chest pain).
● Evidence suggesting cardiac tamponade (eg, hemodynamic compromise). (See "Cardiac

tamponade".)
● A moderate to large pericardial effusion (ie, an end-diastolic echo-free space of more

than 20 mm).
● Immunosuppressed patients.
● Therapy with warfarin or non-vitamin K oral anticoagulants.
● Acute trauma.
● Failure to show clinical improvement following seven days of appropriately dosed

nonsteroidal antiinflammatory drug and colchicine therapy.
● Elevated cardiac troponin, which suggests myopericarditis/perimyocarditis. (See

"Myopericarditis".)
Historically, many clinicians admitted all new cases of acute pericarditis to the hospital, but
this is not necessary. In one report of 300 consecutive patients with acute pericarditis, 15
percent were deemed high risk at presentation and were hospitalized [5]. In the remaining
85 percent of patients who were low risk, outpatient aspirin therapy was effective in 87
percent, and none of these patients had a serious complication (eg, cardiac tamponade) at a
mean follow-up of 38 months.
Although chronic use of glucocorticoids should not be considered as a risk factor in a general
population of patients with acute pericarditis, they were associated with an increased rate of
complications in idiopathic or viral pericarditis [28]. Glucocorticoid therapy given for the
index attack may increase the chance of recurrence, possibly because of its deleterious effect
on viral replication and clearance. (See "Recurrent pericarditis", section on 'Predictors of
recurrence'.)
ESTABLISHING A DEFINITE ETIOLOGY
Because of the relatively benign course associated with the common causes of pericarditis,
along with the relatively low yield of much of the diagnostic testing, it is not necessary to
establish a definite etiology in all patients with acute pericarditis. Initial efforts should focus
on excluding a significant pericardial effusion or cardiac tamponade, and the identification of
patients in whom a more comprehensive evaluation should be performed to exclude causes
that require specific therapy (eg, malignancy, tuberculosis, or purulent pericarditis) [5]. In
addition, among patients at high risk of coronary disease, MI must be ruled out by
appropriate studies. (See "Initial evaluation and management of suspected acute coronary
syndrome (myocardial infarction, unstable angina) in the emergency department".)
The yield of the standard diagnostic evaluation to determine the etiology of acute
pericarditis is relatively low. This was illustrated in three series that included a total of 784
unselected patients who underwent an extensive evaluation [7,28,29]. A specific diagnosis
was established in only 130 patients (17 percent) ( table 5). The most commonly confirmed
diagnoses were:
● Neoplasia – 5 percent
● Tuberculosis – 4 percent
● Autoimmune etiologies – 5 percent
● Purulent pericarditis – 1 percent
In developed countries, unless there is an apparent medical or surgical condition known to

be associated with pericarditis, most cases of acute pericarditis in immunocompetent
patients are due to viral infection or are idiopathic ( table 5) [5,28,30-32]. Acute viral or
idiopathic pericarditis typically follow a brief and benign course after empiric treatment with
antiinflammatory drugs. (See "Acute pericarditis: Treatment and prognosis".)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Pericardial disease".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Pericarditis in adults (The Basics)")
● Beyond the Basics topic (see "Patient education: Pericarditis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
● Epidemiology and etiology – Acute pericarditis (inflammation of the pericardial sac) is

the most common disorder of the pericardium and is seen in approximately 0.1 percent
of hospitalized patients and 5 percent of patients admitted to the emergency
department for nonischemic chest pain. Cases are most commonly idiopathic (most
probably viral in etiology). Other etiologies include bacterial infections, malignancy, and
autoimmune disorders ( table 5). The distribution of etiologies varies with geography
and type of clinical setting (community hospital versus tertiary referral center). (See
'Epidemiology' above.)
● Clinical features – Acute pericarditis can present with a variety of nonspecific signs and
symptoms, depending on the underlying etiology. Common clinical manifestations
include chest pain (typically pleuritic), pericardial friction rub, characteristic ECG
changes (diffuse ST elevation and PR depression), and pericardial effusion. Pericarditis
should also be suspected in a patient with persistent fever and pericardial effusion or
new unexplained cardiomegaly. (See 'Clinical features' above.)
● Diagnostic evaluation – For all patients with suspected acute pericarditis, the initial
evaluation includes a comprehensive history and physical examination, selective blood
work (assessing for markers of inflammation and myocardial damage), chest
radiography, ECG, and echocardiography. Follow-up testing is performed in selected
cases as needed and may include additional laboratory evaluation (eg, blood cultures,
antinuclear antibody titer, HIV and hepatitis C virus serology) and additional cardiac
imaging. (See 'Our approach to diagnostic testing' above.)
● Diagnosis – Acute pericarditis is diagnosed by the presence of at least two of the

following four criteria ( table 4) (see 'Diagnosis' above):
• Typical chest pain (sharp and pleuritic, improved by sitting up and leaning forward).
(See 'Chest pain' above.)
• Pericardial friction rub (a superficial scratchy or squeaking sound best heard with
the diaphragm of the stethoscope over the left sternal border) ( movie 1). (See
'Pericardial friction rub' above.)
• Characteristic changes on the ECG (typically widespread ST-segment elevation)

( waveform 1). (See 'Electrocardiogram' above.)
• New or worsening pericardial effusion. (See 'Echocardiogram' above.)
● Indications for hospitalization – Patients with acute pericarditis with one or more
high-risk features (including fever, subacute course, suspected cardiac tamponade,
immunosuppression, acute trauma, treatment with oral anticoagulation, or elevated
cardiac troponin) are at increased risk for complications and should generally be
admitted to initiate appropriate therapy and to expedite a thorough initial evaluation.
Conversely, patients with uncomplicated (ie, low-risk) acute pericarditis can usually be
evaluated and sent home, with outpatient follow-up. (See 'Assessment of risk and need
for hospitalization' above.)
● Role of testing to determine etiology – Given the relatively benign course associated
with the common causes of pericarditis and the low yield of much diagnostic testing, it
is not necessary to establish a definite etiology in all patients with acute pericarditis.
Initial evaluation should focus on excluding a significant pericardial effusion or cardiac
tamponade and identification of patients in whom a more comprehensive evaluation
should be performed to exclude causes that require specific therapy (eg, malignancy,
tuberculosis, or purulent pericarditis). (See 'Establishing a definite etiology' above.)
Use of UpToDate is subject to the Terms of Use.
REFERENCES
1. Kytö V, Sipilä J, Rautava P. Clinical profile and influences on outcomes in patients

hospitalized for acute pericarditis. Circulation 2014; 130:1601.
2. Chiabrando JG, Bonaventura A, Vecchié A, et al. Management of Acute and

Recurrent Pericarditis: JACC State-of-the-Art Review. J Am Coll Cardiol 2020; 75:76.
3. Imazio M, Cecchi E, Demichelis B, et al. Myopericarditis versus viral or idiopathic acute
pericarditis. Heart 2008; 94:498.
4. Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic
Review. JAMA 2015; 314:1498.
5. Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment of acute pericarditis: a

management program for outpatient therapy. J Am Coll Cardiol 2004; 43:1042.
6. Spodick DH. Pericardial rub. Prospective, Multiple observer investigation of pericardial
friction in 100 patients. Am J Cardiol 1975; 35:357.
7. Zayas R, Anguita M, Torres F, et al. Incidence of specific etiology and role of methods for
specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol 1995; 75:378.
8. Rutsky, EA, Rostand, SG . Pericarditis in end-stage renal disease: Clinical characteristics
and management. Semin Dial 1989; 2:25.
9. Chou TC. Electrocardiography in clinical practice, WB Saunders Company, Philadelphia 1
996.
10. Spodick DH. Arrhythmias during acute pericarditis. A prospective study of 100
consecutive cases. JAMA 1976; 235:39.
11. Chou TC. Electrocardiography in Clinical Practice: Adults and Pediatrics, 4th ed, WB Saun
ders, Philadelphia 1996.
12. Patton KK, Ellinor PT, Ezekowitz M, et al. Electrocardiographic Early Repolarization: A
Scientific Statement From the American Heart Association. Circulation 2016; 133:1520.
13. Spodick DH. Differential characteristics of the electrocardiogram in early repolarization

and acute pericarditis. N Engl J Med 1976; 295:523.
14. Ginzton LE, Laks MM. The differential diagnosis of acute pericarditis from the normal
variant: new electrocardiographic criteria. Circulation 1982; 65:1004.
15. Rutsky EA, Rostand SG. Treatment of uremic pericarditis and pericardial effusion. Am J
Kidney Dis 1987; 10:2.
16. Klein AL, Abbara S, Agler DA, et al. American Society of Echocardiography clinical
recommendations for multimodality cardiovascular imaging of patients with pericardial
disease: endorsed by the Society for Cardiovascular Magnetic Resonance and Society of
Cardiovascular Computed Tomography. J Am Soc Echocardiogr 2013; 26:965.
17. Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/AHA/ASE 2003 guideline for the cli
nical application of echocardiography www.acc.org/qualityandscience/clinical/statement
s.htm (Accessed on August 24, 2006).
18. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and
management of pericardial diseases: The Task Force for the Diagnosis and Management
of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The
European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2015; 36:2921.
19. Imazio M, Demichelis B, Cecchi E, et al. Cardiac troponin I in acute pericarditis. J Am Coll
Cardiol 2003; 42:2144.
20. Spodick DH. Acute cardiac tamponade. N Engl J Med 2003; 349:684.
21. Imazio M, Pivetta E, Palacio Restrepo S, et al. Usefulness of Cardiac Magnetic Resonance
for Recurrent Pericarditis. Am J Cardiol 2020; 125:146.
22. A diagnostic conundrum of a “ring of fire”. Lancet 2023; 401:470.
23. Hyeon CW, Yi HK, Kim EK, et al. The role of 18F-fluorodeoxyglucose-positron emission
tomography/computed tomography in the differential diagnosis of pericardial disease.
Sci Rep 2020; 10:21524.
24. Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of
pericardial diseases. Circulation 2010; 121:916.
25. Imazio M, Brucato A, Derosa FG, et al. Aetiological diagnosis in acute and recurrent
pericarditis: when and how. J Cardiovasc Med (Hagerstown) 2009; 10:217.
26. Imazio M, Brucato A, Barbieri A, et al. Good prognosis for pericarditis with and without
myocardial involvement: results from a multicenter, prospective cohort study.
Circulation 2013; 128:42.
27. Imazio M. Myopericardial diseases: Diagnosis and management, 1st ed, Springer, New Y
ork 2019.
28. Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute

pericarditis. Circulation 2007; 115:2739.
29. Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J. Primary acute pericardial disease:
a prospective series of 231 consecutive patients. Am J Cardiol 1985; 56:623.
30. Maisch B, Ristić AD. The classification of pericardial disease in the age of modern
medicine. Curr Cardiol Rep 2002; 4:13.
31. Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for
acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation
2005; 112:2012.
32. Permanyer-Miralda G. Acute pericardial disease: approach to the aetiologic diagnosis.

Heart 2004; 90:252.
Topic 4940 Version 38.0
GRAPHICS
Distinguishing among life-threatening causes of chest pain: History,

examination, and diagnostic testing
Historical Examination
Diagnosis Electrocardiogram Chest radio
features findings
Acute Substernal/left- Nonspecific ST segment Nonspecific

coronary sided chest May detect elevations, Q May show ev
syndrome pressure or signs of HF waves, new left HF
tightness is bundle branch
common block are evidence
Onset is of AMI
gradual Single ECG is not
Pain radiating sensitive for ACS
to shoulders or Prominent R waves
pain with with ST segment
exertion depressions in V1
increases and V2 strongly
relative risk suggests posterior
"Atypical" AMI
symptoms (eg,
dyspnea,
weakness)
more common
in older adults,
women,
diabetics
Older adults
can present
with dyspnea,
weakness,
syncope, or
ΔMS alone
Aortic Sudden onset Absent upper Ischemic changes Wide medias

dissection of sharp, extremity or in 15% loss of norma
tearing, or carotid pulse Nonspecific ST and knob contour
ripping pain is suggestive T changes in 30% common (up
Maximal Discrepancy 10% have no
severity at in systolic BP
onset >20 mmHg
Most often between right
begins in chest, and left upper
can begin in extremity is

back suggestive
Can mimic Up to 30%
stroke, ACS, with
mesenteric neurologic
ischemia, findings
kidney stone Findings vary
with arteries
affected
Pulmonary Many possible No finding is Usually abnormal Great majorit

embolism presentations, sensitive or but nonspecific normal
including specific Signs of right heart May show ate
pleuritic pain Extremity strain suggestive elevated
and painless exam (eg, RAD, RBBB, hemidiaphra
dyspnea generally RAE) pleural effusi
Often sudden normal
onset Lung exam
Dyspnea often generally
dominant nonspecific;
feature focal
wheezing
may be
present;
tachypnea is
common
Tension Often sudden Ipsilateral Demonstrate

pneumothorax onset diminished or pleural space
Initial pain absent breath
often sharp and sounds
pleuritic Subcutaneous
Dyspnea often emphysema
dominant is uncommon
feature
Pericardial Pain from Severe Decreased voltage May reveal en

tamponade pericarditis is tamponade and electrical heart
most often creates alternans can
sharp anterior obstructive appear with
chest pain shock and significant
made worse by causes effusions
inspiration or jugular Diffuse PR
lying supine venous segment
and relieved by distension, depressions and/or

sitting forward pulsus ST segment
Dyspnea is paradoxus elevations can
common Pericardial appear with acute
effusion can pericarditis
cause friction
rub
Mediastinitis Forceful Ill-appearing; Large majorit

(esophageal vomiting often shock; fever some abnorm
rupture) precedes May hear pneumomed
esophageal (Hamman's) pleural effusi
rupture crunch over pneumothora
Recent upper mediastinum
endoscopy or
instrumentation
increases risk of
perforation
Odontogenic
infection is
possible cause
Coexistent
respiratory and
gastrointestinal
complaints may
occur
ΔMS: altered mental status; ACS: acute coronary syndrome; AMI: acute myocardial infarction; BP:
blood pressure; CABG: coronary artery bypass graft; CK-MB: creatine kinase-MB; CXR: chest
radiograph; ECG: electrocardiogram; HF: heart failure; PCI: percutaneous coronary intervention; PE:
pulmonary embolism; RAD: right axis deviation; RAE: right atrial enlargement; RBBB: right bundle
branch block.
Graphic 54629 Version 4.0
Cardiac auscultation supine and leaning forward
Auscultation of the pericardium: To elicit pericardial rubs, the patient is invited to lean forward (A) or
rest on elbows and knees (B). Both physical maneuvers increase the contact of visceral and parietal
pericardium.
Reproduced from: Heart, Imazio M. Pericardial involvement in systemic inflammatory diseases, 97:1882, Copyright © 2011,
with permission from BMJ Publishing Group Ltd.
Classical four stages of ECG evolution in acute pericarditis
Stage I: diffuse ST elevation with PR depression
Stage II: normalization of ST and PR segments
Stage III: diffuse deep T-wave inversions
Stage IV: normalization of the ECG
ECG: electrocardiogram.
Reprinted by permission from Springer: Myopericardial Diseases, Imazio M (Ed). Copyright © 2016.
Electrocardiogram (ECG) in pericarditis
Electrocardiogram in acute pericarditis showing diffuse upsloping (concave up) ST-segment elevations
seen best here in leads II, III, aVF, and V2 to V6. There is also subtle PR-segment deviation (positive in
aVR, negative in most other leads). ST-segment elevation is due to a ventricular current of injury
associated with epicardial inflammation; similarly, the PR-segment changes are due to an atrial
current of injury, which, in pericarditis, typically displaces the PR segment upward in lead aVR and
downward in most other leads.
Courtesy of Ary Goldberger, MD.
Normal ECG
Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/minute, a PR interval of

0.14 seconds, a QRS interval of 0.10 seconds, and a QRS axis of approximately 75°.
Electrocardiogram features of acute pericarditis versus acute myocardial

infarction
Findings in acute
ECG features Findings in acute MI
pericarditis
ST-segment elevation ST-segment elevation begins ST-segment elevation begins

morphology at J point, rarely exceeds 5 at J point, often exceeds 5
mm, normal concavity mm in height, abnormal
concavity (convex or "dome-
shaped")
ST-segment elevation Widespread ST-segment Anatomical groupings of

distribution elevation in most/all leads leads show ST-segment
Typically most prominent in elevation, which corresponds
inferolateral leads to vascular territory of
infarction
Reciprocal ST-segment changes Usually not seen ST-segment depressions

usually seen in reciprocal
leads
Concurrent ST elevation and T- Unusual unless concomitant Common

wave inversion myocarditis
PR segment changes PR elevation in aVR Rare

PR depression in most/all
other leads
Hyperacute T waves Rare; if seen, due to fusion of Commonly seen at onset of

elevated ST segment and T acute infarction/ischemia
wave
Q waves Not usually new from acute Seen late in course of MI due
pericarditis to transmural injury
QT prolongation Unusual Can be seen
ECG: electrocardiogram; MI: myocardial infarction.
Electrocardiogram (ECG) in an evolving anterior myocardial infarction
Electrocardiogram shows findings typical of an evolving Q-wave anterior MI: loss of R waves in leads
V1 to V3, ST segment elevations in V2 to V4, and T wave inversions in leads I, aVL, and V2 to V5. Sinus
bradycardia (55 beats/min) is present due to concurrent therapy with a beta blocker.
Normal ECG
Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/minute, a PR interval of

0.14 seconds, a QRS interval of 0.10 seconds, and a QRS axis of approximately 75°.
Hyperacute (peaked) T waves
Hyperacute T waves are >5 mm in the limb leads, and usually >10 mm in the precordial leads. They
have a peaked, symmetric morphology.
Early repolarization 12 lead ECG
Early repolarization manifest as inferior J-point slurring and lateral J-point notching, each >1 mm in
two contiguous leads.
Chest radiograph of a pericardial effusion
Cardiomegaly due to a massive pericardial effusion. At least 200 mL of pericardial fluid must
accumulate before the cardiac silhouette enlarges.
Courtesy of Massimo Imazio, MD, FESC.
Pericardial edema and LGE by CMR
(A) Pericardial edema.
(B) Pericardial LGE.
LGE: late gadolinium enhancement; CMR: cardiac magnetic resonance.
Reprinted by permission from Springer: Myopericardial Diseases, Imazio M (Ed). Copyright © 2016.
Indications for invasive workup in acute pericarditis
Pericardiocentesis:
1. Cardiac tamponade
2. Moderate to large effusions refractory to medical therapy and with severe symptoms
3. Suspected bacterial or neoplastic pericarditis
Pericardial biopsy and pericardioscopy (targeted biopsy in specialized center):
1. Relapsing cardiac tamponade
2. Suspected bacterial or neoplastic pericarditis
3. Worsening pericarditis (despite medical therapy) without a specific diagnosis
Courtesy of Dr. Massimo Imazio.
Diagnostic criteria for acute pericarditis and myopericarditis in the clinical

setting
Acute pericarditis (at least two criteria of four should be present)*:
1. Typical chest pain
2. Pericardial friction rub
3. Suggestive ECG changes (typically widespread ST segment elevation)
4. New or worsening pericardial effusion
Myopericarditis:
1. Definite diagnosis of acute pericarditis, PLUS
2. Suggestive symptoms (dyspnea, palpitations, or chest pain) and ECG abnormalities beyond
normal variants, not documented previously (ST/T abnormalities, supraventricular or ventricular
tachycardia or frequent ectopy, atrioventricular block), OR focal or diffuse depressed LV function of
uncertain age by an imaging study
3. Absence of evidence of any other cause
4. One of the following features: Evidence of elevated cardiac enzymes (creatine kinase-MB fraction,
or troponin I or T), OR new onset of focal or diffuse depressed LV function by an imaging study, OR
abnormal imaging consistent with myocarditis (MRI with gadolinium, gallium-67 scanning, anti-
myosin antibody scanning)
Case definitions for myopericarditis include:
Suspected myopericarditis: Criteria 1 plus 2 and 3
Probable myopericarditis: Criteria 1, 2, 3, and 4
Confirmed myopericarditis ¶ : Histopathologic evidence of myocarditis by endomyocardial biopsy o

on autopsy
ECG: electrocardiogram; LV: left ventricular; MRI: magnetic resonance imaging.
* Pericardial effusion confirms the clinical diagnosis, but its absence does not exclude it.
¶ In clinical practice, a confirmed diagnosis would require an endomyocardial biopsy that is not
warranted in self-limited cases with predominant pericarditis.
Reproduced with permission from: Imazio M, Trinchero R. Triage and management of acute pericarditis. Int J Cardiol 2006,
doi:10.1016/j.ijcard.2006.07.100. Copyright © 2006 Elsevier.
Acute pericarditis etiologies: Data from published clinical studies with

unselected populations
Western Europe Africa

[1]
(2007-2012) (1995-2001) [2]
Idiopathic * 516 (55.3%) 32 (13.7%)
Specific etiology 417 (44.7%) 201 (86.3%)
Neoplastic ¶ 85 (8.9%) 22 (9.4%)
Tuberculosis ¶ 4 (<1.0%) 161 (69.5%)
Autoimmune etiologies ¶ 25 (2.6%) Δ 12 (5.2%)
Purulent ¶ 29 (3.0%) 5 (2.1%)
* Most idiopathic cases are likely viral.
¶ As a fraction of the entire sample.
Δ Autoimmune pericarditis can be caused by autoimmune disease or as a complication of myocardial

infarction (MI) or cardiac surgery. In this table, we only report pericarditis caused by autoimmune
disease, while the original paper (Gouriet et al) reports an additional 188 cases related to MI or
cardiac surgery.
Data from:
1. Gouriet F, Levy PY, Casalta JP, et al. Etiology of pericarditis in a prospective cohort of 1162 cases. Am J Med 2015;
128:784.
2. Reuter H, Burgess LJ, Louw VJ, et al. The management of tuberculous pericardial effusion: experience in 233 consecutive
patients. Cardiovasc J S Afr 2007; 18:20.

Acute Pericarditis - Clinical Presentation and Diagnosis - UpToDate

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Acute Pericarditis - Clinical Presentation and Diagnosis - UpToDate

Uploaded by

Copyright:

Available Formats

23/2/24, 14:11 Acute pericarditis: Clinical presentation and diagnosis - UpToDate

Official reprint from UpToDate®

Acute pericarditis: Clinical presentation and diagnosis

Literature review current through: Jan 2024.

Diseases of the pericardium present clinically in one of several ways:

● Acute and recurrent pericarditis

● In an observational study from Finland that included 670,409 cardiovascular admissions

● Electrocardiogram (ECG) changes – New widespread ST elevation and PR depression.

● Pericardial effusion – A pericardial effusion is a common feature of pericarditis but is

Breath-holds during auscultation permit distinction of a pericardial friction rub from a

Typical ECG findings

● Stage 1, seen in the first hours to days, is characterized by widespread ST elevation

● Stage 3 is characterized by the development of diffuse T-wave inversions, generally

Arrhythmias — Sustained arrhythmias are uncommon in acute pericarditis, except in the

● Morphology – The ST-segment elevation in acute pericarditis begins at the J point,

● Distribution – ST-segment elevations in STEMI are characteristically limited to

● Reciprocal changes – Acute STEMI is often associated with reciprocal ST-segment

● Concurrent ST and T-wave changes – ST-segment elevation and T-wave inversions do

STEMI ( waveform 2). Furthermore, the evolution of repolarization abnormalities

● PR segment – PR elevation in aVR with PR depression in other leads due to a

● Other – Hyperacute T waves ( waveform 3), new pathologic Q waves, and QT

● PR deviation and evolution of the ST and T changes strongly favor pericarditis, as

the exception of systemic immune disorders (such as lupus erythematosus or

● Dialysis-associated pericarditis may have a more complex pathogenesis since it is less

● Initial testing in all suspected cases:

• An ECG. (See 'Electrocardiogram' above.)

• Chest radiography. (See 'Chest radiograph' below.)

• Echocardiography, with urgent echocardiography if cardiac tamponade is suspected.

● Selected additional testing – Follow-up testing should be performed on a case-by-case

• Tuberculin skin test or an interferon-gamma release assay if not recently performed.

• Multimodality imaging is an integral part of modern management for pericarditis

• Pericardiocentesis should be performed for therapeutic purposes in patients with

Echocardiogram — Echocardiography is often normal in patients with the clinical

Chest radiograph — Chest radiography is typically normal in patients with acute

Cardiac biomarkers — Acute pericarditis may be associated with increases in serum

Signs of inflammation — Since pericarditis is an inflammatory disease, laboratory signs of

CT may be useful to confirm the diagnosis and to evaluate concomitant pleuropulmonary

In selected cases, 18F-fluorodeoxyglucose (FDG) positron emission tomography/CT may be

Pericardiocentesis and pericardial biopsy — Studies in patients with acute pericarditis

● Pericardiocentesis — In patients with a pericardial effusion, pericardiocentesis or

• Patients with symptomatic effusions and evidence of cardiac tamponade should

• When a significant pericardial effusion is present, a diagnostic pericardiocentesis is

• Pericardiocentesis may also be performed for diagnostic and/or therapeutic

A detailed discussion regarding the performance of pericardiocentesis and the

● Pericardial biopsy — Pericardial biopsy is generally performed as a part of a

● Characteristic changes on the ECG (typically widespread ST-segment elevation)

● New or worsening pericardial effusion.

The diagnosis of acute pericarditis is usually suspected based on a history of characteristic

Myopericarditis or perimyocarditis — The term myopericarditis, or perimyocarditis, is used

ASSESSMENT OF RISK AND NEED FOR HOSPITALIZATION

● Fever (>38°C [100.4°F]).

● Evidence suggesting cardiac tamponade (eg, hemodynamic compromise). (See "Cardiac

● A moderate to large pericardial effusion (ie, an end-diastolic echo-free space of more

● Therapy with warfarin or non-vitamin K oral anticoagulants.

● Failure to show clinical improvement following seven days of appropriately dosed

● Elevated cardiac troponin, which suggests myopericarditis/perimyocarditis. (See

ESTABLISHING A DEFINITE ETIOLOGY

In developed countries, unless there is an apparent medical or surgical condition known to

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

● Basics topics (see "Patient education: Pericarditis in adults (The Basics)")

SUMMARY AND RECOMMENDATIONS