Reimpresión oficial de UpToDate ®

www.uptodate.com © 2019 UpToDate, Inc. y / o sus filiales. Todos los derechos reservados.

Pericarditis aguda: presentación clínica y evaluación diagnóstica.

Autor: Massimo Imazio, MD, FESC
Editor de la sección: Martin M LeWinter, MD
Editor Adjunto: Brian C Downey, MD, FACC

Todos los temas se actualizan a medida que se dispone de nueva evidencia y se completa nuestro proceso de revisión por pares .

Revisión de literatura vigente hasta mayo de 2019. | Este tema se actualizó por última vez el 27 de octubre de 2017.

INTRODUCCIÓN

El pericardio es un saco fibroelástico formado por capas viscerales y parietales separadas por un espacio
(potencial), la cavidad pericárdica. En individuos sanos, la cavidad pericárdica contiene de 15 a 50 ml de un
ultrafiltrado de plasma.

Las enfermedades del pericardio se presentan clínicamente de una de varias maneras [ 1 ]:

● Pericarditis aguda y recurrente.

● Derrame pericárdico sin mayor compromiso hemodinámico.
● Taponamiento cardíaco
● Pericarditis constrictiva
● Pericarditis efusiva-constrictiva

La pericarditis aguda se refiere a la inflamación del saco pericárdico. El término miopericarditis, o

perimyocarditis, se usa para casos de pericarditis aguda que también demuestran inflamación del miocardio; La
miopericarditis se usa para los casos con pericarditis prevalente y función ventricular normal, la perimicocarditis
se usa para los casos con miocarditis prevalente y si la función ventricular se reduce (nuevas anomalías de
movimiento de la pared o función ventricular reducida). La presentación clínica y la evaluación diagnóstica de la
pericarditis aguda se revisarán aquí. La etiología de la pericarditis, el tratamiento y pronóstico de la pericarditis
aguda y otros procesos de enfermedad pericárdica se analizan por separado. (Ver "Etiología de la enfermedad
pericárdica" y "Pericarditis aguda: Tratamiento y pronóstico""Pericarditis recurrente" y "Miopericarditis" y
"Taponamiento cardíaco" y "Pericarditis constrictiva" y "Diagnóstico y tratamiento del derrame pericárdico" .)

EPIDEMIOLOGÍA

La pericarditis aguda es el trastorno más común que afecta al pericardio. Faltan en gran medida los estudios
epidemiológicos, y se desconoce la incidencia y prevalencia exactas de la pericarditis aguda. Sin embargo, la
pericarditis aguda se registra en aproximadamente 0,1 a 0,2 por ciento de los pacientes hospitalizados y en el 5
por ciento de los pacientes ingresados en el Servicio de urgencias por dolor torácico no isquémico [ 2,3 ].

● En un estudio observacional de un área urbana en el norte de Italia, la incidencia de pericarditis aguda fue
de 27.7 casos por 100,000 personas por año [ 4 ].

● En un estudio observacional de Finlandia que incluyó 670,409 ingresos cardiovasculares en 29 hospitales

en todo el país durante un período de 9,5 años, la tasa de incidencia estandarizada para la pericarditis que
requiere hospitalización fue de 3,3 casos por cada 100.000 personas-año [ 3 ].

La pericarditis aguda es un trastorno común en varios entornos clínicos, donde puede ser la primera
manifestación de una enfermedad sistémica subyacente o representar un proceso aislado ( tabla 1 ). En los
países desarrollados, la mayoría de los casos de pericarditis aguda se consideran de origen viral posible o
confirmado, aunque la etiología exacta de la mayoría de los casos sigue sin determinarse siguiendo un enfoque
diagnóstico tradicional [ 5 - 7 ].

Antes de la disponibilidad generalizada de la terapia antirretroviral para tratar la infección con el virus de la
inmunodeficiencia humana (VIH), la enfermedad pericárdica era la manifestación cardiovascular más frecuente
del síndrome de inmunodeficiencia adquirida (SIDA) [ 8,9 ]. Sin embargo, en los países desarrollados con
acceso a la terapia del VIH, los pacientes con infección por VIH que desarrollan pericarditis aguda tienen un
espectro etiológico muy similar al de los pacientes no infectados con VIH. Por el contrario, la infección por VIH y
la tuberculosis persisten como causas principales de pericarditis aguda en los países en desarrollo. (Consulte
"Enfermedades cardíacas y vasculares en pacientes infectados por el VIH", sección "Enfermedad pericárdica" .)

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 [5,10]:

● Chest pain – Typically 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
● Electrocardiogram (ECG) changes – New widespread ST elevation or PR depression
● Pericardial effusion

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.

Determination 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 [11,12]. 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 [6,11-13].

Features of acute pericarditis associated with a higher risk include [11,12]:

● Fever (>38ºC [100.4ºF])

● Subacute course (without acute onset of chest pain)
● Evidence suggesting cardiac tamponade (eg, hemodynamic compromise) (see "Cardiac tamponade")
● A large pericardial effusion (ie, an end-diastolic echo-free space of more than 20 mm)
● Immunosuppression and immunodepressed patients
● A history of therapy with vitamin K antagonists (eg, warfarin) or novel oral anticoagulants
● Acute trauma
● Failure to show clinical improvement following seven days of appropriately dosed NSAID and colchicine
therapy
● Elevated cardiac troponin, which suggests myopericarditis/perimyocarditis

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 [11]. 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 [12]. 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'.)

Chest pain — The vast majority of patients with acute pericarditis present with chest pain (>95 percent of cases)
[11]. The chest pain of pericarditis must always be distinguished from other common and/or life-threatening
causes of chest pain (table 2) 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 from myocardial ischemia, chest pain due to pericarditis is most often sharp and pleuritic in
nature, with exacerbation by inspiration or coughing. One of the most distinctive features is the tendency for a
decrease in intensity when the patient sits up and leans forward [5,14]. 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 [15]. Radiation of chest pain to the trapezius ridge has also been considered to be fairly specific
for pericarditis. However, dull, oppressive pain may occur; in such cases, it is difficult to distinguish pericarditis
from other causes of chest pain [5,14].
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).

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.

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 [16]. In a review of
auscultation and phonocardiography in 100 patients with a pericardial rub, the rub was triphasic in 56 percent of
patients in sinus rhythm, biphasic in 33 percent, and monophasic in 15 percent [16].

Pericardial rubs may be localized or widespread, but are usually loudest over the left sternal border [16]. 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 [14]. 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 [17]. This prevalence is considerably higher than the 35 percent incidence of friction
rubs reported in another series [11].

Suspension of respiration during auscultation permits distinction of a pericardial friction rub from a
pleuropericardial or pleural rub. A pleuropericardial rub results from the 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 can evolve through as many as four stages of changes,
and the temporal evolution of ECG changes can be highly variable [5,14]. The four stages of typical ECG
changes (figure 1) in patients with acute pericarditis include:
 ● Stage 1, seen in the first hours to days, is characterized by diffuse 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 [18].

● 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. Its duration is not well-documented and likely highly variable.

● Stage 4 is represented by normalization of the ECG.

However, pericarditis does not always result in these typical ECG changes. Many patients normalize without
going past stage 1. Moreover, atypical ECG changes are seen in up to 40 percent of patients with acute
pericarditis [11]. 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 'ECG 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 [19]. (See "Pericarditis in renal failure".)

The temporal evolution of ECG changes with acute pericarditis is highly variable from one patient to another [18].
Treatment can accelerate or alter ECG progression. The duration of the ECG changes in pericarditis also
depends upon its cause and the extent of the associated myocardial damage [20].

Sustained arrhythmias are uncommon in acute pericarditis, except in the post-thoracotomy 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 [21]. In a separate report comparing patients with
myopericarditis and simple acute pericarditis, cardiac arrhythmias were also more commonly present in patients
with myopericarditis (odds ratio 17.6, 95% CI 5.7-54.1) [4]. Thus, the presence of atrial or ventricular arrhythmias
is suggestive of concomitant myocarditis or an unrelated cardiac disease.

ECG differentiation from acute myocardial infarction — While both acute pericarditis and acute myocardial
infarction can present with chest pain and elevations in cardiac biomarkers, the electrocardiographic changes in
acute pericarditis differ from those in acute ST elevation MI (STEMI) in several ways (table 3) [22]. 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, V6; inferior leads II, III, aVF) (waveform 2). The pericardium envelops the heart, therefore
the ST changes are more generalized and typically are 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 3A-B), new pathologic Q waves, and QT prolongation are all rarely
seen in patients with acute pericarditis but are more common in acute MI.

ECG differentiation from early repolarization — The early repolarization variant seen on an ECG may be
present in as many as 30 percent of young adults and is often confused with acute pericarditis [23]. Early
repolarization is characterized by ST elevation of 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). As a result, there is elevation of the ST segment itself, which maintains its normal configuration
(waveform 4). In early repolarization, ST elevation is most often present in the anterior and lateral chest leads
(V3-V6), although other leads can be involved. (See "Early repolarization".)

The following electrocardiographic features can be helpful in distinguishing acute pericarditis from early
repolarization:

● 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 have no ST deviations in the
limb leads [24].
 ● PR deviation and evolution of the ST and T changes strongly favor pericarditis, as neither is seen in early
repolarization.

● If the ratio of ST elevation to T wave amplitude in lead V6 exceeds 0.24, acute pericarditis is present
(positive and negative predictive values are both 100 percent) [25].

DIAGNOSTIC EVALUATION

Our approach to diagnostic testing — For a patient who presents with suspected acute pericarditis, we
recommend the following evaluation:

● Initial history and physical examination – This evaluation should consider disorders that are known to
involve the pericardium, such as prior malignancy, autoimmune disorders, uremia, recent myocardial
infarction, 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 [26]. 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.)

The 2003 American College of Cardiology/American Heart Association/American Society of

Echocardiography (ACC/AHA/ASE) guidelines for the clinical application of echocardiography stated
that evidence and/or general agreement supported the use of echocardiography for the evaluation of all
patients with suspected pericardial disease [27]. Similarly, a 2013 expert consensus statement from the
ASE recommends echocardiography for all patients with acute pericarditis [26].

● Selected additional testing – Follow-up testing should be performed on a case by case basis and may
include:

• Blood cultures if fever higher than 38ºC (100.4ºF), signs of sepsis, or a documented, concomitant
bacterial infection (eg, pneumonia).

• Viral studies (eg, culture, PCR, viral serology, etc) are not routinely obtained, since the yield is low and
management is not altered for the vast majority of patients [28].
 • 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".)

• HIV serology.

• Tuberculin skin test or an interferon-gamma release assay (eg, QuantiFERON TB 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.

• 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 cardiac magnetic resonance (CMR) 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) [26,29].

• 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.

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
[11]. (See "Echocardiographic evaluation of the pericardium" and "Diagnosis and treatment of 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 [2,5]. 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) [29]. Such patients
should be considered to have myopericarditis. (See "Myopericarditis", section on 'Laboratory studies'.)
 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.

CMR and/or CT — Computed tomography (CT) may be useful to confirm the diagnosis and especially
evaluate concomitant pleuropulmonary diseases and lymphadenopathies, thus suggesting a possible etiology of
pericarditis (ie, TB, lung cancer) [26]. 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. Computed
tomographic 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).

Cardiac magnetic resonance (CMR) imaging 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).

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 4). 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. (See "Acute pericarditis: Treatment and prognosis", section on 'Adjunctive therapies'.)

● 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 the pericardial space are based upon the presence of an associated effusion, 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 for tuberculosis. (See "Diagnosis and treatment of
pericardial effusion" and "Pericardial disease associated with malignancy".)

• Pericardiocentesis may also be performed for diagnostic and/or therapeutic purposes for large effusions
refractory to medical treatment [30].

• 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 "Diagnosis and treatment of 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 [30,31]. Tissue samples should be sent for cytology, tumor
markers, gram stain, bacterial cultures, and, if tuberculosis is suspected, polymerase chain reaction testing.
(See "Diagnosis and treatment of pericardial effusion", section on 'Pericardial fluid analysis and biopsy'.)

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 upon 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) (table 1) [11]. In addition, among patients at high risk of coronary disease, myocardial
ischemia must be ruled out by appropriate studies.

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 [12,17,28]. 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 1 and table 5) [6,11-13,32-34]. Acute viral or idiopathic pericarditis typically follows a brief and
benign course after empiric treatment with anti-inflammatory drugs. (See "Acute pericarditis: Treatment and
prognosis".)

DIAGNOSIS

Acute pericarditis is diagnosed by the presence of at least two of the following criteria (table 6) [5,14,17,28,33]:

● 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)
● Suggestive 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 [35]. 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 CT or pericardial edema and late gadolinium enhancement on cardiac
magnetic resonance (CMR) [10,35]. (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 [10]. Additional testing, which
typically includes blood work, chest radiography, electrocardiography, and echocardiography, can support the
diagnosis but is frequently normal or unrevealing. The ECG is usually the most helpful test in the evaluation of
patients with suspected acute pericarditis. Echocardiography is often normal, but can be an essential part of the
evaluation if there is evidence of an associated pericardial effusion and/or signs of cardiac tamponade.

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.
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 are
reported as myopericarditis; alternatively, the term perimyocarditis is sometimes used when myocardial
involvement is most prominent. However, in clinical practice, myopericarditis is more common and this term is
often used in both senses. (See "Myopericarditis".)

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

● 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. (See 'Epidemiology' above.)

● Idiopathic cases, most of which are probably viral in etiology, are the most common causes of acute
pericarditis. Other etiologies of acute pericarditis 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.)

● 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 pleuritic chest pain,
pericardial friction rub, and ECG changes, with or without a pericardial effusion. Pericarditis should also be
suspected in a patient with persistent fever and pericardial effusion or new unexplained cardiomegaly. (See
'Clinical features' above.)

● High-risk patients with acute pericarditis should be admitted in order to initiate appropriate therapy and to
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. Conversely, patients with uncomplicated (ie,
low-risk) acute pericarditis can usually be evaluated and sent home, with outpatient follow-up. (See
'Determination of risk and need for hospitalization' above.)
 ● 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 or myocardial damage),
chest radiography, electrocardiography, and echocardiography. Follow-up testing should be performed on a
case by case basis and may include blood cultures, additional bloodwork (eg, ANA titer, HIV serology, etc),
and additional cardiac imaging. (See 'Our approach to diagnostic testing' above.)

● Acute pericarditis is diagnosed by the presence of at least two of the following criteria (table 6) (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.)

• Suggestive changes on the ECG (typically widespread ST segment elevation) (waveform 1). (See
'Electrocardiogram' above.)

• New or worsening pericardial effusion. (See 'Echocardiogram' above.)

● 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 upon 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) (table 1). (See 'Establishing a definite etiology' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Imazio M. Contemporary management of pericardial diseases. Curr Opin Cardiol 2012; 27:308.

2. Spodick DH. Acute cardiac tamponade. N Engl J Med 2003; 349:684.

3. Kytö V, Sipilä J, Rautava P. Clinical profile and influences on outcomes in patients hospitalized for acute
pericarditis. Circulation 2014; 130:1601.

4. Imazio M, Cecchi E, Demichelis B, et al. Myopericarditis versus viral or idiopathic acute pericarditis. Heart
2008; 94:498.

5. Troughton RW, Asher CR, Klein AL. Pericarditis. Lancet 2004; 363:717.

6. Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med 2004; 351:2195.
 7. Little WC, Freeman GL. Pericardial disease. Circulation 2006; 113:1622.

8. Heidenreich PA, Eisenberg MJ, Kee LL, et al. Pericardial effusion in AIDS. Incidence and survival.
Circulation 1995; 92:3229.

9. Chen Y, Brennessel D, Walters J, et al. Human immunodeficiency virus-associated pericardial effusion:

report of 40 cases and review of the literature. Am Heart J 1999; 137:516.

10. Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic Review. JAMA
2015; 314:1498.

11. 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.

12. Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute pericarditis. Circulation 2007;
115:2739.

13. Imazio M, Trinchero R. Clinical management of acute pericardial disease: a review of results and outcomes.
Ital Heart J 2004; 5:803.

14. Spodick DH. Acute pericarditis: current concepts and practice. JAMA 2003; 289:1150.

15. Spodick DH. Acute, clinically noneffusive ("dry") pericarditis. In: Spodick DH: The Pericardium: A Comprehe
nsive Textbook, Marcel Dekker, New York 1997. p.94-113.

16. Spodick DH. Pericardial rub. Prospective, Multiple observer investigation of pericardial friction in 100
patients. Am J Cardiol 1975; 35:357.

17. 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.

18. Spodick, DH. The Pericardium: A Comprehensive Textbook, Marcel Dekker, New York 1997. p.46-64.

19. Rutsky, EA, Rostand, SG . Pericarditis in end-stage renal disease: Clinical characteristics and
management. Semin Dial 1989; 2:25.

20. Chou TC. Electrocardiography in clinical practice, WB Saunders Company, Philadelphia 1996.

21. Spodick DH. Arrhythmias during acute pericarditis. A prospective study of 100 consecutive cases. JAMA
1976; 235:39.

22. Chou TC. Electrocardiography in Clinical Practice: Adults and Pediatrics, 4th ed, WB Saunders, Philadelphi
a 1996.

23. Klatsky AL, Oehm R, Cooper RA, et al. The early repolarization normal variant electrocardiogram:
correlates and consequences. Am J Med 2003; 115:171.
 24. Spodick DH. Differential characteristics of the electrocardiogram in early repolarization and acute
pericarditis. N Engl J Med 1976; 295:523.

25. Ginzton LE, Laks MM. The differential diagnosis of acute pericarditis from the normal variant: new
electrocardiographic criteria. Circulation 1982; 65:1004.

26. 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.

27. Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/AHA/ASE 2003 guideline for the clinical application
of echocardiography www.acc.org/qualityandscience/clinical/statements.htm (Accessed on August 24, 200
6).

28. 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.

29. Imazio M, Demichelis B, Cecchi E, et al. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol 2003;
42:2144.

30. Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of pericardial diseases.
Circulation 2010; 121:916.

31. 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.

32. Maisch B, Ristić AD. The classification of pericardial disease in the age of modern medicine. Curr Cardiol
Rep 2002; 4:13.

33. 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.

34. Permanyer-Miralda G. Acute pericardial disease: approach to the aetiologic diagnosis. Heart 2004; 90:252.

35. 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.

Topic 4940 Version 28.0

GRAPHICS

Causes of pericardial disease

Idiopathic (presumed to be viral, postviral, or immune-mediated)

In most case series, the majority of patients are not found to have an identifiable cause of pericardial disease. Frequently such cases
are presumed to have a viral or autoimmune etiology.

Infectious
Viral - Coxsackievirus, echovirus, adenovirus, Epstein-Barr virus, cytomegalovirus, influenza, varicella, rubella, HIV, hepatitis B,
mumps, parvovirus B19, vaccina (smallpox vaccine)

Bacterial - Mycobacterium tuberculosis (most common cause in countries where tuberculosis is endemic), Staphylococcus,
Streptococcus, Haemophilus, Neisseria (N. gonorrhoeae or N. meningitidis), Chlamydia (C. psittaci or C. trachomatis), Legionella,
Salmonella, Borrelia burgdorferi (the cause of Lyme disease), Mycoplasma, Actinomyces, Nocardia, Tropheryma whippelii,
Treponema, Rickettsia

Fungal - Histoplasma, Aspergillus, Blastomyces, Coccidioides, Candida

Parasitic - Echinococcus, amebic, Toxoplasma

Infective endocarditis with valve ring abscess

Noninfectious
Autoimmune and autoinflammatory

Systemic inflammatory diseases, especially lupus, rheumatoid arthritis, scleroderma, Sjögren syndrome, vasculitis, mixed
connective disease

Autoinflammatory diseases (especially familial Mediterranean fever and tumor necrosis factor associated periodic syndrome
[TRAPS], IgG4-related disease)

Postcardiac injury syndromes (immune-mediated after cardiac trauma in predisposed individuals)

Other - Granulomatosis with polyangiitis (Wegener's), polyarteritis nodosa, sarcoidosis, inflammatory bowel disease (Crohn's,
ulcerative colitis), Whipple's, giant cell arteritis, Behçet syndrome, rheumatic fever

Neoplasm

Metastatic - Lung or breast cancer, Hodgkin's disease, leukemia, melanoma

Primary - Rhabdomyosarcoma, teratoma, fibroma, lipoma, leiomyoma, angioma

Paraneoplastic

Cardiac

Early infarction pericarditis

Late postcardiac injury syndrome (Dressler's syndrome), also seen in other settings (eg, post-myocardial infarction and post-cardiac
surgery)

Myocarditis

Dissecting aortic aneurysm

Trauma

Blunt

Penetrating

Iatrogenic - Catheter and pacemaker perforations, cardiopulmonary resuscitation, post-thoracic surgery

Metabolic

Hypothyroidism - Primarily pericardial effusion

Uremia

Ovarian hyperstimulation syndrome

Radiation

Drugs (rare)

Procainamide, isoniazid, or hydralazine as part of drug-induced lupus

Other - Cromolyn sodium, dantrolene, methysergide, anticoagulants, thrombolytics, phenytoin, penicillin, phenylbutazone,
doxorubicin
References:
1. LeWinter M. Clinical practice. Acute pericarditis. N Engl J Med 2014; 371:2410.
2. Imazio M, Gaita F. Diagnosis and treatment of pericarditis. Heart 2015; 101:1159.
3. Imazio M. Contemporary management of pericardial diseases. Curr Opin Cardiol 2012; 27:308.

Graphic 67851 Version 9.0

Differentiation of life-threatening causes of chest pain

Additional
Historical Examination Chest Additional
Diagnosis Electrocardiogram important
features findings radiograph tests
information

Acute • • Nonspecific • ST segment elevations, • Nonspecific • Troponin • Assume

coronary Substernal/left- • May detect Q waves, new left • May show evidence and/or CK-MB symptoms of
syndrome sided chest signs of HF bundle branch block are of HF elevations ACS within days
pressure or evidence of AMI diagnose AMI or a few weeks
tightness is • Single ECG is not • Single set of PCI or CABG
common sensitive for ACS of biomarkers is from an
• Onset is is not occluded artery
• Prominent R waves
gradual sufficiently or graft
with ST segment
• Pain radiating depressions in V 1 and sensitive to
to shoulders or V 2 strongly suggests rule out AMI
pain with posterior AMI
exertion
increases
relative risk
• "Atypical"
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 in • Wide mediastinum • Can mimic
dissection of sharp, extremity or 15 percent or loss of normal many diseases
tearing, or carotid pulse is • Nonspecific ST and T aortic knob contour depending on
ripping pain suggestive changes in 30 percent is common (up to 76 branch arteries
• Maximal • Discrepancy in percent) involved (eg,
severity at systolic BP >20 • 10 percent have AMI, stroke)
onset mmHg between normal CXR
• Most often right and left
begins in chest, upper extremity
can begin in is suggestive
back • Up to 30
• Can mimic percent with
stroke, ACS, neurologic
mesenteric findings
ischemia, • Findings vary
kidney stone with arteries
affected

Pulmonary • Many possible • No finding is • Usually abnormal but • Great majority are • A high-
embolism presentations, sensitive or nonspecific normal sensitivity D-
including specific • Signs of right heart • May show dimer is
pleuritic pain • Extremity strain suggestive (eg, atelectasis, elevated useful to rule
and painless exam generally RAD, RBBB, RAE) hemidiaphragm, out PE only
dyspnea normal pleural effusion when
• Often sudden negative in
• Lung exam
onset low-risk
generally
patients
• Dyspnea nonspecific; focal
often dominant wheezing may
feature be present;
 tachypnea is
common

Tension • Often sudden • Ipsilateral • Demonstrates air in

pneumothorax onset diminished or pleural space
• Initial pain absent breath
often sharp and sounds
pleuritic • Subcutaneous
• Dyspnea emphysema is
often dominant uncommon
feature

Pericardial • Pain from • Severe • Decreased voltage and • May reveal • Ultrasound
tamponade pericarditis is tamponade electrical alternans can enlarged heart reveals
most often creates appear with significant pericardial
sharp anterior obstructive effusions effusion with
chest pain shock and • Diffuse PR segment tamponade
made worse by causes jugular depressions and/or ST
inspiration or venous segment elevations can
lying supine distension, appear with acute
and relieved by pulsus pericarditis
sitting forward paradoxus
• Dyspnea is • Pericardial
common effusion can
cause friction
rub

Mediastinitis • Forceful • Ill-appearing; • Large majority

(esophageal vomiting often shock; fever have some
rupture) precedes • May hear abnormality:
esophageal (Hamman's) pneumomediastinum,
rupture crunch over pleural effusion,
• Recent upper mediastinum pneumothorax
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 3.0

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.

Graphic 86234 Version 1.0

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 Spinger: Myopericardial Diseases, Imazio M (Ed). Copyright © 2016.

Graphic 115268 Version 2.0

Electrocardiogram (ECG) in pericarditis

Electrocardiogram in acute pericarditis showing diffuse upsloping 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.

Graphic 77572 Version 4.0

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°.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 4.0

Electrocardiogram features of acute pericarditis versus acute myocardial infarction

ECG features Findings in acute pericarditis Findings in acute MI

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

ST segment elevation distribution Widespread ST segment elevation in Anatomical groupings of leads show ST
most/all leads segment elevation, which corresponds
Typically most prominent in inferolateral to vascular territory of infarction
leads

Reciprocal ST segment changes Usually not seen ST segment depressions usually seen in
reciprocal leads

Concurrent ST elevation and T wave Unusual unless concomitant myocarditis Common

inversion

PR segment changes PR elevation in aVR and PR depression Rare

in most/all other leads

Other ECG findings Rare; if seen, due to fusion of elevated Commonly seen at onset of acute
Hyperacute T waves ST segment and T wave infarction/ischemia
Q waves Not usually new from acute pericarditis Seen late in course of MI due to
QT prolongation Unusual transmural injury
Can be seen

ECG: electrocardiogram; MI: myocardial infarction.

Graphic 115285 Version 1.0

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.

Courtesy of Ary Goldberger, MD.

Graphic 81914 Version 3.0

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°.

Courtesy of Ary Goldberger, MD.

Graphic 76183 Version 4.0

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.

Graphic 60464 Version 4.0

ECG of sinus rhythm to Normal electrocardiogram (ECG)

Normal sinus rhythm at a rate of 71 beats/minute, a P wave axis of 45°, and a PR

interval of 0.15 seconds.

ECG: electrocardiogram.

Courtesy of Morton Arnsdorf, MD.

Graphic 58149 Version 5.0

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.

Graphic 83883 Version 2.0

Chest x-ray 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.

Graphic 57640 Version 3.0

Pericardial edema and LGE by CMR

(A) Pericardial edema.

(B) Pericardial LGE.

LGE: late gadolinium enhancement; CMR: cardiac magnetic resonance.

Reprinted by permission from Spinger: Myopericardial Diseases, Imazio M (Ed). Copyright © 2016.

Graphic 115269 Version 2.0

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.

Graphic 69338 Version 1.0

Acute pericarditis etiologies: Data from published clinical studies with unselected populations

Permanyer-Miralda G. Zayas R. et Imazio M. et Reuter H. et Gouriet F. et

et al. al. al. al. al.
(n = 231) (n = 100) (n = 453) (n = 233) (n = 933)

Years 1977-1983 1991-1993 1996-2004 1995-2001 2007-2012

Location Spain Spain Italy Africa Western Europe

Idiopathic 199 (86.0 percent) 78 (78.0 377 (83.2 32 (13.7 percent) 516 (55.0
percent) percent) percent)

Specific etiology 32 (14.0 percent) 22 (22.0 76 (16.8 percent) 201 (86.3 417 (46.0
percent) percent) percent)

Neoplastic 13 (5.6 percent) 7 (7.0 percent) 23 (5.1 percent) 22 (9.4 percent) 85 (8.9 percent)

Tuberculosis 9 (3.9 percent) 4 (4.0 percent) 17 (3.8 percent) 161 (69.5 4 (<1.0 percent)
percent)

Autoimmune 4 (1.7 percent) 3 (3.0 percent) 33 (7.3 percent) 12 (5.2 percent) 197 (21 percent)
etiologies

Purulent 2 (0.9 percent) 1 (1.0 percent) 3 (0.7 percent) 5 (2.1 percent) 29 (3.0 percent)

Data from:
1. Permanyer-Miralda G, Sagrista-Sauleda J, Soler-Soler J. Primary acute pericardial disease: A prospective series of 231 consecutive
patients. Am J Cardiol 1985; 56:623.
2. 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.
3. Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute pericarditis. Circulation 2007; 115:2739.
4. 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.
5. Gouriet F, Levy PY, Casalta JP, et al. Etiology of pericarditis in a prospective cohort of 1162 cases. Am J Med 2015; 128:784.

Graphic 60949 Version 5.0

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 or 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.

Graphic 74376 Versión 7.0

Divulgaciones del contribuyente
Massimo Imazio, MD, Consultor de FESC / Consejos Asesores: SOBI [pericarditis recurrente (Anakinra)]; Kiniksa
[pericarditis recurrente (rilonacept)]. Martin M LeWinter, MD Nada que revelar Brian C Downey, MD, FACC Nada que
revelar

Las revelaciones de los contribuyentes son revisadas para los conflictos de interés por el grupo editorial. Cuando se
encuentran, estos se abordan examinando un proceso de revisión multinivel y los requisitos para que se proporcionen
referencias que respalden el contenido. El contenido referenciado adecuadamente es requerido por todos los autores y debe
cumplir con los estándares de evidencia UpToDate.

Política de conflicto de intereses.