Acute pericarditis (Clinical presentation and diagnostic evaluation)
INTRODUCTION
1.
The pericardium is fibroelastic sac made up of visceral and parietal layers separated by
(potential) space, pericardial cavity. In healthy individuals, pericardial cavity contains 15 to 50
mL of ultrafiltrate of plasma. Pericardial diseases are relatively common in clinical practice
and may have different presentations either as isolated disease or as manifestation of
systemic disorder. Although etiology is varied and complex, pericardium has relatively
non-specific response to these different causes with inflammation of pericardial layers and
possible increased production of pericardial fluid. Chronic inflammation with fibrosis and
calcification can lead to a rigid, usually thickened and calcified pericardium, with possible
progression to pericardial constriction.
2.
Diseases of pericardium present clinically in one of several ways.
A. Acute and recurrent pericarditis
B. Pericardial effusion without major hemodynamic compromise
C. Cardiac tamponade
D. Constrictive pericarditis
E. Effusive-constrictive pericarditis
Acute pericarditis refers to inflammation of pericardial sac. The term myopericarditis is used
for cases of acute pericarditis that also demonstrate myocardial inflammation. 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
3.
disease processes are discussed separately.
EPIDEMIOLOGY
1. Acute pericarditis is the most common disorder involving pericardium. Epidemiologic studies
are lacking, and exact incidence and prevalence of acute pericarditis are unknown. However,
acute pericarditis is recorded in about 0.1 to 0.2% of hospitalized patients and 5% of patients
admitted to the Emergency Department for non-ischemic chest pain.
A. In observational study from an urban area in Northern Italy incidence of acute
pericarditis was 27.7 cases per 100,000 persons per year.
B. In observational study from Finland that included 670,409 CV admissions to 29 hospitals
across country over 9.5-year period, standardized incidence rate for pericarditis
2.
requiring hospitalization was 3.3 cases per 100,000 person-years.
Acute pericarditis is common disorder in several clinical settings, where it may be the first
manifestation of underlying systemic disease or may represent an isolated process (table 1).
In developed countries, most cases of acute pericarditis are considered of possible or
confirmed viral origin, although exact etiology of most cases remains undetermined following
traditional diagnostic approach.
3.
Prior to widespread availability of antiretroviral therapy to treat infection with HIV,
pericardial disease was the most frequent CV manifestation of AIDS. However, in developed
countries with access to HIV therapy, patients with HIV infection who develop acute
pericarditis have etiologic spectrum very similar to non-HIV infected patients. On contrary,
HIV and TB persist as major causes of acute pericarditis in developing countries.
CLINICAL FEATURE
1. Acute pericarditis can present in variety of ways, depending on underlying etiology. Patients
with infectious etiology may present with S/S of systemic infection such as fever and
leukocytosis. Viral etiologies in particular may be preceded by “flu-like” respiratory or GI
symptoms. Patients with known autoimmune disorder or malignancy may present with signs
or symptoms specific to their underlying disorder.
2.
3.
The major clinical manifestations of acute pericarditis.
A. Chest pain – typically sharp and pleuritic, improved by sitting up and leaning forward
B. Pericardial friction rub – a superficial scratchy or squeaking sound best heard with the
diaphragm of the stethoscope over the left sternal border
C. ECG changes – new widespread ST elevation or PR depression
D. Pericardial effusion
Chest pain
A. The vast majority of patients with acute pericarditis present with chest pain (> 95% of
cases). 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
B.
C.
associated with rheumatologic disorder (although in some patients pleuritic chest pain
and pericarditis is initial presentation of SLE).
Chest pain that results from acute pericarditis is typically fairly sudden in onset and
occurs over 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 tendency for decrease in intensity
when patient sits up and leans forward. This position (seated, leaning forward) tends to
reduce pressure on parietal pericardium, particularly with inspiration, and may also
allow for splinting of diaphragm.
However, dull, oppressive pain or radiation of pain to shoulders (particularly trapezius
ridges) may occur; in such cases it is difficult to distinguish pericarditis from other causes
of chest pain. The chest pain of pericarditis must always be distinguished from other
common and/or life-threatening causes of chest pain such as AMI, PE, aortic dissection,
GERD, and musculoskeletal pain.
4.
Pericardial friction rub
A. The presence of pericardial friction rub on PE is highly specific for acute pericarditis
B.
C.
D.
(movie 1). Pericardial friction rubs, which occur during maximal movement of heart
within its pericardial sac, are said to be generated by friction between two inflamed
layers of pericardium. However, this commonly offered explanation for its mechanism
may be oversimplification as patients with pericardial effusion may also have audible
friction rub.
The classic friction rub consists of three phases, corresponding to movement of heart
during atrial systole (which is not heard in patients with Af), ventricular systole, and
rapid filling phase of early ventricular diastole. However, some rubs are present only
during one (one component) or two phases (two components) of cardiac cycle. In review
of auscultation and phonocardiography in 100 patients with pericardial rub, rub was
triphasic in 56% of patients in SR; overall, biphasic rubs were present in 33% and
monophasic rubs in 15%.
Pericardial rubs have superficial scratchy or squeaking quality that is best heard with
diaphragm of stethoscope. They may be localized or widespread, but are usually loudest
over left sternal border. The intensity of rub frequently increases after application of
firm pressure with diaphragm, during suspended respiration, and with patient leaning
forward or resting on elbows and knees. This last maneuver is designed to increase
contact between visceral and parietal pericardium, but is seldom used in practice since it
is cumbersome for patient.
Friction rubs tend to vary in intensity and can come and go over period of hours;
therefore, sensitivity for detection of rub is variable and depends in large part on
frequency of auscultation. Pericardial rubs may be easier to hear in patients without
pericardial effusion, but this finding is not universal and is not well-documented. In
report of 100 patients with acute pericarditis, pericardial rub was present in 34 of 40
(85%) without effusion. This prevalence is considerably higher than 35% incidence of
friction rubs reported in another series.
E.
5.
Suspension of respiration during auscultation permits distinction of pericardial friction
rub from pleuropericardial or pleural rub. A pleuropericardial rub results from friction
between inflamed pleura and parietal pericardium, while pleural rub is result of friction
between inflamed visceral and parietal pleura. As such, pleuropericardial and pleural
rubs can be heard only during inspiratory phase of respiration.
Electrocardiogram
A. Changes in ECG in patients with acute pericarditis signify inflammation of epicardium,
since parietal pericardium itself is electrically inert. However, some causes of pericarditis
do not result in significant inflammation of epicardium and, as such, may not alter ECG.
An illustration of this is uremic pericarditis, in which there is prominent fibrin deposition
but little or no epicardial inflammation. As result, ECG often shows none of changes
associated with pericarditis.
B. ECG in acute pericarditis can evolve through as many as four stages of changes. However,
pericarditis does not always result in significant ECG changes. One series of 300
consecutive patients with acute pericarditis noted typical ECG evolution in 60% of cases.
C. The typical progression of ECG changes in patients with acute pericarditis.
i.
Stage 1, seen in first hours to days, is characterized by diffuse STE (typically concave
up) with reciprocal STD in leads aVR and V1 (waveform 1). There is also atrial
current of injury, reflected by elevation of PR segment in lead aVR and depression
of PR segment in other limb leads and in left chest leads, primarily V5 and V6. Thus,
PR and ST segments typically change in opposite directions. PR segment deviation,
which is highly specific though less sensitive, is frequently overlooked. TP segment
is recommended as baseline for comparison when measuring both PR and ST
segment changes in acute pericarditis.
ii.
Stage 2, typically seen in the first week, is characterized by normalization of ST and
PR segments.
iii.
Stage 3 is characterized by development of diffuse TWI, generally after ST segments
have become isoelectric. However, this stage is not seen in some patients.
iv.
Stage 4 is represented by normalization of ECG or indefinite persistence of TWI
("chronic" pericarditis).
D. The temporal evolution of ECG changes with acute pericarditis is highly variable from
E.
one patient to another. Treatment can accelerate or alter ECG progression. The duration
of ECG changes in pericarditis also depends upon its cause and extent of associated
myocardial damage.
Atypical ECG changes are seen in up to 40% of patients with acute pericarditis. For
example, localized STE and TWI occur before ST-segment normalization in minority of
patients with acute pericarditis without myocardial involvement. These changes can
simulate ECG changes seen in patients with ACS.
F.
Sustained arrhythmias are uncommon in acute pericarditis, except in post-thoracotomy
setting. This was illustrated in review of 100 consecutive patients in which only 7
arrhythmias were identified; all were atrial and all occurred in patients with underlying
heart disease. In separate report comparing patients with myopericarditis and simple
acute pericarditis, cardiac arrhythmias were also more commonly present in patients
with myopericarditis (OR 17.6). Thus, presence of atrial or ventricular arrhythmias is
suggestive of concomitant myocarditis or unrelated cardiac disease.
G. ECG differentiation from acute myocardial infarction
i.
While both acute pericarditis and AMI can present with chest pain and elevations in
cardiac biomarkers, ECG changes in acute pericarditis differ from those in STEMI in
several ways. These distinctions assume that pericarditis does not occur during or
ii.
iii.
iv.
v.
vi.
soon after AMI.
Morphology – STE in acute pericarditis begins at J point, which represents junction
between end of QRS complex (termination of depolarization) and beginning of ST
segment (onset of ventricular repolarization). STE rarely exceeds 5 mm, and usually
retains its normal concavity. In some cases of acute pericarditis, ST segment rises
obliquely in straight line. Although similar patterns can occur with STEMI, typical
finding in STEMI patient is convex (dome-shaped) STE (pattern not characteristic of
acute pericarditis) that may be > 5 mm in height. The basis for these morphologic
differences is not known, but is probably related to the greater injury current
associated with infarction.
Distribution – STE in STEMI are characteristically limited to anatomical groupings of
leads that correspond to localized vascular area of infarct (anteroseptal and
anterior leads V1 to V4; lateral leads I, aVL, V5, V6; inferior leads II, III, aVF). The
pericardium envelops heart, therefore ST changes are more generalized and
typically are present in most leads. In pericarditis, STE in precordial leads is most
commonly seen in V5 and V6, and in decreasing frequency from V4 to V1, while in
limb leads, it is often more evident in leads I and II than in leads III, aVF, and aVL.
Reciprocal changes –STEMI is often associated with reciprocal ST segment changes,
which are not seen with pericarditis except in leads aVR and V1.
Concurrent ST-T changes – STE and TWI do not generally occur simultaneously in
pericarditis, while they commonly coexist in STEMI. Furthermore, evolution of
repolarization abnormalities often takes place more slowly and more
asynchronously among affected leads in pericarditis than in STEMI.
Hyperacute T waves – Peaked T waves (> 10mm high in precordial leads, > 5 mm
high in limb leads), also referred to as hyperacute T waves, can be seen in STEMI
but are not typical of pericarditis. Rarely, fusion of ST segment and T wave into
single monophasic wave in pericarditis can mimic appearance of hyperacute T
waves.
vii.
viii.
ix.
Q waves – Pathologic Q waves, which may occur with extensive injury in STEMI, are
generally not seen in pericarditis. The abnormal Q waves in MI reflect loss of
positive depolarization voltages because of transmural myocardial necrosis.
Pericarditis, on the other hand, generally causes only superficial inflammation.
Abnormal Q waves are not seen unless there is concomitant myocarditis or
preexisting cardiomyopathy or myocardial infarction.
PR segment – PR elevation in aVR with PR depression in other leads due to
concomitant atrial current of injury is frequently seen in acute pericarditis but
rarely seen in STEMI.
QT prolongation – Prolongation of QT interval with regional TWI (in absence of
drug effects or relevant metabolic disorders) favors diagnosis of AMI (or
myopericarditis) over pericarditis alone.
H. ECG differentiation from early repolarization
i.
The early repolarization variant seen on ECG may be present in as many as 30% of
young adults and is often confused with acute pericarditis. Early repolarization is
characterized by STE of J point, which represents junction between end of QRS
complex (termination of depolarization) and beginning of ST segment (onset of
ventricular repolarization). As result, there is STE segment itself, which maintains its
normal configuration (waveform 4). In early repolarization, STE is most often
present in anterior and lateral chest leads (V3-V6), although other leads can be
involved.
ii.
6.
The following ECG features can be helpful in distinguishing acute pericarditis from
early repolarization.
1. STE occur in both limb and precordial leads in most cases of acute pericarditis
(47 of 48 in one study), whereas about 50% of subjects with early
repolarization have no ST deviations in limb leads.
2. PR deviation and evolution of ST and T changes strongly favor pericarditis, as
neither is seen in early repolarization.
3. If ratio of STE to T wave amplitude in lead V6 exceeds 0.24, acute pericarditis is
present (PPV and NPV are both 100%).
Laboratory and imaging findings
A.
Echocardiogram
i.
UCG is often normal in patients with clinical syndrome of acute pericarditis unless
there is associated pericardial effusion. While finding of pericardial effusion in
patient with known or suspected pericarditis supports diagnosis, absence of
pericardial effusion or other UCG abnormalities does not exclude it. In one series of
300 consecutive patients with acute pericarditis, pericardial effusion was present in
180 patients (60%). In most cases effusion was small or moderate in size (79 and
10%) without hemodynamic consequences. Cardiac tamponade was present in only
5% of patients.
B.
Chest x-ray
i.
CXR 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 cardiac silhouette enlarges.
However, acute pericarditis should be considered in the evaluation of patient with
new and otherwise unexplained cardiomegaly.
C. Cardiac biomarker
i.
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 elevated level of Tn-I was detected in 38
patients (32%). Such patients should be considered to have myopericarditis.
D. Signs of inflammation
i.
Since pericarditis is inflammatory disease, laboratory signs of inflammation are
common in patients with acute pericarditis. These include elevations in WBC, ESR,
and serum CRP. While elevation in these markers supports diagnosis, they are
neither sensitive nor specific for acute pericarditis. Additionally, in hyperacute
phase of pericarditis, these markers may remain normal and increased levels may
be found only on follow-up.
DIAGNOSIS
1. The diagnosis of acute pericarditis is usually suspected based on history of characteristic
2.
pleuritic chest pain, and confirmed if pericardial friction rub is present. Pericarditis should
also be suspected in patient with persistent fever and pericardial effusion or new unexplained
cardiomegaly. Additional testing, which typically includes blood work, CXR, ECG, and UCG, can
support diagnosis but is frequently normal or unrevealing. ECG is usually the most helpful test
in evaluation of patients with suspected acute pericarditis. UCG is often normal, but can be
essential part of evaluation if there is evidence of associated pericardial effusion and/or signs
of cardiac tamponade.
Evaluation
A. Initial history and physical examination
i.
This evaluation should consider disorders that are known to involve pericardium,
such as prior malignancy, autoimmune disorders, uremia, recent MI and prior
cardiac surgery. The examination should pay particular attention to auscultation for
pericardial friction rub and signs associated with tamponade.
B. Initial testing.
i.
ECG in all cases.
ii.
CXR in all cases.
iii.
CBC, Tn-I, ESR, and serum CRP.
iv.
Blood cultures if fever > 38ºC or signs of sepsis.
v.
UCG should be performed in all cases, with urgent UCG if cardiac tamponade is
suspected. Even small effusion can be helpful in confirming diagnosis of pericarditis,
although absence of effusion does not exclude diagnosis. In addition, UCG 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 new finding.
vi.
2003 ACC/AHA/ASE guidelines for clinical application of UCG stated that evidence
and/or general agreement supported use of UCG for evaluation of all patients with
suspected pericardial disease. Similarly, 2013 expert consensus statement from ASE
recommends UCG for all patients with acute pericarditis.
C. Additional testing.
i.
ii.
iii.
iv.
v.
D.
E.
F.
G.
Tuberculin skin test or QuantiFERON if not recently performed. QuantiFERON is
most helpful in immunocompromised or HIV positive patients and in regions where
tuberculosis is endemic.
ANA in selected cases (young women, especially those in whom history suggests
rheumatologic disorder). Rarely, acute pericarditis is initial presentation of SLE. It is
important to recognize that positive ANA is non-specific test. A rheumatology
consult should be sought in patients with pericarditis in whom diagnosis of SLE is
being entertained.
HIV serology
CT may be useful to confirm diagnosis and especially evaluate concomitant
pleuropulmonary diseases and lymphadenopathies, thus suggesting possible
etiology of pericarditis (TB, lung cancer). Non-calcified pericardial thickening with
pericardial effusion is suggestive of acute pericarditis. Moreover, with
administration of contrast, enhancement of thickened visceral and parietal surfaces
of pericardial sac confirms presence of active inflammation. CT attenuation values
can help in differentiation of exudative fluid (20 to 60 HU), as found with purulent
pericarditis, and simple transudative fluid (< 10 HU).
CMRI may be performed if UCG is unrevealing but diagnosis of acute pericarditis is
suspected, especially in patients with ongoing fever, poor response to treatment, or
suspicion of hemodynamic compromise.
Multimodality imaging is integral part of modern management for pericarditis and
pericardial diseases. Among multimodality imaging tests, UCG is most often 1st-line test,
followed by CMR and/or CT.
We do not get routine viral survey, since yield is low and management is not altered.
Pericardiocentesis should be performed for therapeutic purposes in patients with
cardiac tamponade.
Pericardiocentesis should be considered for diagnostic purposes in patients suspected of
having malignant or bacterial etiology, or in patients with effusion refractory to medical
therapy.
3.
Clinical diagnostic criteria
A. Acute pericarditis refers to inflammation of pericardial sac. The term myopericarditis, or
B.
perimyocarditis, is used for cases of acute pericarditis that also demonstrate features
consistent with myocardial inflammation.
Because 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 dominant site of
involvement. Cases that involve myocardium in which pericarditis is predominant are
reported as myopericarditis; alternatively, 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.
C. Acute pericarditis
i.
Acute pericarditis is diagnosed by presence of at least two of following criteria
(table 2).
1. Typical chest pain (sharp and pleuritic, improved by sitting up and leaning
forward)
2. Pericardial friction rub (superficial scratchy or squeaking sound best heard with
diaphragm of stethoscope over left sternal border) (movie 1)
3. Suggestive changes on ECG (typically widespread STE)
4. New or worsening pericardial effusion
ii.
While UCG is often normal, and absence of pericardial effusion does not exclude
pericarditis, UCG remains essential part of evaluation if there is evidence of
associated pericardial effusion and/or signs of cardiac tamponade.
D. Myopericarditis
i.
When acute pericarditis is present, myopericarditis can be diagnosed by detection
of one or both of the following in absence of evidence of another cause.
1. Elevation in serum cardiac biomarkers, such as Tn-I
2. New or presumed new focal or global LV systolic dysfunction on imaging
ii.
A more complete discussion of diagnosis of myopericarditis is presented separately.
IDENTIFYING ETIOLOGY
1.
The yield of standard diagnostic evaluation to determine etiology of acute pericarditis is
relatively low. This was illustrated in 3 series that included total of 784 unselected patients
who underwent extensive evaluation. A specific diagnosis was established in only 130
patients (17%) (table 3).
A. Neoplasia – 5%
B. Tuberculosis – 4%
C. Autoimmune etiologies – 5%
D. Purulent pericarditis – 1%
2.
3.
4.
5.
In Western countries, unless there is 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 3). Acute viral or idiopathic
pericarditis typically follows brief and benign course after empiric treatment with
anti-inflammatory drugs.
Because of relatively benign course associated with common causes of pericarditis, it is not
necessary to search for etiology in all patients with acute pericarditis. Initial efforts should
focus upon excluding a significant effusion or tamponade and identification of patients in
whom more comprehensive evaluation should be performed to exclude causes that require
specific therapy (malignancy, TB or purulent pericarditis) (table 1). In addition, among
patients at high risk of CAD, myocardial ischemia must be ruled out by appropriate studies.
Indication for pericardiocentesis and pericardial biopsy
A. Studies in patients with acute pericarditis have reported low yield for diagnostic
pericardiocentesis and pericardial biopsy; however, some authors have advocated for
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 diagnosis of acute pericarditis, it may rarely be necessary in attempt to diagnose
specific etiology.
Pericardiocentesis
A.
B.
C.
In patients with pericardial effusion, pericardiocentesis or surgical drainage can serve
both diagnostic and therapeutic purposes. Among patients with acute pericarditis,
decisions regarding drainage of pericardial space are based upon presence of associated
effusion, its UCG characteristics (size and composition), and clinical significance (causing
hemodynamic compromise).
i.
Patients with symptomatic effusions and evidence of cardiac tamponade should
undergo prompt pericardial drainage.
ii.
When significant pericardial effusion is present, diagnostic pericardiocentesis is
indicated if specific etiology is highly suspected, and diagnosis cannot be reached by
other means. The investigation is especially indicated when neoplastic or bacterial
etiology is suspected because definite diagnosis can only be made by identification
of etiologic agent in 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.
Pericardiocentesis is considered also for large effusions refractory to medical treatment.
Effusions that are small to moderate in size and do not cause hemodynamic compromise
(cardiac tamponade) generally do not require drainage, unless a sample of the effusion
is necessary for diagnostic purposes. Moreover, pericardiocentesis performed
percutaneously has significantly higher complication rate if effusion is not large.
D.
6.
A detailed discussion regarding the performance of pericardiocentesis and the treatment
of pericardial effusions is presented separately.
Pericardial biopsy
A. Pericardial biopsy is generally performed as part of therapeutic procedure (surgical
drainage) in patients with recurrent pericardial effusions and cardiac tamponade after
prior pericardiocentesis (therapeutic biopsy), and as diagnostic procedure in patients
with illness lasting > 3 weeks despite treatment without definite diagnosis. Technical
advances in instrumentation with introduction of pericardioscopy, and in contemporary
virology and molecular biology have improved 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
useful adjunct to conventional laboratory studies in investigation of pericardial samples,
allowing rapid identification of microorganisms otherwise not easily found. Tissue
samples should be sent for cytology, tumor markers, gram stain, bacterial cultures, and,
if tuberculosis is suspected, polymerase chain reaction testing.
DETERMINATION OF RISK AND NEED FOR HOSPITALIZATION
1. Many clinicians admit all new cases of acute pericarditis to hospital, but this may not be
necessary. A patient with uncomplicated acute pericarditis can undergo initial evaluation in
same day hospital facility or clinic, although outpatient follow-up is required. On the other
hand, patients with high-risk features are at increased risk of short-term complications and
2.
3.
4.
have higher likelihood of specific disease. Hospital admission is indicated for high-risk
patients in order to initiate appropriate therapy and thorough etiologic evaluation.
Features of acute pericarditis associated with higher risk.
A. Fever (> 38ºC) and leukocytosis
B. Evidence suggesting cardiac tamponade
C. A large pericardial effusion (echo-free space of > 20 mm)
D. Immunosuppressed state
E. A history of therapy with vitamin K antagonists (warfarin)
F. Acute trauma
G. Failure to respond within 7 days to NSAID
H. Elevated cardiac troponin, which suggests myopericarditis
In one report of 300 consecutive patients with acute pericarditis, 15% were deemed high risk
at presentation and were hospitalized. In remaining 85% of patients who were low risk,
outpatient aspirin was effective in 87%, and none of these patients had serious complication
(cardiac tamponade) at mean follow-up of 38 months.
Although chronic use of glucocorticoids should not be considered as risk factor in general
population of patients with acute pericarditis, they were associated with increased rate of
complications in idiopathic or viral pericarditis. Glucocorticoid given in index attack may
increase chance of recurrence, probably because of its deleterious effect on viral replication.
5.
Gender may also predict likelihood of complications. In series of 453 consecutive cases of
acute pericarditis, women were at increased risk of complications (HR 1.65). A possible
explanation of this finding is higher frequency of autoimmune etiologies (above all connective
tissue diseases) in women.
PROGNOSIS
1. Patients with acute idiopathic or viral pericarditis have good long-term prognosis. Cardiac
tamponade rarely occurs in patients with acute idiopathic pericarditis and is more common in
patients with specific underlying etiology such as malignancy, TB, or purulent pericarditis.
Constrictive pericarditis may occur in about 1% of patients with acute idiopathic pericarditis,
and is also more common in patients with a specific etiology.
2. 15 to 30% of patients with idiopathic acute pericarditis who are not treated with colchicine
develop either recurrent or incessant disease. Immune mechanisms appear to be of primary
importance in majority of cases, and the term "chronic autoreactive" pericarditis has been
used. Risk factors for recurrent pericarditis include lack of response to NSAID, the need for
corticosteroid therapy, and inappropriate pericardiotomy or creation of a pericardial window.
The pathogenesis, course, and treatment of recurrent pericarditis are discussed separately.
SUMMARY AND RECOMMENDATIONS
1. Acute pericarditis (inflammation of the pericardial sac) is the most common disorder of the
pericardium and is seen in about 0.1% of hospitalized patients and 5% of patients admitted to
ED for non-ischemic chest pain.
2. Idiopathic cases, most of which are probably viral in etiology, are the most common causes of
3.
4.
5.
acute pericarditis. Other etiologies of acute pericarditis include any bacterial infections,
malignancy, and autoimmune disorders. The distribution of etiologies varies with geography
and type of clinical setting (community hospital vs. tertiary referral center).
The diagnosis of acute pericarditis is usually suspected based on a history of characteristic
pleuritic chest pain, especially when a pericardial friction rub is present. Pericarditis should
also be suspected in a patient with persistent fever and pericardial effusion or new
unexplained cardiomegaly.
The evaluation of a patient with suspected acute pericarditis includes blood work (assessing
for markers of inflammation or myocardial damage), chest radiography, electrocardiography,
and echocardiography. ECG is often 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 is diagnosed by the presence of at least two of the following criteria.
A. Typical chest pain (sharp and pleuritic, improved by sitting up and leaning forward).
B. Pericardial friction rub (a superficial scratchy or squeaking sound best heard with the
diaphragm of the stethoscope over the left sternal border).
C. Suggestive changes on the electrocardiogram (typically widespread STE).
D. New or worsening pericardial effusion.
6.
7.
Because of relatively benign course associated with common causes of pericarditis, it is not
necessary to search for etiology in all patients. Initial efforts should focus upon excluding
significant effusion or tamponade and identification of patients in whom more
comprehensive evaluation should be performed to exclude causes that require specific
therapy (malignancy, tuberculosis or purulent pericarditis).
A patient with uncomplicated acute pericarditis can undergo initial evaluation in same-day
hospital facility or clinic, although outpatient follow-up is required. Conversely, patients with
high-risk features (high fever, large pericardial effusion, cardiac tamponade, failure to
respond to empiric anti-inflammatory therapy) are at increased risk of short-term
complications and have higher likelihood of specific disease. Hospital admission is indicated
for high-risk patients in order to initiate appropriate therapy and thorough etiologic
evaluation.