Risk of Constrictive Pericarditis After Acute Pericarditis
Massimo Imazio, MD; Antonio Brucato, MD; Silvia Maestroni, MD; Davide Cumetti, MD;
Riccardo Belli, MD; Rita Trinchero, MD; Yehuda Adler, MD
Background—Constrictive pericarditis (CP) is considered a rare, dreaded possible complication of acute pericarditis.
Nevertheless, there is a lack of prospective studies that have evaluated the specific risk according to different etiologies.
The aim of this study is to evaluate the risk of CP after acute pericarditis in a prospective cohort study with long-term
Methods and Results—From January 2000 to December 2008, 500 consecutive cases with a first episode of acute
pericarditis (age, 51?16 years; 270 men) were prospectively studied to evaluate the evolution toward CP. Etiologies
were viral/idiopathic in 416 cases (83.2%), connective tissue disease/pericardial injury syndromes in 36 cases (7.2%),
neoplastic pericarditis in 25 cases (5.0%), tuberculosis in 20 cases (4.0%), and purulent in 3 cases (0.6%). During a
median follow-up of 72 months (range, 24 to 120 months), CP developed in 9 of 500 patients (1.8%): 2 of 416 patients
with idiopathic/viral pericarditis (0.48%) versus 7 of 84 patients with a nonviral/nonidiopathic etiology (8.3%). The
incidence rate of CP was 0.76 cases per 1000 person-years for idiopathic/viral pericarditis, 4.40 cases per 1000
person-years for connective tissue disease/pericardial injury syndrome, 6.33 cases per 1000 person-years for neoplastic
pericarditis, 31.65 cases for 1000 person-years for tuberculous pericarditis, and 52.74 cases per 1000 person-years for
Conclusions—CP is a relatively rare complication of viral or idiopathic acute pericarditis (?0.5%) but, in contrast, is
relatively frequent for specific etiologies, especially bacterial. (Circulation. 2011;124:1270-1275.)
Key Words: constrictive pericarditis ? pericarditis ? prognosis
in particular after tuberculous pericarditis,4whereas it is not
well established after idiopathic and viral acute pericarditis,
the most common causes of acute pericarditis in developed
countries.5–7Unfortunately, there is a lack of prospective
cohort studies, and most data come from retrospective sur-
gery series of patients submitted to pericardiectomy for
permanent chronic constriction.8–10
Clinical Perspective on p 1275
The aim of the present study is to prospectively evaluate
the incidence of constrictive pericarditis after acute pericar-
ditis in a cohort study with a long-term follow-up. To the best
of our knowledge, this is the first prospective study in
contemporary patients with acute pericarditis.
onstrictive pericarditis is a rare but dreaded possible
complication of acute pericarditis.1–4This risk is evident
From January 2000 to December 2008, all consecutive cases with a
first episode of acute pericarditis were recorded and prospectively
studied for outcomes. Baseline features were recorded including age,
gender, presentation of specific features (fever ?38°C, subacute
course), physical (pericardial rubs) and instrumental findings (ECG
changes, pericardial effusion, cardiac tamponade), response to em-
pirical anti-inflammatory drugs at 1 week, and use of corticosteroids.
Response to anti-inflammatory therapy was considered incomplete
in the case of persistence of symptoms with evidence of activity
disease (fever without alternative causes, pericardial rubs, new or
worsening ECG changes, elevated markers of inflammation, and
appearance or worsening of pericardial effusion).
Such features were sought specifically because they have been
reported as possible poor prognostic predictors in patients with acute
Reported diagnostic criteria for acute pericarditis include pericar-
ditic typical chest pain, pericardial friction rubs, widespread ST-
segment elevation or PR depressions not previously reported, and
new or worsening pericardial effusion.2,5,6,11–18A clinical diagnosis
of acute pericarditis was made when at least 2 of these criteria were
present.11–18The presence of elevated markers of inflammation
(C-reactive protein and/or erythrocyte sedimentation rate) was con-
A minimal ST-segment elevation of 1 mm was considered
significant, although no specific recommendations are available on
this issue. The presence of an atrial current of injury, reflected by
Received January 6, 2011; accepted July 14, 2011.
From the Cardiology Department, Maria Vittoria Hospital, Torino, Italy (M.I., R.B., R.T.); Internal Medicine Division, Ospedali Riuniti, Bergamo, Italy
(A.B., S.M., D.C.); and Cardiac Rehabilitation Institute, Chaim Sheba Medical Center, Tel-Hashomer and Sackler Faculty of Medicine, Tel-Aviv and
Misgav ladach Hospital, Jerusalem, Kupat Holim Meuhedet, Israel (Y.A.).
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.
Correspondence to Massimo Imazio, MD, FESC, Cardiology Department, Maria Vittoria Hospital, Via Cibrario 72, 10141 Torino, Italy. E-mail
© 2011 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.orgDOI: 10.1161/CIRCULATIONAHA.111.018580
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, was considered a diagnostic ECG change.
A final diagnosis of idiopathic or viral acute pericarditis was
reached at the end of the diagnostic assessment, which included
chest-x ray, echocardiography, viral serology, and other specific
testing according to the initial clinical presentation. Pericardiocen-
tesis was done when a bacterial or neoplastic etiology was suspected
or in case of cardiac tamponade or severe pericardial effusion
without response to medical therapy after 1 week.
Pericardial injury syndromes included pericarditis resulting from
recent or earlier injury of the pericardium (late post–myocardial
infarction pericarditis, postpericardiotomy syndrome, and posttrau-
matic pericarditis). The initial injury is thought to release cardiac
antigens and stimulate an immune response, eliciting an inflamma-
tory response, which may involve the pericardium, pleura, or both.
On the basis of the presumptive common autoimmune pathogenesis,
pericardial injury syndromes were grouped with connective tissue
A structured follow-up was implemented including serial clinical
visits, ECG, blood chemistry (including C-reactive protein and blood
count), and echocardiograms at least at 1 month, 3 months, and then
every 6 months from the initial episode of acute pericarditis.
Additional investigations were organized according to the patient’s
symptoms and clinical evolution. Case report forms were completed
for each patient (see the online-only Data Supplement). All patients
underwent a basal echocardiographic examination at the time of the
initial clinical diagnosis and regularly at each follow-up visit. The
clinical course was recorded (stable remission, incessant course,
recurrences, cardiac tamponade, persistence of pericardial effusion).
An incessant course was defined as a course with persistence of
symptoms and clinical and instrumental signs of disease activity
without a free interval, whereas recurrence was defined as a situation
in which a new attack occurs after a period of complete disappear-
ance of symptoms and normalization of markers of inflammation if
The following clinical events were considered “adverse events”
during follow-up: recurrent pericardial pain without objective evi-
dence of disease, recurrent pericarditis, cardiac tamponade, and
constrictive pericarditis. Blinded assessment and validation of ad-
verse events were done by an independent committee with 2 experts
on pericardial diseases (see Appendix in the online-only Data
Supplement). Recurrent pericardial pain without objective evidence
of disease20was recorded when recurrent chest pain recognized by
the patient as similar to the previous pericarditic attack was reported
in the absence of other objective evidence of disease activity (fever,
pericardial friction rub, ECG changes, presence/worsening of peri-
cardial effusion, and elevated markers of inflammation). Criteria for
the diagnosis of recurrence included recurrent pain and 1 or more of
the following signs: fever, pericardial friction rub, ECG changes,
echocardiographic evidence of pericardial effusion, and elevation in
the white blood cell count, erythrocyte sedimentation rate, or
C-reactive protein.14–17The diagnosis of cardiac tamponade and
constrictive pericarditis was made with consideration of the combi-
nation of clinical and echocardiographic instrumental data according
to current available guidelines.21,22The presence of effusive-
constrictive pericarditis was suspected in case of pericardial effusion
with constrictive features on echocardiography and/or cardiac mag-
netic resonance imaging. The diagnosis of effusive-constrictive
pericarditis was confirmed when pericardiocentesis failed to de-
crease the right atrial pressure by 50% or to a level ?10 mm Hg after
exclusion of other causes of persistently elevated right atrial pressure
after pericardiocentesis (ie, right heart failure or tricuspid regurgita-
tion).23,24For constrictive pericarditis, clinical suspicion based on
initial physical and echocardiographic evaluation was confirmed by
additional imaging studies (computed tomography, cardiac magnetic
resonance), cardiac catheterization, and, finally, macroscopic and
histology findings from surgical specimens.25All patients had a
surgically confirmed diagnosis of constrictive pericarditis.
Data were expressed as mean?SD for continuous variables and
counts with percentages for categorical variables. Comparisons
between patient groups (idiopathic/viral etiologies versus specific
etiologies) were performed with the Mann-Whitney test for contin-
uous variables and a ?2analysis or Fisher exact test (when the
number of observations obtained for analysis was relatively small)
for categorical variables. Time-to-event distributions were estimated
by the Kaplan-Meier method and compared with the log-rank test. A
P value of ?0.05 was considered to show statistical significance.
Analyses were performed with the software package SPSS 13.0
Incidence rates were computed as the number of new cases of
disease during a period of time divided by the person time at risk.
Person time was the estimate of the actual time at risk in years that
all persons contributed to the study. Confidence intervals for inci-
dence statistics were calculated with the use of MedCalc software,
version 11.5.1 (Mariakerke, Belgium).
The authors had full access to and take full responsibility for the
integrity of the data. All authors have read and agree to the
manuscript as written.
Acute Pericarditis Study Population
In the study period, 500 cases of acute pericarditis (mean age,
51?16 years; 270 men) were recorded. Among them, 416
patients (83.2%; mean age, 50?17 years; 233 men) had a
diagnosis of viral or idiopathic acute pericarditis, and 84
patients (16.8%; mean age, 53?18 years; 37 men) had a
diagnosis of nonviral, nonidiopathic acute pericarditis.
Studied Population Between Viral/Idiopathic and
Comparison of Baseline Characteristics of the
Mean age, y (51?16)
Male gender (n?270)
Fever ?38°C (n?77)
Subacute course (n?22)
Pericarditic chest pain (n?490)
Pericardial rubs (n?175)
ST-segment elevation (n?449)
Pericardial effusion (n?327)
Large pericardial effusion (n?48)
Cardiac tamponade (n?22)
Aspirin or NSAID failure at 1 wk (n?98)
Corticosteroids as initial therapy (n?72)
Data are expressed as mean?SD for continuous variables and numbers and
percentages (in parentheses) for categorical variables. Comparisons between
patient groups (idiopathic/viral etiologies vs specific etiologies) were performed
with the Mann-Whitney test for continuous variables and a ?2analysis for
categorical variables. NSAID indicates nonsteroidal anti-inflammatory drugs.
Overall, C-reactive protein elevation was recorded in 451 of 500 patients
(90.2%) on serial determinations without significant differences between
patients with or without a specific etiology.
*A positive viral serology was recorded in 166 cases (39.9%).
†Specific etiologies included autoimmune causes (pericardial injury syn-
dromes and connective tissue diseases) in 36 patients (7.2%), neoplastic cause
in 25 patients (5.0%), tuberculosis in 20 patients (4.0%), and purulent bacterial
infection in 3 patients (0.6%).
Imazio et al Risk of Constriction After Pericarditis
Serology data supported the diagnosis of viral infection in
166 patients (Coxsackie in 66 patients, Ebstein-Barr virus in
25 patients, cytomegalovirus in 24 patients, parvovirus in 24
patients, influenza/parainfluenza viruses in 15 patients, and
adenovirus in 12 patients). The specific etiologies (nonviral,
nonidiopathic) of acute pericarditis were connective tissue
disease or pericardial injury syndrome in 36 cases (7.2%),
neoplastic pericarditis in 25 cases (5.0%), tuberculosis in 20
cases (4.0%), and purulent pericarditis in 3 cases (0.6%).
Baseline data of the studied population are reported in Table 1.
Follow-Up Data and Risk of
Follow-up data were available for all patients, and no data
were lost at follow-up. During a median follow-up of 72
months (range, 24 to 120 months), patients with a nonviral,
nonidiopathic etiology had a worse event-free survival com-
pared with those with an idiopathic/viral etiology (Figure).
Major adverse events included the following (Table 2):
recurrent chest pain without objective evidence of disease in
85 cases (17.0%), recurrent pericarditis in 152 cases (30.4%),
cardiac tamponade in 22 cases (4.4%), and permanent chronic
constrictive pericarditis in 9 cases (1.8%). Transient constric-
tion was detected by echocardiography in 75 of 500 patients
(15.0%) with resolution within 3 months. Effusive constrictive
pericarditis was recorded in 5 patients. All patients with chronic
constriction had a surgically confirmed diagnosis of constrictive
pericarditis. On histopathological examination of pericardiec-
tomy specimens, 1 patient (11.1% of all cases of permanent
chronic constrictive pericarditis) had normal pericardial thick-
ness. A detailed list of clinical and instrumental data of patients
who developed permanent chronic constrictive pericarditis dur-
ing follow-up is reported in Table 3.
Compared with patients with a specific etiology, patients
with idiopathic/viral acute pericarditis had a lower risk of
each adverse event: recurrent chest pain (14.9% versus
27.4%, respectively; P?0.006), recurrent pericarditis (25.0%
versus 57.1%, respectively; P?0.001), cardiac tamponade
(1.2% versus 20.2%, respectively; P?0.001), and constrictive
pericarditis (Table 2). The risk of constrictive pericarditis was
lower in patients with an idiopathic/viral etiology: 2 cases of
416 patients with idiopathic/viral pericarditis (0.48%) versus
7 cases of 84 patients with a nonviral/nonidiopathic etiology
(8.3%). The incidence rate of constrictive pericarditis was
0.76 cases per 1000 person-years for idiopathic/viral pericar-
ditis, 4.40 cases per 1000 person-years for connective tissue
disease/pericardial injury syndrome, 6.33 cases per 1000
Figure. Event-free survival in patients with (black
line) or without (gray line) a specific (nonidiopathic/
nonviral) etiology of acute pericarditis. Differences
of event-free survivals are evident after 6 months
and increase in the first 48 months. Medians for
survival time in patients with viral/idiopathic etiolo-
gies vs specific etiologies were 88.8 months (95%
confidence interval, 80.0 to 97.6) vs 39.3 months
(95% confidence interval, 28.7 to 50.0), respec-
tively. Recurrent pericardial pain without objective
evidence of disease, recurrent pericarditis, cardiac
tamponade, and constrictive pericarditis were con-
sidered adverse events during follow-up.
Table 2. Adverse Events After a Mean Follow-Up of 60 Months
Recurrent chest pain (n?85)
Recurrent pericarditis (n?152)
Cardiac tamponade (n?22)
Chronic constrictive pericarditis (n?9)
Data are expressed as numbers and percentages (in parentheses). Compar-
ison between patient groups (idiopathic/viral etiologies vs specific etiologies)
were performed with ?2analysis or Fisher exact test (when the number of
observations obtained for analysis was relatively small).
*P values by Fisher exact test.
September 13, 2011
person-years for neoplastic pericarditis, 31.65 cases for 1000
person-years for tuberculous pericarditis, and 52.74 cases per
1000 person-years for purulent pericarditis (Table 4).
Potential Risk Factors for Constrictive Pericarditis
The relative number of patients with constrictive pericarditis
is small, and therefore it was not appropriate to perform a
multivariate analysis. Nevertheless, bivariate analyses were
done to explore potential risk factors for constriction. Patients
who developed constrictive pericarditis during follow-up
showed a higher frequency of specific features compared
with those without such evolution: fever ?38°C (66.7%
versus 14.5%, respectively; P?0.001), incessant course
(55.6% versus 6.9%, respectively; P?0.001), nonidiopathic/
P?0.001), large pericardial effusion (66.7% versus 8.6%,
respectively; P?0.001), cardiac tamponade (44.4% versus
3.7%, respectively; P?0.002), and aspirin/nonsteroidal anti-
inflammatory drug failure at 1 week (66.7% versus 18.7%,
A trend was found toward a higher rate of use of cortico-
steroids (33.3% versus 14.1%) and a lower rate of use of
colchicine (22.2% versus 50.5%) in those who developed
Permanent constrictive pericarditis is a rare, dreaded possible
complication of acute pericarditis that is reported after non-
idiopathic etiologies in particular. A few large series of
patients with constrictive pericarditis diagnosed at pericardi-
ectomy have been described, including 95 patients from
Stanford,8135 patients from the Mayo Clinic,9and 163
patients from the Cleveland Clinic.10The reported frequency
of various causes in these reports, which is influenced by the
selection of cases for referral and surgery, is as follows:
idiopathic/viral in 42% to 49% of cases, after cardiac surgery
in 11% to 37% of cases, after radiation therapy in 9% to 31%
(mainly Hodgkin’s disease or breast cancer), connective
tissue disorder in 3% to 7% of cases, and after bacterial
infection (tuberculous or purulent pericarditis) in 3% to 6% of
Developed Constrictive Pericarditis
Clinical and Instrumental Findings of Patients Who
Mean age, y
Clinical features at presentation
Large pericardial effusion
Medical therapy features
Aspirin or NSAID failure at 1 wk
Corticosteroids as initial therapy
Symptoms of heart failure
Elevated jugular venous pressure
Kussmaul’s sign (lack of an inspiratory
decline in jugular venous pressure)
Nonspecific ST- and T-wave changes
Presence of pericardial calcifications
Pronounced respiratory variations in ventricular
filling, mitral inflow velocity changes ?25%
Dilatation of the inferior vena cava and hepatic
veins (plethora) with absent or diminished
Computed tomographic scan*
Cardiac magnetic resonance imaging*
Increased pericardial thickening and inferior
vena cava plethora
Enhanced ventricular interdependence
Increased right atrial pressure
?Square root? signs in RV and LV diastolic
Equalization of LV and RV diastolic plateau
Mirror-image discordance between RV and
peak LV systolic pressures during inspiration
Data are expressed as numbers and percentages (in parentheses) unless
indicated otherwise. NSAID indicates nonsteroidal anti-inflammatory drugs; RV,
right ventricular; and LV, left ventricular.
*Features with the development of constrictive pericarditis.
Incidence of Constrictive Pericarditis According
Evolution, No. (%)
Pericardial injury syndrome
and connective tissue
diseases; n?36 (7.2%)
Neoplastic; n?25 (5.0%)
Tuberculosis; n?20 (4.0%)
Purulent; n?3 (0.6%)
Incidence rate is assessed as the number of new cases of disease during a
period of time divided by the person time at risk. Person time is the estimate
of the actual time at risk in years that all persons contributed to the study; 95%
confidence intervals (CI) for incidence statistics are calculated.
Imazio et al Risk of Constriction After Pericarditis
cases. Miscellaneous causes (malignancy, trauma, drug-
induced, asbestosis, sarcoidosis, uremic pericarditis) were
also reported in 1% to 10% of cases. More recently, 5 cases
of surgically confirmed cases of constrictive pericarditis after
orthotopic heart transplantation were described.26
Tuberculosis accounted for up to 50% of cases of constric-
tive pericarditis in historical series. Tuberculous pericarditis
is now rare in developed countries (up to 5% of unselected
cases) but remains common in developing countries (where it
is the leading cause of pericarditis), in immigrants (especially
from Africa and Eastern Europe), and in immunosuppressed
patients.4,7,27Tuberculous pericarditis occurs in ?1% to 2%
of patients with tuberculosis and may present clinically in 3
forms: pericardial effusion (80% of cases), constrictive peri-
carditis (5% of cases), or effusive-constrictive pericarditis
(15% of cases).28Pericardial constriction may be a delayed
complication reported even today with a variable rate ranging
from 20% to 60% of all cases, depending on the stage of the
disease, and despite medical therapy.4,7,27,28However, this
disorder may be increasing among immigrants from under-
developed nations and patients with human immunodefi-
ciency virus infection. Other forms of bacterial pericarditis
are now rare. Purulent pericarditis is rare in the modern
antibiotic era and accounts for ?1% of unselected cases with
acute pericarditis.27Nevertheless, for bacterial pericarditis,
the risk of developing constrictive pericarditis is generally
Unfortunately, there are no contemporary prospective data
on the risk of developing constrictive pericarditis after acute
pericarditis in developed countries, and the incidence of the
complication after idiopathic acute pericarditis is not well
assessed. The constrictive evolution is a feared complication
for either the clinician or the patients, especially when the
disease does not respond to conventional therapy, the course
is incessant or recurrent, or the etiology is unknown.
This study on a large sample size of patients with a
long-term follow-up attempts to quantify the risk of develop-
ing constrictive pericarditis after a first attack of acute
pericarditis with a risk assessment according to the etiology.
Overall, the complication is not common (1.8% in the
overall population of acute pericarditis), but the risk is
correlated with the etiology. Such evolution is rare (?0.5%)
in idiopathic or viral acute pericarditis but is not negligible in
other specific etiologies and is very high for bacterial causes:
2.8% for connective tissue disease or pericardial injury
syndrome, 4.0% for neoplastic pericarditis, 20% for tubercu-
lous pericarditis, and 33% for purulent pericarditis. In the
observed study population, the symptoms of constrictive
pericarditis were permanent and often progressive in chronic
cases unless the constrictive pericarditis was surgically
treated with pericardiectomy, whereas constriction was tran-
sient or reversible in 15% of patients with acute pericarditis.
The clinical course with response to anti-inflammatory ther-
apies in these patients implied the presence of constriction
due to inflammation that resolved after standard treatment for
acute pericarditis. On this basis, for patients with newly
diagnosed constrictive pericarditis and without evidence of
chronic constriction, a trial of conservative management with
anti-inflammatory agents for 2 to 3 months is warranted
rather than pericardiectomy.
Patients with idiopathic forms and a recurrent course did
not show a constrictive evolution; these data are consistent
with the previous observation that idiopathic recurrent peri-
carditis does not evolve to constrictive pericarditis19and that
the risk of developing constrictive pericarditis also in the
setting of recurrent pericarditis may be correlated with the
etiology and not the number of recurrences. Such findings
are interesting and suggest that the evolution toward constric-
tive pericarditis may follow a direct pathway correlated with
the response to the specific etiologic agent.
The distinction between recurrent pericarditis and acute
pericarditis directly evolving into constrictive pericarditis is
clinically important. In idiopathic recurrent pericarditis, the
clinical picture is characterized by attacks of pain, fever, and
increased C-reactive protein that resolve, with normalization
of C-reactive protein and disappearance of symptoms, but
then recur after a free interval; this course is generally
benign.5,19On the other hand, the 2 cases of idiopathic acute
pericarditis that we observed evolved directly into constric-
tive pericarditis with an incessant course, with pain and fever
at the beginning and with constriction developing after
several months and becoming the dominant clinical feature.
In conclusion, constrictive pericarditis is a rare complica-
tion of viral or idiopathic acute pericarditis, whereas nonid-
iopathic etiologies (especially bacterial) are correlated with
an increased risk of complications and constrictive pericardi-
tis. Specific features, such as incessant course, large pericar-
dial effusions, and failure of empirical anti-inflammatory
therapy, should warrant a close follow-up because they may
represent potential risk factors for the evolution toward
constrictive pericarditis. In contrast, a recurrent course has a
lower risk of constriction.
Sources of Funding
Funding for the analyses for this study was provided by Maria
Vittoria Hospital, Torino, Italy, and Ospedali Riuniti, Bergamo,
Italy, where data analysis and interpretation were performed.
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Constrictive pericarditis (CP) is a rare but dreaded possible complication of acute pericarditis. This risk is evident after
tuberculous pericarditis in particular, whereas it is not well established after idiopathic and viral acute pericarditis, the most
common causes of acute pericarditis in developed countries. In a prospective cohort study of 500 consecutive cases of acute
pericarditis, after a mean follow-up of 60 months, CP developed in 9 of 500 patients (1.8%): 2 of 416 patients with
idiopathic/viral pericarditis (0.48%) versus 7 of 84 patients with a nonviral/nonidiopathic etiology (8.3%). The incidence
rate of CP was 0.76 cases per 1000 person-years for idiopathic/viral pericarditis, 4.40 cases per 1000 person-years for
connective tissue disease/pericardial injury syndrome, 6.33 cases per 1000 person-years for neoplastic pericarditis, 31.65
cases for 1000 person-years for tuberculous pericarditis, and 52.74 cases per 1000 person-years for purulent pericarditis.
After a long follow-up, the overall number of cases of CP was relatively small (?2%). Patients and clinicians should be
aware that CP is a rare complication of viral or idiopathic acute pericarditis. In contrast, nonidiopathic etiologies (especially
bacterial) are correlated with an increased risk of complications and CP. Warning signs of a possible evolution toward CP
are (1) an incessant course of the disease, (2) a nonidiopathic etiology, (3) large pericardial effusions, and (4) failure of
empirical anti-inflammatory therapy. In contrast, a recurrent course has a lower risk of constriction.
Imazio et al Risk of Constriction After Pericarditis