Acute M yoper ica rd ial

Sy ndromes
Ali Farzad, MDa,b,*, Jeffrey M. Schussler, MDc,d

KEYWORDS
 Pericarditis  Myocarditis  Myopericarditis  Perimyocarditis  Pericardium  Pericardial effusion
 Tamponade

KEY POINTS
 Myocarditis and pericarditis often present with symptoms and findings that overlap with or mimic
acute coronary syndromes.
 Because the treatment of myocarditis and pericarditis is different from that of acute coronary syn-
dromes or myocardial infarction, identification of these and differentiation of them from acute cor-
onary syndromes or myocardial infarction is important.
 Cardiac tamponade, which may occur as a sequela of pericarditis, is a potential emergency.
Although it can often quickly be treated, this is predicated on early and accurate diagnosis.

Video content accompanies this article at http://www.cardiology.theclinics.com.

INTRODUCTION tamponade, and pericardial constriction). The

Acute myopericardial diseases may present as
isolated disease or as a manifestation of a sys-
temic disease. Their clinical presentation varies
but is often associated with chest pain and elec-
trocardiogram (ECG) changes, and can often be
mistaken for acute coronary syndrome (ACS).1
Acute myopericardial syndromes, because of
their unclear presentation and mimicry of other
life-threatening conditions, can be challenging
to manage and, in some cases, can be life-
threatening.
This article reviews the acute myopericardial
syndromes that necessitate emergent evaluation
and treatment, including pericarditis (with
or without myocardial involvement) and its compli-
cations (pericardial effusion, with or without
goal is to help clinicians develop an evidence-
based approach to the evaluation and manage-
ment of these common and complex clinical
syndromes.
ANATOMY AND FUNCTION OF THE
PERICARDIUM
The pericardium is a flask-shaped avascular sac
that surrounds the heart and the roots of the great
vessels. It consists of an outer sac, which is made
of thick and fibrous collagenous connective tissue
(fibrous pericardium), and a double-layered inner
sac (serous pericardium) with visceral and parietal
layers. The visceral layer is thin, adheres to the sur-
face of the myocardium, and reflects over the ori-
gins of the great vessels. The parietal layer has a

Disclosure: The authors have nothing they wish to disclose.

cardiology.theclinics.com

a
Department of Emergency Medicine, Baylor University Medical Center, 3500 Gaston Avenue, Dallas, TX
75246, USA; b Department of Emergency Medicine, Texas A&M College of Medicine, 3302 Gaston Avenue, Dal-
las, TX 75246, USA; c Department of Cardiology, Baylor University Medical Center, Baylor Jack and Jane Ham-
ilton Heart and Vascular Hospital, 621 Hall Street, Dallas, TX 75226, USA; d Division of Cardiology, Department
of Medicine, Texas A&M College of Medicine, 3302 Gaston Avenue, Dallas, TX 75246, USA
* Corresponding author. Department of Emergency Medicine, Baylor University Medical Center, 3500 Gaston
Avenue, Dallas, TX 75246.
E-mail address: Ali.Farzad@BSWHealth.org

Cardiol Clin 36 (2018) 103–114

https://doi.org/10.1016/j.ccl.2017.09.004
0733-8651/18/Ó 2017 Elsevier Inc. All rights reserved.
104 Farzad & Schussler
serosal surface that contacts pericardial fluid in
the pericardial cavity and an opposite surface,
which lines the fibrous pericardium (Fig. 1).
The pericardium separates the epicardium from
other mediastinal structures and attaches to the
diaphragm, sternum, and other structures to limit
displacement of the heart within the chest during
respiration or movement.2 The pericardium also
protects the heart by serving as a physical barrier
to prevent the spread of infection or malignancy.3
The normal pericardial space contains a small
amount of fluid (w25–50 mL of plasma ultrafil-
trate), which lubricates the serosal surface of the
parietal and visceral layers to reduce friction dur-
ing cardiac activity. This fluid equalizes gravita-
tional, hydrostatic, and inertial forces over the
heart to maintain transmural cardiac pressures.2
The pericardium is also metabolically active and
known to produce hormonal modulators of neuro-
transmission and myocardial contractility. The
pericardium fixes the heart to the mediastinum
and maintains ventricular compliance to limit dila-
tation of cardiac chambers. Moreover, the pres-
sure in the pericardial cavity is subatmospheric,
facilitating atrial filling and maintenance of cardiac
pressure.2
Nevertheless, the pericardium is not essential
for life and few adverse consequences follow
congenital absence or surgical removal of the peri-
cardium.2 Presence of an intact pericardium re-
sults in a potential space that can accommodate
only a small reserve volume. The pressure-
volume relation of the pericardium is nonlinear;
hence, small acute pericardial effusions may
cause cardiac tamponade, whereas slow chronic
effusions may stretch the pericardium and not pro-
duce tamponade physiology (Fig. 2). The pericar-
dium has limited elasticity and, once its limit
is reached, the heart must compete with the
intrapericardial fluid for a fixed intrapericardial
volume.2 The mechanical, membranous, and
metabolic functions of the pericardium are sum-
marized in Box 1.
PATHOPHYSIOLOGY OF THE PERICARDIUM
Pericardial heart disease comprises mainly peri-
carditis, which may be an acute, subacute, or
chronic fibrinous, noneffusive, or exudative pro-
cess.2 Response to injury is limited to exudation
of fluid, fibrin, or inflammatory cells. Adhesions
may result during healing that may cause oblitera-
tion of the pericardial space, and later calcifica-
tion.2 Complications include tamponade and
its variants, and constriction, which may be acute,
subacute, or chronic fibrinous.2 Despite a
limited number of clinical syndromes, the pericar-
dium is affected by virtually every category of
disease, including infectious, neoplastic, immune-
inflammatory, metabolic, iatrogenic, traumatic,
and congenital causes.
BACKGROUND/DEFINITIONS/CRITERIA
Clinically, acute pericarditis and myocarditis
commonly coexist. The degree of their respective
involvement in disease is variable, giving rise to
terminology that attempts to accurately describe
clinical presentations. Myopericarditis is defined
as a primarily pericarditic syndrome with concom-
itant myocardial involvement and inflammation.4
Perimyocarditis specifies a primarily myocarditic
syndrome with pericardial involvement.4 In prac-
tice, the two terms are often used interchangeably
and a precise and uniformly adopted definition is
lacking. Typically, inflammation of the pericardium
without involvement of the myocardium or
depressed ejection fraction is referred to as
pericarditis.
Acute pericarditis refers to pericardial inflamma-
tion with acute onset of symptoms. Without treat-
ment, these symptoms can last for 4 to 6 weeks
Fig. 1. Anatomy of the normal
pericardium. (Reproduced with
permission of the Cleveland Clinic
Center for Continuing Education.
Phelan D, Collier P, Grimm R.
Pericardial Disease. Disease man-
agement project (http://www.
clevelandclinicmeded.com/medical
pubs/diseasemanagement/cardiology/
pericardial-disease/). Ó2000-2015
The Cleveland Clinic Foundation.
All rights reserved.)

before resolution. The term incessant pericarditis
is used when symptoms last for greater than 4 to
6 weeks but less than 3 months without remission.
Pericarditis is said to be recurrent or relapsing if
symptoms recur after a previous episode that
completely resolved with treatment. Chronic peri-
carditis lasts more than 3 months (Box 2).3
Acute pericarditis is a clinical diagnosis, made
with at least 2 of the following 4 criteria: (1)
Box 1
Summary of the functions of the pericardium
Mechanical
 Barrier to infection
 Limits displacement of heart
 Maintains pressure-volume relations of the
cardiac chambers and their output; contrib-
utes to ventricular compliance
 Neutralizes effects of respiration and change
in body position
Membranous/serosal
 Lubricates to reduce friction
 Equalizes gravitational, hydrostatic, and
inertial forces
Metabolic
 Immunologic
 Vasomotor
 Fibrinolytic
 Modulates sympathetic neurotransmission
and contractility
Adapted from Hoit BD. Pathophysiology of the Peri-
cardium. Prog Cardiovasc Dis 2017;59(4):343; with
permission.
Acute Myopericardial Syndromes 105
Fig. 2. Pericardial pressure-volume
curves from a rapidly developing
(left) and more slowly developing
(right) effusion. The flat initial
segment of the curves is the pericar-
dial reserve volume, which, once ex-
ceeded, causes a steep increase in
pressure. (From Hoit BD. Pathophys-
iology of the pericardium. Prog
Cardiovasc Dis 2017;59(4):343; with
permission.)
pericarditic chest pain (>85%–90% of cases),
which is typically sharp and pleuritic, and
improved by sitting up and leaning forward; (2)
pericardial friction rub (rare); (3) characteristic
ECG abnormalities; (4) new or worsening pericar-
dial effusion. Acute pericarditis with known
(increased levels of biomarkers of myocardial
Box 2
Myopericardial syndromes: terminology
Acute pericarditis
First attack of pericardial inflammation with
acute onset of symptoms, which usually last
4 to 6 weeks with treatment
Myopericarditis
A primarily pericarditic syndrome with
concomitant myocarditis
Perimyocarditis
A primarily myocardic syndrome with
concomitant pericarditis
Incessant pericarditis
Symptoms last for greater than 4 to 6 months
but less than 3 months without remission
Recurrent/relapsing pericarditis
Symptom recurrence after complete resolu-
tion of previous episode after 4 to 6 weeks
with treatment
Chronic pericarditis
Lasts for longer than 3 months
Adapted from Doctor NS, Shah AB, Coplan N, et al.
Acute pericarditis. Prog Cardiovasc Dis 2017;59(4):349–
59; and Imazio M, Trinchero R. Myopericarditis: etiol-
ogy, management, and prognosis. Int J Cardiol
2008;127(1):17–26; with permission.
106 Farzad & Schussler
damage; ie, troponins) or suspected concomitant
myocardial involvement should be referred to as
myopericarditis. Evidence of new-onset focal or
diffuse reduction of left ventricular function in pa-
tients with positive troponins and clinical criteria
for acute pericarditis suggests predominant
myocarditis with pericardial involvement and
should be referred to as perimyocarditis. The
increased sensitivity of troponin assays and
contemporary widespread use of troponins has
greatly increased the reported number of cases.
EPIDEMIOLOGY
Acute pericarditis is the most common form of
pericardial disease worldwide.5 However, pericar-
ditis accounts for only a small percentage of all
hospital admissions because many low-risk pa-
tients are usually not admitted. Hence, accurate
estimates of incidence and prevalence are un-
known in many populations.6 The mean age of pa-
tients with acute pericarditis ranges from 41 to
60 years, and men are noted to have a 2-fold
greater incidence rate compared with women.7
Pericarditis frequently recurs; about 30% of pa-
tients have recurrence of symptoms within
18 months after a first episode of pericarditis.5,8,9
It is estimated that pericarditis accounts for 5%
of emergency department (ED) admissions for
chest pain–related complaints.6 In-hospital mor-
talities are generally low in developed countries
but increase with age and severe coinfections
and comorbidities.
CAUSE
Acute pericarditis and myocarditis commonly
coexist in the clinical setting because they share
common causal agents, mainly cardiotropic vi-
ruses. Viral infections seem to be the most com-
mon cause of myopericarditis in developed
countries. In developing countries tuberculosis is
a major cause where endemic, and is often asso-
ciated with human immunodeficiency virus (HIV)
infection, especially in sub-Saharan Africa.6 The
cause is varied and depends on the epidemiologic
background, patient population, and clinical
setting. In western Europe and North America,
about 80% to 90% of cases are labeled idiopathic
after a diagnostic evaluation, and most are pre-
sumed to be viral.5 A list of some of the most com-
mon causal agents is broken down by infectious
and noninfectious causes in Table 1. Infectious
causes include viral (most common), bacterial,
viral, fungal, and parasitic causes. Noninfectious
causes include autoimmune, neoplastic, meta-
bolic, drugs, and trauma.
CLINICAL PRESENTATION
History
Patients with acute pericarditis present with
sudden-onset chest pain, which is sharp and usu-
ally in the substernal and precordial area. Pain is
classically worsened with inspiration and is often
positional, increased when supine, and relieved
with sitting or leaning forward. Pain may radiate
to the neck, left shoulder, or jaw. Inflammation of
the phrenic nerve may result in pain in the back
and shoulders.3 Symptoms may be associated
with cough, rhinorrhea, low-grade fever, and dys-
pnea. Patients with underlying malignancy or auto-
immune disorder may present with specific signs
and symptoms or their underlying cause, which
may include fever, fatigue, or weight loss.6
Physical Examination
A thorough physical examination is necessary for
every patient with a suspected myopericardial
syndrome. A pericardial friction rub, thought to
result from friction of inflamed visceral and parietal
layers, produce a squeaky or scratchy high-
pitched sound best heard at the left sternal border
at the end of expiration when the patient is leaning
forward or in a left lateral decubitus position.3 In
contrast with a pleural rub, a pericardial friction
rub is audible throughout the respiratory cycle,
whereas a pleural rub is absent when respiration
is stopped. Only a minority of patients have an
audible rub at presentation, and it tends to vary
in intensity over time, thus serial examinations
may be helpful.10 Despite the poor sensitivity of a
pericardial friction rub, it remains one of the key
diagnostic criteria.10
Tamponade is estimated to develop in 15% of
patients with idiopathic pericarditis. Jugular
venous distention, arterial hypotension, and pul-
sus paradoxus (a decrease in arterial systolic pres-
sure of more than 10 mm Hg with inspiration) are
suggestive of cardiac tamponade. Sinus tachy-
cardia occurs in most patients as a physiologic
response and attempt to maintain cardiac output.
The Kaushal sign is an increase in jugular venous
pressure during inspiration and can be seen in
tamponade.
Electrocardiographic Changes
ECG changes seen in myopericardial syndromes
are attributed to repolarization abnormalities of
the atrium and ventricle in response to epicardial
inflammation, because the parietal pericardium is
electrically inert.6 Commonly taught ECG findings
are diffuse ST-segment elevation without
reciprocal changes, and diffuse PR-segment
 Acute Myopericardial Syndromes 107

Table 1
Causes of acute pericarditis

Infectious Causes
Viral (common) Coxsackie viruses; echoviruses; adenovirus; influenza A and B viruses; enterovirus;
mumps virus; Epstein-Barr virus; HIV; herpes simplex virus; type I varicella zoster
virus; measles; parainfluenza viruses type II; respiratory syncytial virus,
cytomegalovirus ; hepatitis A, B, and C, parvovirus B19
Bacterial Gram-positive and gram-negative species (streptococci, staphylococci,
pneumococci), Mycobacterium tuberculosis
Less common: Legionella, Nocardia, Actinobacillus, Rickettsia, Borrelia burgdorferi
(Lyme disease), Listeria, Leptospira, Chlamydophila psittaci, Treponema
pallidum (syphilis), Coxiella burnetii, Meningococcus spp, Haemophilus spp,
Mycoplasma spp
Fungal (rare) Histoplasma, Blastomyces, coccidiosis, Aspergillus, Candida
Parasitic (rare) Toxoplasma, Entamoeba, Echinococcus
Noninfectious Causes
Autoimmune Systemic lupus erythematous, Sjögrensyndrome, rheumatoid arthritis,
(common) scleroderma, vasculitides–eosinophilic granulomatosis (Churg-Strauss
syndrome), Takayasu disease, Behçet syndrome, sarcoidosis, familial
Mediterranean fever, inflammatory bowel disease, Still disease, mixed
connective tissue disorder, Reiter syndrome, Wegener granulomatosis,
ankylosing spondylitis, giant cell arteritis, dermatomyositis, serum sickness
Neoplastic Primary (mesothelioma), secondary (lung, breast, and so forth)
Metabolic Uremia, myxedema, anorexia nervosa
Drugs Daunorubicin, doxorubicin, cyclophosphamide, 5-fluorouracil, amiodarone,
cyclosporine, mesalazine, clozapine, methysergide, anti–tumor necrosis factor,
hydralazine, procainamide, methyldopa, phenytoin, isoniazid, reserpine
Trauma/ Coronary interventions, permanent pacemaker/implantable cardioverter-
iatrogenic defibrillator implantation, radiofrequency ablation, penetrating,
nonpenetrating trauma, esophageal perforation, rupture
Miscellaneous Amyloidosis, aortic dissection, radiation induced (indirect injury)
Adapted from Doctor NS, Shah AB, Coplan N, et al. Acute pericarditis. Prog Cardiovasc Dis 2017;59(4):349–59; with
permission.

depression (Figs. 3 and 4). However, these classic
findings are insensitive and are reported to be
seen in less than 60% of patients.5 It is estimated
that approximately 90% of patients with acute
pericarditis manifest some type of ECG abnormal-
ity.11 In the past, ECG changes in acute pericar-
ditis have been thought to present in 4 stages.
First, diffuse ST-segment elevation that occurs in
all leads (except for V1 and aVR) with diffuse PR-
segment depression; second, the ST segment
returns to baseline and the T wave flattens; third,
the T wave inverts and there is potential
ST-segment depression; and fourth, the ECG
returns to normal over the course of weeks or
months.11–13
Clinicians are commonly tasked with distin-
guishing the differences between the ECG
changes seen in acute myopericardial syndromes
and other differential diagnoses that can cause
diffuse ST-segment elevations (Box 3). Several
important causes must be considered, including
but not limited to large-territory ST-segment eleva-
tion myocardial infarction (STEMI), (also called
wraparound left anterior descending artery STEMI,
or inferolateral STEMI, in which ST elevation is
seen in multiple leads), ventricular aneurysm, cor-
onary vasospasm, acute perimyocarditis, early
repolarization, left bundle branch block, and
paced rhythms. A method to assist in clinical dif-
ferentiation of these distinct disease processes
has value, because treatment varies based on
the underlying cause. This differentiation can
prove challenging because several different clin-
ical entities can have similar and atypical symp-
toms with comparable ECG abnormalities. Thus,
emergency physicians must focus on the life-
threatening causes of chest pain to avoid misdiag-
nosis and failure to treat these conditions in a
timely manner.
Although there are differentiating ECG patterns,
accurate assessment is imperfect using the
ECG alone because many of the features in
108 Farzad & Schussler

Fig. 3. Twelve-lead ECG of a 47-year-old woman with acute perimyocarditis. The ECG shows sinus bradycardia with
diffuse concave morphology ST-segment elevation compared with the isoelectric T-P segment. ST-segment elevations
are most marked in leads I, II, aVF, and V3 to V5. Note the absence of reciprocal ST-segment depression (excluding
leads aVR and V1) as seen in ST-elevation MI. PR-segment depressions are also seen. (Courtesy of Amal Mattu, MD,
Baltimore, MD.)

perimyocarditis are temporal.10 The focus should
be on identifying ACSs that require urgent or emer-
gent angiography. Reciprocal ST-segment
changes favor STEMI but are not always present.
In contrast with ACS, which may have several
different ST-segment morphologies, concave ST-
segment elevation is typical of acute perimyocardi-
tis. When ST elevation is seen in both leads II and III,
STEMI should be considered when the degree of ST
elevation is greater in lead III than lead II, conversely
the ST-increase in pericarditis is typically greater in
lead II than lead III.12–15 Recent literature by Bischof
and colleagues16 suggests that, when there is ST-
segment elevation in inferior leads, the presence
of any ST depression in lead aVL is highly specific
for coronary occlusion from inferior STEMI and

Fig. 4. Another ECG of acute pericarditis showing sinus tachycardia, diffuse (mild) ST elevation, and marked PR-
segment depression. (Courtesy of Jeffrey Schussler, MD, Baltimore, MD.)
 Acute Myopericardial Syndromes 109

Box 3
Differential diagnosis for diffuse ST-segment elevation seen on 12-lead electrocardiogram with a few
distinguishing factors highlighted

 Large acute ST-segment elevation myocardial infarction (STEMI)

 Diffuse ST-segment elevations, typically with reciprocal ST-segment depression
 Straight, horizontal, convex, or concave ST-segment morphology
 ST-segment elevation in lead III greater than II
 Reciprocal ST depression in aVL in inferior STEMI
 Evolving changes with treatment and time
 Acute perimyocardial syndromes
 Diffuse ST-segment elevation without reciprocal ST depression
 Concave ST-segment morphology
 ST-segment elevation in lead II greater than III, without any ST depression in aVL
 PR-segment depression (not specific)
 Spodick sign (T-P segment downsloping, associated with pericarditis, but not found to be sensitive
or specific)
 ST/T-wave ratio in V6 greater than 0.25
 Early repolarization
 Diffuse ST-segment elevation without reciprocal ST-segment depression
 Fishhook J-point elevation
 Concave ST-segment morphology
 ST-segment elevation in lead II greater than III, without any ST depression in aVL
 No PR-segment depression
 ST/T-wave ratio in V6 less than 0.25
 Ventricular aneurysm
 No reciprocal ST-segment depression
 History of recent myocardial infarction (MI) with Q waves
 Left bundle branch block/paced rhythms
 ST-segment elevation and depression that is discordant to the QRS vector
 Sgarbossa criteria can be used to differentiate from acute MI
 Vasospasm
 No reciprocal ST-segment depression
 May evolve with treatment
From Mattu A. Amal Mattu’s ECG case of the week - October 24, 2016: Differential diagnosis for diffuse ST-segment
elevation. EGCweekly.com. 2016. Available at: https://ecgweekly.com/2016/10/amal-mattus-ecg-case-of-the-week-
october-24-2016/; with permission.

strongly weighs against pericarditis. The temporal
evolution of ECG changes with both entities is highly
variable and changes with treatment and time.
When attempting to distinguish between STEMI
and myopericardial syndrome, providers are
encouraged to know the differences in ECG findings
and consider the factors that strongly favor STEMI
first. A 2-step process that is designed to avoid
misdiagnosis and delay in STEMI diagnosis is pre-
sented in Box 4.
The PR segment has been suggested to be as
important as the ST segment because inflammation
of the subepicardial myocardium causes exagger-
ated atrial repolarization of the thin-walled atrium
and results in PR-segment depression.11,13 Spo-
dick12 published a study in 1974 that identified
PR-segment depression in more than 80% of the
ECGs of patients with diagnosed acute pericarditis.
It has been is suggested that the PR segment can
be used to support the diagnosis of acute
110 Farzad & Schussler

Box 4 pericarditis and may help in differentiating from

2 steps to distinguishing ST-segment elevation
myocardial infarction versus pericarditis in the
emergency department
Step 1. Look closely for factors that rule in
STEMI before thinking of pericarditis. Factors
that strongly favor STEMI:
 Reciprocal ST depression in any lead (except
aVR and V1)
 Convex upward (frowny face) or horizontal/
straight ST-segment morphology
 ST elevation (STE) in lead III greater than
lead II
 Q waves that are known to be new
Step 2. If no factors that strongly favor STEMI,
look for factors that suggest pericarditis:
 Pronounced PR-segment depression in multi-
ple leads (not specific)
Pro tip: when in doubt, do serial ECGs looking
for dynamic changes and consider early inter-
ventional cardiology consultation for coronary
angiography.
From Mattu A. Amal Mattu’s ECG case of the week -
May 20, 2016: ECG findings in pericarditis vs.
STEMI. EGCweekly.com. 2016. Available at: https://
ecgweekly.com/2016/05/amal-mattus-ecg-case-of-the-
week-may-30-2016/; with permission.
other causes of diffuse ST elevation.17 However, cli-
nicians should be aware that PR-segment depres-
sion is not pathognomonic of myopericardial
syndromes, and should be cautious to avoid
making the diagnosis based on this finding alone.5
PR-segment depression can be found in ACS,
especially when atrial infarction is present, and it
can also simply be a normal variant.18 Again, the pri-
mary goal in the ED should be to identify patients
who may benefit from urgent coronary angiography
to avoid delays in time-sensitive diagnosis and
treatment. Emergency physicians should be
cautious not to be biased by anchoring to the diag-
nosis of pericarditis simply based on PR depression
or the ECG alone because it is not specific enough in
isolation. Doing so could result in providers aban-
doning their work-up prematurely to misdiagnose
pericarditis, whereas the patient may still have a
life-threatening cause of the chest pain that goes
undiagnosed and untreated (ie, ACS, PE, or aortic
dissection).
The major electrocardiographic differences be-
tween STEMI, perimyocarditis, and early repolari-
zation are outlined in Tables 2–4. Despite
clinical characteristics that differentiate acute peri-
carditis from acute myocardial infarction (MI),
approximately 15% to 20% of patients presenting
to the ED with pericarditis still require coronary
angiography to make the final diagnosis.19

Table 2
Comparison of electrocardiogram findings to help in distinguishing between ST-segment elevation
myocardial infarction versus myopericardial syndromes, and early repolarization

Comparison of
ECG Findings Acute STEMI Perimyocarditis Early Repolarization
ST-segment Diffuse or localized STE, Usually diffuse STE, Usually precordial STE,
deviation frequently with without reciprocal STD without reciprocal STD
reciprocal STD (except V1 or aVR)
ST-segment Straight, horizontal, Concave upwards (smiley Concave upwards (smiley
morphology convex (frowny face), or face) face)
concave
STE in inferior STE III>II (usually), with STE II>III (almost always), STE II>III without
leads reciprocal STD in aVL without reciprocal STD reciprocal STD in aVL
in aVL
Evolving ECG ST segments and T-wave Unlikely to witness Compare with old ECGs;
changes abnormalities evolve evolving changes unlikely to have
with treatment and during course of ED visit evolving changes
time during course of ED visit
ST/T-wave ratio NA >0.25 <0.25
in V6

Abbreviations: NA, not available; STD, ST depression; STE, ST elevation.

From Mattu A. Amal Mattu’s ECG case of the week - October 24, 2016: Differential diagnosis for diffuse ST-segment
elevation. EGCweekly.com. 2016. Available at: https://ecgweekly.com/2016/10/amal-mattus-ecg-case-of-the-week-
october-24-2016/; with permission.
 Acute Myopericardial Syndromes 111

Table 3
Recommendations for the treatment of acute pericarditis

Recommendations Class Level Reference

Aspirin or NSAIDs are recommended as first-line I A —
therapy for acute pericarditis with gastroprotection
Colchicine is recommended as first-line therapy for I A Bainey & Bhatt,10
acute pericarditis as an adjunct to aspirin/NSAID 2009; and Spodick,11
therapy 1973
Abbreviation: NSAIDs, nonsteroidal antiinflammatory drugs.

Several ECG findings are associated with peri- Echocardiography

cardial tamponade (Fig. 5). Sinus tachycardia is
a common finding and reflects a compensatory re-
action to the decrease in preload and stroke vol-
ume from tamponade in an effort to preserve
cardiac output. A low-voltage QRS is seen in large
pericardial effusions and is often seen before elec-
trical alternans (alternation of the QRS complex
amplitude or axis between beats) manifests. Elec-
trical alternans occurs when there are large peri-
cardial effusions, and the heart swings inside the
distended pericardial sac. Sinus tachycardia in
addition to low-voltage QRS amplitude is a sensi-
tive ECG finding to help in the diagnosis of pericar-
dial effusion.
Imaging and Laboratory Findings
Chest radiograph
Chest radiographs are generally normal in patients
with acute myopericardial syndromes that lack
pericardial effusions or tamponade, because the
cardiac silhouette does not enlarge until at least
300 mL of pericardial fluid have accumulated.6,20
Bedside transthoracic echocardiography provides
simple, noninvasive assessment of the pericar-
dium at presentation to the ED. Video 1 highlights
some of the echocardiographic findings seen in
pericarditis and cardiac tamponade. Although the
presence of a pericardial effusion is common and
supportive of the diagnosis of pericarditis,
absence of an effusion does not exclude the diag-
nosis. Bedside echocardiography is especially
helpful when there are diagnostic dilemmas. For
example, in patients with ST-segment elevation
but with high suspicion for pericarditis, regional
wall motion abnormalities are more strongly sug-
gestive of an ischemic cause. Many patients
have no easily identifiable features, and formal
echocardiography or other diagnostic modalities,
such as coronary angiography, may be needed
when the diagnosis is in doubt.10
Computed tomography and MRI
Computed tomography (CT) and MRI are some-
times used for pericarditis. In the acute setting, CT

Table 4
Commonly prescribed antiinflammatory therapies for recurrent pericarditis

Drug Usual Initial dosea Tx Durationb Taperinga

Aspirin 500–1000 mg every 6–8 h (range, Weeks to Decrease doses by 250–500 mg
1.5–4 g/d) months every 1–2 wkb
Ibuprofen 600 mg every 8 h (range, Weeks to Decrease doses by 200–400 mg
1200–2400 mg) months every 1–2 wkb
Indometacin 25–50 mg every 8 h: start at lower Weeks to Decrease doses by 25 mg every
end of dosing range and titrate months 1–2 wkb
upward to avoid headache and
dizziness
Colchicine 0.5 mg twice or 0.5 mg daily for At least 6 mo Not necessary; alternatively
patients <70 kg or intolerant to 0.5 mg every other day (<70 kg)
higher doses or 0.5 mg once (70 kg) in the
last weeks

Abbreviation: Tx, treatment.

a
Tapering should be considered for aspirin and NSAIDs.
b
Longer tapering times for more difficult, resistant cases may be considered.
112 Farzad & Schussler
Fig. 5. Twelve-lead ECG showing sinus tachycardia, low-voltage QRS complexes, and electrical alternans in a pa-
tient with cardiac tamponade. (Courtesy of Amal Mattu, MD, Baltimore, MD; with permission.)
is sometimes the first test in an ED for the evaluation
of chest pain. It can evaluate for pericardial effusion,
aortic dissection, and coronary artery disease (as
well as other intrathoracic disorders such as pneu-
monia and PE). In addition to the evaluation for the
presence or absence of pericardial fluid, both CT
and MRI can evaluate the pericardium for thick-
ening, which is sometimes seen in the acute phase
of pericarditis but is a concern when more chronic
pericarditis (or constriction) is suspected.
Myocardial biopsy
Biopsy is not typically used in the setting of peri-
carditis but can be used in the confirmation of
myocarditis. Biopsy of the myocardium has an
inherent risk of perforation but this is low in expe-
rienced hands. Typically, biopsy is reserved for in-
stances in which more myocardial dysfunction is
present and acute infectious myocarditis needs
to be proved so that acute treatments can be
tailored to the patient.
TREATMENT
After identification, the treatment of acute myoper-
icarditic conditions is in 2 categories: treatment of
any hemodynamic issues (mainly pericardial effu-
sion and tamponade) and symptomatic relief of
the pericardial pain.
Urgent Treatment of Tamponade Physiology
Pericardiocentesis is the rapid removal of fluid
from the pericardial space and is the gold standard
for treatment of tamponade from any cause,
including pericarditis. This procedure is typically
done in the cardiac catheter laboratory, with
assistance from both fluoroscopy and echocardi-
ography. In the emergency setting, this can be
done at the bedside using sonographic guidance
or (in the case of a code) without imaging.21
Tamponade physiology, when it occurs rapidly,
can be caused by a small amount of pericardial fluid.
In these situations, the risk of percutaneous removal
is higher, and so imaging is helpful in locating the
fluid and guiding its removal.21 In less critical or
time-sensitive settings, or in situations in which
there is recurrence of the effusion, surgical evacua-
tion can be done. The creation of a pericardial win-
dow is as effective in removing acute collections of
fluid as well as preventing their recurrence.21
Symptomatic Treatment of Pericarditis
Treatment of pericarditis is with nonsteroidal anti-
inflammatory medications. Historically, indometh-
acin was used, but most common nonsteroidal
antiinflammatory drugs (NSAIDs) can be used,
such as ibuprofen (typically in full-strength doses
of 800–1600 mg daily) or even intravenous ketoro-
lac.22 Colchicine has recently been added as first-
line therapy with NSAIDs. Colchicine should be
continued for at least 6 months to prevent recur-
rence, because many recurrences are caused by
inadequate dose and duration of initial therapy.6,8
Recurrent pericarditis is treated with a repeat
course of NSAIDs (Tables 3 and 4).
Steroids are not recommended for either the
acute occurrence of pericarditis or recurrence,
although they have been used in rare instances
with intractable pain. The concern is that using
them early in the course of disease may instigate
early recurrence.23

Many patients with acute pericarditis are
admitted to the hospital, but this is more because
a significant percentage of them are initially diag-
nosed as having an acute MI. Most patients with
acute pericarditis do not need to be admitted to
the hospital (if they are correctly identified, and
their pain is managed). Patients with pericardial ef-
fusions who are hemodynamically stable may be
observed for changes in their status. Hypotensive
patients are a medical emergency and should be
admitted.20
Disposition
Major risk factors associated with poor prog-
nosis in acute pericarditis include fever
(>38 C), subacute course (symptoms over
several days without a clear acute onset), evi-
dence of large pericardial effusion, cardiac tam-
ponade, and failure to respond to treatment with
NSAIDs after 7 days.6 Clinical presentations that
suggest an underlying cause or with at least 1
predictor of poor prognosis should warrant hos-
pitalization. Patients without these features can
be managed as outpatients with empiric treat-
ment with antiinflammatory medication and
short-term follow-up after 1 week to assess
response to treatment.
Prognosis
Most patients with acute pericarditis (generally
those with presumed viral or idiopathic causes)
have a good long-term prognosis. Cardiac tampo-
nade and constrictive pericarditis rarely occur in
these patients, and are more common in those
with specific underlying causes, such as malig-
nancy. Constrictive pericarditis is more likely to
occur in autoimmune, immune-mediated, and
neoplastic causes (2%–5%), and highly likely for
bacterial causes (20%–30%), especially with
tuberculosis and purulent pericarditis.6
Approximately 15% to 30% of patients with idio-
pathic acute pericarditis who are not treated with
colchicine develop either recurrent or incessant
disease, whereas colchicine may halve the recur-
rence rate.5,8,9 Patients with myopericarditis have
the potential for a higher rate of complications,
including left ventricular dysfunction and heart
failure.5
SUMMARY
Acute myopericardial syndromes are common in
clinical practice but can be challenging to manage,
with potential life-threatening complications. A
careful clinical history, physical examination, care-
ful ECG interpretation, and application of
Acute Myopericardial Syndromes 113
diagnostic criteria are needed to make an accurate
diagnosis, exclude concomitant disease, and
properly disposition patients. Therapy for acute
pericarditis should be guided per the underlying
cause. For the most common causes (idiopathic
and viral), NSAIDs or aspirin with the addition of
colchicine remains the mainstay of therapy. Pa-
tients with hemodynamic compromise who are
resistant to therapy or have high-risk features
should prompt hospitalization and initiation of
more aggressive therapy.
SUPPLEMENTARY DATA
Supplementary data related to this article can be
found online at https://doi.org/10.1016/j.ccl.2017.
09.004.
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