3. Definition & Terminology
⢠Myopericardial Syndromes include pericarditis, myocarditis, myopericarditi
s, and perimyocarditis.
⢠Acute pericarditis and myocarditis commonly co-exist. The degree of their res
pective involvement is variable,
⢠Myopericarditis is defined as a primarily pericarditic syndrome with concomit
ant myocardial involvement, inflammation, and troponin elevation.
⢠Perimyocarditis is a primarily myocarditic syndrome with concomitant pericar
dial involvement.
4. Definition & Terminology
Pericarditis
⢠Inflammation of the pericardium without myocardial involvement or an associat
ed depressed ejection fraction is referred to simply as pericarditis.
⢠Acute pericarditis refers to pericardial inflammation and an acute onset of sy
mptoms. Without treatment, symptoms may last for 4-6 wk before resolving.
⢠recurrent pericarditis When symptoms recur after a previous episode that co
mpletely resolved with treatment
⢠incessant pericarditis is used when symptoms last for more than 4-6 wk but l
ess than 3 mo without remission.
⢠Chronic pericarditis lasts more than 3 mo
5. Definition & Terminology
Myocarditis
⢠Isolated inflammation of the myocardium is referred to as myocarditis,
which presents with a variable spectrum of disease and degree of ventricular dysfunc
tion.
⢠Acute myocarditis presents with symptoms of heart failure that develop over less
than 3 mo .
⢠chronic myocarditis develops with a less distinct onset of symptoms over a dur
ation greater than 3 mo , Over time, ventricular dysfunction may progress to d
ilated cardiomyopathy. Chronic cases include chronic active (frequent clinical a
nd histologic relapses with ventricular dysfunction) and chronic persistent (persis
tent clinical symptoms and histologic infiltrates without ventricular dysfunction) for
ms of myocarditis.
⢠Fulminant myocarditis is acute myocardial inflammation that presents suddenly
after a distinct viral prodrome. It typically lasts less than 2 wk. Fulminant myocard
itis can lead to electrical instability and cardiogenic shock.
⢠Acute non-fulminant myocarditis is distinguished from fulminant myocarditis in t
hat the onset is less distinct, the heart failure symptoms are less severe, hypotens
ion is less common, and vasopressor and mechanical circulatory support is gener
ally not needed.
6. ⢠The pericardium consists of an outer sac (fibrous pericardium) and a double-l
ayered inner sac (serous pericardium) with visceral and parietal layers.
⢠The thin visceral layer adheres to the surface of the myocardium and is re
flected over the origins of the great vessels.
⢠The parietal layer has a serosal surface (contacts pericardial fluid) and an
opposing surface (lines the fibrous pericardium).
⢠The pericardium provides a physical barrier to prevent the spread of infection
or malignancy.
⢠The pericardial space contains a small amount of fluid (~5-50 mL of plasma )
Anatomy & Pathophysiology
8. ⢠The pericardiumâs response to an injury leads to the exudation of fluid, f
ibrin, and inflammatory cells.
⢠Adhesions may develop during healing that may obliterate the pericardi
al space.
⢠These adhesions may also calcify over time.
⢠The pericardium is affected by virtually every category of disease, inclu
ding infectious, neoplastic, immune-inflammatory, metabolic, iatrogenic,
traumatic, and congenital causes
Anatomy & Pathophysiology
9. Myocarditis
⢠Most of the current data on the pathogenesis of myocarditis are from a
nimal models of post-viral and autoimmune myocarditis.
⢠Most models suggest that myocarditis has 3 phases of progression. Th
e acute phase, which is characterized by host infection, is followed by
a host innate and acquired immunologic response. The acute phase i
nvolves recovery or transition to fibrosis with the development of dilat
ed cardiomyopathy over several wk to mo.
⢠Acute and chronic phases can cause dilated cardiomyopathy and heart
failure
Anatomy & Pathophysiology
10. Epidemiology & Etiology
Pericarditis
⢠Acute pericarditis is the most common form of myopericardial disease
worldwide and accounts for an estimated 5% of nonischemic chest pain
presenting to acute care settings.
⢠The mean age of patients with acute pericarditis is 41-60 y. Men are note
d to have a 2-fold greater incidence compared to women
11. Epidemiology & Etiology
Pericarditis is frequently recurrent. Approximately 20%-30% of patients will experi
ence a recurrence of symptoms within 18 mo of the first episode of pericarditi
s.
12. Epidemiology & Etiology
Myocarditis
⢠The incidence of myocarditis is difficult to estimate due to its range of clinical presentati
ons,
⢠but it is currently reported to be 22 cases per 100,000 persons per year.
⢠The increasing adoption of highly-sensitive troponin assays has dramatically increased
the number of reported cases.
⢠As many as 1%-5% of all acute viral infections may actually involve the myocardium.
⢠Myocarditis occurs in both pediatric and elderly populations, with a median age of 42 y.
13. Epidemiology & Etiology
⢠In developed countries, viruses are the most common presumed etiology of acute myo
pericardial syndromes, and episodes are often preceded by a gastrointestinal or flu-like
illness.
⢠Coronavirus has also been implicated as a common cause in recent cases.
⢠A majority of cases are labeled idiopathic, even after diagnostic evaluation with sophisti
cated immunohistochemical and genomic studies. Most cases are presumed to be viral
in origin or related to an immune response to a virus or other pathogen.
⢠In a prospective study conducted in France, no etiology was found in 55% of cases (n =
933), but approximately 20% were classified as post-cardiac injury syndrome-related.
⢠In developing countries, tuberculosis is the most common cause of acute pericar
ditis and is often associated with human immunodeficiency virus infection, especially in
sub-Saharan Africa.
16. Epidemiology & Etiology
The most common type of myocarditis seen on a myocardial biopsy is lymphocytic m
yocarditis.
The other distinct pathologic types of myocarditis are eosinophilic (associated with h
ypersensitivity reactions to medications and vaccines), giant cell (autoimmune diseas
e), and rarely. granulomatous (ie, sarcoidosis).
17. Pericarditis
⢠Acute pericarditis is a clinical diagnosis that is made with at least 2 of the following 4 cri
teria:
⢠Classic chest pain (>85%-90% of cases) typically described as sharp and pleuritic,
improved by sitting up and leaning forward and worsened by lying back
⢠Pericardial friction rub
⢠Characteristic ECG abnormalities
⢠New or worsening pericardial effusion
Clinical Presentation & Diagnosis
18. Myocarditis
⢠A non-invasive diagnostic test for myocarditis does not currently exist.
⢠many cases are undetected because of subclinical/non-specific presentations or a misse
d diagnosis.
⢠In many cases of early patient presentation, a definitive diagnosis is not possible.
⢠Acute myocarditis is usually a presumptive clinical diagnosis, as a definitive diagnosis re
quires established histological, immunological, and immunohistochemical criteria that
require endomyocardial biopsy.
⢠ECG abnormalities can be highly variable, including ST elevation or depression, suprave
ntricular or ventricular dysrhythmias, and AV blocks.
â˘
⢠Sinus tachycardia is the most typical finding.
Clinical Presentation & Diagnosis
19. Myopericarditis vs. perimyocarditis.
Clinical Presentation & Diagnosis
Myopericarditis perimyocarditis
A presentation consistent with acute
pericarditis with known myocardial
damage (increased troponin values) or
suspected concomitant myocardial
involvement but with maintained
cardiac function.
Evidence of new-onset cardiac
dysfunction in patients with positive
troponins and clinical criteria for
acute pericarditis suggests
predominant myocarditis with
pericardial involvement and should be
referred to as perimyocarditis.
20. Pericarditis
⢠Patients typically present with rapid-onset substernal chest discomfort that is
sharp and pleuritic.
⢠Pain classically worsens with inspiration and is often positional, increasing wh
en the patient is supine and decreasing when he/she is sitting or leaning forw
ard.
⢠Pain may radiate to the neck or jaw, and inflammation of the phrenic nerve m
ay
result in referred pain to the back and shoulders.
⢠Additional symptoms may include cough, rhinorrhea, a low-grade fever, and d
yspnea.
⢠Patients with an underlying malignancy or autoimmune disorder may present
with non-specific signs and symptoms of their primary illness, such as fatigu
e, weight loss, night sweats, etc.
Clinical Presentation & Diagnosis
21. Myocarditis
⢠Often preceded by a viral prodrome of a fever, rash, sore throat, malaise, arthralgias, and
non-specific gastrointestinal or respiratory symptoms.
⢠Patients can present with dyspnea, chest pain, and arrhythmias.
⢠Myocarditis may present with unexpected sudden cardiac death, presumably due to VT or
VF
⢠Bradyarrhythmia and syncope due to a new-onset unexplained heart block may also occur
in both infectious (eg, Lyme disease) and immune-mediated forms of myocarditis.
⢠The clinical presentation of myocarditis may mimic ACS, but unlike with pericarditis, myoc
arditis
will result in profound troponin elevation.
⢠Acute myocarditis in patients with underlying coronary artery disease often results in false-
positive activation of the catheterization suite.
Clinical Presentation & Diagnosis
22. Friction Rub
⢠A pericardial friction rub results from friction between the inflamed visceral and parietal l
ayers of the pericardium, which produces a âsqueaky or scratchyâ high-pitched sound.
⢠It is best auscultated at the left sternal border at end expiration and when the patient is l
eaning forward or in the left lateral decubitus position.
⢠Only a minority of patients with pericarditis have an audible rub at presentation.
⢠This rub tends to vary in intensity over time. Serial examinations are helpful.
⢠Despite the poor sensitivity of a pericardial friction rub, it remains a key diagnostic criter
ion
Clinical Presentation & Diagnosis
27. Clinical Presentation & Diagnosis
Downsloping TP segment seen as an early ECG manifestation in ~30% o
f patients with pericarditis, best visualised in leads II and the lateral prec
ordial leads
spodick sign
28. Pericarditis
⢠Classic findings include a diffuse ST-segment elevation pattern without reciprocal ST-segmen
t depression (excluding leads V1 and aVR) and widespread PR-segment depressions,
but these are insensitive and seen in less than 60% of patients
⢠Classically, ECG changes in patients with acute pericarditis progress through four stages
1) Diffuse ST-segment elevation that occurs in multiple leads (except for V1 and aVR) with diffu
se PR-segment depression.
2) The ST segment returns to baseline, and the T-wave flattens.
3) The T-wave inverts, and there is potential ST-segment depression.
4) The ECG returns to normal over the course of wk or mo
However, patients do not necessarily present with stageable ECG abnormalities and may n
ot progress from one stage to the next in an orderly fashion.
Clinical Presentation & Diagnosis
29. Pericarditis
⢠To distinguish ECG in pericarditis vs early repolarization, consider the following:
⢠The ST/T ratio in V6 can indicate pericarditis vs early repolarization.
⢠A ratio <0.25 favors early repolarization.
⢠A ratio >0.25 favors pericarditis or STEMI.
⢠A notching or irregular J point favors early repolarization, although it is nonspecific;
this indicator is best observed in V4.
Clinical Presentation & Diagnosis
30. Myocarditis
⢠No ECG findings are specific to the diagnosis of myocarditis, and patients with myocard
itis may have normal ECGs or non-specific abnormalities.
⢠The ECG may be concerning for myocardial ischemia, including ST-segment elevation
with reciprocal changes, ST depression, and T-wave inversion.
⢠Other ECG findings include the following:
⢠Sinus tachycardia (most common)
⢠Atrial and ventricular arrhythmias
⢠High-grade AV block
⢠Common in Lyme disease, sarcoidosis, and cases of giant cell myocarditis.
⢠Wide QRS or pathologic Q waves
⢠Associated with a worse prognosis
Clinical Presentation & Diagnosis
31. ⢠CXR : The cardiac silhouette does not increase in size until at least 300 mL of pericardial
fluid has accumulated
⢠Echocardiography
⢠Transthoracic echocardiography provides a simple, non-invasive assessment of the per
icardium at the time of ED presentation and is essential for identifying complications su
ch as tamponade or constrictive pericarditis.
⢠Trivial (only seen in systole)
⢠Small (<10 mm)
⢠Moderate (10-20 mm)
⢠Large (21-25 mm)
⢠Very large (>25 mm)
⢠CT
⢠MRI
Clinical Presentation & Diagnosis
32. Symptomatic treatment of pericarditis.
⢠Acute pericarditis is generally self-limiting when not complicated by pericardial effusion,
constriction, or hemodynamic compromise.
⢠The mainstay treatment is anti-inflammatory medications including NSAIDs in combinati
on with colchicine. Risk of bleeding, hypertension, and renal insufficiency should be con
sidered before initiation.
⢠Ibuprofen (800-1,600 mg daily) and IV ketorolac have replaced the once more com
monly prescribed indomethacin
⢠Aspirin (750-1,000 mg daily, q8h) is the preferred NSAID option in patients with Hx
of ACS
⢠Combination therapy with colchicine is considered first-line treatment for preventing
the recurrence of non-bacterial pericarditis.
⢠Colchicine must be continued for at least 3 mo after a first occurrence of acute peri
carditis to effectively prevent recurrence at 18 mo
Clinical Presentation & Diagnosis
33. The European Society of Cardiology guidelines recommend colchicine for 6 mo in recurrent
pericarditis with level 1A recommendations
Steroids.
⢠Not recommended for ED use as they are associated with an increased risk of recurren
ce
⢠Reserve for patients who do not tolerate NSAIDs or have contraindications to their use,
only after the failure of first-line therapy.
⢠Rarely used in the treatment of intractable pain
⢠Pericardiectomy is a final option for experienced surgical centers after the failure of me
dical therapies
Clinical Presentation & Diagnosis
34. Pericarditis
⢠Most patients with acute pericarditis do not need to be hospitalized. Risk-stratify patient
s to determine disposition.
⢠High-risk features associated with a poor prognosis in acute pericarditis include the foll
owing:
⢠Hypotension
⢠Fever (>38 °C)
⢠A subacute course (symptoms over several d without a clear acute onset)
⢠Evidence of a large pericardial effusion or cardiac tamponade
⢠Failure to respond to treatment with NSAIDs after 7 d
⢠Pericarditis from an underlying causative process (eg, lupus, uremia) or with at least on
e high-risk predictor of a poor prognosis warrants hospitalization.
Clinical Presentation & Diagnosis
35. ⢠Stable patients with intractable pain may be admitted or placed in an observation unit fo
r pain control.
⢠Stable patients without high-risk features can be managed as outpatients with empiric tr
eatment with anti-inflammatory medication and short-term follow-up (1 wk) to assess tr
eatment response.
⢠Discharged patients should receive education with strict follow-up and ED return precau
tions.
⢠Inform patients that acute pericarditis is complicated by recurrences in 20%-30% of
cases, and up to half of patients with a recurrent pericarditis episode may experien
ce more recurrences.
⢠Recommendations for returning to competitive sports suggest waiting until sympto
ms have resolved and diagnostic tests have normalized. A minimal restriction of 3
mo is recommended
Myocarditis
⢠Admit all patients to a monitored bed.
⢠All hemodynamically unstable patients require admission to the ICU.
Clinical Presentation & Diagnosis
American heart association retrospective study Data were collected from a Finnish national registry that included data on all cardiovascular admissions (670409) during 9.5 years in 29 hospitals nationwide. During the study period, there were 1361 admissions for acute pericarditis
Widespread ST-segment elevation, considered characteristic of pericarditis, can be
found in no more than 60%of patientswith acute pericarditis and is more
common in younger male patients, especially in associationwithmyocarditis.3,51
PR depression is especially evident in inferior leads (II, aVF, III) and precordial leads
(V2-V6).