Pericarditis, Endocarditis,

Myocarditis

Dr. SUHAEMI, SpPD, Finasim

The Pericardium

• Two layers - composed of fibrous tissue

– inner visceral layer, attached to epicardium
– outer parietal layer
• stabilizes heart in anatomic position
• protects heart - (contact with
surrounding structures)
The Pericardium

• Can be
– a primary site of disease
– involved in other disease processes that
affect the heart
– affected by other diseases of adjacent
tissue
 The pericardium can permit moderate
changes in cardiac size, however, it cannot
stretch rapidly enough to accommodate
rapid dilation of the heart or accumulation
of fluid w/o increasing
intrapericardial/intracardiac pressure
 Acute Pericarditis
• Acute inflammation of the pericardium
• Origin
– infectious,systemic diseases,malignancy,
radiation,drug toxicity,hemopericardium,other
inflammatory processes in the myocardium or lung
• Pathologic process often involves both the
pericardium and the myocardium
Acute Pericarditis

• Presentation & course may vary

depending on the cause
• syndromes often associated with
– chest pain (pleuritic/postural)
– dyspnea
– pericardial friction rub (with or w/o
evidence of fluid accumulation or
constriction)
– Fever & leukocytosis
 Acute Pericarditis
• Chest x-ray
– may show cardiac enlargement or pleural dx
• ECG
– generalized ST and T wave changes
– characteristic progression (ST elevation, return to
baseline, T wave inversion)
• Echocardiogram
– often normal in inflammatory pericarditis
– may show pericardial effusions
Acute Pericarditis- Causes

• viral infection
– most common coxsackievirus, & echovirus
• also- HIV,influenza,Epstein-Bar, varicella,
hepatitis, mumps
• bacterial infection
– staphylococcus, Strep pneumoniae, B-
hemolytic streptococci, Mycobacterium
tuberculosis, lyme dz
• Fungal infection
• Malignancy
Acute Pericarditis - Causes

• Drugs
– procainamide,hydralazine,minoxidil
• radiation
• connective tissue disease(lupus,rheum)
• uremia
• myxedema
• post-MI (Dressler’s syndrome)
• Idiopathic
Acute Pericarditis -
Clinical Features
• Sudden or gradual onset of sharp or
stabbing chest pain that radiates to the
back, neck, left shoulder, arm, or
trapezial ridge
• Pain aggravated by movement or
inspiration and by lying supine
• sitting up and leaning forward reduces
the pain
Acute Pericarditis -
Clinical Features
• Associated symptoms include;
– low grade intermittent fever, dyspnea,
dysphagia
• transient, intermittent friction rub heard
best at the lower left sternal border or
apex is the most common physical
finding
Acute Pericarditis -
Clinical Features
• Pericardial effusion
– As the pericardium stretches,

• effusions that develop slowly, even large ones,

may not produce hemodynamic changes

• However ….

• those that appear rapidly (even small effusions)

can cause tamponade
Acute Pericarditis -
Clinical Features
• Tamponade
– elevated intrapericardial pressure (>15 mm
Hg), that restricts venous return and
ventricular filling - resulting in decreased
stroke volume /pulse pressure and
increased heart rate/venous pressure
– most common complaints;dyspnea and
decreased exercise tolerance
– common symptoms; weight loss, pedal
edema, ascites
Acute Pericarditis -
Clinical Features
• Tamponade
– Physical Findings; tachycardia, low systolic
BP, narrow pulse pressure, pulsus
paradoxus, neck vein distention, distant
heart sounds, RUQ pain
Acute Pericarditis - Diagnosis

• ST-segment elevation
• Pericarditis w/o other underlying cardiac
disease does not typically produce
dysrhythmias
• Chest x-ray usually normal - but should
be done to rule out other disease
• Echocardiography
Acute Pericarditis - Diagnosis
• Other Tests
– CBC w/diff
– BUN
– Creatinine
– streptococcal serology
– appropriate vial serology
– other serology (antinuclear and anti-DNA
antibodies)
– thyroid function studies
– Sed rate, creatinine kinase levels
w/isoenzymes
Viral Pericarditis

– Most commonly caused by coxsackievirus,

& echovirus
– Can also be caused by HIV, influenza,
Epstein-Bar, varicella, hepatitis, mumps
– Most commonly affects males < age 50
– Diagnosis usually clinical
– rising viral titers in paired sera may be
obtained for confirmation of diagnosis
– cardiac enzymes may be slightly elevated -
indicating myocarditic component
 Viral Pericarditis- Treatment
• Generally symptomatic Tx
• aspirin or NSAIDs
• Corticosteroids -(unresponsive cases)
• Symptoms generally subside over several days to
weeks
• May be recurrences - during first few weeks - months
• Rarely, patients suffer from chronic recurrences
resulting in constrictive pericarditis
• Major early complication - tamponade (< 5% of
cases)
Bacterial Pericarditis

– staphylococcus, Strep, pneumoniae, B-

hemolytic streptococci, Mycobacterium
tuberculosis
– Usually direct result from pulmonary
infection
– patients often present in a critically ill state
– Borrelia burgdorferi (Lyme Disease
organism) can also cause myopericarditis
 Tuberculous Pericarditis
• Rare in developed countries - common elsewhere
• Results from direct lymphatic or hematogenous
spread
• commonly have associated pleural effusions & small
to moderate pericardial effusions
• subacute presentation/non-specific symptoms (fever,
night sweats, fatigue)
• Diagnosis inferred if acid-fast bacilli found elsewhere
• Usual therapy - standard antituberculous drug
• Complication- if therapy unsuccessful- constrictive
pericarditis
 Uremic Pericarditis
• Complication of renal failure
• Occurs in untreated uremia and in stable dialysis
patients
• Presents with or w/o symptoms, typically afebrile
• tamponade is common
• usually resolves with institution or more aggressive
dialysis
• pericardiectomy may become necessary
• indomethacin & systemic glucocorticoids ineffective
for uremic pericarditis
 Neoplastic pericarditis
• Commonly caused by
– breast and renal cell carcinoma, Hodgkin's Disease
and lymphomas
• neoplastic processes involving the pericardium
are the most common cause of pericardial
tamponade in many countries
• presenting symptoms relate to the
hemodynamic compromise of the primary
disease process
• MRI/CT
Neoplastic pericarditis

• Prognosis poor - only small minority

survive >year
• Effusion can be drained,
chemotherapeutic agents or tetracycline
may prevent recurrence
• pericardial windows rarely effective,
partial pericardiectomy from a
subxiphoid incision may be successful
Radiation Pericarditis

• Usually occurs within the first year after

exposure but can be delayed for many
years
• Symptomatic therapy - initial approach
but recurrent effusions and constriction
require surgery
Post MI or Postcardiotomy
Pericarditis
• An inflammatory reaction to transmural
myocardial necrosis that usually occurs
2-5 days after infarction
• typically presents as pain recurrence
• audible rub, repolarization changes
• spontaneous resolution usually occurs
after a few days
• Aspirin, NSAID’s -symptomatic relief
Dressler’s Syndrome

• Occurs weeks to several months after

MI or open heart surgery
• Presentation
– typical pain, fever, malaise, leukocytosis,
elevated sed rate
– large pericardial/pleural effusions common
– Tamponade is rare if Dressler’s after MI,
but more commonly seen in Dressler’s
post-operatively
Dressler’s Syndrome

• NSAID’s
• Corticosteroids
• Recurrences common
Constrictive Pericarditis
Constriction occurs when fibrous
thickening and loss of elasticity of
the pericardium results in
interference of diastolic filling
usually following inflammation
 Cardiac trauma, open heart
surgery, intrapericardial
hemorrhage, fungal or bacterial
pericarditis, and uremic pericarditis
are the most common causes of
constrictive pericarditis (in the past,
tuberculosis was also included)
Constrictive Pericarditis - symptoms

• Symptoms develop gradually and mimic

those of restrictive cardiomyopathy
(CHF, exercise dyspnea, decreased
exercise tolerance)
• chest pain, orthopnea, and paroxysmal
nocturnal dyspnea are uncommon
Physical Exam

• Pedal edema
• hepatomegaly
• ascites
• JVD
• Kussmaul’s sign(^jvp w/insp)
• pericardial knock (early diastolic sound)
heard at the apex
• usually - no friction rub
 Diagnosis
• ECG - may show low voltage QRS complexes
and inverted T waves
• Chest x-ray - 50% of cases show pericardial
calcification
• Doppler echocardiography
• Cardiac CT, MRI
• Consider other diseases - acute pericarditis,
myocarditis, exacerbation of chronic ventricular
dysfunction, or systemic process (eg sepsis)
Treatment

• General supportive care - initial

treatment
• Symptomatic patients - pericardiectomy
• Gentle diuresis
• Treatment with appropriate antibiotics if
agent is Id’d
Endocarditis

• Infective endocarditis is defined as an

infection of the endocardial surface of
the heart, which may include one or
more heart valves, the mural
endocardium, or a septal defect
• Endocarditis can be broken down into
the following categories:
 Native valve (acute and subacute) endocarditis
 Prosthetic valve (early and late) endocarditis
 Endocarditis related to intravenous drug use
Native valve endocarditis (acute
and subacute)

• Native valve acute endocarditis usually

has an aggressive course. Virulent
organisms, such as Staphylococcus
aureus and group B streptococci, are
typically the causative agents of this
type of endocarditis.
• Subacute endocarditis usually has a
more indolent course than the acute
form. Alpha-hemolytic streptococci or
enterococci, usually in the setting of
underlying structural valve disease,
typically are the causative agents of this
type of endocarditis.
Prosthetic valve endocarditis
(early and late)

• Early prosthetic valve endocarditis

occurs within 60 days of valve
implantation. Staphylococci, gram-
negative bacilli, and Candida species
are the common infecting organisms.
Prosthetic valve endocarditis
(early and late)

• Late prosthetic valve endocarditis

occurs 60 days or more after valve
implantation. Staphylococcus
epidermidis, alpha-hemolytic
streptococci, and enterococci are the
common causative organisms.
Endocarditis related to
intravenous drug use

• Endocarditis in intravenous drug abusers

commonly involves the tricuspid valve. S
aureus is the most common causative
organism
• Infective endocarditis generally occurs as a
consequence of nonbacterial thrombotic
endocarditis, which results from turbulence or
trauma to the endothelial surface of the
heart.
Endocarditis

• Increased mortality rates are associated with

increased age, infection involving the aortic
valve, development of congestive heart
failure, central nervous system (CNS)
complications, and underlying disease
• Affects men more than women (2:1 ratio)
• Affects all age groups - however, 50% of
cases in adults over age 50
Endocarditis

• Most common symptoms - fever (90% of

cases) and chills
• Anorexia, weight loss, malaise, headache,
myalgias, night sweats, shortness of breath,
cough, or joint pains are common complaints
• Dyspnea, cough, and chest pain are common
complaints of intravenous drug users who
have infective endocarditis
Endocarditis
• Primary cardiac disease may present
with signs of congestive heart failure
due to valvular insufficiency
• Heart murmurs are heard in
approximately 85% of patients
Endocarditis

 One or more classic signs of infective endocarditis are found

in as many as 50% of patients. They include the following:
 Petechiae - Common but nonspecific finding
 Splinter hemorrhages - Dark red linear lesions in the
nailbeds
 Osler nodes - Tender subcutaneous nodules usually
found on the distal pads of the digits
 Janeway lesions - Nontender maculae on the palms and
soles
 Roth spots - Retinal hemorrhages with small, clear
centers; rare and observed in only 5% of patients.
splinter hemorrhages and purpuric
papules on the foot of a 10 year old
boy with acute bacterial endocarditis
Splinter hemorrhages(Panel A) are normally seen under the fingernails.
They are usually linear and red for the first two to three days and brownish
thereafter.
Panel B shows conjunctival petechiae.
Osler's nodes (Panel C)are tender, subcutaneous nodules, often in the pulp
of the digits or the thenar eminence.
Janeway's lesions (Panel D) are nontender, erythematous, hemorrhagic, or
pustular lesions, often on the palms or soles
 Endocarditis

• baseline studies, such as a complete blood count

(CBC), electrolytes, creatinine, BUN, glucose, and
coagulation panel
• Blood cultures: Two sets of cultures have >90%
sensitivity when bacteremia is present. Three sets
of cultures improve sensitivity and may be useful
when antibiotics have been administered previously
Endocarditis

 Echocardiogram
 Transthoracic echocardiography has a sensitivity
of approximately 60%. Transesophageal
echocardiography has a sensitivity of more than
90% for valvular lesions
Endocarditis

• Empiric antibiotic therapy is chosen

based on the most likely infecting
organisms. Native valve disease usually
is treated with penicillin G and
gentamicin for synergistic treatment of
streptococci
Endocarditis

• Patients with a history of IV drug use

may be treated with nafcillin and
gentamicin to cover for methicillin-
sensitive staphylococci.
Endocarditis

• Infection of a prosthetic valve may

include methicillin-resistant
Staphylococcus aureus; thus,
vancomycin and gentamicin may be
used, despite the risk of renal
insufficiency
Endocarditis

• Rifampin also may be helpful in patients

with prosthetic valves or other foreign
bodies; however, it should be used in
addition to vancomycin or gentamicin.
Endocarditis

 prophylaxis against infective endocarditis in patients

at higher risk. Patients at higher risk include those
with the following conditions:
 Presence of prosthetic heart valve
 History of endocarditis
 History of rheumatic heart disease
 Congenital heart disease with a high-pressure
gradient lesion
 Mitral valve prolapse with a heart murmur
Endocarditis

 prophylaxis in patients before they undergo

procedures that may cause transient bacteremia,
such as the following:
 Ear, nose, and throat (ENT) procedures
associated with bleeding, including dental
manipulations and nasal packing
 Incision and drainage of an abscess
 Anoscopy and Foley catheter placement when a
urinary tract infection is present or suspected
Myocarditis
INTRODUCTION

• As early as 1806 , a persistent inflammatory process

following such an infection (eg, diphtheria) of the
myocardium led to progressive cardiac damage and
dysfunction
• In 1837, the term myocarditis was first introduced as
inflammation or degeneration of the heart by
postmortem
• Endomyocardial biopsy in 1980 allows the sampling
of human myocardial tissue during life and
antemortem diagnosis of myocarditis.
Myocarditis

• Inflammation of the myocardium

• May be the result of systemic disorder
or infectious agent ...usually follows an
upper resp infection
• Pericarditis frequently accompanies
myocarditis
• Drug induced, cytotoxic agents,also,
cocaine
CAUSATION

• A large variety of infections, systemic

diseases, drugs, and toxins have been
associated with the development of this
disease
• Viruses, bacteria, protozoa, and even
worms have been implicated as
infectious agents.
 Infectious Noninfectious

Viruses – Systemic Diseases:

1. Coxsackie B 1. SLE
2. HIV 2. Sarcoidosis
3. Vasculitides(Wegener’s)
4. Celiac disease
Bacterial – Neoplastic infiltration
1. Corynebacterium diphtheriae

Protozoan – Drugs & toxins:

1. Trypanosoma cruzi (Chagas 1. Ethanol
disease) 2. Cocaine
3. Radiation
4. Chemotherapeutic
agents - Doxorubicin
Spirochete
1. Borrelia burgdorferi
Myocarditis

• Bacterial cases include;

– Corynebacterium diphtheriae, Neisseria
meningitides, Mycoplasma pneumoniae,
and B-hemolytic streptococci
• Viral etiologies include;
– coxsackie B, echovirus, influenza,
parainfluenza, Epstein-Barr, and HIV
Pathophysiology

• Several mechanisms of myocardial damage

(1) Direct injury of myocytes by the

infectious agent
(2) Myocyte injury caused by a toxin such as
that
from Corynebacterium diphtheriae
(3) Myocyte injury as a result of infection-
induced immune reaction or
autoimmunity.
Pathophysiology

• Triphasic disease process

Phase I: Viral Infection and

Replication

Phase 2: Autoimmunity and injury

Phase 3: Dilated Cardiomyopathy

Myocarditis -clinical features

• Systemic signs/symptoms (fever,

tachycardia, myalgias, headache, and
rigors)
• chest pain due to coexisting pericarditis
• pericardial friction rub in cases of
concomitant pericarditis
• In severe cases - symptoms of
progressive heart failure (CHF,
pulmonary rales, pedal edema, etc.)
Diagnosis

• Nonspecific ECG changes,

atrioventricular block, prolonged QRS
duration, or ST segment elevation (in
cases of accompanying pericarditis)
• normal chest x-ray
• cardiac enzymes may be elevated
• Differential diagnosis includes cardiac
ischemia or infarction, valvular disease
and sepsis
Normal Myocardium
Borderline Myocarditis
Active Myocarditis
Triphasic disease process.
Treatment

• Supportive care
• If bacterial cause suspected, antibiotics
are appropriate
• Myocardial biopsy may reveal
inflammatory pattern
• Many cases spontaneously resolve
others progress to dilated
cardiomyopathy
Questions ?