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-
Generally symptomatic Tx
Treatment
■ 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
INTRODUCTION

Myocarditis
■ 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
(Lyme disease)
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