DISEASE OF ENDOCARDIUM,

MYOCARDIUM AND
PERICARDIUM

Lucia Krisdinarti
Cardiology Department
Faculty of Medicine GMU/Sarjito Hospital
YOGYAKARTA

1
 TOPICS
INFECTIVE ENDOCARDITIS

MYOCARDITIS

PERICARDITIS

2
Infective endocarditis

3
 Infective Endocarditis
Essential Pathophysiology
characteristics
General definitions Clinical features
and epidemiology
– NVE
Treatment
– I.V. drug abuse
– PVE
Pathogenesis

4
Essential characteristics:
Febrile illness
Persistent bacteremia
Characteristic lesion of microbial infection
of the endothelial surface of the heart
The vegetation
– Variable in size
– Amorphous mass of fibrin & platelets
– Abundant organisms
– Few inflammatory cells

5
General definitions

Acute
– Toxic presentation
– Progressive valve destruction & metastatic infection
developing in days to weeks
– Most commonly caused by S. aureus
Subacute
– Mild toxicity
– Presentation over weeks to months
– Rarely leads to metastatic infection
– Most commonly S. viridans or enterococcus

6
Epidemiology
Case rate may vary between 2-3 cases /100,000
to as high as 15-30/100,000 depending on
incidence of i.v. drug abuse and age of the
population
– 55-75% of patients with native valve endocarditis
(NVE) have underlying valve abnormalities
MVP
Rheumatic
Congenital
ASH or:
i.v. drug abuse

7
Epidemiology ……….

Case rates
– 7-25% of cases involve prosthetic valves
– 25-45% of cases predisposing condition can
not be identified

8
Epidemiology …………..
Adult population
– Rheumatic Heart Disease
20 – 25% of cases of IE in 1970’s & 80’s
7 – 18% of cases in recent reported series
Mitral site more common in women
Aortic site more common in men
– Congenital Heart Disease
10 – 20% of cases in young adults
8% of cases in older adults
PDA, VSD, bicuspid aortic valve (esp. in men>60)

9
Pathology
– NVE infection is largely confined to leaflets
– PVE infection commonly extends beyond
valve ring into annulus/periannular tissue
Ring abscesses
Septal abscesses
Fistulae
Prosthetic dehiscence
– Invasive infection more common in aortic
position and if onset is early

10
 Pathogenesis, Part 1
Damaged endothelium
– undamaged endothelium not conducive to
bacterial colonization
– endothelium can be damaged by high-velocity
flows
– trauma to endothelium can induce
thrombogenesis, leading to nonbacterial
thrombotic endocarditis (NBTE). NBTE is
more receptive to colonization
 Pathogenesis ………….
Microorganism No. %

Streptococcus viridans 289 31.3

Staphylococcus aureus 225 24.4
Negative cultures 152 16.4
Other streptoccal species (e.g. enterococci) 55 5.9

HACEK and diphtheroids 50 5.4

Gram negative bacilli 45 4.8

Strept pneumoniae 18 1.9
Fungi 14 1.5
Others 28 3.0

Berkowitz, FE: Infective endocarditis. IN Nichols EG, Cameron DE, Greeley WJ, et al (eds):
Critical Heart Disease in Infants and Children. St. Louis, Mosby-Year Book, 1995. 12
 Microbiology
S. Viridans
– Most common causative organism
Gram negative bacilli
– Neonates and immunocompromised patients
Prosthetic valves
– Within first year of surgery: Coag-negative staph
– After first year: similar to native valve endocarditis
HACEK organisms
– Hemophilus, Actinobacillus, Cardiobacterium,
Eikenella, Kingella
– Frequently affect damaged valves and can cause
emboli
13
Pathogenesis …………..

Nonbacterial Thrombotic Endocarditis

Endothelial injury
Platelet-fibrin thrombi
Hypercoagulable state
– Lesions seen at coaptation points of valves
Atrial surface mitral/tricuspid
Ventricular surface aortic/pulmonic
Modes of endothelial injury
High velocity jet
Flow from high pressure to low pressure chamber
Flow across narrow orifice of high velocity
– Bacteria deposited on edges of low pressure sink or
site of jet impaction

14
15
 Clinical Features
Interval between index bacteremia & onset
usually < 2 weeks
May be substantially longer in early PVE
Fever most common sign
May be absent in elderly/debilitated pt.
Murmur present in 80 – 85%
Generally indication of underlying lesion
Frequently absent in tricuspid IE
Changing murmur

16
 Classical Peripheral
Manifestations

Less common today

Not seen in tricuspid endocarditis

Petechiae most common

17
Janeway Lesions

18
Splinter Hemorrhage

19
Osler’s Nodes

20
Subconjunctival Hemorrhages

21
Roth’s Spots

22
 Clinical Features ………..
Systemic emboli
Incidence decreases with effective anti-microbial Rx
Neurological sequelae
Embolic stroke 15 – 20% of patients
Mycotic aneurysm
Cerebritis
CHF
Due to mechanical disruption
High mortality without surgical intervention
Renal insufficiency
Immune complex mediated

23
 Diagnosis
Published criteria for diagnostic purposes
in obscure cases
High index of suspicion in patients with
predisposing anatomy or behavior
Blood cultures
Echocardiography
– TTE – 60% sensitivity
– TEE – 80 – 95% sensitive

24
 Duke Criteria
Based on pathological and clinical criteria.
Utilizes microbiological data, evidence of
endocardial involvement, and other phenomenon
associated with infective endocarditis to estimate the
probability of infective endocarditis in a given
patient.
Has been shown to be valid and reproducible in
children

Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization
of specific echocardiographic findings. AM J Med 96:200, 1994

Stockheim JA, Chadwick EG, Kessler S, et al. Are the Duke Criteria superior to the Beth Israel
criteria for the diagnosis of infective endocarditis in children? Clin Infect Dis 27:1451, 1998 25
 Duke criteria
Definitive
– Pathological criteria
Microorganisms, or
Pathologic lesions
– Clinical criteria
2 major criteria, or
1 major and 3 minor criteria, or
5 minor
Possible
– Findings consistent with infective endocarditis that fall short of “definitive” but are
not “rejected”
Rejected
– Firm alternative diagnosis, or
– Resolution of manifestations of endocarditis with antibiotic therapy of 4 days or
less, or
– No pathological evidence of endocarditis at surgery or autopsy with antibiotic
therapy of 4 days or less
26
Duke criteria: Major criteria
Positive blood culture
– Typical microorganism consistent with IE, from two separate blood
cultures
S. viridans, S. bovis, HACEK
community-acquired S. aureus or enterocci (no primary focus)
– Persistently positive cultures
at least two positive cultures, drawn 12 hours apart
all of three, or a majority of four or more cultures (with first and last
sample drawn at least one hour apart
Evidence of endocardial involvement
– Positive echocardiogram
oscillating intracardiac mass on valve or supporting structures, or
myocardial abscess, or
new partial dehiscence of prosthetic valve
– New valvar regurgitation
27
28
Duke criteria: Minor criteria
Predisposition
– Predisposing heart condition or IV
drug abuser
Fever
– > 38.0º C
Vascular phenomena
– arterial emboli, septic pulmonary
infarct, mycotic aneurysm,
intracranial hemorrhage,
conjunctival hemorrhage,
Janeway’s lesion
Immunologic phenomena
– glomerulonephritis, Osler’s
nodes, Roth’s spots, rheumatoid
factors
Microbiologic evidence
– positive blood culture but does
not meet major criteria as noted
Echocardiographic evidence
– consistent with IE but does not
meet major criteria as noted
29
 Goals of Therapy
1. Eradicate infection

2. Definitively treat sequelae of destructive

intra-cardiac and extra-cardiac lesions

30
VIRIDANS STREPTOCOCCI AND STREP. BOVIS
Antibiotic Dosage and route Duration
Aqueous crystalline 12-18 million U/24 h 4 wks
penicillin G sodium IV either continuously
or in 6 = divided doses
or
Ceftriaxone sodium 2g once daily IV or IM 2 wks
Aqueous crystalline 12-18 million U/24 h 2 wks
penicillin G sodium IV either continuously
or in six equally
divided doses
with gentamicin 1 g IM or IV every 8 h 2 wks
sulfate
Vancomycin 30 mg/kg per 24 h IV 4 wks
hydrochloride in two equally divided
doses, not to exceed 2
gram/24h unless serum
levels are monitored
JAMA 1995; 274:1706
Comments
preferred in most patients older than 65 yrs
and in those with impairment of the eighth
nerve or renal function
when obtained 1h after a 20-30 min.
IV infusion or IM injection, serum
concentration of gentamicin of
approximately 3 mcg/mL is desirable;
trough concentration should be < 1 pg/mL
vancomycin therapy is recommended for
patients allergic to beta lactams; peak
serum concentrations of vancomycin should
be obtained one h after completion of the
infusion and should be in the range of
30-45 mcg/mL for twice-daily dosing
31
STAPH. ENDOCARDITIS IN NATIVE VALVES

32
 Prevention

Prophylactic regimen targeted against

likely organism
– Strep. viridans – oral, respiratory, eosphogeal
– Enterococcus – genitourinary, gastrointestinal
– S. aureus – infected skin, mucosal surfaces

33
 Chemoprophylaxis
Adult Prophylaxis: Dental, Oral, Respiratory, Esophageal
Standard Regimen

Amoxicillin 2g PO 1h before procedure or

Ampicillin 2g IM/IV 30m before procedure
Penicillin Allergic
Clindamycin
600 mg PO 1h before procedure or
600 mg IV 30m before
Cephalexin OR Cefadroxil 2g PO 1 hour before
Cefazolin 1.0g IM/IV 30 min before procedure
Azithromycin or Clarithromycin 500mg PO 1h before

34
 Myocardial &
Pericardial Disease
MYOCARDITIS
 Definition

INFLAMMANTORY INFILTRATION
OF THE MYOCARDIUM WITH ASSOCIATED
NECROSIS OR DEGENERATION
OR BOTH
 MYOCARDITIS
CLINICOPATHOLOGY CLASSIFICATION

Topol et all, 2004 Manual Cardiovascular Medicine

ACUTE MYOCARDITIS
65%

FULMINANT MYOCARDITIS
17%

CRHONIC ACTIVE MYOCARDITIS

11%

CHRONIC PERSISTENT MYOCARDITIS

7%
 MYOCARDITIS
ETIOLOGY

Inflammation of myocardium
Can be result of systemic disorder or
infectious agent
Viral-Coxsackie B, echovirus, influenza,
parainfluenza, Epstein-Bar, adenovirus,
parvovirus, hepatitis C virus,and HIV
Bacterial-C. Diptheria, N. meningitidis, M.
pneumonia, M.tuberculosis, and beta-
hemolytic strep
Frequently accompanied with pericarditis
 Etiology (Continued)

Protozoa: Chagas disease, metazoal

myocardial disease
Hypersensitivity (vaccines & drugs):
smallpox, clozapine,tricyclics
Physical agents: Radiation, heat stroke,
hypothermia
 Pathophysiology
Viral phase
Immunological response phase (innate&
acquired immunity components)
Cardiac remodelling phase
 MYOCARDITIS
Clinical Feature

Asymptomatic  chest pain that mimic

ACS
60% have antecedent arthralgia, malaise,
fever, sweat or chill consistent with viral
infection 1 to 2 weeks before onset
Hallmark of heart failure
 MYOCARDITIS
Diagnosis

Sign of acute decompensated heart failure (S3

gallop, central &peripheral oedema,Tachycardia
ECG-nonspecific changes, sinus tachycardia, av
block, prolonged QRS duration, or ST elevation(with
pericarditis)
CXR-Normal
Laboratory finding: Leucocytosis, eosinophillia,
Cardiac Enzymes- may be elevated, rheumatology
screening for SLE, Polymyositis, scleroderma
Differential-ischemia or infarct, valvular disease, and
sepsis
 MYOCARDITIS
MANAGEMENT

Heart Failure management

Arrhythmia management
Exercise Restriction
PERICARDIAL DISEASE
Anatomy and Physiology
Two layer:
– Visceral Pericardium
(serous)
– Parietal Pericardium
(fibrous)
Thin Film of
pericardial fluid
separated two layer
and decrease the
friction
 Anatomy and Physiology
Function of Pericardium:
Fixed the heart within the mediastinum and
limit the motion
Prevent extreme dilatation during sudden rise
of intracardiac volume
Barrier to infection
PERICARDIAL DISEASE

ACUTE PERICARDITIS

PERICARDIAL EFFUSION

CARDIAC TAMPONADE

CONSTRICTIVE PERICARDITIS
 INFLAMMATION OF THE PERICARDIUM AND
ASSOCIATED WITH CHESTPAIN, A FRICTION RUB
AND CHARACTERISTIC ECG CHANGE
ACUTE PERICARDITIS

Topol et all, 2004 Manual Cardiovascular Medicine

Etiology Acute Pericarditis
INFECTIOUS
Viral
Tuberculosis
Pyogenic Bacteria
NONINFECTIOUS
Postmyocardial infarction
Uremia
Neoplastic disease
Radiation-induced
Connective tissue diseases
Drug induced
 -SEVERE & SHARP AND LOCALIZED
Acute Pericarditis
-RETROSTERNAL & LEFT PRECORDIAL AREA
-RADIATED TO BACK&RIDGE OF LEFT TRAPEZIUS
Clinical Features & Diagnostic
.MUSCLE
-WORSE WITH COUGH OR INSPIRATION, LYING
-DECREASE WITH SITTING AND LEANING FORWARD
-PPD TEST Microbacterium culture FOR TB
Diffuse Sttest
-Serologic segment elevation
for screening in Most
conective ECG
tissue
PLEURITIC Lead, exception in aVR
& POSITIONAL
..disease dan V1
CHEST PAIN
Depress
-CXR and PR interval
mammogram
FEVER -Tumor Marker and citology
PERICARDIAL FRICTION RUB
ECG ABNORMALITY
CXR
LABORATORIC STUDY
ECHOCARDIOGRAPHY
 Management of acute
pericarditis
Symptomatic management
Exercise restriction
Hospitalization to determine etiology and observe
for tamponade as well as the effect of treatment
Pain management
NSAID
Ibuprofen 300-800mg every 6-8 hours
Aspirin 300-600mg every 4-6 hours
Indometachin should be avoided in elderly, cause
flow reduction in coronary artery
Gastrointestinal protection must be provided