Yusra Pintaningrum

1 . Endokarditis
2. Perikarditis
3. Myokarditis
ENDOKARDITIS INFEKSIOSA
DEFINITION
• Microbial infection of the endothelial surface of the heart
(including large intrathoracic vessels and intracardiac foreign
bodies)

• The characteristic lesion – the vegetation – is a variably sized

amorphous mass of platelets and fibrin in which abundant
microorganisms and moderate inflammatory cells are enmeshed

• Heart valves – most commonly involved

Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 8 th ed
EPIDEMIOLOGY

• The incidence of IE (1950-2000) at about 3.6 to 7.0 cases per

100,000 patient-years.
• Risk factors in industrialized countries have shifted.
• Frequently in men than in women, with a 2:1 ratio.
Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed

• PHC (1979-2001)
• Annual incidence of 10/10,000 admissions
• Age range from 4-63 yrs; mean of 30 yrs old

Pasaporte B, Pena, A. Association of IE with age: a 21 yr experience.

PHC Journal 2001
TABLE 63-1 PREDISPOSING CONDITIONS AND MICROBIOLOGY
OF NATIVE VALVE ENDOCARDITIS
 Staphyl
ococci
25%

Streptoc *HACEK
Etiologic
occi 50- Agents
group 5-
60% 10%

Others
5%

*Haemophilus parainfluenzae, H. aphrophilus,H. paraphrophilus, H. influenzae,

Actinobacillus, Cardiobacterium hominis, Eikenella Corrodens, Kingella kingae
ESC Guidelines on the prevention, diagnosis, and treatment of infective endocarditis
(2009)
CARDIAC CONDITIONS ASSOCIATED WITH INCREASED RISK
OF INFECTIVE ENDOCARDITIS

DelahayeF, et al. Infective Endocarditis: A Comparison of International Guidelines. Heart 2007;

93: 524–527
 PATHOGENESIS & PATHOPHYSIOLOGY
• A physically damaged endothelium
The valve most types of organism
endothelium • A physically undamaged
endothelium S. aureus

Transient • Unrelated to invasive procedures

bacteraemia • Chewing and tooth brushing

Microbial pathogens • Numerous surface determinants

and host defences • *PMP

*Platelet Microbicidal Proteins

 cardiac valve Endothelial injury

platelet deposition
Microbials with
*MSCRAMMS Adhesion to
platelet
PATHOPHYSIOLOGY

fibronectin
and fibrin
Damaged matrix
Endothelium
Microorganism becomes
progressively incorporated into
the vegetation and multiplies

Endothelial cells b1 family bind

Local Inflamation express integrins circulating
Undamaged of the b1 family fibronectin
Endothelium

Active internalization Provide an adhesive

into valve endothelial surface to circulating
*microbial surface components recognizing cells staphyl.aureus
adhesive matrix molecules
FIGURE 63-3 Digit infarcts in a patient with infective
endocarditis due to Staphylococcus aureus. (Courtesy
of Alan J. Lesse, M.D.)
 Abscess
Definite
vegetation

New
dehiscenc
e of a
prosthesis

Three major criteria echocardiographic findings major

criteria in the diagnosis of IE
DIAGNOSIS
 Leucocytosis

Anemia
Lab Trombositopenia
test

Eleveted ESR
TREATMENT
 Antimicrobial Therapy for Specific Organisms

HACEK Microorganisms

Other Pathogens

Microorganisms Therapy
Amphotericin with 5-fluorocytosine,
Candida species fluconazole

Corynebacteria (diphtheroids) penicillin, vancomycin, aminoglycosides

Enterobacteriaceae (E. coli, Klebsiella,
cephalosporins, carbapenem
Enterobacter, Serratia, Salmonella, Proteus species)
tobramycin + piperacillin, ceftazidime or
Pseudomonas aeruginosa cefipime

Coxiella burnetti doxycycline + hydroxychloroquine

 Response to Therapy
RELAPSE AND RECURRENCE

• Relapse usually occurs within 2 months of discontinuing antibiotic treatment

• < 2% relapse ➔ penicillin-susceptible viridans streptococci

• 8-20% relapse ➔ enterococcal IE

• 4% relapse ➔ S. aureus IE
COMPLICATIONS OF IE
STRUCTURAL HEMODYNAMICS
1. Leaflet rupture 1.Acute valvular regurgitation
2. Flail leaflet 2. Valve obstruction
3. Leaflet perforation 3. Heart failure
4. Abscess
4. Intracardiac shunt
5. Aneurysm
5. Tamponade
6. Fistula
6. Perivalvular regurgitation
7. Prosthetic valve dehiscence
8. Embolization
9. Pericardial effusion
FOLLOW-UP OF ENDOCARDITIS
• Echocardiographic surveillance is MANDATORY:
• Vegetations may enlarge with treatment due to platelet and
fibrin deposition
• Progression of valve destruction = persistent infection
• Abscess may develop despite apparent clinical
improvement
• Ventricular decompensation due to regurgitation is possible
FOLLOW-UP OF ENDOCARDITIS
• Echocardiographic surveillance is MANDATORY:
• Repeat echocardiogram necessary to monitor effect of
medical therapy
• Integrity of valve replacement in setting of active
endocarditis also requires frequent echocardiograms
PREVENTION PRINCIPLES OF THE NEW ESC GUIDELINES
• The existing evidence does not support the extensive use of antibiotic
prophylaxis recommended in previous guidelines.
• Antibiotic prophylaxis should be limited to the highest risk patients.
• The indications for antibiotic prophylaxis for IE should be reduced.
• Good oral hygiene and regular dental review are of particular importance
for the prevention of IE.

ESC Guidelines on the prevention, diagnosis, and treatment of infective endocarditis

(2009)
Perikarditis
 ACUTE PERICARDITIS
• Characterized by typical chest pain, a pathognomonic pericardial friction rub, and
specific electrocardiogram (ECG) changes.
• uncomplicated pericarditis JVP usually normal.
• Ventricular third and fourth heart sounds indicate coexisting myocardial disease.
• Depending on the etiology, there may be fever and other signs of inflammation or
systemic illness.
ECG PERICARDITIS
• In the first stage
ST-segment elevations (upward concavity and seldom
exceed 5 mm in height) typically occur within a few hours of
the onset of chest pain and persist for hours or days.
Depression of the PR segment (except in lead aVR) occurs in
this stage and differentiates acute pericarditis from early
repolarization variants.
• In the second stage
ST segments return to baseline, T waves may appear normal
or exhibit a loss of amplitude.
• In the third stage, tracings show inversion of T waves.
• In the fourth stage, the ECG normalizes in the variably
present
Approximately 50% of patients with acute pericarditis display
all four ECG stages, and variations are common.
Atrial arrhythmias complicate 5% to 10% of cases of acute
pericarditis.
 ECHOCARDIOGRAPHY
• Class I recommendation by the American College of Cardiology (ACC), the American
Heart Association (AHA), and the American Society of Echocardiography (ASE).
• Echocardiography estimates the volume of pericardial fluid, identifies cardiac
tamponade, suggests the basis of pericarditis, and documents associated acute
myocarditis with congestive heart failure.
CHEST RADIOGRAPHY

 In uncomplicated acute pericarditis, the chest radiograph is generally

normal.
However, an enlarged cardiac silhouette may be evident because of a
moderate or large pericardial effusion .
The chest radiograph may provide evidence of tuberculosis, fungal
disease, pneumonia, or neoplasm.
 LABORATORY
 Erythrocyte sedimentation rate and WBC, usually increase in cases of acute
pericarditis.
 Extensive epicarditis occasionally have increases in serum cardiac isoenzymes
suggestive of acute MI.
 Idiopathic pericarditis had increased serum troponin I levels
 Acute MI differential diagnosis because more than half of the patients with
elevated troponin I presented with concurrent ST-segment elevation on ECG.
 THERAPY ACUTE PERICARDITIS
• NSAIDs (eg, ASA 650 mg every 3-4 hours or ibuprofen 300-800 mg every 6 hours)
Prophylaxis GI bleeding : tx. histamine-2 antagonists or PPI.
• Colchicine (1 mg/d, with or without a 2-mg loading dose for 3 months), with NSAIDs
or as monotherapy, is effective for the acute episode, is well tolerated, and may
prevent recurrences.
• Steroid therapy (prednisone 60-80 mg/d) for a week to control pain, with the
dosage tapered carefully.
 RECURRENT PERICARDITIS
• Colchicine may be used as monotherapy for the prevention of recurrent pericarditis.
• Intrapericardial administration of triamcinolone (300 mg/m2) has been shown to
relieve symptoms in patients with recurrent autoreactive myopericarditis.
• Azathioprine (50-100 mg/d) has also been used to prevent recurrent episodes.
• Pericardiectomy should be considered only when repeated attempts at medical
treatment have clearly failed.
 CONSTRICTIVE PERICARDITIS
• Thickened, scarred, and often calcified pericardium limits diastolic filling of the
ventricles.

• Cause of Constrictive pericarditis :

 Acute pericarditis
 Idiopathic
 Cardiac truma and surgery
 Tuberculous and other infectious disease
 Neoplasms (lung and breast)
 Radiation therapy
 Renal Failure
 Connective tissue disease
• Physical findings include ascites, hepatosplenomegaly, edema, and, in long-standing cases,
severe wasting.
• Low QRS voltage, nonspecific T wave changes, and P mitrale are common, but the ECG
findings are nonspecific .
• Atrial fibrillation is seen in approximately one-third of cases, and atrial flutter is seen less
often.
• The cardiac silhouette may be normal or enlarged.
MANAGEMENT CONSTRICTIVE PERICARDITIS
• Pericardiectomy is the definitive treatment for constrictive pericarditis.
• Specific antibiotic (eg, antituberculous) therapy should be initiated before surgery and
continued afterward.
• Diuretics and digoxin (in the presence of atrial fibrillation) are useful in patients who
are not candidates for pericardiectomy because of their high surgical risk.
• Prevention consists of appropriate therapy for acute pericarditis and adequate
pericardial drainage. Although instillation of fibrinolytics (urokinase 400,000 U per
instillation to 1,600,000 U; streptokinase 250,000 IU per instillation to 1,000,000 IU) is
promising, corticosteroids are often ineffective.
MIOKARDITIS
 MYOCARDITIS

 Myocarditis broadly refers to inflammation of the heart muscle

 Inflammation  any form of injury to the heart (ischemic damage,
mechanical trauma, and genetic cardiomyopathies)
 Classic myocarditis  exposure to discrete external antigens
(viruses, bacteria, parasites, and drugs) or internal triggers
(autoimmune activation against self-antigens)
ETIOLOGY

Braunwald’s Heart Disease, 9th Edition

PATHOPHYSIOLOGY

Braunwald’s Heart Disease, 9th Edition

DIAGNOSIS

Braunwald’s Heart Disease, 9th Edition

TREATMENT

Braunwald’s Heart Disease, 9th Edition

THANK YOU