CAUSAL ORGANISMS

F. 05 DISEASESE OF THE HEART Streptococcus o Normal component of the oral cavity flora
CASE 13, 14, 15, & 16 viridanso Most commonly (50%-60% of cases)
Dr. Domantay, Reporting by BLOCK C | August 9, 2017 causes endocarditis of the native, but
previously damaged or abnormal valves
OUTLINE: Staphylococcus o More virulent organism commonly found
I. Infective Endocarditis aureus on the skin
Case 13 o Can infect either healthy or deformed
A. Subacute Infective Endocarditis valves
B. Mechanism o Responsible for 20%-30% of cases
C. Structural alterations (Subacute IE) o Major offender in IE in IV drug users
Enterococci and o Commensals in the oral cavity
II. Noninfected Vegetations HACEK group
Case 14
A. Non Bacterial Thrombotic Endocarditis Haemophilus
B. Mechanism Actinobacillus
C. Other associated conditions Cardiobacterium
D. Structural alterations Eikenella
E. Libman-Sacks Disease (endocarditis of SLE) Kingella
Coagulase-Negative o Most common cause of prosthetic valve
III. Cardiomyopathy Staphylococci endocarditis
Case 15 (CONS)
A. Dilated Peripartum Cardiomyopathy e.g. S. epidermis
B. Mechanism Others include gram-negative bacilli and fungi
C. Structural alteration
 Classic Hallmark of
Case 16 Infective Endocarditis(IE):
A. Hypertrophic Cardiomyopathy o Characterized by large,
B. Mechanism irregular masses on the valve
C. Structural alterations cusps that can extend onto the
D. Complications chordae.
I. INTRODUCTION: INFECTIVE ENDOCARDITIS
o Friable bulky, potentially
INFECTIVE ENDOCARDITIS destructive lesions containing
• microbial infection of the heart valves or the mural fibrin, inflammatory cells, and
1 endocardium bacteria or other organisms
• formation of vegetations composed of thrombotic debris
 Common sites of infection:
2 and organisms
o AORTIC AND
MITRAL VALVE: valves of
• destruction of the underlying tissues
3 the right side of the heart
may be involved (IV Drug
abusers)
TYPES OF INFECTIVE ENDOCARDITIS
ACUTE IE SUB ACUTE IE o Can be single or
Lower virulence multiple sites, and may
Virulence of High virulence involve more than one valve
(eg. Viridans
infecting organisms (eg. S aureus)
streptococci)
Onset Rapid Insidious o Occasionally erode
Deformed valves, into the underlying
Extent of tissue Necrotizing, myocardium and produce an
overall less
damage destructive lesions abscess
destruction
Usually require
Treatment Antibiotics
surgery
 In the figure, acute
 Highly virulent organisms may infect previously normal endocarditis of congenitally
valves bicuspid aortic valve
 Cardiac and vascular abnormalities increase the risk of (caused by S. aureus) with
developing IE extensive cuspal
 Major Antecedent Disorder: Rheumatic Heart destruction; the black arrow
Disease with Valvular Scarring shows an example of ring
 Other antecedent disorders: abscess
o Mitral Valve Prolapse
o Degenerative Calcific Valvular Stenosis
o Bicuspid Aortic Valve (Calcified or not)
o Artificial/Prosthetic Valves
o Unrepaired or Repaired Congenital Defects

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 o Prone to embolization
o May lead to septic infarcts or mycotic aneurysms
secondary to abscesses due to embolic fragments
that contain virulent organisms
 The modified Duke criteria facilitates the evaluation of
individuals with suspected IE that takes into account
predisposing factors, physical findings, blood culture
results, echocardiographic findings, and laboratory
information.

CASE 13

A 23-year old female complains of low-grade fever and myalgia of

three weeks duration. She has a history of rheumatic heart disease.
One month ago, she underwent a dental extraction and she did not
take the antibiotics that were prescribed for her.

Physical Examination:
 Fever
 Pallor
 Small peripheral hemorrhages with slight nodular
character
 Small tender nodules on finger and toe pads
 Subungual linear streaks
 Petechial hemorrhages on conjunctiva, oral mucosa, an
upper extremities
 Mild splenomegaly
 Apical diastolic murmur on cardiovascular exam
 Fundus exam shows oval retinal hemorrhages

Laboratories:
 CBC/PBS: normocytic, normochromic anemia
 UA: microscopic hematuria, growth of penicillin sensitive
Streptococcus viridans on five of six blood cultures

Imaging:
 Vegetations along atrial surface of mitral valve **some previously common clinical manifestations of IE:

A. DIAGNOSIS  JANEWAY LESIONS: erythematous or hemorrhagic nontender

lesions on the palms and soles
SUBACUTE INFECTIVE ENDOCARDITIS  OSLER NODES: subcutaneous nodules in the pulp of the digits
 Characterized by organisms with lower virulence (e.g. Viridans  ROTH SPOTS: retinal hemorrhages in the eyes
streptococci) that cause insidious infections of deformed valves
with overall less destruction B. MECHANISMS IN THE DEVELOPMENT OF THE DISEASE
 Pursue a protracted course of weeks to months
Microbial Invasion
Subacute Infective Patient e.g. S. viridans, HACECK group
Endocarditis
(Dental extraction without antibiotic
One month ago, she underwent medication,
Previous dental extraction
a dental extraction
Surgical procedures,
History of rheumatic heart
disease Contaminated needles,
Abnormal valves
Echo: vegetation along arterial Trivial breaks in the epithelial barriers--
surface of mitral valve gut, oral cavity, skin)
Low grade fever Low grade fever
Detectable murmur Apical diastolic murmur
Influenza-likes syndrome with
Myalgia of three weeks
myalgia
Petechiae located at conjunctiva, Subungual linear streaks Bacteremia
palate, buccal mucosa and oral mucosa and upper (or Fungemia)
extremities extremities microorganism seeding into the
Left upper quadrant pain Mild splenomegaly bloodstream
Hematuria UA: microscopic hematuria
Small peripheral hemorrhage
with Slight nodular character
Osler nodes
Small tender nodules on finger
and toe pads Bacteria goes to the endocardium
Petechial hemorrhage on (Aortic and Mitral Valve)
conjunctiva
Roth spots
Fundus exam shows oval retinal
------------------------------------------------------------------------
hemorrhages

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 A. NON BACTERIAL THROMBOTIC ENDOCARDITIS
History of Rheumatic Heart Disease
Patient most likely has NBTE, a valvular disease.

Already friable  Previous Term: “marantic endocarditis”

valves
 Deposition of small sterile thrombi (non-infected
Exposure of collagen and tissue vegetation) on the leaflet of the cardiac valves
factor
 It is often encountered in debilitated patients, such as those with
cancer or sepsis; hence the previous term marantic
Adherence of endocarditis—root word marasmus, relating to malnutrition
platelets and fibrin
 Vegetations:
o non-invasive
Platelet Fibro Thrombus o do not elicit any inflammatory reaction
o found along the line of closure of the leaflets or cusps
------------------------------------------------------------------------
 Can be a source of SYSTEMIC EMBOLI that produce significant
Platelet Fibro INFARCTS in the BRAIN, HEART, or elsewhere.
Bacteria Thrombus

B. MECHANISM OF PATIENT’S DISEASE

Considering that the patient had a malignancy prior to

Vegetation death, the following explains the mechanism of his
disease.

C. STRUCTURAL ALTERATIONS OF SUB ACUTE IE 1

ADENOCARCINOMA
 SUBACUTE ENDOCARDITIS 5
 Figure 2
NON BACTERIAL
shows endocarditis of TUMOR-DERIVED THROMBOTIC
the Mitral valve MUCIN ENDOCARDITIS
caused by S. viridans
+
o LESSER TISSUE FACTOR
VALVULAR
DESTRUCTION 3 4
than Acute PROCOAGULANT EFFECTS MIGRATORY THROMBOPHLEBITIS
Endocarditis TO THE HEART

o Microscopically,
vegetations exhibit
granulation tissue  There is a striking association of NBTE with mucinous
at their bases adenocarcinoma, potentially relating to procoagulant effects
indicative of of tumor-derived mucin or tissue factor that can also cause
HEALING migratory thrombophlebitis (Trousseau syndrome).

o With time fibrosis, calcification, and chronic  Endocardial trauma (e.g. from an indwelling catheter) is another
inflammatory infiltrates can develop well-recognized predisposing condition, and right-sided valvular
and endocardial thrombotic lesions frwequently track along the
course of the pulmonary artery catheters.
II. Introduction: Noninfected Vegetations
 Non infected (sterile) vegetations occur in nonbacterial
thrombotic endocarditis and the endocarditis of systemic lupus C. OTHER CONDITIONS ASSOCIATED TO THE DISEASE
erythematosus (SLE), called Libman-Sacks endocarditis.
 Frequently occurs concomitantly with:
CASE 14 o deep vein thrombosis
o pulmonary emboli
A 50 year-old man who died of bleeding complications is discussed o or other findings suggesting systemic hypercoagulable
at an autopsy conference owing to peculiar vegetations seen on state.
the mitral valve. He underwent surgery for adenocarcinoma of the
stomach. Shortly before his death, he diagnosed as having a
disseminated intravascular coagulation (DIC); he subsequently
died of bleeding complications.

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D. STRUCTURAL ALTERATIONS IN THE VALVES  3 main functional and pathologic patterns:

 Figure shows a o Dilated Cardiomyopathy (most common (90% of

nearly complete row cases))
of thrombotic o Hypertrophic Cardiomyopathy
vegetations along the o Restrictive Cardiomyopathy (least frequent)
line of closure of the
mitral valve leaflets

 Figure shows
bland thrombus, with
virtually no
inflammation in the
valve cusp (C) or the
thrombotic deposit (t).
The thrombus is only
closely attached to the
cusps (arrow).

 Figure shows
typical lesions on NBTE,
typically exhibits small, bland
vegetations, usually attached
at the line of closure

E. LIBMAN-SACKS DISEASE

 Mitral and tricuspid valvulitits with small, sterile vegetations, CASE 15

occasionally encountered in SLE
A 29 year old female who recently gave birth to a healthy infant
 Locations: undersurface of AV valves, valvular endocardium,
develops dyspnea and swelling of her feet toward the end of the
chords, mural endocardium of atria or ventricles
day. She is nursing her six week old child.
 GROSS: Lesions are small (1-4mm diameter), single or multiple, PE
sterile, pick vegetations with warty (verrucous) appearance
 VS: BP mildly elevated.
 JVP raised with prominent a and v waves.
 MICROSCOPIC: finely granular, fibrinous eosinophilic material  Tender mild hepatosplenomegaly
containing cellular debris including nuclear remnants
 Cardiac apex heaving and displaced outside
midclavicular line
 Associated with: intense valvulitis, characterized by fibrinoid
 Pansystolic apical murmur and systolic murmur
necrosis of the valve substance, and showing the activation of the increasing with inspiration heard in tricuspid area
complement and recruitment of Fc-receptor-bearing cells
 Loud pulmonary component of S2; S3 and S4 gallop
 Fine inspiratory basal crepitant rales at both lung bases
 Pedal edema
II. Introduction: Cardiomyopathy
Labs
CARDIOMYOPATHY
 ECG: premature ventricular contractions
 Implies a principal cardiac dysfunction.
 Heterogeneous group of diseases of the myocardium associated
Imaging
with mechanical and/or electrical dysfunction
 CXR: interstitial pulmonary edema; global
 Usually exhibit ventricular hypertrophy or dilatation
cardiomegaly.
 Causes: frequently are genetic.  Echo/Nuc: cardiomegaly with diminished ventricular
contractility.
 2 Causes:
 Stress test: decreased ejection fraction with stress
o Primary (i.e., predominantly affecting heart)
o Secondary (i.e., part of a larger systemic
disorder)

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A. DILATED PERIPARTUM CARDIOMYOPATHY Microscopic:

 Often subtle and

Patient most likely has DILATED PERIPARTUM
CARDIOMYOPATHY. entirely nonspecific

 It is a special form of dilated cardiomyopathy that can  Most commonly

occur late in pregnancy for several weeks to months there is diffuse
postpartum myocyte
hypertrophy and
 PROGRESSIVE CARDIAC DILATION AND SYSTOLIC variable interstitial
DYSFUNCTION WITH CONCOMITTANT HYPERTROPHY fibrosis
 Presents with heart failure secondary to left ventricular
systolic dysfunction in the absence of any other cause of  Variable myocyte
heart failure hypertrophy
 Interstitial fibrosis -
B. MECHANISM OF THE DISEASE Interstitial fibrosis
(Collagen: blue:
Mechanism: Poorly understood but is probably multifactorial Using Masson
Trichome stain)
 Proposed causes:
a. Pregnancy associated HTN
b. Volume overload
c. Nutritional deficiency
d. Other metabolic derangements CASE 16
e. Poorly characterized immunological reaction

 Recent works: A 21 year old male presents with angina chest pain, dyspnea on
a. Primary defect: a microvascular angiogenic imbalance exertion, and an episode of syncope while playing basketball. The
within the myocardium patient has no history of blue spells, squatting for relief, or
-Leads to functional ischemic injury rheumatic fever in childhood.

*Mouse models: Elevated levels of an antiangiogenic PE

cleavage product of hormone prolactin and peripartum
cardiomyopathy.
*VEGF (which rises late in pregnancy) Blocking prolactin
secretion by bromocriptine in mouse models prevents
peripartum cardiomyopathy, suggesting a potential novel
therapeutic strategy.
C. STRUCTURAL ALTERATIONS OF THE HEART
Labs
Gross:
 Flabby with
Imaging
cardiomegaly (i.e., up to
900 g)
 Poor contractile function
(hypocontracting) and
stasis predispose to
mural thrombi.
 Valves and coronary
arteries are generally
normal
 Evident 4 chamber
A.
hyperthrophy and
dilatation.
 Arrow: Mural thrombus
 VS: pulse bisferious
 JVP normal
 Cardiac apex forceful with strong presystolic impulse
 Systolic thrill palpable over left sternal border
 S4; ejection systolic murmur over left third intercostal
space radiating to base and axilla; murmur increased
by exercise and during forced expiration against a
closed glottis but decreased by squatting
 ECG: left axis deviation due to left ventricular
hypertrophy; Q wave exaggerated in inferior and lateral
precordial leads
 CXR, PA: often normal.
 Echo: asymmetrical septal hypertrophy and
systolic anterior motion of mitral valve; Doppler
may show mitral regurgitation.
 Angio, cardiac: marked thickening of left
ventricular septal wall; small ventricular cavity with
impaired ventricular filling and narrow outflow
tract
HYPERTROPHIC CARDIOMYOPATHY
Patient most likely has HYPERTROPHIC
CARDIOMYOPATHY.

 Characterized by: Myocardial hypertrophy, Poorly compliant

left ventricular myocardium leading to abnormal diastolic
filling
 Intermittent ventricular outflow obstruction
 Clinically heterogenous
 Genetic disorder

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  HCM causes primarily diastolic dysfunction; systolic  MICROSCOPIC:
function is usually preserved.
 It is the leading cause of left ventricular hypertrophy
3 IMPORTANT
unexplained by other clinical or pathologic causes.
FEATURES:
 Massive myocyte
B. MECHANISM OF THE DISEASE
hypertrophy
 Helter-skelter Myocyte
 Pattern of transmission
disarray (disarray of:
o Most are autosomal dominant with variable penetrance.
bundles, individual
myocytes, and
 Caused by:
contractile elements in
a. Mutations of genes encoding sarcomeric proteins:
sarcomeres)
o β-myosin heavy chain mutations (most common)
 Interstitial and
o Cardiac TnT, α-tropomyosin, and myosin-binding protein
replacement fibrosis
C (MYBP-C)
(collagen is blue in this
o 70% to 80% of all cases (main mechanism)
Masson trichrome
stain)
Dean: if asked of the main mechanism, answer: GENETIC!

b. Defective energy transfer from source (mitochondria) of generation

to its site of use (sarcomere)  compensatory hypertrophy
D. POSSIBLE COMPLICATIONS OF THE DISEASE
c. Exaggerated responses of the myocardial fibroblasts to the primary
myocardial dysfunction  interstitial fibrosis -Major feature is reduced stroke volume due to a combination
of impaired diastolic filling and left ventricular outflow tract obstruction.
C. STRUCTURAL ALTERATIONS IN THE HEART
 Focal myocardial ischemia
 GROSS:
 Atrial fibrillation
 Essential feature: Massive myocardial hypertrophy, WITHOUT
VENTRICULAR DILATION!  Stroke (mural thrombi formation)

 Classic pattern: Asymmetric septal hypertrophy  Intractable cardiac failure

o Ventricular septum to the left ventricle free wall
ratio greater than 3:1  Ventricular arrhythmia

 Left ventricular cavity: “Banana-like” by the asymmetric  Death (related to arrhythmia)

bulging of the septum (normal: round to ovoid cavity)
***HCM is one of the most common causes of sudden,
 Most prominent hypertrophy in the sub-aortic region otherwise unexplained death in young athletes

Diagnosis: GROSS
EXAMINATION
 Left ventricular outflow
tract often exhibits a
fibrous endocardial plaque
associated with thickening
of the anterior mitral leaflet
 Result from contact of the
anterior mitral leaflet with
the Septum during
ventricular systole
 Correlate with the
echocardiographic “systolic
anterior motion” of the
anterior leaflet, with
functional left ventricular
Outflow tract Obstruction
during mid- systole.

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 Figure 12-31. Causes and consequences of dilated
and hypertrophic cardiomyopathy. Some dilated
cardiomyopathies and virtually all hypertrophic
cardiomyopathies are genetic in origin. The genetic
causes of dilated cardiomyopathy involve mutations
in any of a wide range of genes. They encode proteins
predominantly of the cytoskeleton, but also the
sarcomere, mitochondria, and nuclear envelope. In
contrast, all of the mutated genes that cause
hypertrophic cardiomyopathy encode proteins of the
sarcomere. Although these two forms of
cardiomyopathy differ greatly in subcellular basis and
morphologic phenotypes, they share a common set of
complications. LV, left ventricle.

Checkpoint!!!

True or False:

1. Dilated cardiomyopathy is the most common cause of sudden unexplained deaths in young athletes.
2. The histologic abnormalities in DCM are specific and usually point to a specific etiology.
3. The essential feature of HCM is massive myocardial hypertrophy, usually without ventricular dilation.
4. The central abnormality in HCM is reduced stroke volume due to impaired systolic filling.
5. Cardiomyopathies are a homogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction.
6. Streptococcus viridans is the most common cause of endocarditis in native, but previously damaged or abnormal valves.
7. Acute endocarditis has lesser valvular destruction than subacute endocarditis
8. Libman-Sacks Disease is an example of an infected endocarditis.
9. IE typically exhibits small, bland vegetations, usually attached at the line of closure
10. IE is often encountered in debilitated patients.

Answers:F-Hypertrophic, F-nonspecific and do not point, T, F-impaired diastolic, F-homogenous; T; F (baliktad); F-Sterile Endocarditis; F-NBTE; F-NBTE

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