Dra. Reyes
October 2015
3.
4.
3.
4.
5.
Forward failure
o Diminished cardiac output
Backward failure
o Damming back of blood in the venous
system
Compensatory changes
1. Pressure or volume stress induces hypertrophyinitially adaptive
2. Ventricular dilation
Major causes:
o Ischemic heart disease
o Hypertension
o Aortic and mitral valve disease
o Myocardial disease
Manifested by:
o Pulmonary congestion
o Edema
Reduced cardiac output causes reduced renal
perfusion, leading to:
o Further salt and water retention
o Ischemic ATN??
o Impairment of waste excretion
Prerenal azotemia
CNS perfusion is reduced
o Hypoxic encephalopathy
o Irritability to coma
B. RIGHT-SIDED HEART FAILURE
Characterized by:
HEART DISEASE
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Arteritis
Emboli
Cocaine-induced vasospasm
3.
Precipitated
by
Relieved by
Prinzmetal variant
Uncommon
Occurs at rest
Unstable/Crescendo
Precipitated by rest
Prinzmetal
Uncomon
Coronary
artery
spasm
Effort
Rest
Unstable
Plaque
disruption with
superimposed
mural
thrombosis
Rest
Rest
B. MYOCARDIAL INFARCTION
3 Patterns:
1. Stable/Typical
Precipitated by effort
Relieved by rest
2.
Caused by
Stable
Most common
Chronic
stenosing
coronary
atherosclerosis
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Plaque
Disruption
Stable angina
>75%
No
Unstable
angina
Variable
Frequent
Transmural
myocardial
infarction
Variable
Frequent
Syndrome
Subendocardial
myocardial
infarction
Sudden death
Variable
Usually
severe
Variable
Frequent
PlaqueAssociated
Thrombus
No
Nonocclusive,
often with
thromboemboli
Occlusive
Widely
variable, may
be absent,
partial/
complete or
lysed
Often small
platelet
aggregates or
thrombi and/or
thromboemboli
Initial event:
o Erosion, ulceration, fissuring rupture or
hemorrhagic expansion of partially stenosing
atheroma (acute plaque change or
disruption)
o Followed by thrombosis
Absence of sudden death
Thrombi may lyse
Fibrinolytic treatment or
spontaneously
vasospasm may relax
Restore viability
Cells poorly contractile (stunned) for 1-2 days
B. SUBENDOCARDIAL INFARCT
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0-1/2
hr
None
Light Microscope
Electron
Microscope
Relaxation of
myofibrils,
glycogen loss,
mitochondrial
swelling
None
Irreversible Injury
- 4 hr
None
4-12 hr
Ocassionally
dark mottling
12-24
hr
Dark
mottling
1-3
days
Mottling with
yellow-tan
infarct center
3-7
days
Hyperemic
border;
central
yellow-tan
softening
7-10
days
10-14
days
2-8
weeks
>2 mos
Maximally
yellow-tan
and soft,
with
depressed
red-tan
margins
Red-gray
depressed
infarct
borders
Gray-white
scar,
progressive
from border
toward core
of infarct
Scarring
complete
Usually none;
variable waviness of
fibers at border
Beginning
coagulation necrosis;
edema; hemorrhage
Ongoing coagulation
necrosis; pyknosis of
nuclei; myocyte
hypereosinophilia;
marginal contraction
band necrosis;
beginning
neutrophilic infiltrate
Coagulation necrosis
with loss of nuclei
and striations;
interstitial infiltrate of
neutrophils
Beginning
disintegration of dead
myofibers, with dying
neutrophils; early
phagocytosis of cells
by macrophages at
intact border
Sarcolemmal
disruption,
mitochondrial
amorphous
densities
Well-developed
phagocytosis of dead
cells, early formation
of fibrovascular
granulation tissue at
margins
Well-established
granulation tissue
with new blood
vessels and collagen
deposition with
decreased cellularity
Dense collagenous
scar
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Clinical Features
Chest pain
Nausea
Diaphoresis
Dsypnea
o ECG changes
o Serum elevation of CKMB
o Troponin I
o Troponin T
o Myoglobin
o Adjunctive for diagnosis
Angiography
Echocardiography
Perfusion scintigraphy
25% of patients experience sudden death secondary
to fatal arrhythmia
o Patients who survive the event, 80-90%
develop complications
Early restoration of flow through the occluded vessel
generates better prognosis via:
o Thrombolysis
o Balloon angioplasty
st
Overall mortality in the 1 year is 30% and thereafter
5-10% per year
Complications depend on:
o Size
o Location of necrosis
o Reserve of functional myocardium
Complications:
Clinical Features
Causes of death
o Chronic heart failure (1/3)
o Renal disease
o Stroke
o Unrelated causes
Hypertensive heart disease increases the risk of
sudden cardiac death
Pathogenesis
Myocyte hypertrophy as a response to increased work
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d.
e.
3.
4.
Cor pulmonale
Pulmonary disorders pulmonary hypertension
right ventricular hyperplasia or dilatation
Morphology:
2.
Clinical Features
Clinical Features:
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Clinical Features:
Generally asymptomatic
Discovered only as midsystolic click
Manifestations:
o Atypical chest pain
o Dsypnea
o Fatigue
o Psychiatric manifestations
Increased risk
o Infective endocarditis
o Mitral valve insufficiency
o Atrial and ventricular arrhythmia
o Sudden cardiac death
Morphology:
Rheumatic fever
o Acute, recurrent inflammatory disease
o Typically occurs 1 to 5 weeks after group A,
-hemolytic streptococcal infection
st
Mainly 5-15 years; adults may suffer the 1 attack
Secondary to host antistreptococcal antibodies crossreactive to cardiac antigens
Diagnosis rests on the:
o Clinical history
o 2 out of 5 major Jones criteria
Death is rare
Most frequently secondary to myocarditis
Valvular involvement leads to deformation, scarring
with permanent dysfunction
st
Clinical features:
Morphology
Aschoff bodies
o Pathognomic foci of fibrinoid necrosis
o With lymphocytes, macrophages and plasma
cells
o Found in many sites, usually the
myocardium
o Slowly replaced by fibrous scar
Valvulitis with formation of beady fibrinous
vegetations (verrucae)
Healed valve shows
o Fibrous thickening of leaflets
o Calcification of fibrous leaflets
o Commisural fusion
o Fishmouth or buttonhole stenosis
o Thickened, fused and shortened mitral valve
chordae
MacCallum plaques
o Subendocardial collections of Aschoff
nodules
o Usually in left atrium
Solitary mitral involvement (65-75%)
Mitral or aortic involvement (20-25%)
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Morphology
Clinical Consequences
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o Weight loss
o Flu-like syndrome
Smaller vegetations, less frequent embolic
complications
Protracted course even without treatment, less fatal
VII. NONBACTERIAL THROMBOTIC ENDOCARDITIS
Marantic endocarditis
Small (1 to 5 mm), sterile, bland brin and platelet
thrombi (vegetations) loosely adherent to valve
leaets (often mitral) along the lines of closure,
without signicant inammation or valve damage
Attributed to systemic hypercoagulability
May embolize to brain, heart, or elsewhere
Occurs in settings of cancer (visceral
adenocarcinomas) or prolonged debilitating illness,
attributed to DIC or hypercoagulability state
A. LIBMAN-SACKS ENDOCARDITIS
Morphology
IE (infective endocarditis)
Aortic Regurgitation
Intrinsic valvular disease
Postinammatory
scarring (rheumatic
disease)
Infective endocarditis
Aortic disease
Degenerative aortic
dilation
Syphilitic aortitis
Ankylosing spondylitis
Rheumatic arthritis
Marfan syndrome
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A. CARDIOMYOPATHY
1. Dilated Cardiomyopathy
Morphology
Cardiomegaly up to 900 gm
Morphology
3. Restrictive Cardiomyopathy
Endomyocardial brosis
Loeffler endocarditis
Endocardial fibroelastosis
Manifestations:
Dyspnea,
Angina,
Near-syncope,
Chronic heart failure
May be asymptomatic
Complications:
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B. MYOCARDITIS
1.
Causes
Dilated
Hypertrophic
Restrictive
<40%
50-80%
45-90%
Impairment of
contractility
(systolic
dysfunction)
Impairment of
compliance
(diastolic
dysfunction)
Impairment
of
compliance
(diastolic
dysfunction)
Idiopathic;
amyloidosis;
radiation
induced
fibrosis
Idiopathic;
alcohol;
peripartum;
genetic;
myocarditis;
hemochromatosis;
chronic
anemia;
doxorubicin
(Adriamycin;
sarcoidosis
Indirect
Ischemic
myocardial
heart
dysfunction
disease;
(not
valvular
cardiomyop
heart
athy)
disease;
hypertensive
heart
disease;
congenital
heart
disease
*Normal approximately 50-65%.
Idiopathic;
genetic;
Friedreich
ataxia;
storage
diseases;
infants
of diabetic
mothers
2.
3.
4.
5.
6.
7.
1.
2.
3.
1.
2.
Pericardial
constriction
Morphology
Hypertensive
heart
disease;
aortic
stenosis
1.
2.
Hypersensitivity Reactions
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3.
Unusually primary
Generally, it is secondary to diseases of adjacent
structures or part of a systemic disorder.
o Viral infections
Lymphocytic inltration
Fuid resorbs if the disease remits
Fibrinous/serobrinous
Hemorrhagic
A. PERICARDIAL EFFUSION
Purulent (Suppurative)
B. HEMOPERICARDIUM
1. Acute Pericarditis
Mostly viral
Serous
Caseous
Secondary to
o Tuberculosis
o Less from mycotic infections
Adhesive Mediastinopericarditis
Constrictive Pericarditis
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3. Rheumatoid Arthritis
Viruses
Pyogenic bacteria
Tuberculosis
Fungi
Other parasites
Presumably Immune-Mediated Reactions
Rheumatic fever
Systemic lupus erythematosus
Scleroderma
Postcardiotomy
Post-myocardial infarction (Dressler) syndrome
Drug hypersensitivity reaction
Miscellaneous
Myocardial infarction
Uremia
After cardiac surgery
Neoplasia
Trauma
Radiation
IX. TUMORS
Probably hamartomas
Circumscribed but poorly encapsulated
Often subendocardial large polypoid accumulations of
adipose tissue
Usually in the
o Left ventricle,
o Right atrium
o Septum
Encroachment on valve function or conduction
pathways
L:R is 4:1
1 to 10 cm diameter, sessile to pedunculated;
Globular and hard to papillary or villous and myxoid
Stellate or globular mesenchymal myxoma cells, with
o Endothelial cells,
o Smooth muscle cells,
o Inammatory cells, in an acid mps matrix
Physical obstruction or wrecking ball trauma to the
atrioventricular valves or embolization
C. RHABDOMYOMAS
Etiology
B. MYXOMAS
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Tetralogy of fallot
o Thalidomide (sleeping pill)
o Excessive alcohol consumption and
cigarette smoking
o Most criticalembryologic development (3 to
8 weeks aog)
A. SHUNTS
Abnormal communication
o Between heart chambers,
o Between vessels,
o Between chambers and vessels
Depending on pressure relationships,
2 Types of Shunts
Other
XI. LEFT-TO-RIGHT SHUNTS: LATE CYANOSIS
A. VENTRICULAR SEPTAL DEFECT
B. OBSTRUCTIONS
Typically
o Coarctation,
o Valvular stenoses,
o Atresias
Do not cause cyanosis
Three types:
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1. Preductal Coarction
o
o
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