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7/28/2019 The Heart 16th March 13
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DR KANWAL ZAHRA
16th March 2013
The Heart
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OVERVIEW
The right side receivesdeoxygenated blood fromthe body and tissues andthen pumps it to the lungsfor oxygenenationIts left side receivesoxygenated blood returningfrom the lungs and pumpsthis blood throughout the
body to supply oxygen andnutrients to the body tissues
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simplified
Cone shaped muscle
Four chambers
Two atria, two ventricles
Two circulations
Systemiccircuit: blood vessels that transport
blood to and from all the body tissues
Pulmonarycircuit: blood vessels that carry blood
to and from the lungs
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simplified
Heart weight:
250 300 g in females
300 350 g in males
0.4 0.5 % of body wt.
Right ventricular wall thickness is 0.3 0.5 cm
1.3 1.5 cm for left ventricle
Cardiomegaley above 500 g is associated with
ischemic changes and termed as cor bovium.
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Coverings of the heart: pericardium
Fibrous pericardium
Serous pericardium (a) Parietal layer (b) Visceral layer = epicardium:
part of heart wall
(Between the layers is pericardial cavity)
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Layers of pericardium and heart wall
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Myocardium
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Cardiac Valves
Tricuspid valve
RA to RV
Pulmonary valve
RV to pulmonary trunk
Mitral (bicuspid) valve
LA to LV
Aortic valve
LV to aorta
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AV (Mitral and tricuspid) valves are composed of:
Annulus, leaflets, chordae tendineae and papillary
muscles
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Semilunar valves (aortic and pulmonic) are
composed of: 3 cusps each with a sinus
3 commissures (corpora arantii)
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Valves are relatively avascular.
ATRIAL SIDE:
Lined by endothelial cells on a thin layer of
collagen and elastin. VENTRICULAR SIDE:
A thicker layer of dense collagen.
Loose myxoid C.T (zona spongiosa) in b/w.
Fibrous and spongiotic regions are of equalthickness.
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Function of AV valves
f l l
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Function of semilunar valves
(Aortic and pulmonary valves)
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Conduction system
SA node (sinoatrial)In wall of RASets basic rate: 70-80
Impulse from SA to atriaImpulse also to AV node via internodalpathwayAV node (In interatrial septum)
AV node through AV bundle(bundle of His)
Into interventricular septumDivide R and L bundle branches
subendocardial branches become(Purkinje fibers)
Contraction begins at apexComposed of specialized myocyteswith fewer interclated discs sndhigher glycogen content
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Blood supply to the heart(theres a lot of variation)
Coronary arteries:
Epicardial coronary arteries
Intramural arteries
Capillary network
Major epicardial coronary arteries are:
Left ant. Descending(LAD)
Left circumflex(LCX)
Both arises from left (main) coronary artery
Right coronary artery
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GROSS EXAMINATION AND TISSUE
HANDLING
ENDOMYOCARDIAL BIOPSIES: taken via Rt. Sidedcardiac catheter
Indications: To moniter heart transplant rejection
Tissue fragments are measured and countedduring gross exam.
Minimum of three preferably four samples ofmyocardium are recommended.
Examination of at least three levels arerecommended. An adequate biopsy must containat least 50% myocardium excluding previousbiopsy sites.
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CARDIAC VALVES: Removed because of
Calcific degeneration or perforation as sequel of
bacterial endocarditis. Mostly received in fragments, if present description of
vegetations and presence and absence of non-surgery
related leaflet destruction should included.
In calcific degeneration, acid decalcification is
required, sections from free edge to annulus.
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For mechanical heart valves, only vegetations
are submitted if present.
For bioprosthetic valves, the valve cusps are also
submitted.
MYOMECTOMY SPECIMENS:
From ventricular aneurysm repair or septal
myomectomy procedures.
Measured, weighed and sectioned at 3mm
intervals perpendicular to endocardial
surface.
All layers of heart should be described.
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HEART EXPLANT SPECIMENS:
Should be weighed
Valves and walls (circumference and diameter)
should be measured
Septal and ventricular configuration
(ventricular hypertrophy etc) should be
described.
Fragments of donor tissue (inflow tract) to
match with recipients anatomy are usually
present in same container.
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CONDUCTING AN AUTOPSY
Examination of the heart includes removing the chest
plate then taking the heart out of the pericardial sac The outside surfaces are examined first and the blood
vessels (coronary arteries) are dissected.
The heart is opened to reveal the internal surfaces
and structures, including the valves and heart muscle
(myocardium).
The muscle is then cut to reveal the surface color,
textures and other features. Finally, tissue sections are prepared to examine under
the microscope.
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Tricuspid and Mitral valves
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Aortic and Pulmonary valves
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PATHOPHYSIOLOGY OF HEART
DISEASES
Failure of pump
Obstruction to flow
Regurgitant flow Shunted flow
Disorders of cardiac conduction
Rupture of heart or a major blood vessel
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HEART FAILURE Often called CHF, when heart unable to pump blood
at a rate sufficient to meet metabolic demands. Compensatory mechanisms which maintain arterial
pressure and perfusion of vital organs include
1- Frank- Starling mechanism: inc filling vol. dilates theheart and inc functional cross bridges formation,enhancing contractility
2- Myocardial adaptations, hypertrophy
3- Activation of neurohumoral systems: Release ofnorepinephrine, activation of renin- angiotensin-aldosterone system , atrial natriuretic peptide,adjust filling vol. and pressure.
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LEFT-SIDED HEART FAILURE
Etiology: IHD, HTN, aortic and mitral valvular
disease, myocardial disease
Morphology: findings depend upon disease
process.
Gross: gross structural abnormalities e.g
myocardial infarcts, deformed, stenotic or
regurgitant valves may be present. Lt. ventricle
is usually hypertrophied often dilated.
M/E: non sp. Mainly myocyte hypertrophy and
varying degree of interstitial fibrosis.
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RIGHT-SIDED HEART FAILURE
Etiology: Lt. sided heart failure, pure Rt. Heartfailure is infrequent, associated with lungdisease so referred as Cor pulmonale (Latincor, heart;pulmnle, of the lungs)
Morphology: varies with cause. Rarelystructural defects(valvular abn, endocardialfibrosis) may be seen. In contrast to Lt. sidedfailure pulm. Congestion is minimal but portaland systemic venous systems may be engorged.
The only finding may be Rt. Atrial or ventriculardilatation.
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CONGENITAL HEART DISEASE
Cardiac development
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CONGENITAL HEART DISEASE
The structural anomalies in CHD fall into three
major categories:
1- Left-to-right shunt
2- Right-to-left shunt 3- Obstruction
LEFT-TO-RIGHT SHUNT:
Most commonly encountered shunts includeASDs, VSDs, Patent ductus arteriosus and
atrioventricular septal defects.
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1- Atrial septal defects (ASDs): classified according to their
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1 Atrial septal defects (ASDs): classified according to theirlocation as:
1- Secundum ASDs: 90% of all, may be single, multiple orfenestrated, near centre of atrial septum.
2- Primum ASDs: 5% of all, adjacent to AV valve. 3- Sinus venosus: 5%, near entrance of sup. vena cava, may be
associated with pulm. Venous return to Rt. atrium.
2-Ventricular septal defects (VSDs):
1- Membranous VSDs: 90% of all, involves the region ofmembranous interventricular septum
2- Infundibular VSDs: Lie below the pulm. Valve
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3- Within muscular septum
Most VSDs are single but those in muscular
septum may be multiple so called Swisscheese septum.
3 P ( i ) d i (PDA)
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3- Patent (persistent) ductus arteriosus (PDA):
Occur if ductus arteriosus remain open after birth, infetal circulation it shunts the blood from pulm.
artery to aorta so bypass the lungs. Produce characteristic harsh murmer described as
machinery like murmer
4- Atrioventricular septal defect (AVSD): results fromfailure of sup. and inf. endocardial cushions of AVcanal to fuse adequately.
Partial AVSD: consisting of primum ASD and cleft ofant. Mitral leaflet, causing mitral insufficiency
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Complete AVSD: large combined AV septal
defect and large common AV valve (hole in
centre of heart). All chambers freelycommunicate inducing vol. hypertrophy.
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RIGHT-TO-LEFT SHUNTS
Cyanosis early in postnatal life (cyanotic heartdiseases) includes:
Tetralogy of Fallot
Transposition of Great Arteries
Persistent Truncus Arteriosus
Tricuspid Atresia
Total Anomalous Pulmonary venous connection
l f ll ( )
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Tetrology of Fallot (TOF) Four cardinal features include:
1- VSD
2- Obstruction to right ventricular outflow tract (subpulmonary
stenosis)
3- An aorta that overrides the VSD
4- Right ventricular hypertrophy
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Morphology: Heart is enlarged and may be
boot-shaped as a result of marked ventricular
hypertrophy,in apical region VSD is usually large, aortic valve usually form
the sup. Border so override the defect and both
ventricular chambers.
Obstruction to Rt. Ventricular outflow is due to
subpulmonic stenosis which can be
accompanied by pulm. Valvular stenosis
Sometimes an aortic valve insufficiency or an
ASD may also be present.
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Transposition of great arteries (TGA)
Produces ventriculoarterial discordance, aorta
arises from Rt. Ventricle and lies ant. To and to
the Rt. of pulm. Artery which originates from Lt.
ventricle
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Condition is incompatible with postnatal life
unless a shunt exists for blood mixing.
The infants out look depends on degree ofblood mixing. Pts with TGA and VSD may have
stable shunts(35%) while those with patent
foramen ovale or PDA have unstable shunts.
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Persistant Truncus Arteriosus Failure of seperation of embryologic TA into aorta and
pulm. Artery. Results in single great artery that receive blood from
both ventricles, give rise to systemic, pulm and coronary
circurlation
T i id A i
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Tricuspid Atresia Complete occlusion of tricuspid valve orifice
Mitral valve is larger than normal and hypoplasia of Rt.Ventricle, Circulation is maintained by RT. to LT. shunt
thru ASD, PFO and a VSD. Inc mortality rate in 1st few wks
or months of life
T l l l
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Total anomalous pulmonary venous
connection
Pulmonary veins fails to join the Lt. atrium Results when common pulmonary vein fails to
develop or become atretic
Fetal development is made possible by primitive
venous channels that drain from lungs into Lt.innominate vein or coronary sinus
PFO or ASD is always present, allowing venous blood
to enter Lt. atrium. Vol. and pressure hypt of Rt. side of heart, dilation of
pulm. trunck. Lt. atrium is hypoplastic but Lt.ventricle is normal in size
Ob i i l li
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Obstructive congenital anomalies Obstruction occur at the level of heart valves or
within a great vessel includes: Stenosis or atresia of aortic or pulmonary valves
Coarctation of the Aorta
Obstruction can also occur within a chamber aswith subpulmonary stenosis in TOF.
Coarctation of the Aorta
2 classic forms are 1- Infantile form 2- Adult form In infantile form there is tubular hypoplasia of
aortic arch proximal to PDA often symptomaticin early childhood
I d lt f th i id lik i f ldi f t j t it
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In adult form there is a ridge like infolding of aorta just oppositeto closed ligamentum arteriosum
It may occur solitary but in 50% of cases accompanied by bicuspidaortic valve and also be associated with aortic stenosis, ASD, VSD,
mitral regurgitation, or berry aneurysms of the circle of Willis inthe brain.
There is cardiomegaly due to left ventricular pressure-overload hypertrophy.
P l St i d At i
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Pulmonary Stenosis and Atresia
obstruction at the pulmonary valve, which may be mild to
severe. Can be isolated or part of a more complex anomaly-either
TOF or TGA.
Right ventricular hypertrophy, poststenotic dilation of thepulmonary artery due to injury of the wall by "jetting"
blood. Subpulmonary stenosis (TOF), the high ventricularpressure is not transmitted to the valve, and thepulmonary trunk is not dilated and may in fact behypoplastic.
When the valve is entirely atretic, there is nocommunication between the right ventricle and lungs. Insuch cases the anomaly is associated with a hypoplasticright ventricle and an ASD; blood reaches the lungsthrough a PDA.
Aortic Stenosis and Atresia
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Aortic Stenosis and Atresia Congenital narrowing and obstruction of the
aortic valve can occur at three locations: valvular, subvalvular, and supravalvular.
valvular aortic stenosis: cusps may be hypoplastic, dysplastic, or abnormal in number.
underdevelopment (hypoplasia) of the leftventricle and ascending aorta, sometimesaccompanied by dense, porcelain-like left
ventricular endocardial fibroelastosis. This iscalled the hypoplastic left heart syndrome, isnearly always fatal in the first week of life, whenthe ductus closes
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Subaortic stenosis : caused by a thickened ring(discrete type) or collar (tunnel type) of dense
endocardial fibrous tissue below the level of thecusps
Supravalvular aortic stenosis: inherited form ofaortic dysplasia. In some cases it results from
deletions on chromosome 7 that include thegene for elastin. Ch. delation cause disruption ofelastin-smooth muscle cell interactions.
Other features of the syndrome include
hypercalcemia, cognitive abnormalities, andhallmark facial anomalies (Williams-Beurensyndrome).
I h i H t Di (IHD)
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Ischemic Heart Disease (IHD)
leading cause of death worldwide for both men
and women (7 million total per year)
results from myocardial ischemia. In 90% of
cases, the cause of myocardial ischemia is
reduced blood flow due to obstructiveatheroscleotic lesions in the coronary arteries.
so termed as coronary artery disease (CAD) or
coronary heart disease. IHD usually presents as one or more of the
following clinical syndromes:
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Myocardial infarction
Angina pectoris
Chronic IHD with heart failure.
Sudden cardiac death.
In addition to atherosclerosis, MI may be caused
by coronary emboli, blockage of small
myocardial blood vessels, and lowered systemic
blood pressure.
Pathogenesis of IHD
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MYOCARDIAL INFARCTION (MI)
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MYOCARDIAL INFARCTION (MI) MI, also known as "heart attack," is the death of cardiac
muscle due to prolonged severe ischemia.FEATURES TIME
Onset of ATP depletion Seconds
Loss of contractility 1 hr
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Evolution of Morphologic Changes in Myocardial Infarction
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Time Gross Features Light Microscope
Electron
Microscope
REVERSIBLE
INJURY0- hr None None Ralaxation of
myofibrils;
glycogen loss;
mitochondrial
swelling
IRREVERSIBL
EINJURY
-4 hr None Usually none; variable
waviness of fibers at border
Sarcolemmal
disruption;mitochondrial
amorphous
densities
4-12 hr Dark mottling (occasional) Early coagulation necrosis;
edema; hemorrhage
Time Gross Features Light Microscope
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12-24 hr Dark mottling Ongoing coagulation necrosis; pyknosis of
nuclei; myocyte hypereosinophilia; marginal
contraction band necrosis; early neutrophilic
infiltrate1-3 days Mottling with yellow-tan infarct
center
Coagulation necrosis, with loss of nuclei and
striations; brisk interstitial infiltrate of
neutrophils
3-7 days Hyperemic border; central
yellow-tan softening
Beginning disintegration of dead myofibers,
with dying neutrophils; early phagocytosis of
dead cells by macrophages at infarct border
7-10 days Maximally yellow-tan and soft,
with depressed red-tan
margins
Well-developed phagocytosis of dead cells;
early formation of fibrovascular granulation
tissue at margins
10-14 days Red-gray depressed infarct
borders
Well-established granulation tissue with new
blood vessels and collagen deposition
2-8 wk Gray-white scar, progressive
from border toward core of
infarct
Increased collagen deposition, with decreased
cellularity
>2 mo Scarring complete Dense collagenous scar
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complications following acute MI
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complications following acute MI
Hypertensive Heart Disease (HHD)
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Hypertensive Heart Disease (HHD) SYSTEMIC (LEFT-SIDED) HYPERTENSIVE HEART DISEASE:
HTN induces Lt. ventricular hypertrophy, initially withoutventricular dilation. The thickness of the left ventricular wallmay exceed 2.0 cm, and the heart weight may exceed 500gm.
M/E the earliest change of systemic HHD is an increase in
the transverse diameter of myocytes. Enlargement oftenaccompanied by interstitial fibrosis.
PULMONARY (RIGHT-SIDED) HYPERTENSIVE HEART DISEASE(COR PULMONALE):
In acute cor pulmonale there is marked dilation of the rightventricle without hypertrophy.
In chronic cor pulmonale the right ventricular wall thickens,sometimes up to 1.0 cm or more.
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More subtle right ventricular hypertrophy may
take the form of thickening of the muscle
bundles in the outflow tract, immediately belowthe pulmonary valve.
Valvular Heart Disease
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Valvular Heart Disease Valvular abnormalities may be congenital or
acquired. Acquired stenoses of the aortic andmitral valves account for approximately two
thirds of all cases.
most frequent abnormalities are: Aortic stenosis: associated with calcification
Aortic insufficiency: usually related to
hypertension and aging. Mitral stenosis: rheumatic heart disease
Mitral insufficiency: myxomatous degeneration
VALVULAR DEGENERATION ASSOCIATED
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WITH CALCIFICATION Calcific Aortic Stenosis:
most common of all, usually the consequence ofage-associated "wear and tear"
Morphology: hallmark of nonrheumatic, calcificaortic stenosis is heaped-up calcified masses within
the aortic cusps, free edges of the cusps are usuallynot involved.
M/E: the layered architecture of the valve is largelypreserved
In contrast to rheumatic aortic stenosis commissuralfusion is not usually seen. The mitral valve isgenerally normal.
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Mitral Annular Calcification
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Mitral Annular Calcification Degenerative calcific deposits can develop in the
peripheral fibrous ring (annulus) of the mitral valve
Grossly, appear as irregular, stony hard, occasionallyulcerated nodules (2-5 mm in thickness) that liebehind the leaflets.
may lead to (1) regurgitation(2) stenosis (3)
arrhythmias occasionally sudden death by penetration of calcium
deposits to a depth sufficient to impinge on theatrioventricular conduction system.
calcific nodules may also provide a site for thrombithat can embolize, can also be the nidus for infectiveendocarditis.
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MITRAL VALVE PROLAPSE (MYXOMATOUS
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(
DEGENERATION) In mitral valve prolapse (MVP), one or both mitral
valve leaflets are "floppy" andprolapse, into the leftatrium during systole.
Characteristic change in MVP is interchordalballooning (hooding) of the mitral leaflets. The
affected leaflets are often enlarged, redundant,thick, and rubbery.
associated tendinous cords may be elongated,thinned, or even ruptured, and the annulus may bedilated.
M/E : attenuation of the collagenous-fibrosa layer ofthe valve, accompanied by marked thickening of thespongiosa layer with deposition of mucoid(myxomatous) material
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RHEUMATIC HEART DISEASE
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RHEUMATIC HEART DISEASE
Rheumatic fever (RF) is an acute, immunologicallymediated, multisystem inflammatory disease that occurs afew weeks after an episode of group A streptococcalpharyngitis.
It may manifest as acute rheumatic carditis which mayprogress over time to chronic (RHD).
Morphology: During acute RF main lesions occur in theheart, called Aschoff bodies, consist of foci of lymphocytesoccasional plasma cells, and plump activated macrophagescalled Anitschkow cells.
These macrophages have abundant cytoplasm and centralround-to-ovoid nuclei in which the chromatin is disposedin a central, slender, wavy ribbon ("caterpillar cells"), andmay become multinucleated.
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Inflammation results in fibrinoid necrosis within thecusps or along the tendinous cords. Overlying thesenecrotic foci are small (1- to 2-mm) vegetations,
called verrucae, along the lines of closure. Subendocardial lesions, exacerbated by regurgitant
jets, may induce irregular thickeningscalled MacCallum plaques, usually in the left atrium.
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In chronic RHD cardinal features are leafletthickening, commissural fusion and shortening,and thickening and fusion of the tendinous cords,creates a "fish mouth" or "buttonhole" stenoses.
Mitral valve is affected alone in 65% to 70% ofcases, aortic valve in another 25% of cases.Tricuspid and the pulmonary valve involvement isinfrequent
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With tight mitral stenosis, the left atrium progressivelydilates and may harbor mural thrombi in the appendageor along the wall, either of which can embolize.
M/E there is organization of the acute inflammation and
subsequent diffuse fibrosis and neovascularization in themitral leaflets that obliterate the avascular leafletarchitecture.
INFECTIVE ENDOCARDITIS
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INFECTIVE ENDOCARDITIS Infective endocarditis (IE) is characterized by colonization
or invasion of the heart valves or the endocardium by a
microbe, leads to the formation ofvegetations. Morphology: hallmark of IE is the presence of friable,
bulky, vegetations containing fibrin, inflammatory cells,and bacteria or other organisms on the heart valves
The vegetations may be single or multiple and may involvemore than one valve. sometimes erode into theunderlying myocardium and produce an abscess (ringabscess).
Emboli may be shed from them at any time; because theembolic fragments may contain large numbers of virulentorganisms, abscesses often develop at the sites where theemboli lodge.
M/E: vegetations of typical subacute IE often have
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granulation tissue indicative of healing. With time,
fibrosis, calcification, and a chronic inflammatory
infiltrate can develop.
PATHOLOGICCRITERIA
Microorganisms, demonstrated by culture or histologic examination, in a vegetation, embolus
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g y g g
from a vegetation, or intracardiac abscess
Histologic confirmation of active endocarditis in vegetation or intracardiac abscess
CLINICALCRITERIA
Major
Blood culture(s) positive for a characteristic organism or persistently positive for an unusual
organism
Echocardiographic identification of a valve-related or implant-related mass or abscess, or
partial separation of artificial valve
New valvular regurgitaionMinor
Predisposing heart lesion or intravenous drug use
Fever
Vascular lesions, including arterial petechiae, subungual/splinter hemorrhages, emboli, septic
infarcts, mycotic aneurysm, intracranial hemorrhage, Janeway lesions
Immunological phenomena, including glomerulonephritis, Osler nodes, Roth
spots, rheumatoid factor
Microbiologic evidence, including a single culture positive for an unusual organism
Echocardiographic findings consistent with but not diagnostic of endocarditis, including
worsening or changing of
a preexistent murmur
NONINFECTED VEGETATIONS
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Nonbacterial Thrombotic Endocarditis (NBTE)
encountered in debilitated patients, striking association
with mucinous adenocarcinomas, procoagulant effectsof tumor-derived mucin or tissue factor.
Endocardial trauma, well-recognized predisposingcondition
Deposition of small sterile thrombi on the leaflets of thecardiac valves. 1 mm to 5 mm in size, and occur singly ormultiply along the line of closure of the leaflets.
M/E : composed of bland thrombi that are looselyattached to the underlying valve, do not elicit anyinflammatory reaction. May be the source of systemicemboli that produce infarcts in the brain, heart.
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Endocarditis of SLE (Libman-Sacks Disease)
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( )
small, sterile vegetations (1-4 mm) have a warty (verrucous)
appearance, located on the undersurfaces of the AV valves,
valvular endocardium, chords, or on the mural endocardium ofatria or ventricles.
M/E: Veg consist of finely granular, fibrinous eosinophilic material
that may contain hematoxylin bodies, remnants of nuclei
damaged by anti-nuclear antigen bodies.
Cardiomyopathies
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Cardiomyopathies cardiomyopathy(literally, heart muscle disease)
produce abnormalities in cardiac wall thicknessand chamber size, and mechanical and/or
electrical dysfunction.
Primarycardiomyopathies: predominantlyconfined to the heart muscle.
Secondarycardiomyopathies: have myocardial
involvement as a component of a systemic ormultiorgan disorder.
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Functional Patterns and Causes
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Functio
nal
Pattern
Ejectio
n
Fractio
n
Mechanisms of
Heart Failure
Causes of Phenotype Indirect Myocardial
Dysfunction (Mimicking
Cardiomyopathy)
Dilated
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( )
Morphology: Heart is usually enlarged, heavy (often
weighing two to three times normal), and flabby, due to
dilation of all chambers. Mural thrombi are common
and may be a source of thromboemboli.
M/E: Non specific
HYPERTROPHIC CARDIOMYOPATHY (HCM)
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( )
MORPHOLOGY: The essential feature of HCM ismassive myocardial hypertrophy, usually without
ventricular dilation. The classic pattern is asymmetric septal
hypertrophy.
On cross-section, the ventricular cavity loses its
usual round-to-ovoid shape and compressed into a"banana-like" configuration by bulging of theventricular septum into the lumen.
M/E : (1) extensive myocyte hypertrophy, with
transverse myocyte diameters frequently greaterthan 40 m (normal, 15 m); (2) haphazarddisarray of bundles of myocytes (termed myofiberdisarray); and (3) interstitial fibrosis.
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RESTRICTIVE CARDIOMYOPATHY (RCM)
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characterized by aprimary decrease in ventricularcompliance, resulting in impaired ventricular filling
during diastole. may be idiopathic or associated with, radiation
fibrosis, amyloidosis, sarcoidosis, metastatictumors, or the deposition of metabolites that
accumulate due to inborn errors of metabolism. Morphology. The ventricles are of approximately
normal size or slightly enlarged, the cavities are notdilated, and the myocardium is firm andnoncompliant. Biatrial dilation is commonlyobserved.
M/E, there may be only patchy or diffuse interstitialfibrosis, which can vary from minimal to extensive.
MYOCARDITIS
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Infectious microorganisms and/or an inflammatory process cause
myocardial injury
INFECTIONSViruses (e.g., coxsackievirus, ECHO, influenza, HIV, cytomegalovirus)
Chlamydiae (e.g., C. psittaci)
Rickettsiae (e.g., R. typhi, typhus fever)
Bacteria (e.g., Corynebacterium diphtheriae, Neisseria meningococcus, Borrelia (Lyme disease)
Fungi (e.g., Candida)
Protozoa (e.g., Trypanosoma cruzi[Chagas disease], toxoplasmosis)
Helminths (e.g. trichinosis)
IMMUNE- MEDIATED REACTIONS
Postviral
Poststreptococcal (rheumatic fever)Systemic lupus erythematosus
Drug hypersensitivity (e.g., methyldopa, sulfonamides)
Transplant rejection
UNKNOWN
Sarcoidosis
Giant cell myocarditis
Morphology: During active phase, heart appear normal
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or dilated, advanced stage the ventricular myocardium is
flabby haveing pale foci or minute hemorrhagic lesions
along with mural thrombi.
M/E: an interstitial mononuclear, predominantly
lymphocytic infiltrate associated with focal myocyte
necrosis, either resolve, leaving no residual changes, or
heal by progressive fibrosis.
Hypersensitivity myocarditis: perivascular infiltrate
composed of lymphocytes, macrophages, and a high
proportion of eosinophils. Giant-cell myocarditis, inflammatory infiltrate containing
multinucleate giant cells interspersed with lymphocytes,
eosinophils, plasma cells, and macrophages
Chagas disease: parasitization of scattered myofibers
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by trypanosomes with an infiltrate of neutrophils,
lymphocytes, macrophages, and occasional eosinophils.
PRIMARY CARDIAC TUMORS
M
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Myxoma
50% of primary tumors, occur in two settings:
Sporadic and familial
Sporadic tumor occurs in middle-aged women
(76%), usually in the left atrium (86%), nearly
always as a single tumor, and without associatedconditions.
familial variety: young people, slightly more
frequent in men, less commonly located in theleft atrium (62%), multicentric, and associated
with extracardiac abnormalities.
Grossly: soft, polypoidal, pale, lobulated masses,
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often attached by a stalk to the septum near the
foramen ovale. A papillary configuration may be
apparent, Calcification may occur, and this seems
to be more common in those located in the right
atrium.
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M/E, round, polygonal, or stellate cells are seen
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surrounded by abundant loose stroma rich in
acid mucopolysaccharides.
Some cells form solid cords and vascular
channels, continuous with the endocardial lining.
Mitoses, pleomorphism, and necrosis are absent
or minimal.
ossification (petrified myxoma), occurrence oftil i ti
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cartilaginous tissue
presence of thymic and foregut remnants,
having well-developed mucin-producing glands.referred as glandular myxoma, can be confusedwith metastatic adenocarcinoma.
development of a thymoma, presumably arisingfrom the thymic remnants.
Other benign tumors and tumorlike
diti
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conditions
Rhabdomyoma and rhabdomyomatosis
Hamartoma of mature cardiac myocytes
Calcified amorphous tumor of the heart (cardiac
CAT) Cystic tumor of the atrioventricular nodal region
Adenomatoid tumor
Papillary fibroelastoma Inflammatory myofibroblastic tumor
Paraganglioma
Primary malignant tumors
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y g
Sarcomas: are exceptionally rare, highly
pleomorphic and unclassifiable.
Of those that can be placed into a specific
category, angiosarcoma is the most common.
Gross: located in the atrium, presents as a largemass
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Metastatic tumors
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Malignant lymphoma is a more common even thanprimary
Any portion of the heart can be involved,conducting system results in heart block.
majority of carcinomas, the primary tumor is in thethoracic cavity or contiguous areas
They reaches the heart by mediastinal lymph nodesand from there extending in a retrograde fashion tothe cardiac lymph vessels.
Tumors spread to the heart by the hematogenousroute are malignant melanoma; carcinomas ofkidney, lung, and breast; choriocarcinomas; andchildhood rhabdomyosarcoma.
http://www.expertconsultbook.com/expertconsult/b/linkTo?type=bookPage&isbn=978-0-323-06969-4&eid=4-u1.0-B978-0-323-06969-4..00005-2--f0100&appID=NGE7/28/2019 The Heart 16th March 13
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