PATHOLOGY OF THE

CARDIOVASCULAR 2
DR IZEIN N C
DEPARTMENT OF ANATOMICAL
PATHOLOGY
NDU
 Outline
• HYPERTENSION
• HYPERTENSIVE HEART DISEASES
• RHEUMATIC FEVER AND RHD
• INFECTIVE ENDOCARDITIS(IE)
 HYPERTENSION(HYPT)
• Is defined as elevated BP. It is a risk factor for
atherosclerosis .
• It is a common health problem with devastating
consequences a times and often remains
asymptomatic until late in its course .
• HYPT is an important Risk factor for both
coronary artery disease and CVA; hypertension
can lead to cardiac hypertrophy and potentially
HF(hypertensive heart disease), aortic
dissection and renal failure
• HYPT. Is a complex, multifactorial disease that
has both genetic and environmental determinants.
• The pathogenic mechanisms of hypertension in
the majority of affected individuals remain largely
unknown, though molecular pathways underlying
blood pressure variations have been recently
elucidated
• A sustained diastolic pressure greater than
90mmHg or a sustained systolic pressure in excess
of 140mmHg is considered to constitute HYPT.
• Based on these criteria screening shows that 25%
of the general population are hypertensive .
• It affects more than 800 million persons
worldwide.
• The prevalence and vulnerability to complications
in areas with age and for unknown reasons are
high in African Americans
 Causes and Types
• 5% of patients have20 HYPT and these group have
underlying renal or adrenal disease(such as 10,
aldosteronism, Cushing syndrome,
pheochromocytoma) , narrowing of the renal
artery(usually by atheromatous plaque-Reno vascular
hypt)or other identifiable cause.
• However, about 95% of HypT is idiopathic (called
essential hypertension).
• This form of hypertension generally does not cause
short-term problems especially when controlled, is
compatible with long life and is asymptomatic, unless
MI,CVA or other complications supervene.
• Thus, this subgroup is often called benign
hypertension
 Causes and Types
• About 5% of hypertensives have a rapidly rising
blood pressure that if untreated, leads to death
within a year or two.
• This is called accelerated or malignant hyPT, a
clinical syndrome characterized by severe
hypT(i.e. systolic Bp over 200mmHg and
diastolic over 120mmHg),renal failure and
retinal hemorrhages and exudates , with or
without papilloedema.
• This can develop in previously normotensive
persons but more often is superimposed on pre-
 Types
1. Essential HYPT.
[Link] HYPT
 Renal
• Acute GN
• Chronic renal disease
• Polycystic disease
• Renin-producing tumors
• Renal artery stenosis
• Renal artery fibromuscular dysplasia
• Renal vasculitis
 Endocrine
• Adrenocortical hyper function(CS, 1 0

aldosterononism CAH, licorice ingestion)

• Exogenous hormones(glucocorticoids, estrogen
inducing pregnancy- induced and oral
contraceptives, sympathomimetics and
tyramine- containing foods, monoamine
oxidase inhibitors)
• Pheochromocytoma
• Acromegaly
• Hypothyroidisim(myxedema)
Cardiovascular
• Coarctation of aorta
• Polyarthritis nodosa(or other vasculitis)
• Increased intravascular volume
• Increased cardiac output
• Rigidity of the aorta
Neurologic
• Psychogenic
• Psychogenic increased intracraninal pressure
• Sleep apnea
 Pathogenesis of HYPT
Arterial hyptertension occurs when
relationship between cardiac output and
TPR is altered.
These factors are well understood for many
of the 20 forms of hypT.
Example in renovasular hypT. RA stenosis
causes decreased glomerular flow and
pressure in the afferent arterioles of the
glomerulus.
• This includes
 Regulation of normal BP:
• Blood pressure level is a complex trait that is
determined by the interaction of multiple
genetic, environmental and demographic
factors that influence cardiac output and
vascular resistance.
• The major factors that determine blood
pressure variation within and between
population include age, gender, body mass
index, and diet, principally sodium intake
Cardiac Output is highly dependent on blood
volume, itself greatly influenced by the whole
body sodium homeostasis.
Peripheral vascular resistance is determined
mainly at the level of the arterioles and is
affected by neural and hormonal factors.
Normal vascular tone reflects the balance between
hormonal vasoconstricting influences (including
angiotensin ii, catecholamine, and endothelin)
and vasodilators(including kinins,prostaglandins
and NO). Resistance vessels also exhibit
autoregulation, whereby increased blood flow
• Other local factors such as pH and hypoxia, and
the alpha and beta-adrenergic systems, which
influence heart rate, cardiac contraction and
vascular tone may be important
• The integrated function of these systems ensures
adequate perfusion of all tissues, despite regional
differences in demand.
• The critical roles of cardiac output tissues and
peripheral resistance in blood pressure
regulation
• BLOOD VOLUME HUMORAL
FACTORS
Constrictors
Dilators -Sodium -
Angiotensiin II -Prostaglandins
• - Mineralocorticoids -Catecholamine
-Kinins
• - Atriopeptin - Thromboxane
- No
 Mechanisms of Essential
hypertension
• Essential hypertension results from an interaction
of genetic and environmental factors that affect
cardiac output peripheral resistance or both.
Genetic Factors
• Clearly play a role in determining blood pressure
levels, as shown by studies comparing blood
pressure in monozygotic and dizygotic twins,
studies of familial aggregation of hypertension,
comparing the blood pressure of biologic and
adoptive siblings and adoption studies .
• Moreover, several single- gene disorders cause
Single- gene disorders cause relatively rare and
severe forms of hypertension through several
mechanisms.
These include
[Link] defects in enzyme involved in aldosterone
metabolism(e.g. aldosterone synthase, 11beta-
hydroxylase, 17 alpha-hydroxylase). These lead to
an adaptive increase in secretion of aldosterone,
increased salt and water reabsorption plasma
volume expansion and ultimately hypertension.
Example include : Glucocorticoid- remediable
aldosteronism (GRA).
2. Mutations in proteins that affect sodium
reabsorption. e.g. mutations in the epithelial
Na+ channel(ENaC) which is a channel highly
regulated by renin-angio tensiin system in the
CCT, responsible for the absorption of the last
2% sodium, thus determining Na balance.
This mutation leads to a moderately severe form
of salt- sensitive hypertension , called liddle-
syndrome caused by increased distal tubular
reabsorption of Na by aldosterone.
.3. Mutations of the
enzyme 11Beta=
HSD2(11beta –
hydroxsteroid
dehydrogenase -2) in
the cell causes
[Link] PHA1
(pseudohypoaldosteronism
type 1) and recessive PHA1
resulting in poor Na
reabsorption at the CCT
4. Gitelman syndrome
occurring at the distal
• Reduced renal sodium exertion in the presence
of normal arterial pressure may well be the key
initiating event in essential hypertension and
indeed, a final common pathway for the
pathogenesis of hypertension.
• Decreased sodium excretion might lead
sequentially to an increase in fluid volume,
increased cardiac output and peripheral
vasoconstriction thereby elevating blood
pressure.
• Alternative hypothesis implicates vasoconstrictive
influences(either factors that induce functional
vasoconstriction or stimuli that induce direct
structural changes in the vessel wall causing
increased peripheral resistance) as the primary
cause of hypertension. Chronic or repeated
vasoconstrictive influences could cause structural
thickening of resistant vessels
 Environmental factors
• These could modify expressions of the genetic
determinants of increased pressure, stress,
obesity, smoking, physical inactivity, heavy
consumption of salt have all been implicated as
exogenous factors in hypertension.
• Evidence linking the level of dietary sodium
intake with prevalence of hypertension in
different population groups is particularly
impressive.
• Moreover in both essential and secondary
hypertension, heavy sodium intake augments
• In summary, essential hypertension is a complex,
multi factorial disorder.
• Although single gene disorders can be responsible
for hypertension in unusual cases , it is unlikely
that a mutation at a single gene locus is a major
cause of essential hypertension in the larger
population.
• It is more likely that essential hypT results from
the combined effect of mutations or
polymorphisms at several gene loci that influence
blood pressure, interacting with a variety of
environmental factors.
Vascular Pathology in Hypertension
Hypertension
1. Accelerates artherogenesis
2. Causes degenerative changes in the walls of
large and medium arteries that potentiate both
aortic dissection and cerebrovascular
hemorrhage
3. HYPT is also associated with two forms of
small blood vessel disease: Hyaline
arteriolosclerosis and hyperplastic
arteriolosclerosis.
Hyaline arteriolosclerosis- a homogenous pink
hyaline thickening of the walls of arterioles with
loss of underlying structural detail with narrowing
of the lumen occurs in elderly patients (whether
normotensive or hypertensive ).
Its more generalized and more severe in
hypertension. Also common in diabetics as part
of the characteristic microangiopathy.
Hyaline arteriolosclerosis is a major
morphological characteristic of benign
nephrosclerosis in which the arteriolar narrowing
causes diffuse impairment of renal blood supply,
loss of nephrons and symmetric contraction of the
• Hyperplastic arteriolosclerosis- related to more
acute and severe elevations of Bp and is
characteristic but not limited to malignant
hypt(diastolic BP > than 120mmHg and systolic
BP >200mmHg).
• Hyperplastic arteriolosclerosis has ‘onionskin’,
concentric laminated thickening of the walls of the
arterioles with progressive narrowing of the
lumina.
• In malignant hypertension, these hyperplastic
changes are accompanied by deposits of fibrinoid
and acute necrosis of the vessel wall referred to as
 HYPERTENSIVE HEART
•
DISEASE
HHD is the response of the heart to the
demands induced by systemic hypertension.
Pulmonary hypertension also causes heart
disease and is referred to as right-side HHD or
cor pulmonale.
SYSTEMIC (LEFT -SIDED)HYPERTENSIVE
HD
• In hypt, hypertrophy of the heart is an adaptive
response to pressure overload that can lead to
myocardial dysfunction , cardiac dilation,
congestive heart failure (CHF)and sudden
death.
The minimal criteria for systemic HHD are the
following
1. Left ventricular hypertrophy(usually concentric),
in the absence of other cardiovascular pathology
that might have induced it and
2.A history or pathologic evidence of hypertension.
The Framingham study established on equivocally
that even mild hypertension( levels only slightly
above above 140/90mmhg) is sufficiently
prolonged, induces left ventricular hypertrophy
 Morphology
• HYPT induces LV pressure overload
hypertrophy without dilation of the LV. The LV
wall is the ratio of its wall thickness to radius
and increase the weight of the heart
disproportionately to increase overall cardiac
size. LVW thickness of the LV wall may
exceed 2.0cm and heart weight exceed 500gm.
• In time , the increased thickness of the LV wall
imparts a stiffness that impairs diastolic filling
and this often induces left atrial enlargement.
 Microscopically
• Earliest change in systemic HHD is increase in
transverse diameter of myocytes, which may be
difficult to appreciate on routine microscopy.
• At more advanced stage, the cellular and
nuclear enlargement become somewhat more
irregular with variation in size among adjacent
cells and interstitial fibrosis occurs
• Depending on the severity, duration and
underlying basis, of the hypertension, and on
the adequacy of therapeutic control, the patient
may
• Enjoy normal longevity and die of unrelated
causes.
• Develop progressive IHD owing to the effects
of HYPT in potentiating atherosclerosis
• Suffer progressive renal damage or CVA or
experience progressive heart failure . The risk
 Pulmonary (right side)hypertensive
heart disease(cor pulmonale)
This consists of right ventricular hypertrophy, dilatation and
potentially failure 20 to pulmonary hypertension caused by
disorders of the lungs or pulmonary vasculature. Pulmonary HHD
is the right-sided counterpart of left-sided(systemic)HHD.
Cor pulmonale may be acute or chronic, depending on the suddenness
of development of the pulmonary hypertension. Chronic cor
pulmonale usually implies right ventricular hypertrophy( and
dilation)20 to prolonged pressure overload caused by obstruction of
the pulmonary arteries or arterioles or compression or obliteration
of septal capillaries(e.g. owing to 10 pulmonary hypT or
emphysema).
Acute cor pulmonale can follow massive pulmonary embolism
 Morphology
• In acute cor pulmonale, there is marked dilation
of the right ventricle without hypertrophy.
• In chronic cor pulmonale, the right ventricular
wall thickens, sometimes upto 1.0 cm or more
and may even come to approximate that of the
left ventricule. There may be thickening of the
muscle bundles in the outflow tract, just below
the pulmonary valve or the moderator band- the
muscle bundle that connects the ventricular
septum to the anterior right ventricular
papillary muscle.
[Link] predisposing to cor pulmonale
• Diseases of the pulmonary, parenchyma
• Chronic obstructive pulmonary disease
• Diffuse pulmonary interstitial fibrosis
• Pneumoconiosis
• Cystic fibrosis
• Bronchiectasis
[Link] of the pulmonary vessels
• Recurrent pulmonary thromboembolism
• Primary pulmonary hypertension
• Extensive pulmonary arteritis (e.g. Wegener
granulomatosis)
• Drug, toxin, orradiation- induced vascular
obstruction
• Extensive pulmonary tumor micro embolism
[Link] affecting chest movement
• Kyphoscoliosis
• Marked obesity(pickwickian syndrome)
• Neuromuscular diseases
[Link] inducing pulmonary arterial
constriction
• Metabolic acidosis
• Hypoxemia
• Chronic altitude sickness
• Obstruction to major airways
 RHEUMATIC FEVER AND
RHD
• RF is an acute immunologically mediated ,
multisystem inflammatory disease that occurs a
few weeks following an episode of group A
streptococcal pharyngitis.
• Acute rheumatic carditis during the active
phase of RF may progress to chronic heart
disease(RHD)
 RHEUMATIC FEVER AND
RHD
The most important consequences of RF are
chronic valvular deformities.
Characterized principally by deforming fibrotic
valvular disease(particularly mitral stenosis),
which produces permanently dysfunction and
severe, sometimes fatal, cardiac problems
decades later.
RF does not follow infections by streptococci at
other sites
• Incidence and mortality rate of RF have declined
remarkably in the past 30 years owing to
improved socio economic conditions, rapid
diagnosis and treatment of strept. pharyngitis and
unexplained decrease in the virulence of group A
streptococci.
• But its still an important public health problem
where there is crowding and depressed economy
in urban areas
 Morphology

• During acute RF, focal inflammatory lesions are

found in various tissues.
• They are most distinctive within the heart where
they are called Aschoff bodies.
• They consist of foci of swollen eosinopjlic collagen
surrounded by lymphocytes(only T cells),
occasional plasma cells and plump macrophages
called ANITSCHKOW CELLS(pathognomonic
of RF).
 Morphology
• These distinctive cells have abundant cytoplasm
and central round-to –avoid nuclei in which the
chromatin is disposed in a central, slender, wavy
ribbon(hence the designation “caterpillar cells”).
• Some of the lager macrophages become
multinucleated to form Aschoff giant cells
 Pancarditis
• During Acute RF, diffuse inflammation and
Aschoff bodies may be found in any of the
three layers of the heart- pericardium,
myocardium or endocardium- hence called
pancarditis.
• In the pericardium, inflammation is
accompanied by a fibrous or serofibrinons
pericardial exudate, described as “bread-and-
butter” pericarditis- which generally resolves
without sequelae.
• The myocardial involvement- myocarditis takes
the form of scattered Aschoff bodies within the
interstitial connective tissues often perivascular.
• The valvular vegetations in RF occur on
concomitant involvement of the endocardium
and the left-sided valves by inflammatory foci
typically results in fibrinoid necrosis within the
cusps or along tendinious cords on which sits
small(1 to2mm)vegetations(verrucae) along the
lines of closure.
• These cause little disturbance to cardiac function.
Subendocardial lesions, perhaps exacerbated by
regurgitation jets, may induce irregular
thickenings called Maccallum plaques usually in
the left atrium.
• Chronic RHD is characterized by organization of
the acute inflammation and subsequent fibrosis. In
participation the valvular leaflets become thick.
• RHD is overwhelmingly the most frequent
cause of mitral stenosis (99% of cases).
• In patients with RHD mitral valve alone is
involved in 65-70% of cases, and mitral and
aortic in about25% of cases.
• Fibrous bridging across the valvular
commissure and calcification created “fish
mouth” or”button hole” stenosis.
• With tight mitral stenosis the left atrium
progressively dilates and may harbor mural
thrombus either in the appendage or along the
wall.
• Long- standing congestive changes in the lungs
may induce pulmonary vascular and,
parenchymal changes and in time, lead to right
ventricular hypertrophy.
• The left ventricule is generally normal with
isolated pure mitral stenosis
 Pathogenesis
• It is strongly suspected that acute rheumatic fever
is a hypersensitivity reaction induced by groupA
streptococci, but the exact pathogenesis remains
uncertain.
• It is thought that antibodies directed against the M
proteins of certain strains of streptococci cross-
react with glycoprotein antigens in the heart, pints
and other tissues.
 Pathogenesis
• The onset of symptoms 2 to 3 weeks after
infection and the absence of streptococci from the
lesions support the concept that RF results from
an immune response against the offending
bacteria.
• Only a minority of infected patients develop RF,
suggesting that genetic susceptibility influences
the hypersensitivity
 Pathogenesis

• The chronic sequelae results from progressive

fibrosis due to both healing of the acute
inflammatory lesions and the turbulence
induced by ongoing valvular deformities
 Clinical features

• RF is characterized by a constellation of
findings that induces as major
manifestations
1. Migratory polyarthritis of the large joints
2. Carditis
3. Subcutaneous nodules
4. Erythema disorder with
5. Involuntary purposeless, rapid marks.
 Clinical features
• The is established by the so called Jones criteria;
• Evidence of a preceding group A streptococcal
infection, with the presence of two of the major
criteria or one major, two minor manifestations
(non specific signs and symptoms that include fever,
arthralgia or elevated blood levels of acute phase
reactants- eg C-reactive protein).
Acute RF typically occurs 10 days to 6 weeks after
an episode of pharyngitis caused by group A
streptococci in about 3% of patients.
Acute RF appears most often in children between
ages 5 and 15, but 20% of 1st attacks occur in
middle to later life.
Though pharyngeal cultures for streptococci are
negative by the time the illnesses begins,
antibodies to one or more streptococcal enzymes,
such as streptolysin O and DNASE B are present
and can be detected in sera of most patients.
The predominant clinical manifestations are those
of Arthritis and Carditis.
Arthritis typically begins with migratory
polyarthritis in which one large joint after another
becomes painful and swollen for a period of days,
and then subsides spontaneously, leaving no
residual disability.
Clinical features related to Acute Carditis includes:
pericardial friction rubs,
weak heart sounds,
tachycardia and
arrhythmias
• Myocarditis may cause cardiac dilation that may
evolve to functional mitral valve insufficiency or
even heart failure.
• Overall, the prognosis for attack is generally good,
and only 1% of patients die from RF
• After an initial attack, there is increased
vulnerability to reactivation of the disease with
subsequent pharyngeal infections and same
manifestations are likely to appear with each
recurrent attack. Carditis is likely to worsen
with each recurrence, and damage is
cummulative. Other hazards are embolization
from mural thrombi and infective endocarditis
superimposed on deformed valves.
• Surgical repair of diseased valves by
increasing the fused mitral valve commissures
and replacement with prosthetic devices has
 INFECTIVE
•
ENDOCARDITIS(IE)
IE, one of the most serious of all infections is
characterized by colonization or invasion of the
heart valves or the mural endocardium by a
microbe, leading to the formation of bulky,
friable vegetations composed of thrombotic
debris and organisms, often associated with
destruction of the underlying cardiac tissues.
Most cases are caused by bacteria(bacterial
endocarditis), though fungi, rickettsiae (q
fever)and chalmydiae have at one time or the
other been responsible for IE.
• Traditionally, IE has been classified on clinical
grounds into Acute and Subacute forms
depending on the range of severity of the
disease and its tempo being determined in large
part by the virulence of the infecting
microorganism and whether underlying cardiac
disease is present
• Acute IE describes a destructive, tumultous
infection frequently of a previously normal heart
valve, with a highly virulent organism, that
leads to death within days or weeks more than
50% of patients may die despites antibiotics and
surgery.
• Subacute IE is caused by organisms of low
virulence in a previously abnormal heart,
particularly on deformed valves.
This disease appears insidiously and pursues a
protracted course of weeks to months even
when untreated with most patients recovering
 Aetiology and Pathogenesis
[Link](previously the major)
[Link] mitral valve(more common now0
[Link] calcific valvular stenosis
[Link] aortic valve(whether calcified or not)
[Link] (prothetic) valves
• Host factors such as neutropenia,
immunodeficiency, malignancy, therapeutic
immunosuppression, DM, alcohol or IV drug
abuse are predisposing influences.
• Others induce platelet- fibrin deposits that
accumulate at site of impairment of jet streams
caused by pre-existing cardiac disease or
indwelling vascular catheters and these may be
important in development of endocanditis
• Endocarditis of native but previously damaged
or otherwise abnormal valves is caused most
commonly(50-60% of cases) by
• [Link] viridans. The more virulent .
• 2.S. aureus commonly found on the skin attacks
either healthy or deformed valves and are
responsible for 10-20% of cases, overall S.
aureus is the major offender in IV drug abusers
Others in the list includes
• 3 HACEK group(haemophilus, Actinobacillus,
cardiobacterium, Eikenella and Kingella), all
commersals in the oral cavity
• [Link] epidermidis, a coagulase negative
staphylococci which most commonly causes
prothetic valve endocarditis.
• 5. Culture-negative endocarditis-because
offending agent is deeply embedded within
enlarging vegetation and not released in blood
• Formost among the factors predisposing to the
development of endocarditis is seeding of the
blood with microbes.
The portal of entry of the agent into the blood
stream may be obvious infection elsewhere, a
dental or surgical procedure that causes transient
bacteraemia, introducing contaminated material
into blood stream by IV drugs abusers or occult
source from the gut, oral cavity or trivial-injuries.
 Morphology
• In both the subacute and acute IE, friable, bulky
and potentially destructive vegetation containing
fibrin, inflammatory cells and bacteria or other
organisms are present on the heart valves.
• The aortic or mitral valves are the most common
sites, though valves of the right heart may be
involved especially in IV during abusers.
• Vegetations may be single or multiple and may
involve more than one valve.
• Vegetation can erode into the underlying
myocardium and produce an abscess cavity(ring
abscess) which is one of the several important
complications.
• Systemic emboli may occur at any time because of
the friable nature of the brain , kidneys,
myocardium and other tissues. Because the
embolic fragments contain large numbers of
virulent organisms, abscesses often develop at the
sites of such infarcts(septic infracts)
• The vegetations of subacute IE are associated in
less valvular destruction than those of acute
endocarditis, although the distinction between
the two forms may be difficult.
• Microscopically, the vegetations of typical
subacute IE often have granulation tissue at their
bases(suggesting chronicity).
With passages of time, fibrosis, calcification and
chronic inflammatory infiltrate may develop.
 Clinical features
• Fever- most consistent sign of IE. But subacute
disease especially in the elderly, fever may be
slight or absent and only manifestations are
sometimes nonspecific fatigue, loss of weight
and flu like syndromes.
• On the other hand acute endocarditis has a
stormy onset with rapidly developing fever,
chills, weakness and lassitude
 Complications
• Generally begin in the first week, and may be
immunologically mediated e.g.
glomerulonephritis, owing to trapping of Ag-Ab
complexes which can cause haematuria,
albuminuria or renal failure.
• Prevention of IE is important and is done by the
prophylactic use of antibiotics in the patient with
some form of cardiac anomaly or artificial valve
who is about to have a dental, surgical or other
invasive procedure.
 Diagnostic Criteria for IE(Duke
Criteria)
Pathological criteria
• -Microorganisms, demonstrated by culture or
histologic examination in a vegetation,
embolises from a vegetation or intracardiac
abscess.
• -Histologic confirmation of active endocarditis
in vegetation or intracardiac abscess
Clinical criteria
Major
• -Positive blood culture(s) indicating characteristic
organism or persistence of unusual organisms.
• -Echocardiographic findings, including valve-
related or implant-related mass or abscess or
partial separation of artificial valve
• -New valvular regurgitation.
Minor
• -Predisposing heart lesion or intravenous drug use.
• -Fever
• -Vascular lesions, including arterial petechiae,
subungal/ splinter usages, emboli, septic infarcts,
myocytic anuerysm, intracranial wages, Janeway
lesions.
• -Immunologic phenomena; including
glomelonephritis, oslers nodes, Roth spots,
rheumatoid factor
• -Microbiologic evidence, including single culture
showing uncharacteristic organism
• -Echocardiographic findings consistent with but not
diagnostic of endocarditis, including new valvular
regurgitation, pericarditis.
Note in Duke criteria, if clinical criteria is used,
- 2 major,
- 1 major plus 3 minor or
- 5 minor criteria are diagnostic.
• -Janeway lesions are small enthematous or
haemorrhage,macular, nontender lesions on the
palms and soles and are the consequence of
septic embolic events.
• -Osler nodes are small, tender subcutaneous
nodules that develop in the pulp of the digits or
occasionally, more proximally in the fingers
and persist for hours to several days
 NONINFCECTED VEGETATIONS
[Link] thrombotic Endocarditic(NBTE)
NBTE is characterized by the disposition of small
masses of fibrin platelets and other blood
components on the leaflets of the cardiac valves. The
lesions are sterile and do not contain microorganisms,
unlike the valvular lesions of IE. NBTE is often
encountered in debilitated patients, such as those
with cancer and sepsis hence the previously used
term marantic endocarditis.
Although the local effect on the valves is usually
unimportant NBTE may achieve clinical significance
by producing emboli and resultant infarcts in the
brain, hearts or elsewhere.
Morphologically
• Sterile , nondestructive and small(1-5mm)
vegetations occurring singly or multiply along the
line of closure of the leaflets or cusps.
Histologically , they are composed of bland
thrombus without accompanying inflammatory
reaction or induced valve damage should the
patient survive the underlying disease,
organization may occur, leaving delicate strands
of fibrous tissue
Pathogenesis
• NBTE frequently occurs concomitantly with
venous thromboses or pulmonary embolism,
suggesting a common origin in a hypercoagulable
state with systemic activation of blood coagulation
such as disseminated intravascular coagulation.
• This may be related to some underlying disease
such as cancer, and in particular ,, mucinous
adenocarcinomas of pancreas.
• The striking association with mucinons
adenocarcinomas in general may relate to the
procoagulant effect of circulating mucin and thus
NBTE can be a part of Trousseau syndrome
• NBTE are also seen occasionally in association
with non mucin-producing malignancy , such as
acute promyelocytic leukaemia, and in other
deblitating diseases or conditions(e.g.
hyperestrogenic states , extensive burns or sepsis)
promoting hypercoagularity.
• Endocardial trauma, as from an indwelling
catheter is a well recognized predisposing
condition and frequently right–sided valvular and
endocardial thrombotic lesions are seen along the
track of a swan- Ganz pulmonary artery catheter
 [Link] as systemic lupus
Erythematosis(Libman sacks Disease)
In SLE mitral and Tricuspid valvulitis with small
sterile vegetations called Libman-sacks
endocarditis is ocassionally encountered.
Morphology
Small, single or multiple , sterile, granular pink
vegetations(1-4mm in diameter).
They may be located on the under surfaces of the
atrioventricular valves, on the valvular
endocardium, on the cords or on the mural
endocardium of atria or ventricules
• Thrombotic heart valve lesions with sterile
vegetations or rarely fibrous thickening
commonly occur with the antiphospholipid
syndrome.
• Circulating antiphospholipid antibodies are
also commonly associated with venous or
aterial thrombosis, recurent pregnancy loss or
thrombocytopenia.
• Mitral value is more involved than aortic.
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