pathology of the heart
TRANSCRIPT
PATHOLOGY OF THE PATHOLOGY OF THE HEARTHEART
DR. HENNY SULASTRY, SpPADR. HENNY SULASTRY, SpPA
Central Diagnostic of Pathology Anatomic Central Diagnostic of Pathology Anatomic M. Hoesin Central General Hospital/ Medicine M. Hoesin Central General Hospital/ Medicine
Faculty of Sriwijaya UniversityFaculty of Sriwijaya University20082008
TerminologyTerminology : : episodic chest painepisodic chest pain caused caused by inadequate oxygenation.by inadequate oxygenation.
Causes include partial or complete Causes include partial or complete interruption of arterial blood flow to the interruption of arterial blood flow to the myocardium.myocardium.
In most cases the cause is In most cases the cause is atherosclerotic atherosclerotic narrowing of the coronary arteries.narrowing of the coronary arteries.
Ischemic Heart DiseaseIschemic Heart Disease
Clinically silent or manifest as angina Clinically silent or manifest as angina pectoris, myocardial infarction, chronic pectoris, myocardial infarction, chronic IHD.IHD.
Risk factorsRisk factors
Life-style Life-style smooking, alkohol smooking, alkohol
Determined genetic factors Determined genetic factors hyperlipidemia, DMhyperlipidemia, DM
Physiological Factor Influence the Expression of Physiological Factor Influence the Expression of IschemiaIschemia
Energy requirmentsEnergy requirments Cardiac muscle has high energy requirmnet, demand high Cardiac muscle has high energy requirmnet, demand high
energy phosphates to maintain membrane integrity and the energy phosphates to maintain membrane integrity and the consentration gradients of sodium, potassium & calciumconsentration gradients of sodium, potassium & calcium
Feature of cardiac muscleFeature of cardiac muscle Poor endogenous fuel reservesPoor endogenous fuel reserves Well vascularizedWell vascularized Aerobic metabolismAerobic metabolism Pattern of myocardial blood flowPattern of myocardial blood flowPerfussion of the myocardial occurs in diastole, systole vessels Perfussion of the myocardial occurs in diastole, systole vessels
are compressed by contractionare compressed by contraction The pattern of flow The pattern of flow learned from Physiology and Internal learned from Physiology and Internal
MedicineMedicine
General Pathology of Ischaemic Myocardial General Pathology of Ischaemic Myocardial InjuryInjury
The time-related functional, biochemical and The time-related functional, biochemical and ultrastructural changes after coronary artery ultrastructural changes after coronary artery occlussion occlussion from animal studies in dogs and from animal studies in dogs and pigs.pigs.
Following have been observed:Following have been observed: Within minutes : cessation of contraction of Within minutes : cessation of contraction of
ischemic areaischemic area Coagulative necrosis over next 12 hoursCoagulative necrosis over next 12 hours Necrosis may be inhibited if blood flow is re-Necrosis may be inhibited if blood flow is re-
establisted within 20-40minestablisted within 20-40min
Biochemical ChangesBiochemical Changes
Fall in oxygen tensionFall in oxygen tension Loss of mitochondrial (aerobic) respirationLoss of mitochondrial (aerobic) respiration Anaerobic glycolysis of glycogen is sole Anaerobic glycolysis of glycogen is sole
sourse energy sourse energy rise in lactate rise in lactate Marked fall in intracellular ATP to zero in 40-Marked fall in intracellular ATP to zero in 40-
60 min60 min Creatine posphate falls to zero within 15 min Creatine posphate falls to zero within 15 min
of ischemiaof ischemia Inhibition myosin ATPase activity by H+Inhibition myosin ATPase activity by H+
STRUCTURAL CHANGES OCCURING IN STRUCTURAL CHANGES OCCURING IN ISCHAEMIC MYOCARDIUMISCHAEMIC MYOCARDIUM
Ultrastructural changesUltrastructural changesMitochondrial and membrane damage (15-Mitochondrial and membrane damage (15-
40 min)40 min)More severe upon reperfusion with More severe upon reperfusion with
swollen muscle cells, accumulation of swollen muscle cells, accumulation of hydrated calcium phosphate in hydrated calcium phosphate in mitochondria and sarcomere disturbance mitochondria and sarcomere disturbance
Ischaemic Heart DiseaseIschaemic Heart Disease(IHD)(IHD)
There are 4 overlapping ischemic There are 4 overlapping ischemic syndromes:syndromes:
1.1. Angina PectorisAngina Pectoris2.2. Myocardial InfarctionMyocardial Infarction3.3. Chronic Ischemic Heart diseasesChronic Ischemic Heart diseases (in (in
elderly patients w/ moderate – severe elderly patients w/ moderate – severe coronary atherosclerosis who insidiously coronary atherosclerosis who insidiously develop CHFdevelop CHF
4.4. Sudden cardiac deathSudden cardiac death is defined as is defined as unexpected cardiac death within 1 hour unexpected cardiac death within 1 hour of symptom onsetof symptom onset
1.1. Stable angina Stable angina The most common form.The most common form. Pain that is precipitated by exertion, Pain that is precipitated by exertion,
relieved by rest or by vasodilators.relieved by rest or by vasodilators. Result from severe narrowing of Result from severe narrowing of
atherosclerotic coronary vesselsatherosclerotic coronary vessels
Angina PectorisAngina Pectoris
Causative lessions are a fixed stenosis of Causative lessions are a fixed stenosis of the lumen of one or more epicardial the lumen of one or more epicardial coronary artery by more than 50%coronary artery by more than 50%
Stenosis morphologyStenosis morphology70% lessions are concentric contain of 70% lessions are concentric contain of
fibrous plaques with small basal lipidfibrous plaques with small basal lipid24% lessions are excentric contain of 24% lessions are excentric contain of
large lipid-pools and fibrouslarge lipid-pools and fibrous
Unstable AnginaUnstable Angina
2. Unstable angina ( Unstable Angina Type 1)2. Unstable angina ( Unstable Angina Type 1) Is prolonged or recurrent pain at restIs prolonged or recurrent pain at rest Indicated myocardial infarctionIndicated myocardial infarction Caused by disruption of an atherosclerotic Caused by disruption of an atherosclerotic
plaque.plaque. Splitting and fissuring of the fibrous cap with Splitting and fissuring of the fibrous cap with
thrombus dispositionthrombus disposition
3. Prinzmetal angina3. Prinzmetal angina ( Unstable Angina Type 2)( Unstable Angina Type 2) Intermittent chest pain at restIntermittent chest pain at rest Caused by vasospasmCaused by vasospasm
Sequential progression of coronary artery lesion morphology, beginning with stable chronic plaque, responsible for typical angina, and leading to the various acute coronary syndromes
Myocardial InfarctionMyocardial InfarctionThe most important cause of morbidity from The most important cause of morbidity from
IHD is one of causes of death.IHD is one of causes of death.Myocardial coagulative necrosis caused by Myocardial coagulative necrosis caused by
coronary artery occlusioncoronary artery occlusion is characteristic. is characteristic.A series of A series of progressive changesprogressive changes involving involving
gross and microscopic appearance of the gross and microscopic appearance of the heart.heart.
Release of myocardial enzymes and other Release of myocardial enzymes and other proteins into bloodstream proteins into bloodstream
A process caused by altered membrane A process caused by altered membrane permeability of necrotic myocardial cells.permeability of necrotic myocardial cells.
The cells involved The cells involved neuthrophills, neuthrophills, macrophages and fibroblasts.macrophages and fibroblasts.
There are There are 2 interrelated types2 interrelated types of of myocardial ischemic necrosis :myocardial ischemic necrosis :
1.1. Transmural InfarctionTransmural Infarction
2.2. Subendocardial InfarctionSubendocardial Infarction
1.1. Transmural InfarctionTransmural Infarction Involving the full thickness of the ventricular Involving the full thickness of the ventricular
wallwall Caused by severe coronary atherosclerosis Caused by severe coronary atherosclerosis
with acute plaque rupture and superimposed with acute plaque rupture and superimposed occlusive thrombosisocclusive thrombosis
PathogenesisPathogenesisSignificant plaques tipically occur in the Significant plaques tipically occur in the
proximal 2cm of the left anterior proximal 2cm of the left anterior descending and left circumflex coronary descending and left circumflex coronary arteriesarteries
In few cases vasospasm and platelet In few cases vasospasm and platelet aggregation without atherosclerotic aggregation without atherosclerotic stenosesstenoses
Initial event Initial event erosion, ulceration, erosion, ulceration, fissuring, rupture, hemorrhagic expansion fissuring, rupture, hemorrhagic expansion of atherosclerosis plaqueof atherosclerosis plaque
Plaques involved in coronary events Plaques involved in coronary events vulnerablevulnerable
Transient changes in blood pressure and Transient changes in blood pressure and platelet reactivityplatelet reactivity
High levels of serum markers of High levels of serum markers of inflammation (CRP) and hypercoagulability inflammation (CRP) and hypercoagulability ( protein C or S defficiency, factor V ( protein C or S defficiency, factor V Leiden)Leiden)
Thrombosis follow the acute plaque and Thrombosis follow the acute plaque and occludes flow the distal tissues occludes flow the distal tissues
The time interval onset of complete The time interval onset of complete myocardial ischemia and the initiation of myocardial ischemia and the initiation of irreversible injury 20-40 minutesirreversible injury 20-40 minutes
If the patient survives If the patient survives thrombi lyse thrombi lyse spontaneouslyspontaneously
Reflow to precariously injured cells may Reflow to precariously injured cells may restore viability but leave the cells poorly restore viability but leave the cells poorly contractile (stunned) for 1 or 2 dayscontractile (stunned) for 1 or 2 days
Nearly all transmural MIs Nearly all transmural MIs affect in left affect in left ventricle; 15% involved the right ventricle ventricle; 15% involved the right ventricle particularly in posterior-inferior left particularly in posterior-inferior left ventricle infarctsventricle infarcts
2. 2. Subendocardial InfarctionSubendocardial Infarction
Limited to the interior one third of the wall of Limited to the interior one third of the wall of the left ventricle and often multifocal.the left ventricle and often multifocal.
Caused by increased cardiac demand in Caused by increased cardiac demand in the setting of limiting supply, the setting of limiting supply, vasospasm,due to diffuse atherosclerosis vasospasm,due to diffuse atherosclerosis diseasedisease
Plaque disruption with overlying thrombus Plaque disruption with overlying thrombus that spontaneously lysesthat spontaneously lyses
Progression of myocardial necrosis after coronary artery occlusion. Necrosis begins in a small zone of the myocardium beneath the endo cardial surface in the center of the ischemic zone.
MorphologyMorphology
Electron MicroscopeElectron Microscope
Reversible phaseReversible phase
- - Glycogen depletionGlycogen depletion
- mitochondrial swelling- mitochondrial swelling
- relaxation of myofibrils- relaxation of myofibrils Irreversible phaseIrreversible phase
- Sarcolemmal disruption- Sarcolemmal disruption
- Mitochondrial amorphous densities- Mitochondrial amorphous densities
Gross changesGross changes
Before 6-12 hoursBefore 6-12 hours usually inapparent usually inapparent 3-6 hours3-6 hours changes occuring changes occuring By 18-24 hoursBy 18-24 hours infarcted tissue is generally infarcted tissue is generally
readily apparent as discrete pale to cyanotic readily apparent as discrete pale to cyanotic areasareas
11stst week week progressively, yellow, softened progressively, yellow, softened 7-10 days7-10 days hyperemic granulation tissue hyperemic granulation tissue 6 weeks6 weeks white fibrous scar white fibrous scar
lnfark myocard, atherosclerosis ruptur, myocardium diganti dengan Jaringan parut berwarna putih keabuan pada ventricel
MicroscopicallyMicroscopically
Within 1 hourWithin 1 hour intercellular edema, myocytes intercellular edema, myocytes become wavy and buckledbecome wavy and buckled
4 hour appearance of neutrophyl in interstitium4 hour appearance of neutrophyl in interstitium 12 – 72 hours after MI12 – 72 hours after MI death myocyte become death myocyte become
hypereosinophilic, loss nuclei, coagulative hypereosinophilic, loss nuclei, coagulative necrosisnecrosis
From 3-7 days after injuryFrom 3-7 days after injury appearance of appearance of macrophages in ischemic area, dead myocytes macrophages in ischemic area, dead myocytes are digested by invading macrophagesare digested by invading macrophages
After 7-10 daysAfter 7-10 days laying down collagen fibers, laying down collagen fibers, granulation tissue progressively replaces necrotic granulation tissue progressively replaces necrotic tissue tissue fibrous scarfibrous scar
Repair complete at 6 weeksRepair complete at 6 weeks
Potongan histologis dari infark myocardial akut
Clinical FeatureClinical Feature
Based mainly inBased mainly in symptoms (chest pain, nausea, diaphories, symptoms (chest pain, nausea, diaphories,
dyspnea)dyspnea) Electrocardiographic changesElectrocardiographic changes Elevation of serum of cardiomyocyte-specific Elevation of serum of cardiomyocyte-specific
proteins release from death cellsproteins release from death cells AngiographyAngiography
ComplicationsComplications
ArrhytmiasArrhytmias CHFCHF Cardiogenic shockCardiogenic shock Ventricular ruptureVentricular rupture Papillary muscle infarctionPapillary muscle infarction Fibrinous pericarditisFibrinous pericarditis Mural thrombosisMural thrombosis Repetitive infarctionRepetitive infarction
Chronic Ischemic Heart DiseaseChronic Ischemic Heart Disease
Is seen typically in elderly patients woth Is seen typically in elderly patients woth moderate to severe multivessels coronary moderate to severe multivessels coronary atherosclerosis who insidiously develop atherosclerosis who insidiously develop CHFCHF
It’s may result from postinfarction cardiac It’s may result from postinfarction cardiac decompensation or slow ischemic myocyte decompensation or slow ischemic myocyte degenerationdegeneration
MicroscopicallyMicroscopically
Myocardium has variable myocyte atrophy Myocardium has variable myocyte atrophy with perinuclear deposition of lipofuscinwith perinuclear deposition of lipofuscin
Myocytolisis of single cells or clusters, Myocytolisis of single cells or clusters, diffuse perivascular and interstitial fibrosisdiffuse perivascular and interstitial fibrosis
Patchy to confluent replacement fibrosis Patchy to confluent replacement fibrosis (scarring)(scarring)
Myocardial Hypertrophy and Heart Myocardial Hypertrophy and Heart FailureFailure
Myocardial hypertrophy is an Myocardial hypertrophy is an adaptive responseadaptive response that increases the contractile strength of the that increases the contractile strength of the myocyte and increase amounts of sarcometric myocyte and increase amounts of sarcometric protein without increase myocyte number under protein without increase myocyte number under condition of hemodynamic overload ( chronic condition of hemodynamic overload ( chronic hypertension, valvular stenosis, valvular hypertension, valvular stenosis, valvular insufficiency, myocardial injury)insufficiency, myocardial injury)
Hypertrophy is a compensatory state of the Hypertrophy is a compensatory state of the heart to maintain cardiac out putheart to maintain cardiac out put
Overtime hypertrophy can lead to Overtime hypertrophy can lead to ventricular dilatation.ventricular dilatation.
A variety of disorders may cause heart A variety of disorders may cause heart failure including ischemic heart disease failure including ischemic heart disease (80%), cardiomyopathies, congenital heart (80%), cardiomyopathies, congenital heart disease.disease.
The majority of patients with CHF have The majority of patients with CHF have ventricular hypertrophyventricular hypertrophy
In most cases In most cases followed by dilation of the followed by dilation of the ventriclesventricles
Multiple factors are involved in the Multiple factors are involved in the development of cardiac hypertrophy development of cardiac hypertrophy including the following :including the following :
1.1. Angiotensin IIAngiotensin II
2.2. Endothelin-1Endothelin-1
3.3. Insulin-likeInsulin-like
4.4. Extracellular matrixExtracellular matrix
5.5. ββ – adrenergic desensitization – adrenergic desensitization
6.6. Calcium homeostasisCalcium homeostasis
7.7. Protooncogene expressionProtooncogene expression
8.8. Fetal gen expressionFetal gen expression
Left-sided heart failure Left-sided heart failure
most common form of heart failuremost common form of heart failure Often occurs secondary to ischemic heart disease Often occurs secondary to ischemic heart disease
and hypertensionand hypertension
● ● Right-sided heart failureRight-sided heart failure
may occur with intrinsic pulmonary disease or may occur with intrinsic pulmonary disease or pulmonary hypertension or secondary to left-sided pulmonary hypertension or secondary to left-sided heart failureheart failure
MicroscopicallyMicroscopically
the damaged myocytes contain a vacuolated the damaged myocytes contain a vacuolated appearance of the cytoplasm due to increased appearance of the cytoplasm due to increased amaunts of glycogen and degenerative changes amaunts of glycogen and degenerative changes due to loss of myofibrilsdue to loss of myofibrils
Hypertensive Heart DiseaseHypertensive Heart DiseaseSystemic (left-sided) Hypertensive Heart Systemic (left-sided) Hypertensive Heart
DiseaseDisease
Diagnosis criteriaDiagnosis criteria : :
Left ventricular hypertrophy typically concentricLeft ventricular hypertrophy typically concentric Absence of other lesions that induce cardiac Absence of other lesions that induce cardiac
hypertrophy ( e.g. aortic valve stenosis aortic hypertrophy ( e.g. aortic valve stenosis aortic coarctaction)coarctaction)
PathogenesisPathogenesis
Myocyte hypertrophic enlargement occurs in Myocyte hypertrophic enlargement occurs in response to increased work.response to increased work.
Myocytes cannot devide Myocytes cannot devide the only way that the only way that cells can augment contractile proteins.cells can augment contractile proteins.
Thickened myocardium reduces left ventricle Thickened myocardium reduces left ventricle compliance compliance impairing diastolic filling while impairing diastolic filling while increasing oxygen demand.increasing oxygen demand.
Myocyte hypertrophy increases the distance for Myocyte hypertrophy increases the distance for oxygen and nutrient diffusion from adjacent oxygen and nutrient diffusion from adjacent capillariescapillaries
Coronary atherosclerosis + hypertension Coronary atherosclerosis + hypertension add add element of ischemiaelement of ischemia
MorphologyMorphology
The left ventricular wall is thickened (>2cm)The left ventricular wall is thickened (>2cm) Heart weight is increased ((>500gm)Heart weight is increased ((>500gm) Myocyte and muclei are enlargedMyocyte and muclei are enlarged Long-term Long-term diffuse interstitial fibrosis, focal diffuse interstitial fibrosis, focal
myocyte atrophy, degeneration myocyte atrophy, degeneration Resulting left ventricle chamber dilatation and Resulting left ventricle chamber dilatation and
wall thinningwall thinning
Hypertensive Heart DiseaseHypertensive Heart DiseasePulmonary (Right-Sided) Heart DiseasePulmonary (Right-Sided) Heart Disease
(Cor Pulmonale)(Cor Pulmonale)
Cor Pulmonale (CP) is the right-sided counterpart Cor Pulmonale (CP) is the right-sided counterpart to systemic hypertensive heart diseaseto systemic hypertensive heart disease
BasicallyBasically causes right ventricular causes right ventricular hypertrophy ventricular pathology hypertrophy ventricular pathology excludedexcluded
Acute CPAcute CP refers to right ventricular dilatation refers to right ventricular dilatation after massive pulmonary embolizationafter massive pulmonary embolization
Chronic CPChronic CP result from chronic right result from chronic right ventricular pressure overloadventricular pressure overload
Hypoxemia and acidosisHypoxemia and acidosis vasoconstriction in pulmonary vasoconstriction in pulmonary vasculaturevasculature exacerbates exacerbates pulmonary pulmonary hypertensionhypertension
MorphologyMorphologyOften Often ≥ 1 cm, dilatation or both are present.≥ 1 cm, dilatation or both are present.Can cause tricuspid regurgitationCan cause tricuspid regurgitationThe left side of the heart The left side of the heart normal normalPulmonary arteriolar wall thickening and Pulmonary arteriolar wall thickening and
artherosclerosis occur.artherosclerosis occur.
Rheumatic Heart DiseaseRheumatic Heart DiseaseCollagen Vascular DiseasesCollagen Vascular DiseasesBacterial EndocarditisBacterial EndocarditisNonbacterial Thrombotic EndocarditisNonbacterial Thrombotic EndocarditisMitral Valve ProlapseMitral Valve Prolapse
Acquired Valvular and Endocardial Acquired Valvular and Endocardial DiseaseDisease
Rheumatic feverRheumatic fever
DefinitoinDefinitoin multisystem inflammatory disorder multisystem inflammatory disorder with major cardiac manifestations and sequelae, with major cardiac manifestations and sequelae, in children between 5 and 15 years of age.in children between 5 and 15 years of age.
1-4 weeks after an episode of tonsilitis or other 1-4 weeks after an episode of tonsilitis or other infection caused by group infection caused by group A A ß-hemolytic ß-hemolytic streptococci.streptococci.
Etiology Etiology Immunologic origin. Immunologic origin. The postulate The postulate result of streptococcal antigens result of streptococcal antigens
that elicit an antibody response reactive to that elicit an antibody response reactive to streptococcal organism as well as to human streptococcal organism as well as to human antigens in the heart and others tissues.antigens in the heart and others tissues.
Rheumatic FeverRheumatic Fever
1.1. Acute Rheumatic FeverAcute Rheumatic Fever
2.2. Chronic Rheumatic FeverChronic Rheumatic Fever
Acute Rheumatic FeverAcute Rheumatic Fever ARF is a multisystem disease of childhood that ARF is a multisystem disease of childhood that
occurs following an acute streptococcal infection occurs following an acute streptococcal infection usually pharyngitis (“sore throat”)usually pharyngitis (“sore throat”)
Diagnosis is based in clinical hystory and 2 of 5 major Diagnosis is based in clinical hystory and 2 of 5 major (Jones) criteria, minor criteria (include fever, (Jones) criteria, minor criteria (include fever, arthralgia, leukocytosis ).arthralgia, leukocytosis ).
Strephococcus pyogenes from group Strephococcus pyogenes from group A A ß-hemolytic ß-hemolytic streptococci.streptococci.
ARF affects the pericardium, myocardium,ARF affects the pericardium, myocardium, endocardium and valves endocardium and valves pancarditispancarditis
Clinical feature Clinical feature learned in Pediatric learned in Pediatric MedicineMedicine
PathogenesisPathogenesis
The immune reaction to streptococcal The immune reaction to streptococcal antigen is idiosyncratic, seen in 3% antigen is idiosyncratic, seen in 3% patiensts with a streptococcal sore throat.patiensts with a streptococcal sore throat.
The antibodies produced are directed The antibodies produced are directed against streptococcal cell wall components against streptococcal cell wall components (fibrillary M protein) and cross-react with the (fibrillary M protein) and cross-react with the following target tissues :following target tissues :
• Heart muscleHeart muscle• Heart valve connective tissueHeart valve connective tissue• Thymic cellsThymic cells• Human glomerular basement membraneHuman glomerular basement membrane• Neuronal cytoplasm in sub-thalamic and Neuronal cytoplasm in sub-thalamic and
caudate nuclei in the braincaudate nuclei in the brain• SkinSkin• LymphocytesLymphocytes
Characteristic features in the acute Characteristic features in the acute phase:phase:
Aschoff bodies Aschoff bodies pathognomonic pathognomonicTransient fibrinous pericarditis contain Transient fibrinous pericarditis contain
Aschoff bodiesAschoff bodies Inflammatory valvulitis Inflammatory valvulitis beady fibrinous beady fibrinous
vegetation (verrucae)vegetation (verrucae)
Microscopically:Microscopically:
1.1. MyocadialMyocadial changeschanges, 2 histological pattern :, 2 histological pattern : Non specific myocarditisNon specific myocarditis : edema, inflammatory : edema, inflammatory
cells and rarely a small-vessel arteritiscells and rarely a small-vessel arteritis Specific granulomatous myocarditisSpecific granulomatous myocarditis : present : present
throughout the heart but most commonly in throughout the heart but most commonly in the interventricular septum the interventricular septum
Focus granulomatous called Focus granulomatous called Aschoff NoduleAschoff Nodule Aschoff nodules contain : necrosis fibrinoid, Aschoff nodules contain : necrosis fibrinoid,
aschoff giant cells (multinucleated aschoff giant cells (multinucleated macrophages), Anitschkow myocytes ( cell macrophages), Anitschkow myocytes ( cell with a characteristic bar of chromatin and owl with a characteristic bar of chromatin and owl eye nucleuseye nucleus
Aschoff bodyAschoff body
Classic lession (patognomonic) of rheumatic Classic lession (patognomonic) of rheumatic fever fever
an area of focal interstitial myocardial an area of focal interstitial myocardial inflammation inflammation
that is characterized by fragmented collagen that is characterized by fragmented collagen and fibrinoid necrosis materials in the central and fibrinoid necrosis materials in the central surounded by large cells (surounded by large cells (Anitschkow myocitesAnitschkow myocites) ) and multinucleated giant cell macrophages and multinucleated giant cell macrophages ((Aschoff cellsAschoff cells) and lymphocytes mostly T ) and lymphocytes mostly T helper cells.helper cells.
With time the the Aschoff nodule regresses to a With time the the Aschoff nodule regresses to a small scarsmall scar
Other anatomic changes Other anatomic changes PancarditisPancarditis
1. Pericarditis 1. Pericarditis inflammation of the pericardium may inflammation of the pericardium may
result in pericardial,pleural or others result in pericardial,pleural or others serous effusions.serous effusions.
2. Myocarditis 2. Myocarditis inflammation of the inflammation of the myocardium may lead to cardiac failure, myocardium may lead to cardiac failure, the cause of most deaths occuring during the cause of most deaths occuring during the early stages of acute rheumatic the early stages of acute rheumatic fever.fever.
3. Endocarditis3. Endocarditis inflammation of inflammation of endocardial, lead to valvular damageendocardial, lead to valvular damage
PancarditisPancarditis
2. Pericardium2. Pericardium changeschanges: :
shaggy fibrinous deposits on the visceral shaggy fibrinous deposits on the visceral and parietal surfaces and parietal surfaces ‘bread-and –butter’‘bread-and –butter’ pericarditispericarditis
3. Endocardium and valves changes3. Endocardium and valves changes : :
valve leaftlets inflammed and valve leaftlets inflammed and edematous edematous deposition of tiny fibrin deposition of tiny fibrin nodules along the leaflets termed verrucous nodules along the leaflets termed verrucous endocarditisendocarditis
Chronic Rheumatic HeartChronic Rheumatic Heart DiseaseDisease
Long term structural damageLong term structural damage Diffuse fibrosis causing Diffuse fibrosis causing thickened, shrunken, thickened, shrunken,
less pliableless pliable The valve leaftlets or cups of the affected The valve leaftlets or cups of the affected
valvesvalves fibrous adhessions fibrous adhessions stenosis stenosis Most common in mitral valves and oartic valveMost common in mitral valves and oartic valve The mitral valve The mitral valve have “ have “fish mouth”fish mouth”
appearanceappearance Complication Complication bacterial endocarditis, mural bacterial endocarditis, mural
thrombi, congestive heart failure, adhesive thrombi, congestive heart failure, adhesive pericarditis.pericarditis.
Characteristic features of the chronic Characteristic features of the chronic (or healed ) valve:(or healed ) valve:
Fibrous thickening of leafletsFibrous thickening of leafletsBridging fibrosis across valve commisuresBridging fibrosis across valve commisures fishmouth/ button hole stenosisfishmouth/ button hole stenosisThickened, fused and shortened chordaeThickened, fused and shortened chordaeCalsification in the fibrous leaftletsCalsification in the fibrous leaftletsSubendocardial collections of Aschoff Subendocardial collections of Aschoff
nodules nodules Mc Callum plaques Mc Callum plaques
Rheumatic endocarditis Rheumatic endocarditis occurs in areas occurs in areas subject to greatest hemodynamic stress, such as subject to greatest hemodynamic stress, such as the points of valve closure and the posterior wall the points of valve closure and the posterior wall of the left atrium of the left atrium MacCallum plaque.MacCallum plaque.
Early stageEarly stage valve leaflets are red and valve leaflets are red and swollen, tiny, warty, bead-like, rubbery swollen, tiny, warty, bead-like, rubbery vegetation (verrucae) form along the line of vegetation (verrucae) form along the line of closure of valve leaflet.closure of valve leaflet.
Late stageLate stage fibrotic healing, the valve become fibrotic healing, the valve become thickened, fibrotic, deformed, fusion of valve thickened, fibrotic, deformed, fusion of valve cups, calsification cups, calsification are grouped under the term are grouped under the term rheumatic heart disease.rheumatic heart disease.
The diseases involve :The diseases involve :
1.1. Mitral valve Mitral valve involved in 65%-70% of involved in 65%-70% of cases.cases.
2.2. Combine aortic and mitral valve Combine aortic and mitral valve 20%- 20%-40% of cases afffected a long the mitral 40% of cases afffected a long the mitral valve.valve.
3.3. Tricuspid and pulmonary valve Tricuspid and pulmonary valve less less frequently affected a long the mitral valve frequently affected a long the mitral valve and the aortic valves in 5% cases.and the aortic valves in 5% cases.
4.4. Pulmonary valve Pulmonary valve rarely. rarely.
Chronic Rheumatic Heart Disease “ fish mouth or Button hole”
. Endokarditis rematik katup mitral. Tonjolan-tonjolan multipel berwarna kelabu, berbentuk mirip kulit (verukosa) tampak pada bagian penutupan katup: dikelilingi oleh deposit-defosit fibrin yang baru terjadi (merah)
EndocarditisEndocarditis
Cardiac disorders are marked mainly by Cardiac disorders are marked mainly by valve vegetationsvalve vegetations
Major examples :Major examples :
1.1. Infective endocarditisInfective endocarditis
2.2. Nonbacterial thrombotic endocarditisNonbacterial thrombotic endocarditis
3.3. Endocarditis associated with SLE Endocarditis associated with SLE ((Libman-Sacks endocarditisLibman-Sacks endocarditis))
Infective Endocarditis Infective Endocarditis
Bacterial, fungal, infection of the Bacterial, fungal, infection of the endocardium endocardium involvement of valvular involvement of valvular surfaces.surfaces.
Characteristics include large, soft, friable, Characteristics include large, soft, friable, easily detacted easily detacted vegetations vegetations consisting of consisting of fibrin intermshed inflammatory cells and fibrin intermshed inflammatory cells and bacteria.bacteria.
Complication Complication ulceration, perforation, ulceration, perforation, rupture of chordae tendineae.rupture of chordae tendineae.
Classification Classification 1.1. Acute endocarditisAcute endocarditis pathogens is highly virulent organism such as pathogens is highly virulent organism such as
Staphylococcus aureus (50% of cases).Staphylococcus aureus (50% of cases). Clinically rapidly developing fever with rigor, Clinically rapidly developing fever with rigor,
malaise weakness.malaise weakness. Death occurs in days to weeks in 50%- 60% of Death occurs in days to weeks in 50%- 60% of
cases.cases.
2. Subacute (bacterial)endocarditis2. Subacute (bacterial)endocarditis by less by less virulent organisms such as Streptococcus virulent organisms such as Streptococcus viridans ( more than 50% cases), occur in viridans ( more than 50% cases), occur in congenital heart disease or preexisting valvular congenital heart disease or preexisting valvular heart disease.heart disease.
PathogenesisPathogenesisBacteriemia are prerequisites that can come Bacteriemia are prerequisites that can come
from infections from elsewhere in the body, from infections from elsewhere in the body, intravenous drug abuse, dental or surgical intravenous drug abuse, dental or surgical procedures, injury to gut, urinary tract, procedures, injury to gut, urinary tract, oropharynx or skin, neutropenia and oropharynx or skin, neutropenia and immunosuppressionimmunosuppression
Endocarditis bacterial can occurs on normal Endocarditis bacterial can occurs on normal valves and in certain valvular and others valves and in certain valvular and others cardiac condition ( CHD, VSD, CRHD )cardiac condition ( CHD, VSD, CRHD )
MorphologyMorphology Friable 0.5-2.0 cm, microba laden vegetationFriable 0.5-2.0 cm, microba laden vegetation Bulky (1-2cm)Bulky (1-2cm) Vegetations are typically on the downstream Vegetations are typically on the downstream
margin of a jet lession margin of a jet lession Acute infective endocarditis has a large Acute infective endocarditis has a large
vegetations can cause embolic complicationvegetations can cause embolic complication Subacute infective endocarditis tend to be small Subacute infective endocarditis tend to be small
vegetationsvegetations Ring abcessRing abcess
Valvular involvementValvular involvement Mitral valveMitral valve Mitral valve along with the aortic valveMitral valve along with the aortic valve Tricuspid valve Tricuspid valve 50% cases, most caused by 50% cases, most caused by
staphylococcal infectionstaphylococcal infection..
• ComplicationsComplications Distal embolizationsDistal embolizations Septic infarctsSeptic infarcts Focal necrotizing glomerulitis Focal necrotizing glomerulitis caused by caused by
immune complex disease or by septic emboliimmune complex disease or by septic emboli
Endokarditis infektif. Suatu massa trombotik polipoid yang baru (“vegetasi) tampak pada garis penutupan katup aorta.
Nonbacterial thrombotic Nonbacterial thrombotic endocarditisendocarditis
Marantic endocarditisMarantic endocarditisOccurs in settings of Occurs in settings of
cancer(adenocarcinomas), prolonged cancer(adenocarcinomas), prolonged debilitating ilness, DICdebilitating ilness, DIC
Morphology:Morphology:Small (1-5mm) sterile, bland fibrin, platelet Small (1-5mm) sterile, bland fibrin, platelet
thrombithrombiVegetations can embolize systemicallyVegetations can embolize systemically
Endocarditis associated with SLE Endocarditis associated with SLE ((Libman-Sacks endocarditis)Libman-Sacks endocarditis)
Pathogenesis uncertainPathogenesis uncertain Affected in mitral and tricuspid valvesAffected in mitral and tricuspid valves Findings : fibrinoid necrosis, mucoid Findings : fibrinoid necrosis, mucoid
degeneration, small, fibrinous, sterile degeneration, small, fibrinous, sterile vegetationsvegetations
Comparison of the lesions in the four major forms of vegetative endocarditis. The acute rheumatic heart disease (RHD) is marked by a flow of small, warty verrucae along the lines of the valve leaflets. Infective endocarditis (lE) typically shows large irregular and destructive masses that can extend onto the chordae. Nonbacterial thrombotic endocarditis (NBTE) typically shows small, bland vegetations, usually attached at the line of closure. One or many may be present. Libman-Sacks endocarditis ( has small or medium-sized