CVS1-K14 Histopathology of Cardiovascular System

CVS K14
CARDIOVASCULAR
SYSTEMS
Dr. dr. T. Ibnu Alferally, M.Ked(PA),Sp.PA. D. Bioet
Dr. dr. Betty, M.Ked(PA),Sp.PA.
DEPARTEMEN PATOLOGI ANATOMI

FAKULTAS KEDOKTERAN USU
MEDAN - 2021
2 TUJUAN INSTRUKSIONAL
UMUM
Mahasiswa mampu menjelaskan
tentang :
1. Histopatologi jenis-jenis penyakit / kelainan pada
organ jantung
2. Patogenesis Infeksi jantung
3. Patogenesis penyakit/ kelainan pericardium
Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

3 TUJUAN INSTRUKSIONAL
KHUSUS
1. Mahasiswa mampu menjelaskan patogenesis dan
gambaran makroskopis / mikroskopis jenis-jenis
penyakit jantung
gambaran mikroskopis Endocarditis
gambaran mikroskopis Hydropericardium dan
Hemopericardium
gambaran mikroskopis Pericarditis, Tuberculosis
Pericarditis, Bacterial Pericarditis.

4

5 Types of Heart Disease
1. Ischaemic Heart Disease (IHD)

2. Hypertensive HD (systemic & pulmonary)
3. Valvular HD
4. Non-ischemic (primary) myocardial disease
5. Congenital HD

6 ISCHAEMIC HEART DIASEASE (±80%)
HYPERTENSIVE HEART DIASEASE ( 9%)
RHEUMATIC HEART DIASEASE ( 2-3 %)
HEART CONGENITAL HEART DIASEASE (2 %)
DISEASE ENDOCARDITIS BACTERIALIS ( 1-2 %)
SYPHILLIS HEART DIASEASE ( 1%)
COR PULMONALE DIASEASE ( 1 %)
OTHERS ( 5%)
3/28/2021
Departemen Patologi Anatomi FK USU - CVS K14
CORONARY HEART
DISEASE
Coronary heart disease …
8
Arteriosclerotic heart disease
Angina pectoris
Myocardial infarction (MCI)

9
ARTERIOSCLEROTIC HEART DISEASE
 Atherosclerotic coronary artery
 Diffuse myocardial fibrotic  occasionally cardiac valve fibrotic
MORPHOLOGY :
Atherosclerotic Ischaemic Myocardial fibrotic
Brown Atrophy Marked as

Brownish-yellow granular diffusely (accumulates in
heart muscle)  contained lipofuscin (complexes of
lipid & protein)
Arteriosclerotic heart disease …
10
The heart become:

 Small
 Normal
 Enlarged
Disorder of cardiac valve:

 Mitral valve fibrotic
 Chordae tendineae fibrotic / calcification

11 Gross appearance of heavily
fibrotic & calcified cardiac valve
Fibrotic

12 ANGINA PECTORIS
Intermittent chest pain caused by transient,

reversible myocardial ischaemic
UNSTABLE
TYPICAL / STABLE PRINZMETAL / ANGINA
ANGINA VARIANT, PECTORIS
PECTORIS ANGINA (cressendo
angina )
13
3/28/2021

14
Pathogenesis
Myocardial hypoxia
 Artherosclerotic coronary arteri

 Syphilis heart disease
 Polyarthritis nodosa
 Aorta valve insufficiency
 Anemia
Hypoxia caused of: Paroxismal myocardial

 Occlusion of arteries hypoxia imposed by
 Coronary artery vasospasm exercise

Schematic of coronary artery lesions
15

MYOCARDIAL INFARCTION
16
(MCI)
Popularly called heart “attack “
Development of an area of myocardial necrosis

caused by local ischaemia
Coroner insufficiency caused by :

Coronary atherosclerosis (99%)
Thrombosis & Emboli
Vascular diseases
Osteum occlusion caused by
syphillis
Arteriosclerosis occlusion &
Hypotension 3/28/2021

Myocardial infarction (MCI) …
17 Types
Transmural Sub-endocardial
(full/nearly full) (non-transmural)
Inner 1/3 - 1/2 wall
Incidence & Risk Factor
 Any age, risk ↑  age ↑

 ♀ : protected during reproductive age
 Estrogen ↓ (after menopause)  HD ↑

TRANSMURAL
INFARCT
18
SUB-ACUTE APICAL INFARCT

With RESORPTION of
MUSCLE & MURAL THROMBI
INTRA-MURAL
INFARCT

19
HEALED INFARCT

20
ACUTE TRANSMURAL
MYOCARD INFARCT
With RUPTURE
CARDIAC
TAMPONADE

Pathogenesis
21
• Basic : Coronary Arterial Occlusion
• Severe coronary atherosclerosis
• Acute atherosclerotic plaque change
(rupture)
• Superimposed pletelet activation
• Thrombosis & vasospasm
Consequence:
Myocardial Response
• Cessation of aerobic glycolysis  anaerobic
glycolysis 
• Inadequate product of phosphate
(Creatine phos & ATP)
• Acc. lactid acid
22
Schematic of sequential
progression of coronary
artery lesions &
various acute coronary
syndromes

23
TYPES & DEGREES OF

CORONARY ATHEROSCLEROTIC
NARROWING OF OCCLUSION

25
Distribution of infarcts
Right Left anterior

coronary descending
artery artery
(30-40 %) (40-50 %)
Left circumflex
artery
(15-20 %)

Progression of myocardial necrosis after coronary artery occlusion
26

30

31

32 Complications
 Papillary muscle dysfunction (infarcted papillary
muscle  may rupture)
 External rupture of the infarct  cardiac
tamponade
 Rupture of the intraventricular septum
 Mural thrombi  potential sources for systemic
emboli
 Ventricular fibrotic & aneurysms

HYPERTENSIVE
HEART DISEASE
34 HYPERTENSIVE HEART DISEASE
Diagnosis based on:
Left ventricular hypertrophy with a history of

hypertension
Excluded
 Aortic stenosis
 Primary hypertropic cardiomyopathy

Hypertensive heart disease …
35 Morphology
 Concentric hypertrophy (symetric,

circumferential > 450 gm)
 Size:
Early: Normal  dilated
Microscopic
• Myocytes >>
• Nuclei: large, hyperchromatic,
boxcar shaped

Hypertensive heart disease …
36
HYPERTROPHIE &
DILATATION of LV
THROMBUS
IN LEFT ATRIAL
HYPERTROPHIE of RV & LV
ANTERO-SEPTAL INFARCT

VALVULAR HEART
DISEASE
38
RHEUMATIC HEART DISEASE
Acute
Immunologically mediated
Multisystem inflammatory disease
 group A streptococcal pharyngitis after an
interval of a few weeks

Rheumatic heart disease …
Rheumatic Fever may cause
39
HD in acute phase Chronic valvular

(Acute rheumatic deformities
carditis)
 Only 3% group A streptococcal pharyngitis  RF

Initial  ↑ reactivation with subsequent pharyngeal
infections
 Ab >< M protein  cross reaction with glycoprotein :

 Heart
 Joints & others
 Onset : 2-3 weeks after infection Streptococci (-) in

lesion

40

41
ASCHOFF BODY
ADHESIVE PERICARDITIS
& FOCAL CALCIFICATION

42
THROMBUS
(Almost filling LA)

43 Morphology
Acute Rheumatic Fever
 Inflammatory infiltrates in :
 Synovium
 Joint
 Skin
 Heart (most importantly)  fibrosis  deformities
 Lung
 Initial tissue reaction : focal fibrinoid necrosis

44

Acute Rheumatic Carditis (ARC)
45  Characteristic :
Inflammatory in 3 layers of heart (Pancarditis)
 Hallmark of ARC : (Aschoff bodies)
Multiple foci of inflammation within connective tissue of

heart
Central focus fibrinoid necrosis
Surrounded by :
• Mononucleous
• Anitschkow cells
• (large histiocyte, vesicular nuclei, abundant basophilic
cytoplasm)
PERICARDIAL
46 INVOLVEMENT
Manifested grossly &
microscopically :
 Fibrinous pericarditis
 Serous/Sero-sanguineous
effusion

47 Endocardium
 Valvular inflammation tends to : mitral & aortic valves
 The valve predisposes :
Small vegetations (valve closure) = verrucous
endocarditis

Arthritis of the large joints
48
 Self limited, does not  chronic deformity
Pulmonary
 Manifested by chronic inflammation & fibrinous inflammation of

pleural surface
Skin
 Subcutaneous nodules / erythema

marginatum
RHEUMATIC FEVER
49
MIGRATORY ARTHRITIS
ERYTHEMA ANNULARE
SUB-CUTANEOUS NODULES
SYDENHAM’S CHOREA
50
Infective Endocarditis
Infection of the cardiac valve /mural surface of

the endocardium  thrombotic
(debris+organism) [term vegetation]
Caused by bacteria
Acute Sub-acute
Previously abnormal valve
High virulence
Low virulence
(Staph. Aureus)
(α-Hemolytic Streptococcus)
Infective Endocarditis …
51
 Bacteriemia
 IV Drug Abuse
Etiology  Dental Surgery
 Catheter
 Brushing teeth
Risk Pre-existing cardiac

abnormal
• Prosthetic heart valves
• I V drug abuser
52
Morphology
 Vegetations :
 Bacteria or other organism
 Single / multiple
 May involved : > 1 valve
 Most common : Aortic & Mitral
 RV valve  drug abuser
 Fungal  ↑↑

53
Acute Endocarditis
 Classic vegetation
 Begins : small excrescences
 indistinguishable from NBTE (Non Bacterial

Thrombotic Endocarditis)
 Infection may extend through :
abscess peri-valvular
Valve  myocardium 
(ring abscess)
 Microscopic :
 Bacterial, fibrin, blood
 Extends beyond avasc valve  neutrophil response
 Systemic emboli  brain, kidney, myocard  infarct  abscesses

54
EMBOLUS & INFARCT
(Vessel of ocular fundus)
PETECHIA
CLUBBING FINGERS
MYCOTIC ANEURYSMS of
SPLENIC ARTERIES
& INFARCT OF SPLEEN
(SPLENOMEGALY)

PERICARDIAL
DISEASE
56 PERICARDITIS
Cause :
 Virus, pyogenic bacteria,
mycobacteria, fungi
 Secondary to :
 Acute myocard infarct
 Cardiac surgery
 Radiation to the mediastinum
 Uremia
 RF, SLE, metastatic malignancies

57 Pericarditis may :
1. Immediate hemodynamic
complications
2. Resolve  sequelae (-)
3. Progress to chronic fibrosing process

Morphology
58
Acute pericarditis
 Patients with uremia / acute RF : fibrinous, shaggy
(bread & butter pericarditis)
 Viral : fibrinous
 Acute Bacterial : fibrinopurulent
 Tuberculous : caseous
 Metastases : shaggy fibrinous
Acute fibrinous / fibrinopurulent  resolve, sequelae (-)

Extensive suppuration / caseation  chronic pericarditis

59 Chronic pericarditis
Appearance ranges :
 Delicate adhesions – dense, fibbrotic scars
that obbliterate the pericardial space
Constrictive pericarditis

Complications
60
1. Constrictive pericarditis
2. Obliterate pericarditis (Focally /
diffuse)
3. V. Cava compression, causes :
 Ascites
 Hepatosphlenomegaly
4. DC

61
Pericardial Effusions
Serous Serosanguineous Chylous
CvHD Blunt chest Mediastinal

Hypoalbumiemia trauma lymphatic
Malignancy obstruction

Hemopericardium
62
 Separately from hemorrhagic pericardium effusion
 Pure blood :
 Ruptured aortic aneurisma
 Ruptured myocard infarct
 Penetrating trauma injection
 Cardiac Tamponade  DEATH

63

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CVS K14

DEPARTEMEN PATOLOGI ANATOMI

3. Patogenesis penyakit/ kelainan pericardium

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

1. Ischaemic Heart Disease (IHD)

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

HYPERTENSIVE HEART DIASEASE ( 9%)

RHEUMATIC HEART DIASEASE ( 2-3 %)

HEART CONGENITAL HEART DIASEASE (2 %)

DISEASE ENDOCARDITIS BACTERIALIS ( 1-2 %)

SYPHILLIS HEART DIASEASE ( 1%)

COR PULMONALE DIASEASE ( 1 %)

Arteriosclerotic heart disease

Myocardial infarction (MCI)

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Atherosclerotic Ischaemic Myocardial fibrotic

Brown Atrophy Marked as

The heart become:

Disorder of cardiac valve:

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Intermittent chest pain caused by transient,

Departemen Patologi Anatomi FK USU - CVS K14

 Artherosclerotic coronary arteri

Hypoxia caused of: Paroxismal myocardial

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Development of an area of myocardial necrosis

Coroner insufficiency caused by :

Departemen Patologi Anatomi FK USU - CVS K14

Incidence & Risk Factor

 Any age, risk ↑  age ↑

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

SUB-ACUTE APICAL INFARCT

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

TYPES & DEGREES OF

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Right Left anterior

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Left ventricular hypertrophy with a history of

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

 Concentric hypertrophy (symetric,

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

HD in acute phase Chronic valvular

 Only 3% group A streptococcal pharyngitis  RF

 Ab >< M protein  cross reaction with glycoprotein :

 Onset : 2-3 weeks after infection Streptococci (-) in

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Departemen Patologi Anatomi FK USU - CVS K14 3/28/2021

Acute Rheumatic Fever