Cardio Vas Cul Er

CARDIOVASCULER
DEPARTEMEN PATHOLOGY ANATOMIC

MEDICAL FACULTY
USU – MEDAN
2008
Types of Heart Disease
1. IHD
2. Hypertensive HD (systemic & pulmonary)
3. Valvular HD
4. Nonischemic (primary) myocardial disease
5. Congenital HD
2 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

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 %)
3 OTHERS ( 5%)
Departemen Pathology Anatomy - Cardiovascular 5/4/2018
CORONARY HEART DISEASE
CORONARY HEART DISEASE
ARTERIOSCLEROTIC MYOCARDIAL
ANGINA PECTORIS
HEART DISEASE INFARCTION

ARTERIOSCLEROTIC HEART DISEASE
 Atherosclerotic coronary artery
 Diffuse myocardial fibrotic  occasionally cardiac valve
fibrotic
MORPHOLOGY
Atherosclerotic Ischaemic Myocardial fibrotic
Marked as
Brown Atrophy
Brownish-yellow granular diffusely (accumulates in the heart
muscle) contained lipofuscin (complexes of lipid & protein)
ARTERIOSCLEROTIC HEART DISEASE
The heart is become:
 Small
 Normal
 Enlarged
Disorder of cardiac valve :

 Mitral valve fibrotic
 Chordae tendineae fibrotic or calcification

Gross appearance of heavily fibrotic and
calcified cardiac valve

ANGINA PECTORIS
Intermittent chest pain caused by transient, reversible myocardial

ischaemic
TYPICAL / STABLE PRINZMETAL / UNSTABLE

ANGINA PECTORIS VARIANT, ANGINA PECTORIS
ANGINA (cressendo angina )

10 5/4/2018
Departemen Pathology Anatomy - Cardiovascular
Pathogenesis
Myocardial hypoxia
 Artherosclerotic coronary arteri

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

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

MYOCARDIAL INFARCTION
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
12 5/4/2018
Departemen Pathology Anatomy - Cardiovascular
Types
Transmural Sub-endocardial
(full/nearly full) (non-transmural)
Inner 1/3 – ½ wall
Incidence & Risk Factor
 Any age, risk ↑  age ↑

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

Pathogenesis
• 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
Distribution of infarcts
Right coronary Left anterior

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

Evolution Of Morphologic Changes in Myocardial
Infarction
Time Gross Feature Light Microscopic Electron
Findings Microscopic
Findings
Reversible Injury
< ½ hr None None Relaxation of
myofibrils; glycogen
loss; mitochondrial
swelling
Irreversible Injury
½ -4 hr None Usually none; variable Sacrolemmal
waviness of fibers at disruption;
border mitochondrial
amorphous densities
4 -12 hr Occasionally dark Beginning coagulation
mottling necrosis; edema;
haemorrhage
Evolution Of Morphologic Changes in Myocardial
Infarction
Time Gross Feature Light Microscopic Findings
18 – 24 hr Dark mottling Coagulation necrosis; “contraction
band” necrosis at periphery of
infarct; neutrophilic infiltrate
1 - 3 days Mottling with yellow-tan infarct center Complete coagulation necrosis of
myofibers; heavy neutrophilic
infiltrate
3 - 7 days Hyperemic border; central yellow-tan Beginning disintegration of dead
softening myofibers, with dying neutrophils;
early phagocytosis of dead cells by
macrophages at infarct border
7 - 10 days Maximally yellow-tan & soft, with Well-developed phagocytosis of
depressed red-tan margins dead cells; early formation of
fibrovascular granulation tissue at
margins

Time Gross Feature Light Microscopic Findings
10 - 14 days Red-gray depressed infarct borders Well-established granulation tissue

with new blood vessels & collagen
deposition
2 – 8 wk Gray-white scar, progressive from Increase collagen deposition, with
border toward core of infarct decreased cellularity
> 2 month Scarring complete Dense collagenous scar

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
HYPERTENSIVE HEART DISEASE
Diagnosis based on:
Left ventricular hypertrophy with a history of hypertension
Excluded
 Aortic stenosis
 Primary hypertropic cardiomyopathy

Morphology
 Concentric hypertrophy (symetric, circumferential
> 450 gm)
 Size:
 Early: Normal  dilated
Microscopic
• Myocytes >
• Nuclei: large, hyperchrom, boxcar shaped

29 5/4/2018
VALVULAR HEART DISEASE
RHEUMATIC HEART DISEASE
 Acute, immunologically mediated, multisystem

inflammatory disease  group A streptococcal pharyngitis
after an interval of a few weeks

Rheumatic Fever may cause
HD in acute phase Chronic valvular

(Acute rheumatic carditis) deformities
 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

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

Acute Rheumatic Carditis (ARC)
 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 involment
Manifested grossly &

microscopically :
 Fibrinous pericarditis
 Serous/Sero-sanguineous
effusion

Endocardium
 Valvular inflammation tends to : mitral & aortic valves

 The valve predisposes :
Small vegetations (valve closure) = verrucous endocarditis

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

pleural surface
Skin
 Subcutaneous nodules / erythema marginatum

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)
 Bacteriemia
 IV Drug Abuse
Etiology
 Dental Surgery
 Catheter
 Brushung teeth
Risk Preexisting cardiac abnormal
• Prosthetic heart valves

•I V drug abuser

Morphology
 Vegetations :
 Bacteria or other organism
 Single / multiple
 May involved : > 1 valve
 Most common : Aortic & Mitra
 RV valve  drug abuser
 Fungal  ↑↑

Acute Endocarditis
 Classic vegetation
 Begins : small excrescences
 indistinguishable from NBTE (Non Bacterial Thrombotic
Endocarditis)
 Infection may extend through :
Valve  myocardium  abscess peri-valvular (ring abscess)
 Microscopic :
 Bacterial, fibrin, blood
 Extends beyond avasc valve  neutrophil response
 Systemic emboli  brain, kidney, myocard  infarct  abscesses

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

Pericarditis may :
1. Immediate hemodynamic complications

2. Resolve  sequelae (-)
3. Progress to chronic fibrosing process

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

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

Pericardial Effusions
Serous Serosanguineous Chylous
CvHD Blunt chest trauma Mediastinal

Hypoalbumiemia Malignancy lymphatic
obstruction

Hemopericardium
 Separately from hemorrhagic pericardium effusion
 Pure blood :
 Ruptured aortic aneurisma
 Ruptured myocar infarct
 Penetrating trauma inj
 cardiac tamponade  death

CARDIAC TUMORS
Metastatic Neoplasms
 More common than primary

 10% of disseminated cancer
 Most involves :
 Pericardium  caused : pericarditis & hemorrhagic effusion
Most common primary neoplasms that metastasize :

• Carcinoma lung & breast
Via:
• Melanoma
• Lymphoma, leukemia
• Lymphatic
• Venous
57 Departemen Pathology Anatomy - Cardiovascular • Arterial channels 5/4/2018
Large metastatic carcinoma in left atrium that was continuous with
tumor in left pulmonary vein
 This mass simulated an

atrial myxoma by
echocardiography.
The primary tumor was

mucoepidermoid
carcinoma of left
submaxillary gland.

Primary Neoplasms
 Rare
 Most common:
 Myxoma
 Lipoma
 Papillary elastofibromas
 Rhabdomyomas
 Angiosarcomas
 Rhabdomyosacomas

Gross appearance of cardiac myxoma.
The lesion has a polypoid shape and a hemorrhagic
appearance.

Cardiac myxoma showing tumor cells concentrating
beneath the surface, surrounded by a highly myxoid
stroma

Cardiac myxoma.
The concentric arrangement of tumor cells around
endocardium-lined spaces is characteristic of the entity.

Glandular myxoma
(Gross appearance)
 Note the myxoid quality &

extensive hemorrhage

Glandular myxoma
(Microscopic appearance)
The epithelium is tall columnar and contains intracytoplasmic mucin.

This rare type of myxoma should not be confused with metastatic adenocarcinoma
Gross appearance of a large angiosarcoma
of the heart

Primary synovial sarcoma of heart showing
typical biphasic appearance

High-grade sarcoma of heart, not further
classifiable
It is not unusual for these tumors to show a ring of epithelioid large

67
tumor
Departemen Pathology Anatomy cells in a perivascular location.
- Cardiovascular 5/4/2018

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CARDIOVASCULER

DEPARTEMEN PATHOLOGY ANATOMIC

2 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

HYPERTENSIVE HEART DIASEASE ( 9%)

RHEUMATIC HEART DIASEASE ( 2-3 %)

SYPHILLIS HEART DIASEASE ( 1%)

COR PULMONALE DIASEASE ( 1 %)

5 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

Atherosclerotic Ischaemic Myocardial fibrotic

Disorder of cardiac valve :

7 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

8 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

Intermittent chest pain caused by transient, reversible myocardial

TYPICAL / STABLE PRINZMETAL / UNSTABLE

9 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

 Artherosclerotic coronary arteri

Hypoxia caused of: Paroxismal myocadial

11 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

Popularly called heart “attack “

Development of an area of myocardial necrosis caused by local

Coroner insufficiency caused by :

Incidence & Risk Factor

 Any age, risk ↑  age ↑

13 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

• Basic : Coronary Arterial Occlusion

Right coronary Left anterior

19 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

22 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

10 - 14 days Red-gray depressed infarct borders Well-established granulation tissue

> 2 month Scarring complete Dense collagenous scar

23 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

25 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

Left ventricular hypertrophy with a history of hypertension

27 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

28 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

 Acute, immunologically mediated, multisystem

31 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

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 lesion

Acute Rheumatic Fever

 Initial tissue reaction : focal fibrinoid necrosis

36 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

 Hallmark of ARC : (Aschoff bodies)

Multiple foci of inflammation within connective tissue of heart

38 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

Manifested grossly &

39 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

 Valvular inflammation tends to : mitral & aortic valves

40 Departemen Pathology Anatomy - Cardiovascular 5/4/2018

 Self limited, does not  chronic deformity

 Manifested by chronic inflmmation & fibrinous inflammation of

 Subcutaneous nodules / erythema marginatum

Infection of the cardiac valve /mural surface of the endocardium 

Previously abnormal valve

Risk Preexisting cardiac abnormal

• Prosthetic heart valves