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

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Departemen Pathology Anatomy Cardiovascular

5/16/16

ISCHAEMIC HEART DIASEASE
(±80%)
HYPERTENSIVE HEART
DIASEASE ( 9%)
RHEUMATIC HEART DIASEASE
( 2-3 %)

HEART
DISEASE

CONGENITAL HEART DIASEASE
(2 %)
ENDOCARDITIS BACTERIALIS
( 1-2 %)
SYPHILLIS HEART DIASEASE
( 1%)
COR PULMONALE DIASEASE ( 1
%)

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Departemen Pathology Anatomy OTHERS
Cardiovascular

( 5%)

5/16/16

CORONARY HEART DISEASE .

CORONARY HEART DISEASE ARTERIOSCLEROTIC HEART DISEASE 5 ANGINA PECTORIS Departemen Pathology Anatomy Cardiovascular MYOCARDIAL INFARCTION 5/16/16 .

ARTERIOSCLEROTIC HEART DISEASE Atherosclerotic coronary artery Diffuse myocardial fibrotic  occasionally cardiac valve fibrotic MORPHOLOGY Atherosclerotic Ischaemic Brown Atrophy Myocardial fibrotic Marked as Brownish-yellow granular diffusely (accumulates in the heart muscle) contained lipofuscin (complexes of lipid & protein) 6 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

ARTERIOSCLEROTIC HEART DISEASE The heart is become: Small Normal Enlarged Disorder of cardiac valve : Mitral valve fibrotic Chordae tendineae fibrotic or calcification 7 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

Gross appearance of heavily fibrotic and calcified cardiac valve 8 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

ANGINA PECTORIS Intermittent chest pain caused by transient. ANGINA Departemen Pathology Anatomy Cardiovascular UNSTABLE ANGINA PECTORIS (cressendo angina ) 5/16/16 . reversible myocardial ischaemic TYPICAL / STABLE ANGINA PECTORIS 9 PRINZMETAL / VARIANT.

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Pathogenesis Myocardial hypoxia  Artherosclerotic coronary arteri  Syphilis heart disease  Polyarthritis nodosa  Aorta valve insufficiency  Anemia Hypoxia caused of: Occlusion of arteries  Coronary artery vasospasm 11 Departemen Pathology Anatomy Cardiovascular Paroxismal myocadial hypoxia imposed by exercise 5/16/16 .

MYOCARDIAL INFARCTION Popularly called heart “attack “ Development of an area of myocardial necrosis caused by local ischaemia Coroner insufficiency caused by : 12 Coronary atherosclerosis (99%) Thrombosis & Emboli Vascular diseases Osteum occlusion caused by syphillis Arteriosclerosis occlusion & Hypotension Departemen Pathology Anatomy Cardiovascular 5/16/16 .

risk ↑  age ↑ ♀ : protected during reproductive age Estrogen ↓ (after menopause)  HD ↑ 13 Departemen Pathology Anatomy Cardiovascular 5/16/16 .Type s Transmural (full/nearly full) Sub-endocardial (non-transmural) Inner 1/3 – ½ wall Incidence & Risk Factor Any age.

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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 .

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Distribution of infarcts Right coronary artery (30-40 %) Left anterior descending artery (40-50 %) Left circumflex artery (15-20 %) 19 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

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mitochondrial swelling None Usually none. of fibers at border mitochondrial amorphous densities Irreversible Injury ½ -4 hr 21 Departemen Pathology Anatomy Cardiovascular 4 -12 hr Occasionally dark Beginning 5/16/16 .Evolution Of Morphologic Changes in Myocardial Infarction Time Gross Feature Light Microscopic Findings Electron Microscopic Findings Reversible Injury < ½ hr None None Relaxation of myofibrils. Sacrolemmal variable waviness disruption. glycogen loss.

“contraction band” necrosis at periphery of infarct.7 days Hyperemic border. neutrophilic infiltrate 1 . central yellow-tan softening Beginning disintegration of dead myofibers. heavy neutrophilic infiltrate 3 . with dying neutrophils.3 days Mottling with yellow-tan infarct center Complete coagulation necrosis of myofibers. early phagocytosis of dead cells by macrophages at infarct border 7 Departemen Pathology Anatomy -Cardiovascular 10 days Maximally yellow-tan & Well-developed 5/16/16 .Evolution Of Morphologic Changes in Myocardial Infarction Time 18 – 24 hr 22 Gross Feature Light Microscopic Findings Dark mottling Coagulation necrosis.

Time 10 .14 days 2 – 8 wk > 2 month 23 Gross Feature Light Microscopic Findings Red-gray depressed infarct borders Well-established granulation tissue with new blood vessels & collagen deposition Gray-white scar. progressive from border toward core of infarct Increase collagen deposition. with decreased cellularity Scarring complete Dense collagenous scar Departemen Pathology Anatomy Cardiovascular 5/16/16 .

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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 25 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

HYPERTENSIVE HEART DISEASE .

HYPERTENSIVE HEART DISEASE Diagnosis based on: Left ventricular hypertrophy with a history of hypertension Excluded Aortic stenosis Primary hypertropic cardiomyopathy 27 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

hyperchrom. circumferential > 450 gm) Size: Early: Normal  dilated Microscopic • Myocytes > • Nuclei: large.Morphology Concentric hypertrophy (symetric. boxcar shaped 28 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

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VALVULAR HEART DISEASE .

immunologically mediated. multisystem inflammatory disease  group A streptococcal pharyngitis after an interval of a few weeks 31 Departemen Pathology Anatomy Cardiovascular 5/16/16 .RHEUMATIC HEART DISEASE  Acute.

Rheumatic Fever may cause HD in acute phase (Acute rheumatic carditis) Chronic valvular 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 32 Departemen lesion Pathology Anatomy Cardiovascular 5/16/16 .

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Morphology Acute Rheumatic Fever Inflammatory infiltrates in : Synovium Joint Skin Heart (most importantly)  fibrosis  deformities Lung Initial tissue reaction : focal fibrinoid necrosis 36 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

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vesicular nuclei. abundant basophilic cytoplasm) Departemen Pathology Anatomy Cardiovascular 5/16/16 .Acute Rheumatic Carditis (ARC) Characteristic : Inflammatory in 3 layers of heart (Pancarditis) Hallmark of ARC : (Aschoff bodies) 38 Multiple foci of inflammation within connective tissue of heart Central focus fibrinoid necrosis Surrounded by : • Mononucleous • Anitschkow cells (large histiocyte.

Pericardial involment Manifested grossly & microscopically : Fibrinous pericarditis Serous/Serosanguineous effusion 39 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

Endocardium  Valvular inflammation tends to : mitral & aortic valves  The valve predisposes : Small vegetations (valve closure) = verrucous endocarditis 40 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

does not  chronic deformity Pulmonary  Manifested by chronic inflmmation & fibrinous inflammation of pleural surface Skin Subcutaneous nodules / erythema 41 marginatum Departemen Pathology Anatomy Cardiovascular 5/16/16 .Arthritis of the large joints  Self limited.

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Aureus) Departemen Pathology Anatomy Cardiovascular Low virulence (α-Hemolytic Streptococcus) 5/16/16 .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 43 High virulence (Staph.

Bacteriemia Etiology IV Drug Abuse Dental Surgery Catheter Brushung teeth Risk Preexisting cardiac abnormal • Prosthetic heart valves •I V drug abuser 44 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

Morphology Vegetations : Bacteria or other organism Single / multiple May involved : > 1 valve Most common : Aortic & Mitra RV valve  drug abuser Fungal 45  ↑↑ Departemen Pathology Anatomy Cardiovascular 5/16/16 .

kidney. myocard  infarct  abscesses 46 Departemen Pathology Anatomy Cardiovascular 5/16/16 . fibrin. blood Extends beyond avasc valve  neutrophil response Systemic emboli  brain.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.

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PERICARDIAL DISEASE .

PERICARDITIS Caus e : bacteria.  Virus. SLE. metastatic malignancies 49 Departemen Pathology Anatomy Cardiovascular 5/16/16 . pyogenic mycobacteria. fungi  Secondary to : Acute myocard infarct Cardiac surgery Radiation to the mediastinum  Uremia  RF.

Pericarditis may : 1. Progress to chronic fibrosing process 50 Departemen Pathology Anatomy Cardiovascular 5/16/16 . Immediate hemodynamic complications 2. Resolve  sequelae (-) 3.

shaggy (bread & butter pericarditis) Viral : fibrinous Acute Bacterial : fibrinopurulent Tuberculous : caseous Metastases : shaggy fibrinous 51 Acute fibrinous / fibrinopurulent  resolve.Morphology Acute pericarditis Patients with uremia / acute RF : fibrinous. sequelae (-) Extensive suppuration / caseation  chronic pericarditis Departemen Pathology Anatomy Cardiovascular 5/16/16 .

Chronic pericarditis Appearance ranges : Delicate adhesions – dense. fibbrotic scars that obbliterate the pericardial space Constrictive pericarditis 52 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

causes :  Ascites  Hepatosphlenomegaly 4.Complications 1. Cava compression. Constrictive pericarditis 2. DC 53 Departemen Pathology Anatomy Cardiovascular 5/16/16 . V. Obliterate pericarditis (Focally / diffuse) 3.

Pericardial Effusions

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Serous

Serosanguin
eous

Chylous

CvHD
Hypoalbumiemia

Blunt chest trauma
Malignancy

Mediastinal
lymphatic
obstruction

Departemen Pathology Anatomy Cardiovascular

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Hemopericardium

Separately from hemorrhagic pericardium

effusion
Pure blood :
Ruptured aortic aneurisma
Ruptured myocar infarct
Penetrating trauma inj

 cardiac tamponade  death

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CARDIAC TUMORS

• Venous leukemia Departemen Pathology Anatomy • Arterial 5/16/16 Cardiovascular channels .Metastatic Neoplasms More common than primary 10% of disseminated cancer Most involves : Pericardium  caused : pericarditis & hemorrhagic effusion 57 Most common primary neoplasms that metastasize : • Carcinoma lung & Via: breast • Melanoma • Lymphatic • Lymphoma.

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. 58 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

Primary Neoplasms Rare Most common: Myxoma Lipoma Papillary elastofibromas Rhabdomyomas Angiosarcomas Rhabdomyosacomas 59 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

The lesion has a polypoid shape and a hemorrhagic appearance.Gross appearance of cardiac myxoma. 60 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

Cardiac myxoma showing tumor cells concentrating beneath the surface. surrounded by a highly myxoid stroma 61 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

Cardiac myxoma. 62 Departemen Pathology Anatomy Cardiovascular 5/16/16 . 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 63 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

Glandular myxoma (Microscopic appearance) 64 The epithelium is tall columnar and contains intracytoplasmic mucin. Departemen Pathology Anatomy 5/16/16 Cardiovascular This rare type of myxoma should not be confused with .

Gross appearance of a large angiosarcoma of the heart 65 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

Primary synovial sarcoma of heart showing typical biphasic appearance 66 Departemen Pathology Anatomy Cardiovascular 5/16/16 .

not further classifiable 67 It is not unusual for these tumors to show a ring of epithelioid large tumor Departemen Pathology Anatomy .High-grade sarcoma of heart. Cardiovascular 5/16/16 .cells in a perivascular location.

THANK YOU 68 Departemen Pathology Anatomy Cardiovascular 5/16/16 .