CARDIOVASCULER

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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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 %)

OTHERS ( 5%)

CORONARY HEART DISEASE

CORONARY HEART DISEASE

ARTERIOSCLEROTIC HEART DISEASE

ANGINA PECTORIS

MYOCARDIAL INFARCTION

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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 Departemen Pathology Anatomy lipid & protein) 9/6/2013 Cardiovascular

ARTERIOSCLEROTIC HEART DISEASE

The heart is become: Small Normal Enlarged Disorder of cardiac valve : Mitral valve fibrotic Chordae tendineae fibrotic or calcification

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Gross appearance of heavily fibrotic and calcified cardiac valve

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ANGINA PECTORIS
Intermittent chest pain caused by transient, reversible myocardial ischaemic

TYPICAL / STABLE ANGINA PECTORIS

PRINZMETAL / VARIANT, ANGINA

UNSTABLE ANGINA PECTORIS

(cressendo angina )
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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

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Paroxismal myocadial hypoxia imposed by exercise

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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
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Types
Transmural (full/nearly full) Sub-endocardial (non-transmural)
Inner 1/3 wall Incidence & Risk Factor
Any age, risk age : protected during reproductive age Estrogen (after menopause) HD

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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 %)

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Evolution Of Morphologic Changes in Myocardial Infarction

Time Gross Feature Light Microscopic Findings Electron Microscopic Findings

Reversible Injury
< hr None None Relaxation of myofibrils; glycogen loss; mitochondrial swelling

Irreversible Injury
-4 hr None Usually none; variable waviness of fibers at border Sacrolemmal disruption; mitochondrial amorphous densities

4 -12 hr

Occasionally dark mottling

Beginning coagulation necrosis; edema; haemorrhage

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Evolution Of Morphologic Changes in Myocardial Infarction

Time 18 24 hr Gross Feature Dark mottling Light Microscopic Findings Coagulation necrosis; contraction band necrosis at periphery of infarct; neutrophilic infiltrate Complete coagulation necrosis of myofibers; heavy neutrophilic infiltrate Beginning disintegration of dead myofibers, with dying neutrophils; early phagocytosis of dead cells by macrophages at infarct border

1 - 3 days

Mottling with yellow-tan infarct center

3 - 7 days

Hyperemic border; central yellow-tan softening

7 - 10 days

Maximally yellow-tan & soft, with depressed red-tan margins

Well-developed phagocytosis of dead cells; early formation of fibrovascular granulation tissue at margins

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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 Increase collagen deposition, from border toward core of with decreased cellularity infarct Scarring complete Dense collagenous scar

> 2 month

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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

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HYPERTENSIVE HEART DISEASE

HYPERTENSIVE HEART DISEASE

Diagnosis based on: Left ventricular hypertrophy with a history of hypertension Excluded
Aortic stenosis Primary hypertropic

cardiomyopathy

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Morpholog y
Concentric hypertrophy (symetric, circumferential

> 450 gm) Size:

Early: Normal dilated

Microscopic Myocytes > Nuclei: large, hyperchrom, boxcar shaped

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VALVULAR HEART DISEASE

RHEUMATIC HEART DISEASE

Acute, immunologically mediated, multisystem

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

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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
32 Departemen Pathology Anatomy Cardiovascular 9/6/2013 Onset : 2-3 weeks after infection Streptococci (-) in

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Morpholog y
Acute Rheumatic Fever
Inflammatory infiltrates in :

Synovium Joint Skin Heart (most importantly) fibrosis deformities Lung

Initial tissue reaction : focal fibrinoid necrosis

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Acute Rheumatic Carditis (ARC)

Characteristic :

Inflammatory in 3 layers of heart (Pancarditis)

Hallmark of ARC : (Aschoff bodies)

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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) Departemen Pathology Anatomy Cardiovascular 9/6/2013

Pericardial involment
Manifested grossly & microscopically :
Fibrinous pericarditis Serous/Sero-

sanguineous effusion

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Endocardium
Valvular inflammation tends to : mitral & aortic valves The valve predisposes :

Small vegetations (valve closure) = verrucous endocarditis

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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
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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

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High virulence (Staph. Pathology Aureus) Departemen Anatomy Cardiovascular

Low virulence (-Hemolytic Streptococcus)

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 Bacteriemia

Etiolog y

IV Drug Abuse Dental Surgery

Catheter
Brushung teeth

Risk

Preexisting cardiac abnormal

Prosthetic heart valves I V drug abuser

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Morphology
Vegetations :
Bacteria or other organism Single / multiple May involved : > 1 valve

Most common : Aortic & Mitra

RV valve drug abuser Fungal

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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
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PERICARDIAL DISEASE

PERICARDITIS

Caus e: Virus, pyogenic bacteria, mycobacteria,

fungi Secondary to : Acute myocard infarct Cardiac surgery Radiation to the mediastinum Uremia RF, SLE, metastatic malignancies
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Pericarditis may :

1. Immediate hemodynamic complications 2. Resolve sequelae (-) 3. Progress to chronic fibrosing process

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

Constrictive pericarditis

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Complication s

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

Serous
CvHD Hypoalbumiemia

Serosanguine ous
Blunt chest trauma Malignancy

Chylous
Mediastinal lymphatic obstruction

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Hemopericardiu m
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

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 & Via: breast Melanoma Lymphatic Lymphoma, leukemia Venous Departemen Pathology Anatomy Arterial channels Cardiovascular

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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.

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Primary Neoplasms
Rare

Most common:
Myxoma Lipoma Papillary elastofibromas Rhabdomyomas Angiosarcomas Rhabdomyosacomas

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

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

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

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Glandular myxoma (Gross appearance)

Note the myxoid

quality & extensive hemorrhage

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Glandular myxoma (Microscopic appearance)

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The epithelium is tall columnar and contains intracytoplasmic mucin. This rare type of myxoma should not be confused with metastatic Departemen Pathology Anatomy - Cardiovascular 9/6/2013 adenocarcinoma

Gross appearance of a large angiosarcoma of the heart

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Primary synovial sarcoma of heart showing typical biphasic appearance

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High-grade sarcoma of heart, not further classifiable

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It is not unusual for these tumors to show a ring of Departemen Pathology Anatomy epithelioid large tumor cells in a perivascular location. 9/6/2013 Cardiovascular

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