CV-1

Normal aorta - intima

CV-2

Minimal amount of fatty streaks and dots (difficult to see).

CV-3

Fatty dots that have become confluent in some areas in the ascending aorta.

CV-4

Atheromatous plaque of aorta showing confluent elevated yellow granular surface in intima.  Uncomplicated plaques.

CV-5

Cross section shows that the atheromatous lesion is related to fatty and atheromatous deposits with fibrous cap of the intima.  Notice that the buffy brown elastic muscular media becomes attenuated under the atheromatous plaque.

CV-6

An oil red 0 stain staining fat.  The red areas are fatty being atheromatous deposits and the white areas around the intercostal arterial ostea are fibrous plaques.

CV-7

Complicated atherosclerosis showing ulceration of the plaques superimposed with thrombotic deposition.  Note the whitish fibrous plaques and wrinkling of intimal surface.

CV-8

Transverse sections of normal coronary artery embedded in the epicardial fat, which obscures the vascular wall in the illustration

CV-9

Multiple cross sections of coronary artery showing extensive atherosclerosis, and recent thrombotic occlusion in some segments.  There is variation between different sections in morphologic appearanceand severity (degree of lumen narrowing).

CV-10

Severe coronary atherosclerosis with old thrombotic occlusion which has undergone organisation and been replaced by semi-translucent fibrous tissue.  Many segments have pinpoint lumens (recanalization).

CV-11

Abdominal aneurysm with rupture.

CV-12

In situ view showing retroperitoneal hemorrhage involving the left paracolic region due to ruptured aneurism.

CV-13

Atherosclerotic aortic aneurysm which has been opened and has exposed the lumen, which is filled with a massive amount of thrombus.  Notice severe degree of complicated atherosclerotic change in the segment above the aneurysm.

CV-14

Cross section of lower abdominal aorta and common iliac artery showing aortic aneurysm (fusiform in shape) with mural thrombosis resulting in marked lumen stenosis.  The old thrombus tends to become yellow-brown and semitranslucent due to disintegration of blood elements.

CV-15

Massive extrapleural hematoma of left chest due to rupture of thoracic aortic aneurysm.

CV-16

There are two thoracic aneurysms with the proximal one ruptured.  Extensive atherosclerotic changes in mural thrombi are present. The underlying process may be syphilitic in nature.

CV-17

A dissecting aneurysm shown in the thoracic aorta. 

CV-18

A close-up view of dissecting aortic hematoma (same case as CV 17).  Notice that the inner flap is thicker, as the lesion commonly is present between middle and outer 1/3 layer.

CV-19

Dissecting aortic aneurysm with intimal tear in the ascending aorta (pointer).  It may have torn through the adventitia as well.

CV-20

A typical spiral intimal tear of dissecting aneurysm in the ascending aorta.  The flap is readily demonstrable by aortography during life.  The tear may account for aortic valvular insufficiency.  Circumferential dissecting may result in coronary insufficiency.

CV-21

Severe degree of atherosclerosis with dilation and aneurysm formation of ascending aorta and thoracic aorta, typical for syphilitic aortitis.

CV-22

The so-called "tree-bark" appearance of intima of syphilitic aortitis.  What kind of tree is it?

CV-23

An interlobar renal artery is occluded by an atheromatous embolus that contains cholesterol (clefts left in tissue following lipid extraction during processing), foreign body reaction and some fibrosis.

CV-24

Gangrene of the third and fifth toes with atrophic skin change in peripheral circulatory insufficiency due to occlusive atherosclerosis.

CV-25

Saddle embolus in pulmonary artery -- where is the source of such massive thrombotic emboli?

CV-26

Acute myocardial infarct shown on this septal cut, which demonstrates yellow mottling.  The red-brown change is due to incomplete fixation.

CV-28

Close-up view of thrombotic occlusion and atherosclerotic change of the coronary  artery.

CV-29

Recent myocardial infarction (10-14 days) involving the left lateral ventricular wall and papillary muscle.  The necrotic tissue remains pale and yellow, and is bordered by hyperemic and cystic zone as a result of resorption of necrotic tissue and inflammatory hyperemia. Compare to the uniform brown muscle seen at the apex.

CV-30

Close up view of typical acute MI ofhours' duration showing yellow necrotic tissue and passive hyperemia.  Abrupt distinction between infarcted and non-infarcted tissue.

CV-31

Acute MI of two days duration.  The necrotic myocardial fibers are hypereosinophilic, granular and fragmented with loss of nuclei.  Intense neutrophilia is present in the interstitium.  Two adjacent atrophic but viable myofibers are present in the field.

CV-32

A roughened brown patch with a linear tear on the epicardial surface is the site of rupture due to transmural infarction.

CV-33

Hemopericardium as seen in-situ.  The pericardium is opened to reveal blood in the cavity, surrounding the heart.

CV-34

Infarct, two weeks prior to death, showing resorption of necrotic fibers, replacement by fibroblasts.  There is mixed neutrophil and monocyte infiltration.  Residual necrotic muscle fibers are still identifiable.

CV-35

Close-up view of rupture of a left ventricular infarct.  Note the sinuous tract that opens at the epicardial surface.  The infarcted myocardium exhibits yellow color.

CV-37

Recent myocardial infarct involving the left myocardial apical region, showing thinning of the wall, and presence of an overlying mural thrombus.  The ventricle is dilated.

CV-39

Mural thrombus in the posterior wall, where dilatation has developed consequent to an infarct.

CV-40

Marked left ventricle dilatation and endocardial fibroelastosis.  Notice the diffuse thinning of the ventricular wall.

CV-41

Marked endocardial fibrosis and thin myocardial wall.

CV-42

Focal endocardial and myocardial fibrosis in an area of old infarct, which has resulted in a ventricular aneurysm.

CV-43

Ventricular aneurysm as seen on external view.

CV-44

An infarct, ventricular aneurysm and rupture of the posterior papillary muscle consequent to a recent infarct

CV-45

An old septal infarct that exhibits white fibrous scar.

CV-46

Rupture of papillary muscle consequent to infarction

CV-47

Concentric hemorrhagic necrosis of left ventricle that developed during extracorporeal circulation for valvular repair.  The coronary angiogram demonstrates paucity of intramyocardial vessels.  Such a lesion develops as a result of inadequate perfusion.  Following infarction, reperfusion results in hemorrhagic appearance.

CV-48

Interstitial myocardial fibrosis.  May be seen in chronic ischemic heart disease or hypertension.

CV-50

Cross section demonstrates marked left ventricular thickening and obliteration of the ventricular lumen, thus, a concentric hypertrophy, typical longstanding hypertension.

CV-51

Fine granularity of renal cortex due to underlying arteriolo-nephrosclerosis, which is the result of longstanding hypertension.

CV-52

Arteriolosclerosis of renal arterioles showing eosinophilic hyaline deposits subendothelially.  Notice renal tubular atrophy and interstitial fibrosis.

CV-53

An onion-skin like intimal thickening of a small muscular artery, seen in accelerated or malignant hypertension.

CV-54

The "flea-bitten" kidney exhibiting punctate hemorrhages seen in malignant hypertension.

CV-55

Necrotizing arteritis (fibrinoid necrosis) of glomerular afferent arteriole and ischemic glomerulus in malignant hypertension.

CV-56

Apoplexy - hypertensive hemorrhage in the internal capsule with rupture into the ventricle

CV-57

Adrenal cortical adenoma (functional) - there is atrophy of adjacent adrenal cortex.  A cause of “secondary” hypertension, potentially curable by surgery.

CV-58

Coarctation of aorta

CV-59

Pheochromocytoma of adrenal medulla showing hemorrhagic features in the tumor tissue.

CV-61

Rheumatic mitral stenosis with marked left atrial dilatation and endocardial fibrosis.  Valve viewed from atrial aspect.

CV-62

Chronic rheumatic mitral valvulitis with stenosis, which can pass a probe of 3.5 cm circumference.  Notice the fibrous thickening and fusion of chordae tendineae.

CV-63

Chronic rheumatic mitral valvulitis showing fibrous shortening of the leaflets, and retraction of cordae; consequently, insufficiency of the valve.

CV-64

Rheumatic mitral stenosis leading to marked left atrial dilatation.  A huge (aboutcm diameter) ball thrombus is attached to the atrial wall.  Dislodgement of such mural thrombus will completely and fatally obstruct the mitral orifice.

CV-65

Acute rheumatic valvulitis, with dew-drop like verrucae along the valvular Margin.

CV-66

Acute superimposed upon chronic mitral rheumatic valvulitis.  Notice the vegetations on the valve and some fibrous thickening of the valve leaflets, as well as the chordae.

CV-67

Aortic rheumatic valvulitis - notice the thickening  and fusion of the leaflets.

CV-68

Fibrinous pericarditis of rheumatic pancarditis.

CV-69

Acute rheumatic valvulitis showing fibrin (acellular, eosinophilic) deposition on the denuded endocardial surface.  Underneath are proliferative lesions of Aschoff bodies with moderate edema of the tissue of the valve.

CV-70

High magnification of Aschoff body showing the nuclear peculiar features of Anitschow myocytes

CV-71

An exudative and proliferative Aschoff body.  Notice the eosinophilic fibrinoid necrosis of collagen (or exudate), edema of the tissue (wide spaces between the cells) and the so-called Anitschow myocytes showing typical caterpillar-like nuclear chromatin pattern or "owl-eye" appearance when seen on cross sections. Multinucleation of these cells may occur.

CV-73

A marantic thrombus on a normal mitral valve leaflet.

CV-74

Subacute bacterial endocarditis showing thrombotic deposition on deformed aortic valve.

CV-75

Thickened aortic valves of rheumatic origin, superimposed with subacute bacterial endocarditis that presents a large amount of thrombotic vegetation

CV-76

Close-up view of thrombotic vegetation gingerly attached to the closure margin of aortic valves.

CV-79

Colonies of bacteria embedded in fibrin meshwork, and acute inflammatory exudates in subacute bacterial endocarditis.

CV-81

A metastatic pyemic abscess in myocardium.

CV-82

Calcific aortic stenosis showing rigidity and thickening of the aortic valve.

CV-83

Calcific aortic stenosis with severe distortion due to deposits in the sinus of Valsalva of bicuspid aortic valves.

CV-84

Marked endocardial fibroelastosis.