FIGURE 6.1

A normal medium-sized artery in transverse section. The wall is composed mainly of smooth muscle (van Geison).

FIGURE 6.2

A scanning electron microscope view of an artery and vein. The artery (above – small arrow) has a smaller lumen and endothelium that is aligned to the direction of the rapid flow. In contrast, the vein (below – large arrow) has a large capacitance and polygonal endothelial cells.

FIGURE 6.3

The anterior surface of the heart has a yellowish area, which is a full-thickness infarct of the left ventricle. It lies in the territory of the left anterior descending coronary artery which is occluded by thrombosis. There is surrounding inflammation and a fibrinous exudate on the surface, a common response to tissue necrosis.

FIGURE 6.4

A kidney with two sunken areas in its midzone. These are scars due to old healed cortical infarcts.

FIGURE 6.5

Propagation of thrombus in a vein.

FIGURE 6.6

The hilum of a lung showing pulmonary arteries containing large red thromboemboli derived from the leg veins.

FIGURE 6.7

Multiple recent infarcts in both kidneys in a patient with atrial fibrillation, atrial thrombosis and systemic embolism.

FIGURE 6.8

An artery occluded by loose fibrous tissue within which there are slits formed by crystals of cholesterol derived from an atheromatous plaque. This shows that that the occlusion is due to organized athero-embolism.

FIGURE 6.9

A section of kidney tissue from a patient who died after multiple long-bone fractures. It shows two renal glomeruli stained to reveal fat (red). The glomerular capillaries are plugged with fat globules which, being fluid at body temperature, have passed through the pulmonary capillaries.

FIGURE 6.10

A medium-sized artery from a middle-aged man showing early arteriosclerosis. The intima is thickened and there is reduplication of the internal elastic lamina. This has caused thinning of the media: compare with Figure 6.1.

FIGURE 6.11

An electron micrograph of a renal arteriole showing advanced arteriolosclerosis. The medial smooth muscle cells are largely replaced by amorphous proteinaceous material. This is derived from retention of plasma proteins combined with some basement membrane-type proteins synthesized in situ.

FIGURE 6.12

Autoregulation allows the cardiac, cerebral and renal circulations to maintain constant flow over a wide range of pressure. Arteriosclerosis due to age and hypertension shifts this curve to the right and renders tissues susceptible to ischaemia if blood pressure falls. Conversely, malignant hypertension is rare in the elderly and in those with longstanding hypertension.

FIGURE 6.13

A piece of aorta opened out to show that the smooth endothelial surface is largely replaced by ulcerated confluent atheromatous plaques with adherent thrombus.

FIGURE 6.14

An aortogram showing a tortuous aorta with an irregular outline due to severe atheroma, which has also caused narrowing of the renal arteries.

FIGURE 6.15

An aorta with severe atheroma which has narrowed the origins of one renal artery. The diminished blood flow has caused shrinkage of the kidney on that side due to ischaemic atrophy.

FIGURE 6.16

A histological section of iliac artery showing extreme narrowing due to a large atheromatous plaque.

FIGURE 6.17

A histological section through an atheromatous plaque stained to show lipid as red. Beneath the lumen (right) there is a pale collagenous fibrous cap beneath which the media is replaced by a lipid rich atheromatous plaque around which there is some fibrosis and chronic inflammation.

FIGURE 6.18

Early events in the formation of an atheromatous plaque.

FIGURE 6.19

Stages in the development of an atheromatous plaque. It is believed that those with a thin overlying collagenous cap are more likely to crack and ulcerate and trigger thrombosis.

FIGURE 6.20

Schematic diagram of lipoprotein pathways. VLDL = very low density lipoprotein; IDL = intermediate density lipoprotein; LDL = low density lipoprotein; HDL = high density lipoprotein.

FIGURE 6.21

Intracellular cholesterol metabolism. ACAT = Acyl-CoA: Cholesterol acyltransferase; LDL = low density lipoprotein.

FIGURE 6.22

Interaction between risk factors and cells. LDL = low density lipoprotein; PDGF = platelet-derived growth factor.

FIGURE 6.23

A histological section through a fatty streak in the aorta of a child stained to show fat red. The fatty streak consists mainly of groups of lipid-containing foam cells in the intima.

FIGURE 6.24

A renal interlobar artery in early established hypertension. There is intimal thickening but the predominant feature is hypertrophy of the muscular media causing increased wall to lumen ratio. This causes increased response to prevailing pressor stimuli – the ‘vascular amplifier’.

FIGURE 6.25

Advanced arteriosclerosis in a renal radial artery in an elderly subject with longstanding benign hypertension. The intima is grossly thickened by excess matrix proteins including collagen and elastic tissue. There has been almost complete loss of the medial smooth muscle, presumably due to atrophy.

FIGURE 6.26

This transverse slice of the left ventricle shows gross hypertrophy that is present in some hypertensive patients.

FIGURE 6.27

A section of kidney showing fibrinoid necrosis and thrombosis of arterioles (stained red). A small radial artery shows intimal proliferation probably due to a healing response which causes extreme narrowing.

FIGURE 6.28

The kidneys in acute malignant hypertension are swollen and their surfaces show small haemorrhages.

FIGURE 6.29

A peripheral blood smear showing red blood cells fragmented due to intravascular thrombosis in malignant hypertension.

FIGURE 6.30

A section of kidney from a case of polyarteritis showing a damaged glomerulus and a radial artery which in its lower part shows fibrinoid necrosis. There is intense surrounding inflammation.

FIGURE 6.31

A saccular atheromatous aneurysm of the descending aorta in the typical position above the iliac arteries. Its lumen contains abundant soft thrombus.

FIGURE 6.32

The heart is enlarged due to longstanding hypertension and the aorta is diffusely affected by severe atheroma and arteriosclerosis. It is dilated due to an aneurysm and elongated.

FIGURE 6.33

The ascending arch and descending aorta from a 26-year-old man, who died of a dissecting aneurysm. The transverse intimal tear is just above the aortic valve and the cause is the narrowing (coarctation) at the aortic arch.

FIGURE 6.34

Another case showing that the haematoma is within the layers of the aorta.

FIGURE 6.35

The low power view (left) shows that the elastic fibres (stained black) have fragmented and the higher power view (right) shows that the spaces are filled with connective tissue mucins (stained blue).

FIGURE 6.36

The ascending aorta severely dilated due to a syphilitic aneurysm. The intimal surface is covered by white thickenings that give rise to a ‘tree bark’ appearance.

FIGURE 6.37

An electron micrograph showing a renal glomerular capillary with the endothelial cell cut tangentially to reveal the presence of round pores which give rise to a highly permeable fenestrated endothelium.

FIGURE 6.38

An electron micrograph showing a capillary in the cerebral cortex. It contains a red blood cell. There are two endothelial cells whose cytoplasm is non-fenestrated. The endothelial cells overlap and there is a tight junction between the cells seen as a black line. This is characteristic of a less permeable endothelium.

FIGURE 6.39

‘Pitting’ oedema of the lower legs demonstrated clinically.

FIGURE 6.40

A sectioned lung showing spontaneous pulmonary haemorrhage in disseminated intravascular coagulation.

FIGURE 6.41

Metabolic and circulatory effects of cardiogenic shock. BP = blood pressure; DIC = disseminated intravascular coagulation; ARDS = acute respiratory distress syndrome.

FIGURE 6.42

Some effects of hypoxia.

FIGURE 6.43

Spontaneous serosal haemorrhages in a case of meningococcal shock with DIC.

FIGURE 6.44

Outcomes of leg vein thrombosis.

FIGURE 6.45

A histological section of a coronary artery from a case of stable angina. The residual lumen is an eccentric tiny slit. The artery is severely narrowed by an atheromatous plaque filled with amorphous lipid material. It is surrounded by collagen (stained green).

FIGURE 6.46

A transverse section through the long axis of the heart showing transmural myocardial infarction. The recently infarcted tissue is the shaded area.

FIGURE 6.47

The top panel shows a histological section depicting a ruptured atheromatous plaque which has precipitated luminal thrombosis. The bottom panel shows the propagated thrombus it has caused.

FIGURE 6.48

Global subendocardial myocardial infarction. The recently infarcted tissue is the shaded area.

FIGURE 6.49

A transverse section through the heart showing global subendocardial infarction. In addition the anterior portion also shows a transmural regional myocardial infarction.

FIGURE 6.50

A large myocardial infarct at 5 days showing the colour changes associated with coagulative necrosis.

FIGURE 6.51

A histological section showing a zone of dark red myocytes with coagulative necrosis next to a zone of pale staining viable myocytes that have retained their nuclei and cytoplasmic striations.

FIGURE 6.52

A heart with a previous myocardial infarct that has stretched to form an aneurysm which contains mural thrombus.

FIGURE 6.53

Cardiac tamponade which shows gross distension of the pericardial sac by blood. The pericardium has been incised to reveal a mass of fresh blood clot.

FIGURE 6.54

A chest X-ray showing enlargement of the heart cause by heart failure. There are streaky opacities in both lung fields due to pulmonary oedema due to left ventricular failure. ECG leads are also visible.

FIGURE 6.55

The interior of the left ventricle showing the aortic valve at the top and the posterior surface of the anterior mitral valve leaflet. The head of the infarcted papillary muscle has been ruptured and avulsion of the attached chordae tendineae caused mitral incompetence.

FIGURE 6.56

A histological section of myocardium showing a focus of lymphocytic myocarditis.

FIGURE 6.57

A grossly enlarged heart showing a marked globular shape in dilated cardiomyopathy.

FIGURE 6.58

An echocardiogram shows that all four chambers are dilated with thin walls.

FIGURE 6.59

The myocardium in dilated cardiomyopathy shows vacuolation of myocytes and diffuse fibrosis.

FIGURE 6.60

A grossly hypertrophied left ventricle in hypertrophic cardiomyopathy with some asymmetrical hypertrophy.

FIGURE 6.61

A focus of abnormal hypertrophied myocytes in hypertrophic cardiomyopathy. There is an irregular arrangement showing disarray and this is associated with interstitial fibrosis.

FIGURE 6.62

A mitral valve with severe shortening and thickening of the cusps and shortening and fusion of the chordae tendineae.

FIGURE 6.63

The mitral, aortic and tricuspid valves visualized through the atria. There is mitral stenosis and severe aortic stenosis.

FIGURE 6.64

A floppy mitral valve viewed through the atrium showing soft thickened and stretched cusps bulging into the atrium.

FIGURE 6.65

Two aortic valves surgically removed for calcific aortic stenosis. This occurred prematurely because the valves were congenitally bicuspid.

FIGURE 6.66

Syphilitic aortitis causing thickening and stretching of the aortic root and aortic incompetence.

FIGURE 6.67

Vegetations on an infected aortic valve in subacute bacterial endocarditis. The valve is thickened, scarred and fused at the commissures due to previous rheumatic damage.

FIGURE 6.68

Subacute infective endocarditis in the aortic valve in a dilated
heart. The spleen is also enlarged and shows an infarct due to embolism.

FIGURE 6.69

Echocardiogram showing the heart in ventricular systole. The thickened and scarred cusps and chordae tendineae are visible. The mitral valve remains open during systole indicating regurgitation which was confirmed by colour Doppler studies.

FIGURE 6.70

A mitral valve removed at operation. It is thickened, calcified and the orifice is reduced to a slit by fusion of the commissures due to rheumatic scarring. It is rigid and can neither open or close. A large friable vegetation protrudes into the orifice.

FIGURE 6.71

The valve flap of the prosthetic mitral valve replacement is jammed with thrombus. It can neither open nor close fully.

FIGURE 6.72

The anterior surface of the heart with the pericardium opened to reveal a fibrinous pericarditis.

FIGURE 6.73

An opened atrium showing a myxoma as a soft ovoid gelatinous mass on a stalk which may obstruct the mitral valve or give rise to embolism.

FIGURE 6.74

This plastic flap valve has been surgically removed because it was jammed by formation of thrombus.

FIGURE 6.75

The ventricles of the heart removed at operation during the transplantation procedure. The atria have been left to anastomose to the new organ.

FIGURE 6.76

Diffuse chronic inflammation and myocyte damage indicate severe acute rejection of the allograft.

FIGURE 6.77

A methenamine silver stained preparation showing septate fungi with dichotomous branching morphologically consistent with Aspergillus.

FIGURE 6.78

The heart is embedded in a white tumour mass consisting of diffuse large B-cell lymphoma occupying most of the mediastinum.

FIGURE 6.79

A surgically excised coarctation showing a tight stenosis of the aortic arch.