Chapter7 Diseases of Cardiovascular System
OBSERVATIONAL METHODS OF SPECIMEN
Heart. (Fig.7-01) The normal heart assumes cone form flatted slightly in front and back; its size resembles one’s right fist, and the heart of an adult
man weights 240gm in females and 270gm in males. The inner endocardium
and outer epicardium is smooth. The expected thickness of the free wall of the
right ventricle is 0.3-0.4cm and that of the left ventricle 0.8-1.2cm. The
perimeter of mitral valve is l0cm, of tricuspid valve l2cm, of aortic valve
7.5cm and of pulmonary valve 8.5cm. The valve is very thin; the cordae
tendineae is fine and long with full of flexibility.
Gross examination. Note the size, morphology, color and smooth degree of
the heart. Section surface: To observe whether each heart cavity is dilated, the
thickness, degree of hardness and color and luster of the cardiac muscle is
changed, and there are myocardial infarct, hemorrhage and scar formation;
whether the endocardium is smooth, whether there are mural thrombi and
hemorrhagic point in the endocardium; whether the perimeter of each valve is
changed; whether there are edema, thickness and/or scarring, ulcer and
perforation in the valve; whether there are adhered vegetations in valve and
how is its quantity, size, morphology, color and arrangement; whether the
cordae tendineae is thickness, shortening and fusion; whether the papillary
muscle is hypertrophy; whether there are defect in the auricular and
ventricular septum; whether the foramen ovale is closed and pathological
changes in the coronary artery.
Light microscope examination. Note whether there is inflammation, what
kind of inflammation and characteristic lesions on each layer of heart wall;
whether the myocardial cells are hypertrophy, atrophy, and whether cross
striation is clear; whether the pigment and the other foreign materials are
deposited in the myocardial plasma; whether the endothelial cells are integrity
and there are mural thrombi in the endocardium, and the adhered vegetations
in valve constitute with what kinds of composition.
Blood vessel. Three basic structural constituents make up the walls of
blood vessels: endothelium, smooth muscle, and connective tissue. They are
arranged in concentric layers (or tunicas) - an intima, a media, and an
adventitia - most clearly distinguished in the larger vessels. Arteries are
divided into three types: ?Large or elastic arteries, including aorta and its
major branches; ?Medium-sized or muscular arteries(such as the coronary or renal arteries), also referred to as distributing arteries; and ?Small arteries
(usually less than 2 mm in diameter).
Gross examination. To observe that whether the shape (such as saccular protrusion, fusiform expansion, flexion and tubercle, etc.), thickness and
hardness of blood vessel are changed; whether the vascular intima is smooth
and has the sclerosis plaque; whether the vascular lumen is narrow, and
thrombus and the other foreign materials.
Light microscope examination. (Fig. 7-02a,b) To observe whether the
vascular endothelial are integrity, and there are intimal thickness and
deposition of abnormal materials in the intima; whether the elastic fibers are
break, increase or decrease, and the smooth muscle cells have what kind of
changes in the media; and whether there is inflammation in each layer of
vascular wall and narrow of the lumen.
1. To grasp the basic pathological changes of atherosclerosis; the
characteristics of pathological changes of atherosclerosis of coronary and
brain artery; and the type, pathological changes and consequence of the
coronary heart disease.
2. To grasp the pathological changes and outcome of main organs of the
primary hypertension, and the relationship between atherosclerosis and
3. To grasp the basic pathological changes of rheumatic disease and the
pathological changes of rheumatic heart disease; to master the pathological
features of chronic valvular heart disease and its influence on
4. To be familiar with the pathological changes and its consequence of
5. To understand the concept, pathological changes and its consequence of
myocarditis and cardiomyopathy.
Gross specimen Tissue section
Atherosclerosis of the aorta Atherosclerosis of the aorta Atherosclerosis
Atherosclerosis of the brain Coronary atherosclerosis
Myocardial infarction Myocardial infarction Coronary heart
Hypertensive heart disease Arteriolar nephrosclerosis Primary hyper- tension
Arteriolar nephrosclerosis Hyaline degeneration of the
Brain hemorrhage Necrotizing arteriolitis
Rheumatic endocarditis Rheumatic endocarditis Rheumatic heart
Rheumatic pericaditis Rheumatic myocarditis
Mitral valve stenosis Valvlar vitium of
Mitral valve stenosis and
Acute bacterial endocarditis Acute bacterial endocarditis Infective endo- carditis
Subacute bacterial endocar- Subacute bacterial endocar-
Dilated cardiomyopathy Hypertrophic cardiomyopathy Cardiomyopathy
Hypertrophic cardiomyopathy Keshan disease
Viral myocarditis Myocarditis
KEY POINTS OF SPECIMEN OBSERVATION
Basic pathologic changes
(1) Gross morphology
?Fatty streak and spot: Multiple yellow, flat spots, flatten or slightly
raised, are visible on the tunica intima of the arteries. Some of the spots
coalesce into enlongated streaks
?Fibous plaque: Yellow or porcelain white (wax drop shape) plaque
slightly raised above the surrounding intimal surface.
?Atheromatous plaque: The plaque appears white or whitish yellow,
slightly raised and impinge on the lumen of the artey. On section, the
superificial portion of these lesions at the luminal surface tend to be firm
and white (the fibrious cap) and the deep portions yellow or whitish
yellow and soft, the centers contain yellow, grumous debris. Its bottom is
atrophied media. The atheroma may complicate ulceration or
?Complicated lesions: Hemorrhage into a plaque; focal rupture or gross
ulceration; thrombosis; calcification; aneurysm; media weakening; and
the lumen is narrowed in different degree.
?Fatty streak: A collection of lipid-filled foam cells in the intima.
?Fibrous plaque: The surface of plaque is the fibrous cap under that
contains smooth muscle cells, macrophages, foam cells, and extracellular
lipid and matrix.
?Atheroma: The surface layer of atheroma is hyaline degenerated fibrous
cap, the deep layer is lots of amorphism necrotic mass in which has
cholesterol crystal and calcium salt, and the bottom and edge of lesion
has granulation tissue, a little of foam cells, mononuclear cells and
Case abstract: Male, 55-year-old. He suffered the intermittent substernal
ache and/or precordial chest ache accompanying with the short breath and
heartthrob for 4 years. In the last 2 months, the symptoms were more serious.
3 hours ago, paroxysmal acute angina pectoris was happened after hard work
and the radiating pain was emitted to left shoulder and arm. Myocardial
infarct was diagnosed by electrocardiogram, showing pathologic Q waves in
leads V1-V5. The emergency treatment didn’t work. Patient was dead. Serious
atherosclerosis of the aorta and its main branches, coronary artery, the circle
of Willis and myocardial infarct of the left ventricle wall were observed in
(?)Atherosclerosis of the aorta
Gross specimen: (Fig. 7-03a, b) There are many grey and yellow plaques,
slight elevated on tunica intima of the aorta. Pin-size yellow flecks are fatty
streak, gray hunch is fibrous plaque; yellow white one is atheromatous plaque.
What is the main pathological change and where is the most serious lesion?
What complications are there?
Tissue section: (Fig. 7-04a,b, c) First, ascertain the tunica intima of the aorta and to observe the characteristic lesions of the intima.(a)Plenty of foam cells
congregated under endothelium, which is fatty streak.(b) Fibrous plaque. The
surface of intima is fibrous cap, under which there are plenty of foam cells. (c)
Atheromatous plaque. Local intemia thicken apparently; surface of intima is
fibrous cap with hyaline degeneration. The light stained area is necrotic
substance, cholesterol crytstal and calcification under the cap. Media is
compressed and become thinner.
Question: What kinds of complicated lesions are there in atherosclerosis of
the aorta? Which is the most feared?
(?) Coronary atherosclerosis
Gross specimen: (Fig.7-05a,b) It is coronary artery sliced transversely or vertically ?Note the characteristics lesions in the tunica intima; ?Note the
changes of the lumen.
Tissue section: (Fig. 7-06a,b) ?Note the changes of thickness and lumen;
?Note characteristics lesions in the vascular wall.
Question: What is the most dangerous lesion of coronary atherosclerosis for
(?) Atherosclerosis of the basal artery
Gross specimen: (Fig. 7-07) Opened or unopened the basal artery (some with the brain tissue). ?See through the adventitia; there is yellow white plaques
on intima; ?Wall thichen with luminal narrowing. Question: What kind of influence does atherosclerosis of the brain on the cerebral cortex? What outcome could it be? What kinds of clinical
manifestation are there?
(?) Myocardial infarction
Gross specimen: (Fig.7-08a, b) Horizontal section of the heart.(a) Gray
infarctive focuses are visible at anterial wall of left ventricle and anterior
1/3 of interventrical septum, which involve all layers.(b)It is left ventricular
aneurysm. The wall of left ventricle become thin, protrude, complicated from
Question: What complications and results may be having?
Section: (Fig. 7-09a, b, c) To ascertain and observe the region of damage.(a)
Light microscope of 1 day of myocardial infarct.The cytoplasm of myocytes
are granular with loss of nuclei and striations; and cytoplasm of some
myocytes are coagulative and hypereosinophilic showing wave-like striation.
Interstitial vessels dilate and congest. (b) Necrotized cardiac muscle cells
dissolve presenting netlike. (c)In the seventh days，peripheral granulation
tissues grow into replacing the infarct.
Question: What are the reasons of myocardial infarct? What are the main manifestations in clinic? Which complications and results may be having?
2. Primary hypertension
Basic pathologic changes
The following pathological changes could be seen at the stage 2, 3 or
complications stage respectively.
(1) Gross morphology
? Wall of arterioles thicken and is sclerosis, and the lumen is narrow;
? Wall of small artery thicken, and lumen contracts in different degree;
? Large artery: often accompanying atherosclerosis.
?Heart: concentric hypertrophy or eccentric hypertrophy of the left
?Kidney: primary granular atrophy of the kidney. The kidneys are reduced
in size, and the cortical surfaces show fine, even granularity. On cut
surface, the renal cortex becomes thin, and dividing line between the
cortex and medulla is not clear.
?Brain: edema, cerebral softening or cerebral lacunar infarct, and
?Retina: arteriosclerosis of the central artery, papilledema, ratinal
exudates and hemorrhage.
? The artery
1) Benign hypertension
? The vascular lesion consists of a homogenous, pink, hyaline
thickening of the walls of arterioles with loss of underlying
structural detail and narrowing of the lumen.
? Elastic fibers and collagenous fibers in the intima of the small artery
(musclar artery) increase; the internal elastic laminas reduplicate;
and smooth muscle cells and elastic fibers in the media increase.
2) Malignant hypertension: fibrinoid necrosis of arterioles, proliferation
of smooth muscle cells of the small artery yielding “onion-skin”
?Kidney: focal atrophy and disappearance of nephrons, hyperplasia of the
connective tissue and infiltration of the lymphocytes in the interstitial.
The rest glomeruluses are hyprothy accompanying with the renal tubules
dilation and protein cast formation in the tubular lumen.
?Brain: cerebral edema, focal liquefactive necrosis and hemorrhage.
(?) Benign hypertension
Case abstract: Female, 55-year-old. She often suffered headache and
dizziness for 6 years, and these symptoms aggravated after emotional
excitement and hard work. In recent one year, she occasionally felt the chest
distress and palpitation, amount of urine increased, and the blood pressure
was 200/130mmHg(26.7/17.3kPa). Urinary albumin (+), chest-X-ray:
hypertrophy of the heart as “boot” shape. One day ago, she suddenly fainted at working and the left limbs paralyzed. The emergency treatment didn’t work.
Patient was dead.
(1) Hypertensive heart disease (HHD)
Gross specimen: (Fig. 7-10) To pay attention to observe the size, shape of the
heart, thickness of the ventricular wall, and the changes of papillary muscles,
valves and cavity of the left ventricles.
Question: How do these changes of the heart take place? What influence will it
make on human body?
Tissue section: (Fig. 2-07) To observe the change of the cardiac muscles and think of the causation of these changes.
(2) Arteriolar nephrosclerosis
Gross specimen: (Fig. 7-11) ?How do the size, shape and surface of the kidney change? ?What changes have happened in the renal cortex and medulla?
?Do the renal pelvis and its surrounding tissues have any changes? ?What
characteristics does transected small artery have?
Tissue section: (Fig.7-12a,b) The afferent glomerular arteriole suffered
homogeneous, red-stained hyaline degeneration, and vascular wall thicken with
stricture or obstruction of the lumen; wall of interlobular arteries thicken,
lumen of that stricture. Some of glomeruli suffered fibrosis, hyaline
degeneration，corresponding glomeruli atrophy, disappear and is replaced by
fibrous tissue. Other glomeruli suffered compensatory hypertrophy; renal
tubule dilate，and protein cast can be seen.
Question: What serious consequence, can be caused by pathologic changes of
the kidney and what are the clinical manifestations?
(3) Brain Hemorrhage
Gross specimen: (Fig. 7-13) Note the position, scope of the hemorrhage in
the brain tissue, and then to infer the patient’s clinical manifestations.
(4) Hyaline degeneration of the spleen artery
Gross specimen: (Fig. 7-14) To observe carefully the changes of the central
arterial wall in the white pulp.
(?) Malignant hypertension (Accelerated hypertension)
Tissue sections:(Fig. 7-15a,b) (a) Interlobular arteries suffered fibrinoid
necorsis. (b) Hyperplastic ateriolosclerosis is identified with its onion-skin,
concentric, laminated thickening of the walls of arterioles, caused by
increase of smooth muscle and collagen fibers in the wall of interlobular
Question: What are the characteristic lesions of arteriole and small atery? What manifestations would patient show? What is the main cause of death?
3. Rheumatism heart disease (RHD)
Basic pathologic changes
?Alteration and exudative stage
There are mucoid degeneration of connective tissue matrix, fibrinoid
necrosis of collagen and a little of serous fluid and infiltration of plasma
?Proliferative stage (granulomatous stage)
The basic pathological change is formation of Aschoff body (rheumatic
body or rheumatic granuloma).
Aschoff body is large, round or oval, consists of central fibrinoid
necrosis with a perimeter of Aschoff cell (rheumatic cell), lymphocyte,
plasma cell and monocyte.
Aschoff cells have abundant basophilic cytoplasm and single or multiple central round-to-ovoid nuclei in which the chromatin is disposed in the
central zone. In cross section these nuclei have an “owl eye” appearance,
and when cut longitudinally they resemble a “caterpillar”.
?Scar stage (healing stage)
The rheumatic granuloma is replaced by the fibroblast, and finally
become fibrous scar.
?Hereinabove pathological changes could appear at the same time.
?The rheumatic lesion in tunica serosa is mainly serous and/or fibrinous
(1) Gross morphogogy
It mainly involves the mitral valve. Vegetations (verrucae) are visible
along the line of closure of the valve leaflet. The valve leaflets become
fibrous thickening, hardening or fusion. The irregular MacCallum
plaques may be visible in the left atrium.
?Rheumatic myocarditis: the myocardial interstitium inflammation, the
heart may dilate.
?Rheumatic pancarditis: cor villosum or hydropericardium could be seen.
?Rheumatic endocarditis: the vegetations are white thrombus, composed
of pink platelet trabeculae and dark-red fibrin.
?Rheumatic myocarditis: scattered Aschoff bodies within the interstitial
connective tissue, often perivascular. Besides, degeneration, exudation
and focuses of scar may be seen.
?Rheumatic pancarditis: a fibrinous or serofibrinous inflammation.
(?) Rheumatic endocarditis
Case abstractFemale, 10 years old. She had fever and migratory joint ache for 2 months, palpitation and hard breath for 1 week. She also sufferen from
lower extremities edema, hepatomegly and splenomegly, ascitis, and
pink-white froth sputum was coughed. She was dead after effectless treatment.
Gross specimen: (Fig. 7-16a,b) (a) Acute rheumatic endocarditis. The mitral valve is thin. There is a row of small irregular, warty gray vegetations
(verrucae) on the line of closure of atrial surface of mitral valve; cordae
tendineae thicken. (b) Recurrent rheumatic endocarditis. The mitral valve and
the tendinous cords thicken apparently, a few of small brown warty
vegetations are visible alone the line of closure of valve leaflet.
Tissue section: (Fig. 7-17) First to recognize the valve and to observe the pathological changes of the valve.
Question: What is the essence of the lesion? What kind of serious results will
be happened if the lesion relapsed?
Tissue section: (Fig. 7-18a,b) The myocardial interstitium especially besides vessels has circumscribed collection of cells, the Aschoff body.
Question: What’s lesion in this stage? How many stage of lesions in the