Chapter six

Cardiovascular System Disease

Section 1 Atherosclerosis (AS)

Definition
Atherosclerosis is a disease of large and medium
sized arteries, characterised by lipid deposition and
fibrosis.
fibrosis
 atherosclerosis

Arteriosclerosis arteriolosclerosis

medial calcification
Aetiology and Pathogenesis

Hard risk factors

1. Abnormality of blood lipid LDL↑ HDL↓
2. Hypertension
3. Smoking
4. Diseases which can cause secondary hyperlipemia
Soft risk factors
5. obesity
6. Genetic factors
7. Less exercise and others
 pathogenesis
 Response to injury hypothesis
 Lipid infiltration/insudation hypothesis
 Clonal proliferation hypothesis
Foam cells
Pathologic change

Fatty streaks or dots

Fibrous plaque

Atheromatous plaque

Complicated lesion
Morphology
Fatty streaks and dots

Lipid infiltrate to intima from the plasma

macroscopically, flat or slightly elevated yellow
streaks or dots. Microscopically, accumulation of lipid
in smooth muscle cells and macrophages——foam
cells accumulation.

Fatty streaks and dots usually formed in early age,

although they may evolve
Fatty streaks
 Fibrous plaque
 Grossly a elevated flat or round lesion (0.3-
1.5cm) whitish-yellow or waxy white.
 Microscopically, foam cells aggregate to
form a plaque, with slightly central
necrosis. The surface fibrous tissue
proliferate to form a fibrous cap.
Fibrous plaque
Fibrous plaque
Grossly a elevated flat or round lesion (0.3-1.5cm) whitish-yellow
or waxy white. In large lesions, the central portion is frequently
soft containing degenerated and necrotic tissue, free fat and
visible cholesterol crystals. Microscopically, the cholesterol
appears as clear, elongated, fusiform clefts because the crystals
have been dissolved out in preparation of the section, a core of
amorphous extracellular lipids. It typically is composed of a
superficial fibrous cap containing smooth muscle cells , scattered
leukocytes, and dense connective tissue overlying a cellular zone
with smooth muscle cells, macrophages, and T lymphocytes; and
a central necrotic core containing dead cells, lipid, cholesterol
clefts, lipidladen foam cells (macrophages and smooth muscle
cells), and plasma proteins. In the periphery are proliferating small
blood vessels attempting to organize the plaque.
Atheromatous plaque (atheroma)
 Grossly, the soft yellow nodules
 Microscopically, besides the aggregation
of foam cells, there severe necrosis in the
centre of the plaque with the formation
of cholesterol crystals, which are clear,
elongated, fusiform clefts. (The lipid
substance was dissolved by solvents
during the staining process.)
Atheromatous
plaque
Atheromatous plaque
Atheromatous plaque
The soft yellow nodules is an atheroma. In advanced
lesions, ulceration of atheroma and superimposed
thrombi may be seen. The internal elastic lamina is
frayed and fragmented, and in places, it may be absent.
Calcium salts become deposited in the atheromatous
lesions, and form thin, brittle, calcified plates, which
may crack easily.
The atheromatous lesions are much more prevalent in
the abdominal than in the thoracis aorta. Their
distributions is patchy, at point of stress. e.g., vessels
on the posterior wall of the aorta and at the point of
branching of major vessles.
Complicated lesion
Hemorrhage into the plaques
Atheromatous ulceration
Superimposed thrombi
Formation of an aneurysm
 Complicated lesions

 Hemorrhage into the plaque: induced by the

rapture of the plaque or the damage of the
trophic blood vessels.
 Ulceration: rapture of the plaque, which can
induce thrombosis or embolism secondarily.
Thrombosis over the plaque
Producing occlusion of the lumen, or, in the case of
small thrombi may organize, become incorporated into
the intima, and contribute to growth of the plague.
Calcification and ulceration
 Formation of an aneurysm: the disordered artery
dilated because of thinning and weakening of the
media adjacent to the large plaque.
Narrowing of the lumen, resulting in ischemia.
Obstruction of small vessels, caused by the plaque itself or
one of its complications may lead to serious ischemic effects—
e.g., sudden death or myocardial in farct, with involvement of
the coronary arteries, infarct of the brain in cerebral
atherosclerosis, and hypertension with renal arterial disease.
The Leriche syndrome, occurring chiefly in men and
characterized by ischemic effects in the lower limbs.
Symptomatic atherosclerotic disease most often relates to the
heart, brain, kidneys, lower extremities, and small intestine.
Atherosclerosis
Atheromatous
ulceration
Calcification
Atherosclerosis lesions in main arteries

1. Aorto-atherosclerosis

2. Coronary
3. Carotid and Cerebral atherosclerosis
4. Renal atherosclerosis

Atherosclerotic contracted kidney

5. Artery of extremity

6. Mesenteric artery
 Section 2 Coronary atherosclerosis and coronary
heart disease

Coronary atherosclerotic heart disease≈ Coronary heart

disease. Besides of the atherosclerosis, the vasopasm,
thrombosis can also induce coronary heart disease, which
usually is called ischemic heart disease, including angina
pectoris, myocardial infarction, sudden cardiac death,
fibrous myocardium.

The left anterior descending branch, which is responsible for

blood supply for anterior wall of left ventricle and 2/3
anterior part of the interventricle septum, is most frequently
Angina pectoris

Angina pectoris is episodic chest pain caused by ischemia of the

myocardium, which commonly radiates from the substernal and
left pectoral regions to the left shoulder and medial aspect of the
left arm.
Typical or stable angina pectoris: a predictable angina that
occurs at a fixed level of exercise, as a result of an increased
demand in myocardial work.
Variant angina: this is angina at rest or, some cases, awakens
the patient from sleep caused by an increase in the coronary
vasomotor tone
Unstable angina pectoris: the frequence of the angina increases
gradually.
 Myocardial infarctions

Myocardial necrosis result from the break of coronary blood supply

Types
Subendocardial myocardial infarction
Limited to the inner one third of the ventricular wall
Transmural myocardial infarction

Infarction of full thickness of ventricular wall

Occlusion of the anterior descending branch of the left coronary artery
produces an infarct of the anterior part of the interventricular septum,
the apical and anterior part of the wall of the left ventricles.
Various coronary frequencies The sites of regional
arteries infarction

Left anterior 40-50% Anterior and apical

descending coronary left ventricle,
artery anterior 2/3 of the
interventricular
septum
Left circumflex 15-20% Lateral wall of left
coronary artey ventricle

Right coronary 30-40% Posterior wall of the

artery left ventricle
Posterior 1/3 of the
interventricular
septum.
Pathologic change

6 hours
8~9 hours
After 4 days
The necrotic muscles fibres are swollen, hyalinized, and lacking
their striations and nuclei, leukocytes abundantly infiltrate the area.
After 7 days
Granulation tissue formation

2-8 weeks
The healing of myocardial infarcts is by scar tissue, replacing the
destroyed muscle, which does not regenerate.
Complications

(1) Functional disorder of papillary muscle

(2) Rupture of the heart
(3) Ventricular aneurysm
(4) Mural thrombosis
(5) Acute pericarditis

cardiogenic shock, arrhythmias

Fibrosis of the myocardium

Sudden cardiac death

 Section 3 Primary Hypertension

Primary hypertension is so called because these seemed to be no

primary lesion.

systolic pressure ≥140mmHg

diastolic pressure ≥90mmHg

Secondary hypertension ( symptomatic hypertension)

Aetiology and Pathogenesis

1. Genetic factors
2. Diet Na+
3. Vocation, social and psychological stress

Renin —— Angiotensin —— Aldosterone

Cases of high blood pressure commonly are divided into primary
(essential) and secondary (symptomic) types. The less common
secondary type is a result of renal disease (such as chronic
pyelonephritis and glomerulnnephritis), renal artery stenosis ,
cerebral or cardiac vascular disease, or endocrine lesions, such
as an adrenal or pituitary tumor.
The common essential type of hypertension is so called because
these seemed to be no primary lesion. It has been recognized
that renal arteriolar sclerosis is an almost constant postmorten
finding in essential hypertension. The arteriolar sclerosis is often
a generalized change, particularly common is the spleen,
pancreas, adrenal glands, and brain, but it is only in the kidneys
that arteriolar sclerosis and hypertension seem to be closely
associated.
 Types and pathologic change

Benign hypertension 3 stages

1. Dysfunctions stage
spasm of arteriole
2. Artery systemic changes
Arteriolosclerosis
musle arteriole fibrosis
elastic musclar artery AS

Arteriolosclerosis (Hyaline degeneration of arteriole)

3. Organs change
Hypertensive heart disease
kidney of hypertension

Primary granular contracted kidney

brain change

cerebral hemorrhage

Retinal change
malignant hypertension

Hyperplastic arteriosclerosis

Necrotizing arteriolitis
Section 4 Rheumatism

Laryngopharynx Group A beta-hemolytic streptococci

Allergic disease

Connective tissue, Aschoff body

Affects the heart, arteries, joints, skin, subcuteneous tissues and

the nervous system

rheumatic fever
Aetiology and Pathogenesis

It generally is agreed that is occurs after infection with Group A

beta-hemolytic streptococci.
streptococci The lesions of rheumatism are not the
result of direct infection by these organisms but represent an
allergic or hypersensitivity reaction.

Ab-Ag crossing reaction

Pathologic change

1. Nonspecific inflammation

1. granulomatous inflammation 3 stages

Alternative and degeneration stage
proliferative stage
Around the fibrinoid necrotic foci the proliferation of histocytic cells,
forming a granuloma. In their charcteristic form, as may be seen in the
myocardium, each of these minute nodules of proliferation inflammaties
is known as an Aschoff body.
body
Fibrosis or healing stage
Different organs rheumatic lesions

Carditis
Rheumatic heart disease
Chronic rheumatic heart disease
Endocarditis
the mitral valve vegetation
Myocarditis
Aschoff bodies
Rheumatic pericarditis
Rheumatic arthritis

Erythema annullare

Subcutaneous nodules

Rheumatic arteritis

Chorea minor
Section 6 Valvular vitium of the heart

Mitral stenosis

Rheumatic inflammation

Apex of heart, diastole murmur

left atrium failure → lung congestion → right heart failure →

systemic congestion

X ray: pear like heart

 Mitral insufficiency

Combined with mitral stenosis

Apex of heart, systole murmur

left heart failure → lung congestion → right heart failure →

systemic congestion
 Aortic stenosis

aortic valve, ejective murmur

left atrium failure → lung congestion → right heart failure →

systemic congestion

Angina pectoris, pulse pressure ↓

X ray: boot like heart

 Aortic insufficiency

aortic valve, diastole murmur

left atrium failure → lung congestion → right heart failure →

systemic congestion

Pulse pressure ↓ water-hammer pulse, pistol shot sound

Valvular vitium of the heart result from a healed or chronic
valvulitis or, occasionally, are congenital malformations. The
results of imflammation in the valves are seen as thickening,
adhesions, retraction, and shortening of the leaflets. There may
be a narrowing of the valve opening (stenosis), or closure of the
valve may be insufficient so that leakage (regurgitation) occur
through it. Valvalar insufficiency and stenosis may be produced
by the same deformity. Valve deformities are common on the left
side of the heart (aortic and mitral) but are uncommon on the
right side (tricuspid and pulmonary).
Mitral stenosis
Mitral stenosis is one of commonest valve deformities and almost
invariably is caused by rheumatic inflammation. Fibrous thickening,
adhesions, and retraction of valve leaflets with bridging and
calcification across the commissures and chordae are thickened,
fused, and shortened, May produce all degrees of stenosis. The
orifice may be narrowed to a tiny slit “fish mouth” or “button hole”
stenosis. The rigidity and retraction usually cause some insufficiency
of the valve as well.
Inceased work of the left atrium will compensate for a mild mitral
stenosis. A more severe uncompensated stenosis results in
increased pressure and stasis in the pulmonary circulation and
increases the work of the right ventricle. Thus left atrial dilatation,
chronic passive congestion of the lungs, and right ventricular
hypertrophy constantly accompany any great degree of mitral
stenosis. In pure stenosis, the left ventricle is normal or small in size.
Clinically left heart failure and right heart failure X-ray shows the
heart like a pear.
6.2 Mitral insufficiency
Mitral insufficiency essentially caused by rheumatic endocarditis
and secondery by SBE, and occasionally by congenital heart
disease. Regurgitation through the mitral valve is most often a
relative insufficiency resulting from the dilatation of the mitral
ring accompanying a dilatation of the left ventricle, but
insufficiency also may be caused by shortening and retraction of
the leaflets and chordae tendineae. If regurgitation is severe, one
finds left atrial dilatation along with hypertrophy of the left and
right ventricles. X-ray shows the heart like a ball.
6.3 Aortic stenosis
Aortic stenosis may occur as a pure lesion, but frequently it is
associated with aortic insufficiency. Noncalcific valvular sterosis
ususally is caused by rheumatic fever. Congenital valvular and
subaortic stenosis also occur.
Bicuspid aortic valve is sometimes associated with aortic stenosis.
Calcific aortic stenosis is attributed mainly to rheumatic fever.
However, when it occurs in advanced age; particularly in the
absence of lesions in other valves, it is ragarded as atherosclerotic
in origin. Healed bacterial endocarditis, especially related to
Brucella organisms, is a possible cause. Left ventricular failure,
hypertrophy, and dilatation (poststenotic dilation of the aortic root)
result from the stenosis. Angina pectoris appears frequently
because of a reduced coronary blood flow syncope with increase
risk of (in hypertrophied myocardium) sudden death and chronic
heart failure. The differences of pressure pulse pressure and
systemic diastolic pressure are diminishing. X –ray show the heart
like boots.
Aortic insufficiency
Regurgitation through the aortic valve during diastole may result
from dilatation of the aortic ring or from changes in the leaflets
themselves. Dilatation of the ring may accompany dilatations of
the rest of the heart ,or it may result from disease such as
syphilitic aortitis and Marfan syndrom. Changes in the leaflets are
commonly caused by syphilitis or rheumatic fever and SBE. The
leaflets may be simply affected or distorted at the commissure,
but often the whole leaflets is thickened, with rounded edges and
distinct shortening and retraction.
Diastolic regurgitation through the aortic valve is accompanied
by a significant fall of systemic diastolic pressure and hence a
high pulse pressure ( the differences between the higher pulse
pressure and lower diastolic pressure are increasing). Severe
hypertrophy and dilatation of the left ventricle result from the
extra work. Fibrosis of the endocardium, with formation of
endocardial “pockets”, caused by the regurgitating blood, is a
characteristic feature. Angina pectoris may result from
coronary insufficiency (related to low diastolic pressure). And
an increased demand of the hypertrophied heart for more
oxygen. In turn left heart failure, pulmonary atery, congestion
high pressure and right heart failure . Clinically around blood
vessels sign. X-ray shows that heart like a ball.