Arteriosclerosis

THERE HAS BEEN MUCH CONFUSION IN THE USE
of the terms arteriosclerosis and atherosclerosis. Arteriosclerosis
is a diffuse lesion which often affects long
segments of the arterial tree in which there is usually a
combination of hypertrophic and fibrous changes in the
entire thickness of all layers of the arterial wall. The media
and adventitia are commonly affected by this disease
process. Atherosclerosis is the term used for atheroma
of arteries. It is typically patchy with a focal lesion of
the intima with degeneration. There are also plaques of
atheroma jutting into the lumen of the vessel obstructing
the flow of blood.

I. DISEASES CAUSING ARTERIOSCLEROSIS
A. Hypertensive Arteriosclerosis
Prolonged hypertension causes the walls of the affected
arteries to become firmer and thicker, and the lumen are
often wider than normal. Arteries appear to be generally
enlarged and they may become somewhat tortuous. These
changes can be seen especially in the retinal arteries
(hypertensive retinopathy), kidneys, pancreas, and other
organs. The lumen of minute arterial branches, however,
are often diminished owing to thickening of the intima.
Microscopic examination shows that the arterial wall
is generally thickened with a proliferation of connective
tissue cells and formation of new tissue both in the
intima and the media. There is a considerable amount
of concentric fibrous thickening, often without atheroma
formation. In the thickening of media there may be
distinct evidence of muscular increase, but in most cases
the muscle fibers are found to be undergoing replacement
by fibrous tissue leading to distinct fibrosis of the media.
There is, however, true muscular hypertrophy. In young
subjects with severe kidney disease and severe hypertension,
hypertrophy of the media occurs before secondary
fibrosis has appeared. This hypertrophy is similar to
hypertrophy of the myocardium in response to the
increased workload imposed by the high pressures. In the
thickened intima, there is distinct hypertrophy and
hyperplasia of the longitudinal muscle layer next to the
internal elastic lamina. A reactive increase in the supporting
elements of the vessel wall occurs in both muscle and
elastic tissue. This occurs in response to increased blood
pressure. This type of musculoelastic hyperplasia can be
arrested by some antihypertensive agents.

With hypertensive arteriosclerosis the walls of small
vessels become swollen and hyaline and its lumen may be
diminished. These changes may be observed in end-stage
kidney disease caused by severe hypertension and nephritis.
In advanced cases there are lesions of a more severe type
in which patchy necrosis of the arterial wall occurs
along with fibrous infiltration and thrombosis. A typical
finding in patients with malignant hypertension is fibrinoid
necrosis of arteries in the kidney and other organs.
These hemorrhagic changes are classically observed in the
retinal arteries that are severely damaged by malignant
hypertension and reflect the extensive pathologic changes
that occur in other organs including the kidney and brain.
Cerebral hemorrhage may also occur. Epistaxis is not
uncommon and red blood cells exuding from kidney
lesions are also found in the urine.

B. Monckeberg’s Sclerosis — Calcification
of the Media
Calcification is frequent in the arterial system. A striking
degree of calcification is that which occurs in the media
of arteries, particularly in the elderly. Calcification of
the media is far more common in large arteries such as the
iliac and femoral arteries. Lime salts are deposited in the
middle media in these patients and elevated blood pressure
may be recorded, but the mean arterial pressure is normal.
This condition is not caused by hypertension nor does it
cause hypertension. This is essentially a senile change that
rarely leads to senile gangrene.

C. Endarteritis Obliterans
Endarteritis obliterans is a reaction of the arterial wall to
an irritant which approaches it from the outermost lining
of the adventitia. This process may be initiated by syphilis
in which the main lesions are endarteritis and periarteritis
of the small arteries in association with infiltration of
lymphocytes and plasma cells around them.
These lesions affect the vasa vasorum, the small arterioles
that feed the media with blood. The aortic arch is also
commonly affected by syphilitic lesions. The arch immediately
above the aortic valve is usually involved leading to
weakness of the arterial wall and aneurysm formation of
the ascending part of the aortic arch. Syphilis commonly
damages the aortic valve and dilates the aortic valve ring
causing severe aortic regurgitation. The aortic arch shows
thickened plaques and irregularity of the surface with
formation of aneurysmal depressions. Narrowing of the
orifices of the coronary artery at their origin from the
aorta (ostia) may occur and cause angina. Syphilitic lesions
may also affect the pulmonary arteries causing right heart
strain and heart failure. The arterial damage by syphilis is
therefore not considered a true form of arteriosclerosis
and is regarded as a specific disease of the arteries that
includes vasculitis.

D. Thromboangiitis Obliterans
This disease process is a segmental vasculitis that affects
the peripheral arteries, veins, and nerves of the arms and
legs. The renal, coronary, and cerebral vessels may also be
involved. Thromboangiitis obliterans is sometimes called
Buerger’s disease as he was the first to described it in 1908
in 11 amputated limbs.
The pathologic process of this disease is distinct from
atheroma and arteriosclerosis. This condition is fortunately
rare and occurs in young persons usually less than age 40
who are cigarette smokers. The pathologic process consists
of highly cellular thrombi composed of polymorphonuclear
leukocytes forming micro abscesses. Occasionally
multinuclear giant cells are observed. The inflammatory
infiltrate affects the vascular wall, but the internal elastic
lamina remain intact. There is usually considerable fibrosis
of the media and adventitia. Similar changes may be
present in the accompanying veins and phlebitis of the
superficial veins of the arms and legs may be a prominent
feature. It is important to note that atherosclerosis and
arteriosclerosis are two distinct diseases that cause disturbances
in arteries, not veins.
Thromboangiitis obliterans is common in Asia and
rare in North America and western Europe. Most patients
have symptoms before age 40 and more than 80% occur
in men. Patients may complain of cold hands and feet
(Raynaud’s phenomenon) and develop digital ulcerations
and gangrene. Several diseases may cause similar
symptoms and signs including scleroderma, lupus erythematosus,
mixed connective tissue disease, and antiphospholipid
antibody syndrome. These diseases must be
excluded before considering thromboangiitis obliterans
as the diagnosis.
Diagnosis is based on the age of onset before age of
40, history of tobacco use, physical examination demonstrating
distal limb ischemia, and exclusion of other conditions
mentioned above. Angiography may show segmental
lesions.
Treatment includes cessation of cigarette smoking.
Biopsy of lesions may prove difficult to heal and reconstructive
surgery is often not feasible because of the
segmental lesions that may be present.

II. ATHEROSCLEROSIS
The word ‘‘atheroma’’ is derived from the Greek stem
‘‘athere,’’ meaning porridge or gruel. When a plaque of
atheroma is cut, one can see a gelatinous, thick, porridgelike
material that contains cholesterol and other fatty
material. The plaque of atheroma involves the intima
and the middle wall of the artery. Apart from a rich fat
content, the plaque has a preponderance of smooth muscle
cells that are derived from the media. These smooth
muscle cells are believed to be very important in the
formation and growth of the plaque. Substances such as
cholesterol and products released from blood platelets
stimulate the smooth muscle cells to proliferate, thus
enlarging the plaque.

The intima of the artery in contact with the blood is
smooth. When atherosclerosis occurs, a plaque of atheroma
juts into the lumen of the artery. The silky smooth
lining of the arteries is damaged by the force of blood as it
moves through arteries that are elastic and constantly
moving in pulsation. With every pulse wave, the arterial
wall yields and stretches; over many years some damage
must occur. The damage is partially repaired by small
blood particles (platelets), which clump together and
plug the damaged surface. These platelet plugs form a
temporary patch, just like the plug of coagulated blood
that forms when you nick yourself and a very small clot
forms. In the coronary arteries or aorta, small clots are
commonly formed on the lining. Presumably, these clots
are involved in the repair of injuries to the smooth lining
of the arteries. These small blood clots are somehow
welded into the lining as hard, thickened areas (fibrous
plaques). The artery tries to strengthen its wall during
this repair job.

The plaques of atheroma are sometimes smooth,
bumpy, large, rough, and even ulcerated. Because the
vessel wall gets hard (sclerosed), the term used for the
disease is atherosclerosis. A heart
attack is caused by blockage of a coronary artery, and such
a blockage is usually due to one or more of the following:

A blood clot forms on a plaque of atheroma. Lipid
rich plaques are prone to rupture but can be fissured
or ulcerated and this often leads to clotting; the term
atherothrombosis describes this serious complication of
atheroma. See the chapter Atheroma/Atherosclerosis.

A large plaque of atheroma nearly completely blocks
the artery.

Small blood particles (platelets) may stick to the surface
of the plaque in clumps similar to sludge in pipes; the
clumped material may dislodge and be moved downstream
by the blood and may block a smaller artery.

A coronary artery may go into spasm, especially at the
site of a plaque, blocking the vessel for a few minutes or
a few hours (coronary artery spasm).

An increase in adrenaline can be produced under the
influence of stress or other inciting factors causing
clumping of platelets that may lead to clot formation;
excess adrenaline from any source can also produce
electrical disturbances in the heart, especially ventricular
fibrillation; in fibrillation the heart muscle stops contracting
and quivers therefore no blood is pumped,
causing cardiac arrest.


The exact mechanism that leads to the formation of
blockage by atheroma has defied medical research for
the past 60 years; it is certain that a high level of LDL
cholesterol, particularly oxidized LDL (bad) cholesterol,
initiates and perpetuates atheroma formation and
progression.

Atherosclerosis causes blockage of arteries and is the
cause of heart pain, angina, heart attacks, and death
from coronary heart disease; blockage of arteries by
atherosclerosis is the basic cause of heart attacks,
stroke, aneurysm of the aorta, and poor circulation in
the legs.

In the western world, the UK, Europe, Ireland, and
Russia atherosclerosis is the most common disease affecting
men aged 35–80 and women after age 55. Death due
to atherosclerosis is several times more common than all
forms of cancer. The underlying atherosclerotic disease of
the coronary arteries leads to more deaths than any other
disease in industrialized countries. This disease is much
more common in young men than women. Women
are fortunately protected from atherosclerosis up to age 55
because of estrogens. Because men commonly die from
heart attacks between age 40 to 60, the disease in the
left anterior coronary artery has been appropriately labeled
‘‘the widow-maker.’’

For more information visit Jigfo.com, the no.1 source of information.