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Myocardial Hypertrophy and Heart Failure

Adaptive response that augments myocyte
contractile strength  compensatory response
to hemodynamic overload  chronic
hypertension or valvular stenosis (pressure
overload), myocardial injury, valvular
insufficiency (volume overload).
Cardiac hypertrophy compensates for
hemodynamic overloading of the heart.
 Hypertrophic responses feature
enlargement of cardiac myocytes and
accumulation of sarcomeric proteins,
without an increase in the number of
cardiac myocytes  a compensatory and
potentially reversible, but faced with
persistent stress, the myocardium
becomes irreversibly enlarged and dilated.
 Increases cardiac workload for a
prolonged period or produces structural
damage may eventuate in myocardial
Cardiac Failure
 Ischemic heart disease  chronic left ventricular
failure with/out history of infarction or angina.
 Pathologic examination :
Atherosclerotic narrowing of the coronary
arteries and diffuse myocardial fibrosis.

Cardiac failure occurs when hypertrophy of

surviving muscle can no longer compensate for
progressive loss of myocardial cells.
Severe myocytolysis in end-stage heart failure. myocytes
show loss of myofibrils, giving the cells a marked
vacuolated appearance. Only a thin rim of contractile
cytoplasm is present
Myocardial Infarction
 Severe atherosclerotic narrowing of one
or more coronary arteries.
 A fresh thrombus overlying an
atherosclerotic plaque is found in 40–90%
of cases.
 Thrombosis  precipitated by slowing and
turbulence of blood flow in the region of a
plaque or by ulceration of a plaque.
Coronary atherosclerosis, plaque formation
produce marked surface irregularity
Dating of a Myocardial Infarct
Elapsed TimeGross or Naked Eye Features (at Autopsy)

0–12 hours : Usually none

12–24 hours : Softening, irregular pallor
 Loss of striations
 Cytoplasmic eosinophilia
 Nuclear pyknosis
 Mild edema
 Occasional neutrophils
1–3 days : Pale infarct surrounded by a red (hyperemic) zoneAs
above, plus:
 Nuclear lysis
 More neutrophils
 Inflammatory capillary dilatation
 4–7 days : Pale or yellow (caused by liquefaction by
neutrophils), definite red marginAs above, plus:
 Liquefaction of muscle fibers
 Neutrophils
 Macrophages remove debris
 Ingrowth of granulation tissue from margins
 7–14 days : Progressive replacement of yellow infarct by
red-purple (granulation) tissueAs above, plus:
 Disappearance of necrotic muscle cells
 Reduced numbers of neutrophils
 Macrophages, lymphocytes
 Beginnings of fibrosis and organization of granulation tissue
 2–6 weeks : Becomes gray-whiteAs above, plus:
 Development of fibrous scar
 Decreasing vascularity
 Contraction of scar
 The necrotic
myocardial fibers,
which are eosinophilic
and devoid of cross
striations and nuclei,
are immersed in a
sea of acute
inflammatory cells.
 Atherosclerosis is thickening of the artery
resulting from deposition of specific
atheromatous lesions.
 “Arteriosclerosis" is a nonspecific term that
denotes thickening and loss of elasticity
("hardening") of the Arteries from Any
 Changes Associated with Aging and
Hypertension Often Lead to

 The basic abnormality in atherosclerosis is

the deposition of complex lipids in the
intima. The cause is uncertain.
Risk Factors for Atherosclerotic
Arterial Disease
 Increasing age: Significant disease is rare under 30 years.
 Morbid obesity: >30% over ideal body weight.
 Lack of physical exercise: Incidence greater in persons with
sedentary occupations; regular exercise (20 minutes twice weekly)
decreases risk.

Highly significant factors

1. Male sex :
Males are affected more than females; female incidence increases
after menopause; sex incidence is equal after age 65 years.
2. Family history:
History of ischemic heart disease in a parent or sibling under age 55
3. Hyperlipidemia:
Major risk factor under 45 years of age.
Specific lipoproteins involved in increased risk :
Total cholesterol >6 mmol/L (>240 mg/dL)
Total triglyceride >2.8 mmol/L (>250 mg/dL)
LDL-cholesterol >4.2 mmol/L (>160 mg/dL)
Low HDL-cholesterol: <0.9 mmol/L (<35 mg/dL)

4. Hypertension
 The major risk factor in patients over 45 years of age :
Hypertensives have a fivefold increased risk compared
with normotensive persons.
 Cigarette smoking : Ten cigarettes per day increases
the risk threefold; cessation of smoking decreases risk
to normal after 1 year.
 Diabetes mellitus : Both type I and type II diabetes
mellitus are associated with a twofold increase in risk.
The Fatty Streak
 Fatty streaks are thin, flat, yellow streaks
in the intima. They consist of
macrophages and smooth muscle cells the
cytoplasm of which has become distended
with lipid (to form foam cells).
The Fibrous Atheromatous Plaque
 Basic lesion of clinical atherosclerosis  three zones:
(1) A fibrous cap under the endothelium, consisting of
dense collagen and scattered smooth muscle cells
and macrophages
(2) Lipid zone, which consists of foam cells (lipid-
laden macrophages and smooth muscle cells) and
extracellular lipid and debris
(3) Basal zone, composed of proliferated smooth
muscle cells and connective tissue. Different plaques
contain varying amounts of these three layers; some
are mainly fibrous, and others are predominantly fatty.
 The fibrous atheromatous plaque appears
grossly as a yellow-white elevation on the intimal
surface of the artery.
 In cut section, the center of the plaque consists
of semisolid yellow material
 Microscopically, the three zones are
recognizable and are of varying thickness in
different plaques. Needle-shaped cholesterol
crystals are commonly present in the lipid zone.
Severe atherosclerosis and a recent thrombus in
the narrowed lumen
Thromboangiitis Obliterans
(Buerger's Disease)
 Thromboangiitis obliterans is characterized by
segmental involvement of small and medium-
sized arteries, mainly in the lower extremities.
The lesion frequently involves adjacent veins
and nerves.
 In the acute phase, there is marked swelling and
neutrophilic infiltration of the entire
neurovascular bundle. Thrombosis is common.
Healing by fibrosis and organization of thrombi
produces thick cord-like vessels with occluded
 Progressive ischemia of the lower limbs produces
intermittent claudication, with pain in the calf muscles
precipitated by exercise and relieved by rest. As the
disease progresses, the amount of exercise necessary
to produce pain (called the claudication distance)
decreases, leading to progressively greater disability.
 With severe disease, pain is present at rest along with
trophic changes in the skin, culminating in dry gangrene.
 The disease is progressive. Abstinence from smoking
frequently results in remissions, but it is not uncommon
for these patients to continue smoking cigarettes even as
disease progresses to extreme disability and amputation
of their limbs.
Buerger's Disease
 Thrombophlebitis is a common phenomenon in infected
wounds or ulcers and characteristically involves the
superficial veins of the extremities. The affected vein is
firm and cord-like and shows signs of acute inflammation
(pain, redness, warmth, swelling). This type of thrombus
tends to be firmly attached to the vessel wall; they rarely
form emboli.
 Rarely, thrombophlebitis occurs in multiple superficial leg
veins (thrombophlebitis migrans) in patients with visceral
cancers, most commonly pancreatic and gastric cancer
(Trousseau's syndrome). Mucins and other cancer cell
products have been shown to possess thromboplastin-
like activity.
Varicose Veins
 Abnormally dilated and tortuous veins
occur in several sites—in the legs, rectum
(hemorrhoids), esophagus (varices in
portal hypertension), or spermatic cord
(varicocele). They are associated with
increased pressure in the affected vessels,
obstruction to adequate venous drainage,
or increased blood flow in the affected
 In the legs, varicose veins involve superficial saphenous
venous system :
(1) Obstruction to the deep veins of the leg, with the
superficial varicose veins representing the collateral
venous drainage
(2) Incompetence of the valves in the saphenous veins
and in the perforating veins that normally prevent flow of
blood from the deep to the superficial veins.
 Mechanism involving valve incompetence is responsible
for most cases of varicose veins. The cause of valve
incompetence is unknown but is probably a degenerative
Clinical Features
 Varicose veins are visible in the leg as markedly
dilated tortuous veins whose distribution
depends upon which valves are incompetent.
They are associated with obesity and
pregnancy, and there may be a familial
 Varicose veins produce adverse cosmetic
effects and chronic aching and swelling, and
they serve as sites for recurrent
thrombophlebitis, stasis dermatitis, and skin
ulceration. Stasis ulcers typically occur in the
region of the ankle.
Varicose Veins of the legs
 Severe varicosities of
the superficial leg
veins have led to
stasis dermatitis and
 About 70% are present at birth. The skin, liver, and brain are
common sites, but any organ may be involved.
 Hemangiomas composed of well-formed vascular spaces lined by
endothelial cells that show no cytologic atypia.

 Capillary hemangiomas are usually found in the skin and mucous
membranes as small (< 1 cm), red to blue plaques or nodules. Most
grow slowly with the growth of the individual. One specific type
(strawberry hemangioma) grows rapidly during the first few months
of life and then regresses (80% regress completely by 5 years).
 Cavernous hemangiomas occur in skin as well as in the viscera,
forming a soft spongy mass that may reach 2–3 cm in size. They
grow slowly.
Cavernous hemangiomas
 Cavernous lymphangioma (cystic hygroma) :
benign tumor that occurs mainly in the neck in
infancy, causing considerable enlargement of
the neck. It is common in Turner syndrome. The
larger tumors may obstruct delivery through the
birth canal.
 Lymphangiomas also occur in the mediastinum
and retroperitoneum in adults.
 Lymphangiomas can grow to large size, making
complete surgical removal difficult. They do not
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