CARDIOVASCULAR SYSTEM

ANATOMY AND PHYSIOLOGY. The heart is a muscular

pump that ejects blood into the vascular tree with sufficient
pressure to maintain optimal circulation. The average weight of
heart in an adult male is 300-350 gm while that of an adult
female is 250-300 gm. It is divided into four chambers: a right
and a left atrium both lying superiorly, and a right and a left
ventricle both lying

*HEART FAILURE
Heart failure is defined as the pathophysiologic state in
which impaired cardiac function is unable to maintain an
adequate circulation for the metabolic needs of the tissues of the
body. It may be acute or chronic. The term congestive heart
failure (CHF) is used for the chronic form of heart failure in
which the patient has evidence of congestion of peripheral
circulation and of lungs (page 89). CHF is the end-result of
various forms of serious heart diseases.
Heart failure may be caused by one of the following factors,
either singly or in combination
1. INTRINSIC PUMP FAILURE. The most common and
most important cause of heart failure is weakening of the
ventricular muscle due to disease so that the heart fails to
act as an efficient pump. The various diseases which may
culminate in pump failure by this mechanisms are:
 i) Ischaemic heart disease
ii) Myocarditis
iii) Cardiomyopathie
iv) Metabolic disorders e.g. beriber
v) Disorders of the rhythm e.g. atrial fibrillation and
flutter

2. INCREASED WORKLOAD ON THE HEART. Increased

mechanical load on the heart results in increased
myocardial demand resulting in myocardial failure.
Increased load on the heart may be in the form of pressure
load or volume load.

i) Increased pressure load may occur in the following

states:

A) Systemic and pulmonary arterial

hypertension.
b) Valvular disease e.g. mitral stenosis, aortic valve
disease.
c) Chronic lung diseases.
ii) Increased volume load occurs when a ventricle is
required to eject more than normal volume of the
blood
Resulting in cardiac failure. This is found in the
following conditions:
A) Valvular insufficiency
b) Anaemia
c) Thyrotoxicosis
d) Arteriovenous shunts
e) Hypoxia due to lung diseases.
. IMPAIRED FILLING OF CARDIAC
CHAMBERS. Decreased cardiac output and cardiac
failure may result from defect in filling of the heart
as occurs in the following conditions:

i) Cardiac tamponade e.g. haemopericardium,

hydro- pericardium.
ii) Constrictive pericarditis.

Types of Heart Failure

Heart failure may be acute or chronic, right-sided or

left-sided, and forward or backward failure.

ACUTE AND CHRONIC HEART FAILURE.

Depen- ding upon whether the heart failure
develops rapidly or slowly, it may be acute or
chronic.

Acute heart failure. Sudden and rapid

development of heart failure occurs in the following
conditions:
 i) Larger myocardial infarction
ii) Valve rupture
iii) Cardiac tamponade
iv) Massive pulmonary embolism
v) Acute viral myocarditis
vi) Acute bacterial toxaemia.
In acute heart failure, there is sudden reduction in
cardiac output resulting in systemic hypotension but
oedema does not occur and a state of cardiogenic
shock and cerebral hypoxia develops.
Chronic heart failure. More often, heart failure
deve- lops slowly as observed in the following
states:
i) Myocardial ischaemia from atherosclerotic
coronary artery disease
ii) Multivalvular heart disease
iii) Systemic arterial hypertension
iv) Chronic lung diseases resulting in hypoxia and
pulmonary arterial hypertension v) Progression
of acute into chronic failure.
v) ) Progression of acute into chronic failure.
vi) In chronic heart failure, compensatory
mechanisms like tachycardia, cardiac dilatation
and cardiac hyper- trophy try to make
adjustments so as to maintain adequate cardiac
output. This often results in well-maintained
 arterial pressure and there is accumulation of
oedema.

LEFT-SIDED AND RIGHT-SIDED HEART FAILURE. Though

heart as an organ eventually fails as a whole, but functionally,
the left and right heart act as indepen- dent units. From clinical
point of view, therefore, it is helpful to consider failure of the
left and right heart separately. The clinical manifestations of
heart failure result from the accumulation of excess fluid
upstream to the left or right cardiac chamber whichever is
initially affected .
Left-sided heart failure. Left-sided heart failure is initiated by
stress to the left heart. The major causes are:
i) Systemic hypertension
ii) Mitral or aortic valve disease (stenosis)
iii) Ischaemic heart disease
iv) Myocardial diseases e.g. cardiomyopathies, myocar-
ditis.
V) Restrictive pericarditis.

The clinical manifestations of left-sided heart failure

Result from accumulation of fluid upstream in the lungs
And from decreased left ventricular output. Accordingly,
The major pathologic changes are as under:
I) Pulmonary congestion and oedema causing dysp- noea and
orthopnoea .
II) Decreased left ventricular output causing hypo- perfusion and
diminished oxygenation of tissues e.g. in kidneys causing
ischaemic acute tubular necrosis , in brain causing hypoxic
encephalopathy , and in skeletal muscles causing muscular
weakness and fatigue.
Right-sided heart failure. Right-sided heart failure occurs
more often as a consequence of left-sided heart failure.
However, some conditions affect the right ventricle primarily,
producing right-sided heart failure. These are as follows:
i) As a consequence of left ventricular failure.
ii) Cor pulmonale in which right heart failur occur
iii) Pulmonary or tricuspid valvular disease.
iv) Pulmonary hypertension secondary to pulmonary
thromboembolism.
v) Congenital heart disease with left-to-right shunt.
Whatever be the underlying cause, the clinical
manifestations of right-sided heart failure are upstream
of the right heart such as systemic and portal venous
congestion, and reduced cardiac output. Accordingly, the
pathologic changes are as under:
 *CARDIAC HYPERTROPHY AND DILATATION
The heart may undergo compensatory enlargement in the form
of hypertrophy, dilatation, or both, so as to prevent or postpone
heart failure.
Ultimately, however, myocardial reserve capacity to withstand
any further compensatory burden is exceeded and cardiac failure
supervenes that ends in death.
Compensatory Hypertrophy-
Hypertrophy of the heart is defined as an increase in size and
weight of the myocardium. It generally results from increased
pressure load while increased volume load (e.g. valvular
incompetence) results in hypertrophy with dilatation of the
affected chamber due to regurgi- tation of the blood through
incompetent valve. The atria may also undergo compensatory
changes due to increased workload.
The basic factors that stimulate the hypertrophy of the
myocardial fibres are not known. It appears that stretching of
myocardial fibres in response to stress induces the cells to
increase in length. The elongated fibres receive better nutrition
and thus increase in size. Other factors which may stimulate
increase in size of myocardial fibres are anoxia (e.g. in coronary
athero- sclerosis) and influence of certain hormones (e.g.
catecholamines, pituitary growth hormone).
CAUSES. Hypertrophy with or without dilatation may involve
predominantly the left or the right heart, or both sides.
Left ventricular hypertrophy. The common causes of left
ventricular hypertrophy are:
i) Systemic hypertension
ii) Aortic stenosis and insufficiency
iii) Mitral insufficiency
iv) Coarctation of the aorta
v) Occlusive coronary artery disease
vi) Congenital anomalies like septal defects and patent
ductus arteriosus
Vii) Conditions with increased cardiac output e.g. thyro-
Oxicosis, anaemia, arteriovenous fistulae.
Right ventricular hypertrophy. Most of the causes of right
ventricular hypertrophy are due to pulmonary artiral
hypertension. These are:
I)Pulmonary stenosis and insufficiency
II)Tricuspid insufficiency
III) Mitral stenosis and/or insufficiency
III) Chronic lung diseases e.g. chronic emphysema,

COMPENSATORY DILATION
Quite often, hypertrophy of the heart is accompanied by cardiac
dilatation. Stress leading to accumulation of excessive volume
of blood in a chamber of the heart causes increase in length of
myocardial fibres and hence cardiac dilatation as a
compensatory mechanism.
CAUSES. Causes of accumulation of excessive volume of blood
within the cardiac chambers may result in dilatation of the
respective ventricles or both. These are:
i) Valvular insufficiency (mitral and/or aortic insuffi-
ciency in left ventricular dilatation, tricuspid and/or
pulmonary ii) Left-to-right shunts e.g. in VSD
ii) Conditions with ii) Left-to-right shunts e.g. in VSD
iii) Conditions with high cardiac output e.g. thyrotoxi-
cosis, arteriovenous shunt
iv) Myocardial diseases e.g. cardiomyopathies, myocar-
ditis
v) Systemic hypertension. cardiac output e.g. thyrotoxi-
cosis, arteriovenous shunt
Iv) Myocardial diseases e.g. cardiomyopathies, myocar- ditis
V) Systemic hypertension.insufficiency in right ventricular
dilatation)

CONGENITAL HEART DISEASE

Congenital heart disease is the abnormality of the heart
present from birth. It is the most common and important form
of heart disease in the early years of life and is present in
about 0.5% of newborn children. The Inci- dence is higher in
premature infants. The cause of congenital heart disease is
unknown in majority of cases. It is attributed to multifactorial
inheritance involving genetic and environmental influences.
Classification of Congenital Heart Diseases.
1. MALPOSITIONS OF THE HEART
II. SHUNTS (CYANOTIC CONGENITAL HEART
DISEASE)
A. Left-to-right shunts (Acyanotic or late cyanotic group)
1. Ventricular septal defect (VSD) (25-30%)
2. Atrial septal defect (ASD)(10-15%)
3. Patent ductus arteriosus (PDA) (10-20%)

B. Right-to-left shunts (Cyanotic group)

1. Tetralogy of Fallot (6-15%)
2. Transposition of great arteries (4-10%)
3. Persistent truncus arteriosus (2%)
4. Tricuspid atresia and stenosis(1%)

III. OBSTRUCTIONS
 (OBSTRUCTIVE CONGENITAL HEART DISEASE)
1. Coarctation of aorta(5-7%)
2. Aortic stenosis and atresia(4-6%)
3. Pulmonary stenosis and atresia(5-7%) .

ISCHAEMIC HEART DISEASE

Ischaemic heart disease (IHD) is defined as acute or chronic
form of cardiac disability arising from imbalance between the
myocardial supply and demand for oxygenated blood. Since
narrowing or obstruction of the coronary arterial system is the
most common cause of myocardial anoxia, the alternate term
‘coronary artery disease (CAD)’ is used synonymously with
IHD. IHD or CAD is the leading cause of death in most
industrialised countries (about one-third of all deaths) and
somewhat low incidence is observed in the developing
countries. Men develop IHD earlier than women and death rates
are also slightly higher for men than for women until the
menopause.

ETIOPATHOGENESIS

IHD is invariably caused by disease affecting the coronary

arteries, the most prevalent being athero- sclerosis accounting
for more than 90% cases, while other causes are responsible for
less than 10% cases of IHD. Therefore, it is convenient to
consider the etiology of IHD under three broad headings:
i) Coronary atherosclerosis;
ii) Superadded changes in coronary atherosclerosis;
iii) Non-atherosclerotic causes.

MYOCARDIAL INFARCTION
Acute myocardial infarction (MI) is the most important
consequence of coronary artery disease. Many patients may die
within the first few hours of the onset, while remainder suffer
from effects of impaired cardiac function. A significant factor
that may prevent or dimi- nish the myocardial damage is the
development of collateral circulation through anastomotic
channels over a period of time. A regular and well-planned
exercise programme is likely to encourage good collateral
circulation.

INCIDENCE. In industrialised countries, MI accounts for 10-

25% of all deaths. Due to the dominant etiologic role of
coronary atherosclerosis in MI, the incidence of MI correlates
well with the incidence of atherosclerosis in a geographic area.
Age. MI may virtually occur at all ages, though the incidence is
higher in the elderly. About 5% of heart attacks occur in young
people under the age of 40 years, particularly in those with
major risk factors to develop atherosclerosis like hypertension,
diabetes mellitus, cigarette smoking, familial
hypercholesterolaemia etc.

Sex. Males throughout their life are at a significantly

Higher risk of developing MI as compared to females.
Women during reproductive period have remarkably
Low incidence of MI, probably due to the protective
Influence of oestrogen. The use of oral contraceptives
Is associated with high risk of developing MI. After
Menopause, this sex difference gradually declines but
The incidence of disease among women never reaches
That among men of the same age.

HYPERTENSIVE HEART DISEASE

Hypertensive heart disease or hypertensive cardio- myopathy is
the disease of the heart resulting from systemic hypertension of
prolonged duration and manifesting by left ventricular
hypertrophy. Even mild hypertension (blood pressure higher
than 140/90 mm Hg) of sufficient duration may induce
hypertensive heart disease. It is the second most common form
of heart disease after IHD. As already pointed out, hyper-
tension predisposes to atherosclerosis. Therefore, most patients
of hypertensive heart disease have advanced coronary
atherosclerosis and may develop progressive IHD. Amongst the
causes of death in hypertensive patients, cardiac decompensation
leading to CHF accounts for about one-third of the patients;
other causes of death are IHD, cerebrovascular stroke, renal
failure following arteriolar nephrosclerosis, and dissecting
aneurysm of the aorta.
PATHOGENESIS. The pathogenesis of systemic hyper-
tension is discussed later (page 670). Pathogenesis of left
ventricular hypertrophy which is most commonly caused by
systemic hypertension is described here.
Stimulus to hypertrophy of the left ventricle is pressure overload
in systemic hypertension. The stress of pressure on the
ventricular wall causes increased production of myofilaments,
myofibrils, other cell organelles and nuclear enlargement. Since
the adult myocardial fibres do not divide, the fibres are hyper-
trophied. However, the sarcomeres may divide to increase the
cell width.

COR PULMONALE
Cor pulmonale (cor = heart; pulmonale = lung) or pulmo- nary
heart disease is the disease of right side of the heart resulting
from disorders of the lungs. It is charac- terised by right
ventricular dilatation or hypertrophy, or both. Thus, cor
pulmonale is the right-sided counter- part of the hypertensive
heart disease described above. Depending upon the rapidity of
development, cor pulmonale may be acute or chronic:
■ Acute cor pulmonale occurs following massive pulmonary
embolism resulting in sudden dilatation of the pulmonary trunk,
conus and right ventricle.
■ Chronic cor pulmonale is more common and is often preceded
by chronic pulmonary hypertension , The various chronic lung
diseases causing chronic pulmonary hypertension and
subsequent cor pulmonale are:
i) Chronic emphysema;
ii) Chronic bronchitis;
iii) Pulmonary tuberculosis;
iv) Pneumoconiosis;
v) Cystic fibrosis;
vi) Hyperventilation in marked obesity (Pickwickian
syndrome); and
vii) Multiple organised pulmonary emboli.
PATHOGENESIS. Chronic lung diseases as well as diseases
of the pulmonary vessels cause increased pulmonary vascular
resistance and increased pulmo- nary blood pressure (pulmonary
hypertension). Pulmo- nary hypertension causes pressure
overload on the right ventricle and hence right ventricular
enlargement.
Initially, there is right ventricular hypertrophy, but as cardiac
decompensation sets in and right heart failure ensues, dilatation
of right ventricle occurss
PATHOLOGIC CHANGES. In acute cor pulmonale, there is
characteristic ovoid dilatation of the right ventricle, and
sometimes of the right atrium. In chronic cor pulmonale, there is
increase in thickness of the right ventricular wall from its normal
3 to 5 mm upto 10 mm or more. Often, there is dilatation of the
right ventricle too.

RHEUMATIC FEVER AND RHEUMATIC

HEART-
DEFINITION-
Rheumatic fever (RF) is a systemic, post-streptococcal,
non-suppurative inflammatory disease, principally
affecting the heart, joints, central nervous system, skin
and subcutaneous tissues. The chronic stage of RF
involves all the layers of the heart (pancarditis) causing
major cardiac sequelae referred to as rheumatic heart
disease (RHD). In spite of its name suggesting an acute
arthritis migrating from joint to joint, it is now well
known that it is the heart rather than the joints which is
first affected. William Boyd years ago gave the dictum
‘rheumatism licks the joint, but bites the whole heart’.
INCIDENCE
The disease appears most commonly in children between
the age of 5 to 15 years when the streptococcal infection
is most frequent and intense. Both the sexes are affected
equally, though some investigators have noted a slight
female preponderance.
The geographic distribution, incidence and severity of RF
and RHD are generally related to the frequency and
severity of streptococcal pharyngeal infection. The
disease is seen more commonly in poor socio-economic
strata of the society living in damp and overcrowded
places which promote interpersonal spread of the
streptococcal infection. Its incidence has declined in the
developed countries as a result of improved living
conditions and use of antibiotics in streptococcal infec-
tion. But it is still common in the developing countries of
the world like in India, Pakistan, some Arab coun- tries,
parts of Africa and South America.
CLINICAL FEATURES
The first attack of acute RF generally appears 2 to 3 weeks after
streptococcal pharyngitis, most often in children between the
age of 5 to 15 years. With subse- quent streptococcal
pharyngitis, there is reactivation of the disease and similar
clinical manifestations appear with each recurrent attack. The
disease generally pre- sents with migratory polyarthritis and
fever. However, RF has widespread systemic involvement and
no single specific laboratory diagnostic test is available.
Therefore, for diagnosis, the following set of guidelines called
revised Jones’ criteria are followed. These criteria are divided
into major and minor.
A. Major criteria are:
1.Carditis
2.Polyarthritis
3.Chorea (Sydenham’s chorea)
4.Erythema marginatum
5.Subcutaneous nodules
B. Minor criteria are:
1. Clinical findings (arthralgia, fever)
2. Laboratory findings (elevated ESR, raised C-reactive
protein, leucocytosis).

MYOCARDIAL DISEASE
Involvement of the myocardium occurs in three major forms of
diseases already discussed-ischaemic heart disease, hypertensive
heart disease and rheumatic heart disease. There are two other
broad groups of myocardial diseases considered here:
I. Myocarditis i.e. inflammatory involvement of the
myocardium; and
II. Cardiomyopathy i.e. a non-inflammatory myocardial
involvement with unknown (primary) or known
(secondary) etiology.
MYOCARDITIS
Inflammation of the heart muscle is called myocarditis.
MYOCARDITIS
It is a rather common form of heart disease that can occur at any
age. Its exact incidence is difficult to ascer- tain as the
histological examination has been confined to autopsy material
only. Reports from different studies have estimated the incidence
of myocarditis in 1 to 4% of all autopsies.
A number of classifications of myocarditis have been proposed
in the past as follows:
■Interstitial and parenchymatous type, depending upon whether
the inflammation is confined to interstitial tissue or the
parenchyma;
 Etiologic Classification of Myocarditis.
1. INFECTIVE MYOCARDITIS
1. Viral myocarditis
2. Suppurative myocarditis
3. Toxic myocarditis
4. Infective granulomatous myocarditis
5. Syphilitic myocarditis
6. Rickettsial myocarditis
7. Protozoal myocarditis
8. Helminthic myocarditis
9. Fungal myocarditis

III. IDIOPATHIC (FIEDLER’S) MYOCARDITIS

1. Diffuse type
2. Giant cell (idiopathic granulomatous) type

IV. MYOCARDITIS IN CONNECTIVE TISSUE

DISEASES
1. Rheumatoid arthritis
2. Lupus erythematosu
3. Polyarteritis nodosa
4. Dermatomyositis
5. Scleroderma
 V. MISCELLANEOUS TYPES OF MYOCARDITIS
1. Physical agents
2.Chemical aagent
3.Drugs
4.Immunologic agent
5.Metabolic derangements

CARDIOMYOPATHY
Cardiomyopathy literally means disease of the heart muscle but
the term was originally coined to restrict its usage to myocardial
disease of unkown cause. The WHO definition of
cardiomyopathy also excludes heart muscle diseases of known
etiologies. However, the term cardio- myopathy has been
loosely used by various workers for myocardial diseases of
known etiology as well e.g. alcoholic cardiomyopathy, amyloid
cardiomyopathy, ischaemic cardiomyopathy etc. This
controversy is resolved by classifying all cardiomyopathies into
two

Broad groups:
a) Primary cardiomyopathy; and
b) secondary cardiomyopathy i.e. myocardial disease
with nown underlyining cause

Classification of Cardiomyopathies.

1. PRIMARY CARDIOMYOPATHY
1. Idiopathic dilated (or congestive) cardiomyopathy
CARDIOMYOPATH
2. Idiopathic hypertrophic cardiomyopathy
i) Obstructive type
ii) Non-obstructive type
3. Idiopathic restrictive (or obliterative or infiltrative)
cardio- myopathy
1) Cardiac amyloidosis
ii) Endocardial fibroelastosis
iii) Endomyocardial fibrosis
iv) Loeffler’s endocarditis (fibroplastic parietal
endocarditis with peripheral blood
eosinophilia)
II. SECONDARY CARDIOMYOPATHY

1.Nutritional disorders (e.g. alcoholic cardiomyopathy,

beriberi heart disease)
2.Toxic chemicals (e.g. cobalt, arsenic, lithium,
hydrocarbons)
4. Drugs (e.g. emetrine, cyclophosphamide,
adriamycin, catechola- mines)
 5. Metabolic diseases (e.g. cardiac amyloidosis,
haemochromatosis, glycogen storage diseases)
6. Neuromuscular diseases (e.g. Friedreich’s ataxia,
muscular dystrophies)
7. Infiltrations (e.g. leukaemia, carcinomas)
Connective tissue diseases (e.g. rheumatoid arthritis,
lupus
Erythematosus, systemic sclerosis, dermatomyositis)

PERICARDIAL DISEASE
Diseases of the pericardium are usually secondary to, or
associated with, other cardiac and systemic diseases.
They are broadly of 2 types:
I. Pericardial fluid accumulations
II. Pericarditis
PERICARDIAL FLUID ACCUMULATIONS
Accumulation of fluid in the pericardial sac may be watery or
pure blood. Accordingly, it is of 2 types: hydropericardium
(pericardial effusion) and haemo- pericardium.
Pericarditis
• Acute pericarditis refers to inflammation of the pericardial sac.
• Acute pericarditis is the most common disorder involving the
pericardium.
 VALVULAR DISEASES AND DEFORMITIES
Valvular diseases are various forms of congenital and acquired
diseases which cause valvular deformities. Many of them result
in cardiac failure. Rheumatic heart disease is the most common
form of acquired valvular disease. Valves of the left side of the
heart are involved much more frequently than those of the right
side of the heart. The mitral valve is affected most often,
followed in descending frequency, by aortic valve, and
combined mitral and aortic valves. The valvular deformities may
be of 2 types: stenosis and insufficiency. Stenosis is the term
used for failure of a valve to open completely during diastole
resulting in obstruction to the forward flow of the blood.
Insufficiency or incompe- tence or regurgitation is the failure of
a valve to close completely during systole resulting in back flow
or regurgitation of the blood.
The congenital valvular diseases have already been. Described .
Various acquired valvular diseases that may deform the heart
valves are listed below:
1. RHD, the commonest cause
2. Infective endocarditis
3. Non-bacterial thrombotic endocarditis
4. Libman-Sacks endocarditis
5. Syphilitic valvulitis
6. Calcific aortic valve stenosis
 7. Calcification of mitral annulus
8. Myxomatous degeneration (floppy valve syndrome)
9. Carcinoid heart disease.
The major forms of vegetative endocarditis involving the valves
have already been described. Others alongwith the consequences
of these valvular diseases in the form of stenosis and
insufficiency of the heart valves are described below.
MITRAL STENOSIS
Mitral stenosis occurs in approximately 40% of all patients with
RHD. About 70% of the patients are women. The latent period
between the rheumatic carditis and development of symptomatic
mitral stenosis is about two decades.
MITRAL INSUFFICIENCY
Mitral insufficiency is caused by RHD in about 50% of patients
but in contrast to mitral stenosis, pure mitral insufficiency
occurs more often in men (75%). Subsequently, mitral
insufficiency is associated with some degree of mitral stenosis.
AORTIC STENOSIS
Aortic stenosis comprises about one-fourth of all patients with
chronic valvular heart disease. About 80% patients of
symptomatic aortic stenosis are males. It is of 2 main types: non-
calcific and calcific type, the latter being more common.
1. Non-calcific aortic stenosis. The most common cause of non-
calcific aortic stenosis is chronic RHD. Other causes are
 congenital valvular and subaortic stenosis and congenitally
bicuspid aortic valve .
2. Calcific aortic stenosis. Calcific aortic stenosis is the more
common type. Various causes have been ascribed to it. These
include healing by scarring.
AORTIC INSUFFICIENCY
About three-fourth of all patients with aortic insufficiency are
males with some having family history of Marfan’s syndrome.
The characteristic physical findings in a patient of aortic
insufficiency are awareness of the beatings of the heart,
poundings in the head with each heart beat, low diastolic and
high pulse pressure, rapidly rising and collapsing water hammer
pulse (Corrigan’s pulse), booming ‘pistol shoť sound over the
femoral artery, and systolic and diastolic murmur heard over the
femo- ral artery when it is lightly compressed (Durozier’s
■sign). Sometimes, angina pectoris occurs due to increased
myocardial demand or due to coronary insufficiency.
PATHOLOGY OF ANGIOPLASTY AND VASCULAR
GRAFT
Nowadays, with the development of surgical and non- surgical
therapeutic interventions in coronary artery disease, it has been
possible to study the pathology of native as well as grafted
vessel. These include study of coronary artery in balloon
angioplasty and surgically grafted vessel in coronary bypass.
BALLOON ANGIOPLASTY
Balloon angioplasty is a non-surgical procedure that employs
percutaneous insertion and manipulation of a balloon catheter
into the occluded coronary artery. The balloon is inflated to
dilate the stenotic artery which causes endothelial damage,
plaque fracture, medial dissection and haemorrhage in the
affected arterial wall. At this stage, unstable angioplasty is
liable to be associated with acute coronary syndromes
After 3-6 months of angioplasty, 30-40% cases of satisfactorily
dilated vessel lumen are followed by reste- nosis. The restenosis
is multifactorial in etiology that includes smooth muscle cell
proliferation, extracellular matrix and local thrombosis.

VASCULAR GRAFT
Synthetic or autologous grafts are used to replace or bypass
diseased arteries. Most frequently used is autologous graft of
saphenous vein which is reversed (due to valves in the vein) and
transplanted.
For coronary artery bypass graft surgery, the graft may be
reversed saphenous vein or internal mammary artery which is
closest to the operative area of heart. Long-term follow-up of
bypass surgery has yielded following observations on pathology
of grafted vessel:
1. In a reversed saphenous vein graft, long-term lumi- nal
patency is 50% after 10 years. Pathologic changes which
develop in grafted vein include thrombosis in early stage,
intimal thickening and atherosclerosis with or without
complicated lesions.
2. Internal mammary artery graft, however, has a patency of
more than 90% after 10 years.
3. Atherosclerosis may also develop in native coronary artery
distal to the grafted vessel.

TUMOURS OF HEART
Tumours of the heart are classified into primary and
secondary, the latter being more common than the former.

PRIMARY TUMOURS
Primary tumours of the heart are quite rare, found in 0.04%
of autopsies. In decreasing order of frequency, the benign
tumours encountered in the heart are: myxoma, lipoma,
fibroelastoma, rhabdomyoma, haemangioma and
lymphangioma. The malignant tumours are still rarer, the
important ones are: rhabdomyosarcoma, angiosarcoma and
malignant

SECONDARY TUMOURS
Metastatic tumours of the heart are more common than the
primary tumours. About 10% cases with dissemi- nated
cancer have metastases in the heart. Most of these result from
haematogenous or lymphatic spread. In descending order of
frequency, primary sites of origin are: carcinoma of the lung,
breast, malignant lymphoma, leukaemia and malignant
melanoma. Occasionally, there may be direct extension of a
primary intrathoracic tumour such as carcinoma of the lung
into the peri- cardium and into the cardiac chambers.