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MYOCARDIAL INFARCTION

INTRODUCTION:-

•  Myocardial infarction (MI) is the most important and feared 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 diminish the myocardial damage is the development of collateral circulation through anastomotic channels over a period of time.
•  A regular and well-planned exercise programme encourages good collateral circulation and improved cardiac performance.

INCIDENCE:-
 In developed countries, acute MI accounts for
10-25% of all deaths. Due to the dominant etiologic role of
coronary atherosclerosis in acute MI, the incidence of acute
MI correlates well with the incidence of atherosclerosis in a
geographic area.

Age:-
 Acute 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 and
dyslipidaemia including familial hypercholesterolaemia.

Sex:-
 Males throughout their life are at a significantly higher
risk of developing acute MI as compared to females. Women
during reproductive period have remarkably low incidence of
acute MI, probably due to the protective influence of oestrogen.
The use of oral contraceptives is associated with high risk of
developing acute MI. After menopause, this gender difference
gradually declines but the incidence of disease among women
never reaches that among men of the same age.

ETIOPATHOGENESIS:-
 The etiologic role of severe coronary
atherosclerosis (more than 75% compromise of lumen)
of one or more of the three major coronary arterial
trunks
in the pathogenesis of about 90% cases of acute MI is well
documented by autopsy studies as well as by coronary angiographic
studies. A few notable features in the development of
acute MI are as under:
1. Myocardial ischaemia Myocardial ischaemia is brought
about by one or more of the following mechanisms:
i) Diminished coronary blood flow e.g. in coronary artery
disease, shock.
ii) Increased myocardial demand e.g. in exercise, emotions.
iii) Hypertrophy of the heart without simultaneous increase
of coronary blood flow e.g. in hypertension, valvular heart
disease.
2. Role of platelets Rupture of an atherosclerotic plaque
exposes the subendothelial collagen to platelets which
undergo aggregation, activation and release reaction. These
events contribute to the build-up of the platelet mass that may
give rise to emboli or initiate thrombosis.
3. Acute plaque rupture In general, slowly-developing
coronary ischaemia from stenosing coronary atherosclerosis of
high-grade may not cause acute MI but continue to produce
episodes of angina pectoris. But acute complications in
coronary atherosclerotic plaques in the form of superimposed
coronary thrombosis due to plaque rupture and plaque
haemorrhage is frequently encountered in cases of acute MI:
i) Superimposed coronary thrombosis due to disruption of
plaque is seen in about half the cases of acute MI. Infusion
of intracoronary fibrinolysins
in the first half an hour of
development of acute MI in such cases restores blood flow in
the blocked vessel in majority of cases.
ii) Intramural haemorrhage is found in about one-third cases
of acute MI.
Plaque haemorrhage and thrombosis may occur together
in some cases.
4. Non-atherosclerotic causes About 10% cases of acute
MI are caused by non-atherosclerotic factors such as coronary
vasospasm, arteritis, coronary ostial stenosis,
embolism,
thrombotic
diseases, trauma and outside compression as
already described.
5. Transmural versus subendocardial infarcts There
are some differences in the pathogenesis of the transmural
infarcts involving the full thickness of ventricular wall and the
subendocardial (laminar) infarcts affecting the inner subendocardial
one-third to half
i) Transmural (full thickness) infarcts are the most common
type seen in 95% cases. Critical coronary narrowing
(more than 75% compromised lumen) is of great significance in
the causation of such infarcts. Atherosclerotic plaques with
superimposed thrombosis and intramural haemorrhage are
significant in about 90% cases, and non-atherosclerotic causes
in the remaining 10% cases.
ii) Subendocardial (laminar) infarcts have their genesis in
reduced coronary perfusion due to coronary atherosclerosis
but without critical stenosis (not necessarily 75% compromised
lumen), aortic stenosis or haemorrhagic shock. This is because
subendocardial myocardium is normally least well perfused
by coronaries and thus is more vulnerable to any reduction
in the coronary flow. Superimposed coronary thrombosis
is frequently encountered in these cases too, and hence the
beneficial role of fibrinolytic treatment in such patients.

TYPES OF INFARCTS :-
Infarcts have been classified in a
number of ways by the physicians and the pathologists:
1. According to the anatomic region of the left ventricle involved,
they are called anterior, posterior (inferior), lateral,
septal and circumferential, and their combinations
like anterolateral,
posterolateral (or inferolateral) and anteroseptal.

2. According to the degree of thickness of the ventricular wall
involved, infarcts are of two types 
i) Full-thickness or transmural, when they involve the entire
thickness of the ventricular wall.
ii) Subendocardial or laminar, when they occupy the inner
subendocardial half of the myocardium.

3. According to, the age of infarcts they are of two types:
i) Newly-formed infarcts called as acute, recent or fresh.
ii) Advanced infarcts called as old, healed or organised.

LOCATION OF INFARCTS:-


Infarcts are most frequently located in the left ventricle. Right ventricle is less susceptible
to infarction due to its thin wall, having less metabolic requirements  and is thus adequately nourished by the thebesian vessels. 
Atrial infarcts, whenever present, are more often in the right atrium, usually accompanying the infarct
of the left ventricle.
Left atrium is relatively protected from infarction because it is supplied by the oxygenated blood in the left atrial chamber.
The region of infarction depends upon the area of obstructed blood supply by one or more of the three coronary arterial trunks.

Accordingly, there are three regions of myocardial infarction:-

1. Stenosis of the left anterior descending coronary artery is the
most common (40-50%). The region of infarction is the anterior
part of the left ventricle including the apex and the anterior
two-thirds of the interventricular septum.
2. Stenosis of the right coronary artery is the next most frequent
(30-40%). It involves the posterior part of the left ventricle
and the posterior one-third of the interventricular septum.
3. Stenosis of the left circumflex coronary artery is seen least
frequently (15-20%). Its area of involvement is the lateral wall
of the left ventricle.