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Family
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Preview of Understanding Angina & Heart Attacks
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How your heart works
The heart is a muscular pump in the chest which is
constantly working, pumping blood around your body, day and night,
from the cradle to the grave. It contracts and relaxes 100,000 times
a day, and all of this work needs a good blood supply of its own – which
is provided by the coronary arteries.
The basic function of the heart is to pump red blood,
which is rich in oxygen and nutrients, through large arteries to the
rest of the body. When the oxygen has been extracted by the tissues,
veins carry the blood which is now blue and low in oxygen back to the
heart.
There are two sides to the heart, each of which acts as a separate pump.
The two halves are sub-divided into two chambers, four in all. The upper
ones, the atria, act as collecting reservoirs and the lower ones, the
ventricles, contract to pump the blood on. The right side of the heart
receives blood through veins coming from all over the body and pumps
it through the lungs so it can pick up oxygen. The left side collects
blood returning from the lungs and pumps it round the body to the tissues
which need oxygen.
In order to reach all the different organs and muscles,
blood has to be pumped at high pressure, as you will certainly know if
you have ever cut an artery – the blood spurts everywhere! To do
this the heart is very strong and, unlike the muscles in our legs, for
example, it doesn’t become fatigued. The heart muscle does, however,
require a very good blood supply and this is provided by the coronary
arteries and their branches.
Diagram
showing the heart and circulation with veins (blue) draining
the blood back to the heart where it is pumped to the lungs and
back to the rest of the body through the arteries (red). Inset:
diagram of the capillary network in tissues such as skin or muscle,
with oxygen and other nutrients passing through the capillary
walls to the cells. |
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The heart
receives blue ‘deoxygenated’
blood and pumps it through the lungs and then back out, red ‘reoxygenated’,
into the body |
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External
view of the heart. |
Internal
view of the heart. |
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The coronary arteries
The coronary arteries come off the aorta – the
main blood vessel from the heart – just as it leaves the pumping
chamber, the left ventricle, so they are the first arteries to receive
blood high in oxygen. The two arteries, the right and the left, are relatively
small (3–4 mm in diameter). They pass over the surface of the heart,
meeting each other at the back almost forming a circle. When this pattern
of blood vessels was first seen by the ancients, they thought it looked
like a crown and so they used the Latin name we have today – the
coronary arteries.
As these arteries are so important, doctors are familiar
with all their branches and the variations that can arise from one person
to another. The left coronary artery has two main branches, called the
anterior descending and the circum-flex, which in turn have other branches
of their own. It supplies most of the left ventricle which is the more
muscular of the two ventricles because it has to pump blood around the
whole of the body. The right coronary artery is usually smaller and supplies
the underside of the heart and the right ventricle, the chamber that
pumps blood to the lungs.
The coronary arteries are similar in structure to all
other arteries, but are different in one way – blood can only flow
through these vessels into the heart muscle between beats
as it relaxes. While the heart muscle is contracting, the pressure is
too great to allow any blood to pass through the heart muscle itself.
This means that the heart requires a very efficient network of fine blood
vessels within the heart muscle.
In CHD, the coronary arteries become narrowed (rather
like a water pipe becomes ‘furred up’ in a hard water area),
and the heart muscle becomes starved of the blood and oxygen it needs.
At rest this may not matter, but if the heart tries to work harder than
normal – for example, if you walk up stairs – the coronary
arteries may not be able to keep up with the demand for oxygen, and you
get a pain in your chest (see Angina). If you rest for a while, the pain
will usually go away. If a coronary artery becomes completely blocked
by a blood clot, the area of the heart muscle it serves will die (see
Heart attack).
Diagram
of the heart showing the left and right coronary arteries arising
from the aorta and branching over the surface of the heart. |
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Atheroma
Hardening of the arteries, atheroma and atherosclerosis
are all the same thing. When you are born, your blood vessels are flexible
and elastic and the blood can flow through them with ease. Early in adult
life, however, fat deposits can start to form on the walls of the arteries.
They gradually build up, forming lumps which protrude into the middle
of the artery, and so reduce the blood flow.
The extent of these changes and the rate at which they
occur are affected by the level of fat (technically called lipid) in
the blood, especially one called low-density lipoprotein cholesterol,
or LDL for short. People who have high blood levels of LDL cholesterol
are more likely to develop severe atheroma, but some changes may be present
in all of us by the time we reach middle age.
As the patches of atheroma (or plaques) grow, they
thicken and weaken the wall of the artery and progressively reduce the
amount of blood which can flow through it. This process can affect any
organ, so that atheroma of the arteries to the brain can lead to a stroke,
to the limb, gangrene and, to the heart, a heart attack.
The process of hardening of the arteries is curiously
patchy throughout the body, and partic-ularly so in the coronary arteries.
The narrowing can just affect one coronary artery or part of one, or
it can affect the artery throughout its length, and this may be important
in deciding what treatment would suit you best.
In CHD, doctors often talk of one-, two- or three-vessel
disease; this refers to whether the three main branches are affected,
that is to say, the two main branches of the left coronary artery and
the right coronary artery. In general, one- or two-vessel disease may
be treated with medicines or angioplasty, whereas three-vessel disease,
which affects all the major coronary arteries, usually requires bypass
surgery.
Diagram
of blood cells flowing down diseased coronary arteries (seen
from left to right with increasing fat deposits obstructing flow). |
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Thrombosis
Thrombosis is the medical term for a clot, the natural
process that comes into play to stop us bleeding when we injure ourselves.
To stop the blood clotting at the wrong time, we also all have chemicals
circulating in our blood which are natural anticoagulants or blood thinners.
When a blood vessel is damaged, a whole series of chemicals is released
close by, activating the blood and causing it to clot. In the case of
coronary disease, a clot forms, not because of an outside injury, but
as a result of damage to the lining of the artery caused by the fat that
has built up in its wall.
Normally, the lining of our arteries is smooth and
does not provide any focus on which a clot can form. When atheroma develops
the lining is no longer smooth and, where there are breaks in the surface,
small cells from the blood called platelets stick to these breaks and
help to seal them. Providing the breaks are small, no harm results, but
where the artery is critically narrowed even a small clot can have an
important effect on blood flow. We now know that such a process is the
cause of sudden deterioration in angina – so-called unstable angina.
In a heart attack a rather different process is probably
responsible. The fatty deposit in the artery does not just contain fat
but is also surrounded by scar tissue caused by the cholesterol itself.
This forms a fibrous cap over the top of the deposit which is much more
rigid than the rest of the artery. Any sudden stress can cause this cap
to split, creating a wider area of damage to the wall of the artery.
This results in a much larger clot forming, one that usually blocks the
artery altogether. Blood cannot then reach the heart muscle beyond this
clot and so that section of muscle dies.
Thrombosis, then, is one of the central problems in
coronary heart disease. It is the cause of most cases of sudden deterioration
in angina and of most heart attacks. As we shall see, the newer and highly
effective treatments for coronary heart disease work by removing these
clots and preventing their recurrence. We have complex and expensive
drugs which can dissolve a clot in a heart attack, and simple, equally
effective drugs such as aspirin which can prevent them forming in the
first place.
We are trying to find out what factors make some people
more likely to form blood clots than others. An increased tendency to
clot may be one of the as yet undiscovered reasons why we in the UK are
more susceptible to coronary heart disease.
Fat
deposits form on the walls of the artery |
Scar
tissue forms a fibrous cap over the fat deposits |
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The
cap is rigid and splits creating a wider area of damage |
A
large clot forms to seal the damaged area; this blocks the artery |
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Coronary
thrombosis. |
The heart attack
A heart attack is the final result when the diseased
coronary artery becomes completely blocked by a clot, or thrombus. The
heart muscle, or myocardium, beyond the clot is suddenly starved of blood
and oxygen, and becomes painful, a pain that becomes more intense as
the minutes pass. Unless the clot disperses by itself, which doesn’t
often happen, this area of heart muscle dies within 5 to 10 minutes,
resulting in a fully blown heart attack, or myocardial infarction (MI)
to give it its technical name.
The actual size of the heart attack and the amount
of damaged muscle depends on a number of factors. The first is the size
of the artery: the bigger the artery that is blocked the bigger the area
of damage. The second is that the area of damage is generally greater
when other coronary arteries are also diseased. Finally, the size of
the heart attack depends on whether the area of muscle has developed
any collateral blood supply. If other collateral arteries have developed
to supply the threatened area, the resultant damage is much less. Regular
exercise is a good stimulus to the formation of collateral vessels, which
is one reason why it forms such an important part of the treatment programmes
of people with CHD.
The immediate effect of the damage to the muscle, apart
from pain, is that the heart no longer pumps as effectively as before,
and the blood pressure may fall, leading to faintness and sweating or
nausea. The other major problem in the early stages is that the injury
to the muscle causes irregularities of heart rhythm, or cardiac arrhythmias.
These irregularities can be life-threatening and lead to a so-called
cardiac arrest. As a result of the dangers of these arrhythmias, it is
vital that the heart is monitored closely in the first 48 hours or so,
and this is usually carried out in hospitals in cardiac care units (CCUs
for short). Fortunately, such complications are rare after the first
two to three days, and that is when most people can go to the main ward
to recover before going home.
After a heart attack, the body begins to repair the
damage straight away. Cells remove the dead or damaged muscle and fibrous
or scar tissue is formed, a process which takes about six to eight weeks.
The scar itself is strong, but unfortu-nately the heart muscle that has
been lost cannot be replaced and some weakening of the heart is an inevitable
result. For most people with a small heart attack this makes very little
difference to the overall performance of the heart as a pump. If a larger
area of muscle is damaged, however, the heart becomes enlarged, and can
no longer pump effectively, a condition we call heart failure.
The heart
attack: a blocked artery with damaged heart muscle beyond. Some
collateral blood vessels can already be seen supplying the damaged
area. |
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The end result
Heart failure can be caused by many diseases affecting
the heart, especially high blood pressure, but, in this country, CHD
is probably the most common cause. When the heart stops pumping properly,
the lungs become congested with blood, leading to breathlessness. Congestion
of the rest of the body also leads to fluid retention, which makes the
ankles and legs swell. For many years the mainstay of treatment has been
the drugs called diuretics or ‘water tablets’, which get rid
of the excess fluid in the body and lungs. Now, however, we have a new
class of drug called the ACE (angiotensin-converting enzyme) inhibitors
which are even more effective, particularly in reducing the breathlessness.
The other result of the scarring of heart muscle is
that it can interfere with the electrical processes responsible for maintaining
the normal heart rhythm, and so lead to irregularities, or cardiac arrhythmias.
The most common of these is called atrial fibrillation, which is usually
treated with digoxin, an old drug derived from the foxglove. Other irregularities
can be treated with drugs such as beta-blockers – one of the most
useful drugs in CHD – and newer drugs are also now available. See
the Family Doctor book Understanding Heart Failure.
What happens with time
Coronary heart disease is a gradual and unpredictable
condition. The fatty deposits in the arteries may build up very slowly
over the course of 20 or 30 years. For most of this time there are no
symptoms and angina only becomes a problem when one or more of the coronary
arteries narrow by more than 70 per cent and blood flow to that part
of the heart muscle becomes affected.
As the process is so slow the heart can find ways of
overcoming the changes by developing new blood vessels called collaterals.
The coronary arteries in effect form a network of blood vessels around
the heart and, when one is narrowed, one of the other branches expands
to help the area of heart muscle affected.
Although the build-up of coronary atheroma is slow,
a clot can occur at any time. People who experience only occasional angina
may get a sudden worsening of their condition – unstable angina –
or develop a heart attack. Fortunately this doesn’t happen very
often; only about five per cent of people with angina per year experience
such a deterioration.
What is much more worrying is the fact that a heart attack can occur ‘out
of the blue’ in someone who has never been aware that he or she
has a heart condition at all. This can happen because quite a small fatty
deposit, one that causes no real problem in terms of blood flow, can
suddenly split and a clot can block off the artery.
We are now beginning to understand this process rather better and there
are a number of drugs which seem able to stop it happening.
| CASE
HISTORIES |
Arthur, aged 64
Three months ago, Arthur found he was getting a pain in his chest
whenever he walked up stairs or when he walked up the hill
to his home, especially on cold days. His GP told Arthur he
had angina and started him on treatment with a regular anti-anginal
medicine called atenolol – Arthur now feels well again
and has no symptoms.
John, aged 52
John was a keen athlete and ran marathons. His father died
of a heart attack (MI) when he was 64. John had been feeling
quite well, but he collapsed with chest pain and died suddenly
during a 10-mile run. A postmortem examination revealed that
the cause of death was a heart attack. |
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KEY POINTS
- To function as a pump, the heart muscle is critically
dependent on the coronary arteries for a good blood supply
- In CHD, the coronary arteries become narrowed
by fatty deposits or atheroma
- Narrowing of the coronary arteries can starve
the heart muscle of oxygen and this results in the pain of angina
- A heart attack results when a diseased coronary
artery is blocked completely by a clot, and the heart muscle beyond
can die
- After a heart attack the damaged muscle heals
by forming a scar; providing it is not too big complete recovery
can be expected
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