The Heart Essay, Research Paper
CONTENTS
3 Introduction
4 The Human Heart
5 Symptoms of Coronary Heart Disease
5 Heart Attack
5 Sudden Death
5 Angina
6 Angina Pectoris
6 Signs and Symptoms
7 Different Forms of Angina
8 Causes of Angina
9 Atherosclerosis
9 Plaque
10 Lipoproteins
10 Lipoproteins and Atheroma
11 Risk Factors
11 Family History
11 Diabetes
11 Hypertension
11 Cholesterol
12 Smoking
12 Multiple Risk Factors
13 Diagnosis
14 Drug Treatment
14 Nitrates
14 Beta-blockers
15 Calcium antagonists
15 Other Medications
16 Surgery
16 Coronary Bypass Surgery
17 Angioplasty
18 Self-Help
20 Type-A Behaviour Pattern
21 Cardiac Rehab Program
22 Conclusion
23 Diagrams and Charts
26 Bibliography
INTRODUCTION
In today’s society, people are gaining medical knowledge at
quite a fast pace. Treatments, cures, and vaccines for various
diseases and disorders are being developed constantly, and yet,
coronary heart disease remains the number one killer in the
world.
The media today concentrates intensely on drug and alcohol
abuse, homicides, AIDS and so on. What a lot of people are not
realizing is that coronary heart disease actually accounts for
about 80% of all sudden deaths. In fact, the number of deaths
from heart disease approximately equals to the number of deaths
from cancer, accidents, chronic lung disease, pneumonia and
influenza, and others, COMBINED.
One of the symptoms of coronary heart disease is angina
pectoris. Unfortunately, a lot of people do not take it
seriously, and thus not realizing that it may lead to other
complications, and even death.
THE HUMAN HEART
In order to understand angina, one must know about our own
heart. The human heart is a powerful muscle in the body which is
worked the hardest. A double pump system, the heart consists of
two pumps side by side, which pump blood to all parts of the
body. Its steady beating maintains the flow of blood through the
body day and night, year after year, non-stop from birth until
death.
The heart is a hollow, muscular organ slightly bigger than a
person’s clenched fist. It is located in the centre of the chest,
under the breastbone above the sternum, but it is slanted
slightly to the left, giving people the impression that their
heart is on the left side of their chest.
The heart is divided into two halves, which are further
divided into four chambers: the left atrium and ventricle, and
the right atrium and ventricle. Each chamber on one side is
separated from the other by a valve, and it is the closure of
these valves that produce the “lubb-dubb” sound so familiar to
us. (see Fig. 1 – The Structure of the Heart)
Like any other organs in our body, the heart needs a supply
of blood and oxygen, and coronary arteries supply them. There are
two main coronary arteries, the left coronary artery, and the
right coronary artery. They branch off the main artery of the
body, the aorta. The right coronary artery circles the right side
and goes to the back of the heart. The left coronary artery
further divides into the left circumflex and the left anterior
descending artery. These two left arteries feed the front and the
left side of the heart. The division of the left coronary artery
is the reason why doctors usually refer to three main coronary
arteries. (Fig. 2 – Coronary Arteries)
SYMPTOMS OF CORONARY HEART DISEASE
There are three main symptoms of coronary heart disease:
Heart Attack, Sudden Death, and Angina.
Heart Attack
Heart attack occurs when a blood clot suddenly and
completely blocks a diseased coronary artery, resulting in the
death of the heart muscle cells supplied by that artery.
Coronary and Coronary Thrombosis2 are terms that can refer to a
heart attack. Another term, Acute myocardial infarction2, means
death of heart muscle due to an inadequate blood supply.
Sudden Death
Sudden death occurs due to cardiac arrest. Cardiac arrest
may be the first symptom of coronary artery disease and may occur
without any symptoms or warning signs. Other causes of sudden
deaths include drowning, suffocation, electrocution, drug
overdose, trauma (such as automobile accidents), and stroke.
Drowning, suffocation, and drug overdose usually cause
respiratory arrest which in turn cause cardiac arrest. Trauma may
cause sudden death by severe injury to the heart or brain, or by
severe blood loss. Stroke causes damage to the brain which can
cause respiratory arrest and/or cardiac arrest.
Angina
People with coronary artery disease, whether or not they
have had a heart attack, may experience intermittent chest pain,
pressure, or discomforts. This situation is known as angina
pectoris. It occurs when the narrowing of the coronary arteries
temporarily prevents an adequate supply of blood and oxygen to
meet the demands of working heart muscles.
ANGINA PECTORIS
Angina Pectoris (from angina meaning strangling, and
pectoris meaning breast) is commonly known simply as angina and
means pain in the chest. The term “angina” was first used during
a lecture in 1768 by Dr. William Heberden. The word was not
intended to indicate “pain,” but rather “strangling,” with a
secondary sensation of fear.
Victims suffering from angina may experience pressure,
discomfort, or a squeezing sensation in the centre of the chest
behind the breastbone. The pain may radiate to the arms, the
neck, even the upper back, and the pain may come and go. It
occurs when the heart is not receiving enough oxygen to meet an
increased demand.
Angina, as mentioned before, is only temporarily, and it
does not cause any permanent damage to the heart muscle. The
underlying coronary heart disease, however, continues to progress
unless actions are taken to prevent it from becoming worse.
Signs and Symptoms
Angina does not necessarily involve pain. The feeling varies
from individuals. In fact, some people described it as “chest
pressure,” “chest distress,” “heaviness,” “burning feeling,”
“constriction,” “tightness,” and many more. A person with angina
may feel discomforts that fit one or several of the following
descriptions:
- Mild, vague discomfort in the centre of the chest, which
may radiate to the left shoulder or arm
- Dull ache, pins and needles, heaviness or pains in the
arms, usually more severe in the left arm
- Pain that feels like severe indigestion
- Heaviness, tightness, fullness, dull ache, intense
pressure, a burning, vice-like, constriction, squeezing
sensation in the chest, throat or upper abdomen
- Extreme tiredness, exhaustion of a feeling of collapse
- Shortness of breath, choking sensation
- A sense of foreboding or impending death accompanying
chest discomfort
- Pains in the jaw, gums, teeth, throat or ear lobe
- Pains in the back or between the shoulder blades
Angina can be so severe that a person may feel frightened,
or so mild that it might be ignored. Angina attacks are usually
short, from one or two minutes to a maximum of about four to
five. It usually goes away with rest, within a couple of minutes,
or ten minutes at the most.
Different Forms of Angina
There are several known forms of angina. Brief pain that
comes on exertion and leave fairly quickly on rest is known as
stable angina. When angina pain occurs during rest, it is called
unstable angina. The symptoms are usually severe and the coronary
arteries are badly narrowed. If a person suffers from unstable
angina, there is a higher risk for that person to develop heart
attacks. The pain may come up to 20 times a day, and it can wake
a person up, especially after a disturbing dream.
Another type of angina is called atypical or variant angina.
In this type of angina, pain occurs only when a person is resting
or asleep rather than from exertion. It is thought to be the
result of coronary artery spasm, a sort of cramp that narrows the
arteries.
Causes of Angina
The main cause of angina is the narrowing of the coronary
arteries. In a normal person, the inner walls of the coronary
arteries are smooth and elastic, allowing them to constrict and
expand. This flexibility permits varying amounts of oxygenated
blood, appropriate to the demand at the time, to flow through the
coronary arteries. As a person grows older, fatty deposits will
accumulate on the artery walls, especially if the linings of the
arteries are damaged due to cigarette smoking or high blood
pressure.
As more and more fatty materials build up, they form plaques
which causes the arteries to narrow and thus restricting the flow
of blood. This process is known as atherosclerosis. However,
angina usually does not occur until about two-thirds of the
artery’s diameter is blocked. Besides atherosclerosis, there are
other heart conditions resulting in the starvation of oxygen of
the heart, which also causes angina.
The nerve factor – The arteries are supplied with nerves,
which allow them to be controlled directly by the brain,
especially the hypothalamus – an area at the centre of the brain
which regulates the emotions. The brain controls the expanding
and narrowing of the arteries when necessary. The pressures of
modern life: aggression, hostility, never-ending deadlines,
remorseless, competition, unrest, insecurity and so on, can
trigger this control mechanism.
When you become emotional, the chemicals that are released,
such as adrenaline, noradrenaline, and serotonin, can cause a
further constriction of the coronary arteries. The pituitary
gland, a small gland at the base of the brain, under the control
of the hypothalamus, can signal the adrenal glands to increase
the production of stress hormones such as cortisol and adrenaline
even further.
Coronary spasm – Sudden constrictions of the muscle layer in
an artery can cause platelets to stick together, temporarily
restricting the flow of flow. This is known as coronary spasm.
Platelets are minute particles in the blood, which play an
essential role both in the clotting process and in repairing any
damaged arterial walls. They tend to clump together more easily
when the blood is full of chemicals released during arousal, such
as cortisol and others.
Coronary spasm causes the platelets to stick together and to
the wall of the artery, while substances released by the
platelets as they stick together further constrict the blood
vessels. If the artery is already narrowed, this can have a
devastating effect as it drastically reduces the blood flow.
(Fig. 3 – Spasm in a coronary artery)
When people are very tense, they usually overbreathe or hold
their breath altogether. Shallow, irregular but rapid breathing
washes out carbon dioxide from the system and the blood will become
over-oxygenated. One might think that the more oxygen in the blood
the better, but overloaded blood actually does not give up oxygen
as easily, therefore the amount of oxygen available to the heart is
reduced. Carbon dioxide is present in the blood in the form of
carbonic acid, when there is a loss in carbonic acid, the blood
becomes more basic, or alkaline, which leads to spasm of blood
vessels, almost certainly in the brain but also in the heart.
ATHEROSCLEROSIS
The coronary arteries may be clogged with atherosclerotic
plaques, thus narrowing the diameter. Plaques are usually
collections of connection tissue, fats, and smooth muscle cells.
The plaque project into the lumen, the passageway of the artery,
and interfere with the flow of blood. In a normal artery, the
smooth muscle cells are in the middle layer of the arterial wall;
in atherosclerosis they migrate into the inner layer. The reason
behind their migration could hold the answers to explain the
existence of atherosclerosis. Two theories have been developed for
the cause of atherosclerosis.
The first theory was suggested by German pathologist Rudolf
Virchow over 100 years ago. He proposed that the passage of fatty
material into the arterial wall is the initial cause of
atherosclerosis. The fatty material, especially cholesterol, acts
as an irritant, and the arterial wall respond with an outpouring of
cells, creating atherosclerotic plaque.
The second theory was developed by Austrian pathologist Karl
von Rokitansky in 1852. He suggested that atherosclerotic plaques
are aftereffects of blood-clot organization (thrombosis). The clot
adheres to the intima and is gradually converted to a mass of
tissue, which evolves into a plaque.
There are evidences to support the latter theory. It has been
found that platelets and fibrin (a protein, the final product in
thrombosis) are often found in atherosclerotic plaques, also found
are cholesterol crystals and cells which are rich in lipid. The
evidence suggests that thrombosis may play a role in
atherosclerosis, and in the development of the more complicated
atherosclerotic plaque. Though thrombosis may be important in
initiating the plaque, an elevated blood lipid level may accelerate
arterial narrowing.
Plaque
Inside the plaque is a yellow, porridge-like substance,
consisting of blood lipids, cholesterol and triglycerides. These
lipids are found in the bloodstream, they combine with specific
proteins to form lipoproteins. All lipoprotein particles contain
cholesterol, triglycerides, phospholipids, and proteins, but the
proportion varies in different particles.
Lipoproteins
Lipoproteins all vary in size. The largest lipoproteins are
called Chylomicra, and consist mostly of triglycerides. The next in
size are the pre-beta-lipoproteins, then the beta lipoproteins. As
their size decreases, so do their concentration of triglycerides,
but the smaller they are, the more cholesterol they contain. Pre-
beta-lipoproteins are also known as low density lipoproteins (LDL),
and beta lipoproteins are also called very low density lipoproteins
(VLDL). They are most significant in the development of atheroma.
The smallest lipoprotein particles, the alpha lipoproteins, contain
a low concentration of cholesterol and triglycerides, but a high
level of proteins, and are also known as high density lipoproteins
(HDL). They are thought to be protective against the development of
atherosclerotic plaque. In fact, they are transported to the liver
rather than to the blood vessels.
Lipoproteins and Atheroma
The theory is that lipoproteins pass between the lining cells
of the arteries and some of them accumulate underneath. All except
the chylomicra, which are too big, have a chance to accumulate. The
protein in the lipoproteins are broken down by enzymes, leaving
behind the cholesterol and triglycerides. These fats are trapped
and set up a small inflammatory reaction. The alpha particles do
not react with the enzymes are returned to the circulation.
RISK FACTORS
There are several risk factors that contribute to the
development of atherosclerosis and angina: Family history,
Diabetes, Hypertension, Cholesterol, and Smoking.
Family History
We all carry approximately 50 genes that affect the function
and structure of the heart and blood vessels. Genetics can
determine one’s risk of having heart disease. There are many cases
today where heart disease runs in a family, for many generations.
Diabetes
Diabetics are at least twice as likely to develop angina than
nondiabetics, and the risk is higher in women than in men. Diabetes
causes metabolic injury to the lining of arteries, as a result, the
tiny blood vessels that nourish the walls of medium-size arteries
throughout the body, including the coronary arteries, become
defective. These microscopic vessels become blocked, impeding the
delivery of blood to the lining of the larger arteries, causing
them to deteriorate, and artherosclerosis results.
Hypertension
High blood pressure directly injures the artery lining by
several mechanisms. The increased pressure compresses the tiny
vessels that feed the artery wall, causing structural changes in
these tiny arteries. Microscopic fracture lines then develop in the
arterial wall. The cells lining the arteries are compressed and