The Heart Essay Research Paper CONTENTS3

The Heart Essay, Research Paper


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


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


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.


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


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)


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.


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 (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


- 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


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


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.


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.


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 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.


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.


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.


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

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