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About heart attacks

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About heart attacks


A heart attack occurs when the supply of oxygen-rich blood to the heart is
disrupted, usually by a blood clot in one of the coronary arteries that supply
the heart with blood. The heart is composed of a special type of muscle
that never rests and therefore has high oxygen requirements. When the
heart muscle is deprived of oxygen for even a brief period of time, the
myocardial tissue begins to die (infarct). Medically, heart attacks are
known as myocardial infarctions.

Coronary artery disease is the leading cause of heart attacks in the United
States, accounting for more than half of all cardiovascular events in men and
women under the age of 75. Atherosclerosis is the leading cause of coronary
artery disease. Sometimes called "hardening of the arteries,"
atherosclerosis is characterized by fatty plaque deposits that gradually
block arteries, causing them to lose their suppleness. A blood clot can
form after such a plaque deposit ruptures.
Heart attacks can occur both with and without warning signs. Many people
experience episodes of cardiac ischemia before a heart attack. Ischemia
describes a lack of oxygen-rich blood. Ischemia may have no symptoms
(silent ischemia) or it may be accompanied by a type of chest pain known as
angina. In many cases, angina occurs at predictable times, usually during
periods of activity when the heart's oxygen requirements are increased,
such as after exercise. If the angina occurs at irregular or unpredictable
times, and is not associated with exertion, it is known as unstable angina.
This is a dangerous warning sign that a heart attack may be imminent.
Depending upon the severity of the attack and of the subsequent scarring,
as well as how rapidly the person gets access to medical service, a heart
attack can lead to:
• Full recovery, occurring in the majority of patients

• Heart failure, a chronic condition in which at least one chamber of


the heart is not pumping well enough to meet the body’s demands
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• Electrical instability of the heart, which can cause a potentially


dangerous abnormal heart rhythm (arrhythmia)

• Cardiac arrest, in which the heart stops beating altogether, resulting


in sudden cardiac death in the absence of immediate medical attention

• Cardiogenic shock, a condition in which damaged heart muscle cannot


pump normally and enters a shock-like state that is often fatal

• Death
The location of the damage in the heart muscle is also important. Different
coronary arteries supply different areas of the heart, thus the severity of
the damage depends upon which artery was blocked, the extent of the
blockage and how much of the heart muscle depended on that blocked
artery.
A heart attack is not the same thing as cardiac arrest, even though many
people use the terms interchangeably. Cardiac arrest occurs when the
heart actually stops beating and pumping blood. It is usually caused by an
abnormal heart rhythm that causes the heart's main pumping chambers
(e.g., ventricles) to quiver and contract irregularly (ventricular fibrillation).
The term “massive heart attack” is also mistakenly used to describe
cardiac arrest, but they are not the same thing. A heart attack may lead
to cardiac arrest, but these are separate events.

This invention relates to methods and products to abate coronary artery blockage in
men and in women. These methods include administering a combination of natural
hormones, including human growth hormone or recombinant human growth
hormone, one or more sex hormones, such as testosterone, estrogen or
progesterone and other naturally occurring hormones, as appropriate.
The methods and products of this invention are disclosed in part in U.S. Pat. No.
5,855,920, issued Jan. 5, 1999, entitled TOTAL HORMONE REPLACEMENT
THERAPY. The entire text of the '920 patent is incorporated herein by this reference.
However, in abating coronary artery blockage in men and women, the methods of
this invention additionally call for administering sufficient T3 thyroid supplement to
maintain the body temperature of males and females with such blockage above
about 97.6.degree. F. upon awakening, and is in the range of about 98.7.degree. F. to
about 99.0.degree. F. during the afternoon hours. In addition, in treating males with
coronary artery blockage, and with below optimal testosterone levels, these methods
call for administering natural testosterone in gel form, preferably applied topically to
under arm pits.
In treating a human male or female subject who has blockage of coronary arteries, a
treating physician preferably obtains the subject's records, including, where available,
MRI, CAT scan, angiogram and all other pictorial and visual documentation of the
blockage. The treating physician then measures the subject's total cholesterol, HDL,
LDL, and triglyceride levels, and the subject's hormones in terms of growth hormone
level as reflected through IGF-1 level, melatonin level, thyroid hormone level, thymus
hormone level, adrenal hormone of DHEA level and pregnenolone level, and the
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subject's sex hormone(s) level (in males, testosterone; in females, progesterone and
estrogen).
In treating males or females presenting with coronary artery blockage, all of these
hormones, if below optimal levels, would be administered to increase their
bloodstream levels to optimal, as that term is used in the '920 patent. In addition, in
male human subjects requiring testosterone supplement, testosterone would be
administered in natural form, i.e. in gel form, not in synthetic form, such as
testosterone types with prefixes or suffixes.
In both male and female human subjects, the hormones administered include
sufficient T3 thyroid supplement, in addition to the regular T4 and T3 thyroid
supplements, to insure that the subject's body temperature is at or above about
97.6.degree. F. upon awakening, and is in the range of about 98.7.degree. F. to about
99.0.degree. F. during afternoon hours.
The treatment continues until the coronary artery blockage has abated, as
determined by tests such as MRI, CAT scan and/or angiogram
Role of atherosclerosis in heart attacks
Atherosclerosis is the single most deadly disease in the United States. At one
time, researchers used to think of arteries as roughly analogous to
plumbing pipes. In recent years, however, our understanding of arteries,
and arterial disease, has been greatly enhanced. In fact, arteries are
muscular organs that contract along with the heart to enhance blood flow
and help maintain blood pressure.
Arteries are highly sensitive to a number of chemicals and hormones that
help regulate their function. These chemicals act upon, and are sometimes
excreted by, the inner lining of the artery, or the endothelium. Researchers
have learned that long before atherosclerosis becomes clinically apparent,
this thin layer of cells has already been damaged and the earliest plaque
deposits have already formed. Indeed, atherosclerosis often begins in
early childhood, and it rarely is limited to the coronary arteries. In most
cases, if a person has atherosclerotic plaque deposits in their coronary
arteries, other arteries are also affected.
The underlying defect, or cause, of atherosclerosis often remains
unknown. However, researches have made great strides forward in
understanding the process by which damage to the endothelial cells early
in life can later evolve into a heart attack as an adult. It is now thought
that the atherosclerotic process is mediated by immune-related
inflammation. LDL cholesterol molecules also play an important role in the
development of atherosclerosis.
According to this theory, arteries are damaged, which provokes a local
immune response at the site of the injury. White blood cells gather at the site
of the injury and begin to secrete chemical messengers that cause
inflammation. This is a normal immune system reaction that occurs in an
inappropriate place. At the same time, the protective endothelial layer has
been compromised, allowing LDL "bad" cholesterol cells to migrate into
the inner layer of the artery. This further aggravates the injury, which
causes more white blood cells to gather. Other fatty materials in the
bloodstream (e.g., triglycerides) also begin to gather at the injury. Together,
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these materials combine to form a lipid foam. This foam forms fatty
streaks.

Over time, these fatty streaks grow larger, eventually attracting circulating
blood platelets and evolving into plaque deposits on the inside of the artery
wall. Not all plaque deposits pose the same threat. Some plaque deposits
develop a relatively hard "shell" of minerals in a process called calcification.
These types of plaque are considered to be stable plaques. They are less
likely to rupture and cause a heart attack. Other types of plaque are known
as unstable plaques, which, in comparison to stable plaques, have the
following:
• A larger fatty core
• More white blood cells encased within
• A thinner, softer, more unpredictable coating that might be stripped
off without warning
The exact trigger of a plaque rupture is unknown. However, it can occur as
a result of a strong, fast blood flow, especially during heavy exertion or
emotional stress, when the coating is thin and the core of fat/white blood
cells is particularly full.
During a plaque rupture, the fatty core of the plaque deposit is exposed to
circulating blood, while pieces of the plaque travel downstream into the
artery. At this point, several different events might occur. The site of the
plaque rupture might attract platelets, which start a clotting cascade and
form a blood clot (thrombosis). This blood clot may grow big enough to
obstruct blood flow. Alternatively, it may break off and travel down the
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artery until it becomes lodged in a smaller


artery. Finally, the pieces of the plaque may
themselves become trapped in an artery,
blocking blood flow. Any of these scenarios
results in a heart attack. The severity of the
attack will depend on which coronary artery is
blocked, how dependent the heart muscle was
on that source of blood supply and the extent
of the blockage.
Researchers have found that almost 80
percent of first-time heart attack patients had ruptured plaque located
both where the heart attack occurred and at other, distant sites.
Researchers concluded that a heart attack is often not the result of one,
discrete area of plaque damage. It may be separate areas of plaque
rupture that combine to make the heart less stable and therefore
vulnerable to a heart attack, a concept known as (pancoronaritis).

Heart attacks may also be caused by a coronary artery spasm, a temporary


constriction of an artery in the heart.
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Signs and symptoms of heart attacks
Just as some people experience no symptoms during silent ischemia, some
people can have a silent heart attack without knowing it. Up to 25 percent
of heart attacks are symptom-free. The absence of symptoms,
however, does not mean the absence of damage to the heart muscle.
Unfortunately, people having a silent heart attack are unaware that they
need to seek proper treatment immediately, and additional heart-related
events or damage may occur.

The majority of people who suffer a heart attack experience symptoms


that are often severe and frightening. Recognizing these symptoms and
realizing their importance is crucial. The vast majority (90 percent or
more) of heart attack-related deaths in patients under age 55 occur
outside of the hospital. Medical experts believe this is often due to the
patient's lack of recognition of the situation. Younger people tend to
ignore symptoms, whereas an older person may be more willing to call 9-
1-1 at the first sign of trouble. Whatever the case, the sooner the
symptoms of a heart attack are recognized and appropriate treatment is
administered, the better the outlook for survival – both in the near future
and over the long term. Symptoms of a heart attack may include:
• Chest pain that is unrelieved by rest and often spreads or radiates
through the upper body to the arms, neck, shoulders or jaw

• Chest-area pressure, discomfort or squeezing sensation that may


be either constant or intermittent

• Shortness of breath or shallow breathing


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• Heart palpitations, in which the heartbeat is fast, strong or obviously


irregular

• Abnormally weak and/or fast pulse

• Fainting (syncope) or loss of consciousness

• Feeling tired or fatigued

• Sweating, often with heavy chills

• Nausea or upset stomach

• Gray facial color


Women tend to have different heart attack symptoms than men. Although
they may experience shortness of breath, weakness, unusual fatigue and
cold sweats, they may not experience chest pain. They may instead feel
pain high in the abdomen or chest, or in the back, neck or jaw. They may
also experience dizziness. Many women have reported symptoms of unusual
fatigue, sleep disturbances, shortness of breath, indigestion and anxiety in
the weeks leading up to their heart attack.
Although one or a combination of these symptoms may indicate the onset
of a heart attack, they may be due to other conditions as well. As a
general rule, it is better to be safe than sorry. If a heart attack is
suspected and any of these symptoms are present, this may indeed be a
sign of a serious lack of oxygen-rich blood supply to the heart. Emergency
medical help should be sought immediately. Physicians usually advise
stricken individuals to first call 9-1-1, then to chew an aspirin (“regular”
aspirin, not non-aspirin pain relievers such as acetaminophen) and wash it
down with a glass of water while waiting for help to arrive.

Prevention methods for heart attacks


Risk factor modification is a major goal of prevention, both for first attacks
and repeat heart attacks. Patients are urged to reduce behaviors that are
associated with heart attack, such as smoking, and adopt healthy lifestyle
habits that have been shown to prevent heart attacks, such as exercising
and eating a heart-healthy diet. By altering these risk factors, it may be
possible to slow the progression of atherosclerosis, which is the leading
cause of heart attacks.
The American Heart Association (AHA) recommends that people have their
blood pressure, body mass index (BMI), waist circumference and pulse checked at
least every two years, beginning at age 20. Cholesterol tests and glucose tests
are to be checked at least every five years. Such risk factors, according to
the AHA, can be used to estimate the risk of developing heart disease within
a 10-year period.

Specific recommended changes include:


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• Improving your cholesterol ratio. A person’s total cholesterol level


(which includes LDL cholesterol, HDL cholesterol and triglycerides)
should be no more than 200 milligrams per deciliter and no more
than five times the HDL level. Key strategies for reducing levels of
total cholesterol, LDL cholesterol and triglycerides are to eat a
heart-healthy diet and to exercise regularly. If these strategies do
not reduce total cholesterol levels, a physician may prescribe
cholesterol-reducing drugs (e.g., statins). Strategies for increasing levels
of HDL cholesterol include eating monounsaturated fats in moderation,
decreasing the amount of saturated fat, limiting alcohol use and
starting an exercise program.

• Exercising regularly. Exercise can be an excellent tool in the both


prevention of heart disease and improving quality of life for heart
patients. Physically, it can slow or even reverse the process of
atherosclerosis, as well as lower blood pressure and reduce
cholesterol levels. Emotionally, it can reduce levels of stress and
depression.

• Achieving and maintaining a healthy weight. Obesity and being


overweight are major risk factors for a host of serious health
conditions, including coronary artery disease, high blood pressure, diabetes,
heart attack and stroke. Some weight control methods include
limiting calories, increasing activity, counseling, medication and
surgical interventions.

• Eating a heart-healthy diet. Modern research has consistently


supported the idea that health is largely determined by what people
choose to eat. Certain B-vitamins and minerals have been shown to be
helpful to heart health. Omega-3 fatty acids found in certain fish (e.g.,
tuna, salmon and sardines) may keep arteries healthy and elastic.
Saturated fats and tropical oils (palm and coconut oil), however, have
been shown to be harmful, because they can speed up the
development of coronary artery disease, atherosclerosis and
obesity. Trans fat, in particular, has been linked to damage to the
heart.

• Quitting smoking and avoidnig all second–hand smoke. Tobacco


smoking is a major cause of coronary artery disease and cardiac
arrest. According to the United States Centers for Disease Control and
Prevention (CDC), from 1995 to 1999, nearly 450,000 people in the
United States died prematurely from smoking. Of these, nearly
150,000 deaths were attributed to cardiovascular diseases and
nearly 125,000 were attributed to lung cancer. The CDC also
estimates that second–hand smoke was responsible for more than
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35,000 deaths from ischemic heart disease (and 3,000 deaths from lung
cancer) annually during the same five-year period.

• Controlling blood pressure. Individuals with high blood pressure


(hypertension) are at greater risk of heart attack and other
problems resulting from cardiovascular disease. Current research
suggests that hypertension can bring on changes in genes involved in
heart function. This contributes to a process known as remodeling,
where there is enlargement and weakening of the heart’s left
ventricle (left ventricular hypertrophy). Cells involved in heart muscle
contraction become impaired and eventually self-destruct, leading
to heart failure. Hypertension can be controlled through taking blood
pressure medications, self-monitoring, eating a heart-healthy, low-
salt diet, and engaging in regular exercise. People are also
encouraged to have regular check-ups with their physician.

• Controlling diabetes. People with diabetes may be more likely to


develop heart-related diseases. Good glucose control is essential for
all diabetics, as well as weight loss and a healthy diet. All type 1
diabetics will require insulin therapy, while type 2 diabetics can be
treated with a number of additional medications that help control
glucose levels. Non-insulin drugs used to treat type 2 diabetes
include metformin and acarbose.

• Learning and practicing stress management techniques. Stress,


excessive anger and fatigue can lead to high-risk practices such as
overeating, smoking, high blood pressure (hypertension) and a lack
of exercise. In addition, chronic stress may be a direct contributor to
poor heart health because it produces increases in blood pressure
that could become permanent. Anxiety has also been linked to an
increased risk for future health problems in men who have suffered
a heart attack.

• Avoiding high levels of homocysteine by getting enough B-vitamins.


There is considerable debate over the role of homocysteine in heart
disease. Homocysteine is an amino acid that is produced as a
byproduct of other chemical reactions in the body. Numerous
studies have shown that people with elevated homocysteine are at
greater risk for heart attack, stroke and other cardiovascular
problems. However, researchers have been unable to determine if
elevated homocysteine levels are caused by heart disease, or if
they cause heart disease. Also, two large, well-designed studies
have recently shown that moderately lowering homocysteine among
people with diabetes and existing heart disease had no effect on
lowering risk for cardiovascular events.

At this point, the AHA has not identified elevated homocysteine as a


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major risk factor for heart disease and does not recommend
widespread use of folic acid and vitamin B supplements to lower
homocysteine. However, because of the association between
homocysteine and heart disease, people are advised to obtain these
important nutrients through a healthy diet that includes fruits,
vegetables, whole grain and fortified grain products. Additionally,
people who have a family history or personal history of heart
disease but lack other well-defined risk factors, such as smoking or
obesity, should consider monitoring their homocysteine levels. In
the event of elevated homocysteine (above 15 mmol/L),
supplementation to lower homocysteine should only be done under
the supervision of a physician to ensure the patient's safety. Folate
supplements, for example, may mask a true vitamin B-12
deficiency. In addition, studies find that these supplements may
increase the risk of artery re-narrowing (restenosis) following
revascularization procedures such as balloon angioplasty and stenting.

• Recognizing and treating chronic depression. Depression has been


linked with a higher risk of developing high blood pressure, heart
disease and having a heart attack. Depression is associated with
heart disease in several ways, including a risk of abnormal heart
rhythms (arrhythmias), alteration of the amount of blood flowing to
the coronary arteries, increased risk of blood clots (“sticky” platelets), and
increased risk of sudden cardiac death. A recent study of the anti-
depressant drug sertraline found that it was a safe and effective
therapy in patients having a recent heart attack or unstable angina.
It has also been shown to have anti-clotting properties.
There is a great deal of information in the media about different vitamins,
mineral, nutrients and other substances and their supposed affect on
heart health. For instance, there are conflicting reports on whether high
doses of vitamin E can protect arteries and prevent heart attacks and
strokes, or whether high doses of vitamin E can actually damage the
heart. Aspirin therapy, which may be prescribed for a patient after a heart
attack, has also been touted as way to prevent a first heart attack. While
recent research supports the theory, there are risks to the regular use of
aspirin, including gastrointestinal bleeding. Patients with no history or
significant risk of heart disease should discuss with their physician if the
risks associated with aspirin outweigh the potential benefits.

It is unfortunate that up to two-thirds of post-attack patients do not make


lifestyle changes. It is estimated that up to one-third of fatal heart attacks
could be prevented with the proper pre-attack medical treatments and
lifestyle modifications. Even after one heart attack, the chances of
avoiding future attacks can be increased with appropriate preventive care.
People who have had a heart attack, or are at risk of having one, are
encouraged to remember that their lifestyle choices can have a major
impact on their heart health. Patients should always consult their
physicians before making any changes to their diet or activity levels.
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Much attention has also been given to the possible benefits of moderate
alcohol consumption in lowering the risk of heart attacks and heart
disease in general At this point, medical experts do not recommend that
non-drinkers begin drinking alcohol for better cardiovascular health.
Research is still being done to clarify the relationship between alcohol and
the heart. However, findings in recent years have suggested that
moderate alcohol consumption may offer some people a degree of
protection against heart disease. Moderate drinking is defined as no more
than one drink per day for women and no more than two drinks per day
for men. One drink is equal to the following: 12 ounces of beer or wine
cooler, 5 ounces of wine or 1.5 ounces of 80-proof liquor.

Patients should discuss alcohol consumption with their physicians. In


general, patients should follow established, proven wellness strategies.
The earlier in life a patient modifies his or her habits, the better the
chances of lowering or even eliminating certain risk factors for heart
attack.
Diagnosis methods for heart attacks
When a patient has symptoms of a heart attack, the physician will promptly
evaluate the patient’s medical history and run tests such as:
• Electrocardiogram (EKG). A recording of the heart’s electrical activity
as a graph, or series of wave lines, on a moving strip of paper or
video monitor. The highly sensitive electrocardiograph machine
helps detect heart irregularities, disease and damage by measuring
the heart’s rhythms and electrical impulses.

• Blood tests. These can be used to detect the presence of certain


markers that are released following a heart attack. These include
troponin, myoglobin, creatine phosphokinase (CPK) and creatine kinase MB.
Once the patient is stabilized, the final diagnosis of whether the patient
actually had a heart attack can take several days. Tests that may be run
during this time include:
• Radionuclide imaging. A branch of nuclear medicine that introduces
small, harmless amounts of radioactive materials (“tracers”) into the
body. A special gamma camera is then used to scan the radioactive
tracers and create visual images of the heart.
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• Echocardiogram of the heart. This test uses sound waves to track the
structure and function of the heart. A moving image of the patient’s
beating heart is played on a video monitor, allowing the physician to
study the heart’s thickness, size and function. The image also
shows the motion pattern and structure of the four heart valves.
During this test, a Doppler ultrasound may also be done to evaluate
blood flow within the heart, revealing any potential leakage
(regurgitation) or narrowing (stenosis) of the heart valves.