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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
• 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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35,000 deaths from ischemic heart disease (and 3,000 deaths from lung
cancer) annually during the same five-year period.
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.
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.
• 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.