It was a cold Saturday night in middle class America. Bob had
spent most of the day working in the yard, and watching his favorite
college football team play their annual rivalry game. It seemed to
Bob that this was a good departure for the never ending pressure
at work. Bob and his lovely wife Jan enjoyed eating out every Saturday
night and were regulars at their favorite high cholesterol eatery. After
a large meal Bob and Jan returned home an were relaxing when Bob
started to experience severe chest pains and was rushed to the ER.
Bob was examined, test were run, and then suddenly the pain started
to subside. The doctor then told Bob he had been a victim of Angina!
Bob was initially pleased, but the doctor quickly dashed his enthusiasm
by explaining that Angina can be a leading indicator of a heart attack.
So what is Angina and what can be done to avoid this condition?
Angina is recurring chest pain that originates under the
breastbone or sternum, often spreading to the neck, jaw,
arms, and upper back. The nature of the pain varies, but
it is usually described as a sensation of pressure, tightness,
heaviness, or choking, and it is often accompanied by shortness
of breath. Severe angina may feel like a heart attack, but it is a
temporary condition that does not cause permanent damage.
It does, however, signal increased risk of heart attack.
Angina occurs when the heart muscle is not getting enough oxygen.
The most common cause is atherosclerosis, a narrowing of the coronary
arteries due to deposits of fatty plaque. The narrowed arteries may be
able to deliver enough oxygen rich blood to the heart muscle to carry
on normal activities. But when the heart must work harder, such as
during unaccustomed physical exertion or periods of stress, the heart
muscle becomes starved for oxygen, a condition called ischemia.
A heavy meal or exposure to cold may also precipitate angina because
blood flow is diverted from the coronary arteries to other parts of the body.
Some people experience angina while resting or even sleeping. This
unprovoked, or variant, angina is sometimes caused by spasm in the
coronary artery, usually at the site of fatty deposits. More often, it is
classified as unstable angina, and is a warning sign of impending heart
attack.
Other Causes of Chest Pain
Indigestion, esophageal spasms, heartburn, and panic attacks are
among the many non-cardiac causes of chest pains. An overactive
Thyroid, or hyperthyroidism, can also cause irregular heart beats
and chest pain. Pericarditis, an inflammation of the sac surrounding
the heart, should be ruled out, as should structural problems, such
as a broken rib. Asthma, a collapsed lung, and other pulmonary
disorders can also produce shortness of breath similar to that
of angina.
Diagnosis
There is no specific test for angina, but a doctor can usually tell whether
or not the pain arises from the heart by asking three key questions: What
provokes the discomfort? What is it like? And what alleviates it? Angina
is suspected when there are other cardiovascular risk factors, such as
cigarette smoking, a family history of heart attack, elevated blood pressure
and cholesterol levels, diabetes, and so on. During a physical examination,
the doctor listens carefully to the heart for any abnormal sounds or beats.
Routine tests include an electrocardiogram (ECG), blood pressure
measurement, blood and urine tests, and a chest X-ray. If the doctor
suspects angina, additional tests may be ordered to evaluate any chance
of heart disease or a hidden heart condition.
An exercise stress test can usually confirm that physical exertion brings on
ischemia. The test is sometimes combined with echocardiography, examination
using high frequency sound waves, or nuclear scanning, in which thallium or
another radioactive substance is injected into the blood stream and then
tracked by special gamma cameras. These last two tests can often pinpoint
the areas of heart muscle that are deprived of blood.
A more invasive procedure, cardiac catheterization, is needed to make a
precise diagnosis of coronary artery disease. In the examination, a thin,
flexible tube is inserted into an artery in the leg (or less commonly, in the arm)
and threaded to the heart. A dye is then injected into the coronary arteries to
make them visible on X-rays.
Natural Therapies for Angina
From a natural point of view, there are two primary remedial goals in the
treatment of angina:
* Improving the blood supply to the heart
* Improving energy metabolism within the heart
These goals are linked, because increased blood flow means improved
energy metabolism and vice versa. The treatment goals are best
accomplished by a careful blend of nutrition (e.g., carnitine, pantethine,
CoQ10, and magnesium) and herbs like hawthorn and khella which improve
the delivery and utilization of oxygen to the heart muscle. In severe cases,
EDTA chelation therapy may be a fitting alternative to angioplasty or
coronary bypass.
Carnitine, CoQ10, Pantethine, Magnesium, Hawthorne, Khella,
and Chelation Therapy
The heart utilizes fats as its major metabolic fuel. It converts free fatty acids
into energy, much as an automobile uses gasoline. Defects in the use of fats
by the heart greatly increase the risk of atherosclerosis, heart attacks, and
angina pains. Explicitly impaired utilization of fatty acids by the heart results
in accumulation of high concentrations of fatty acids within the heart muscle.
This then makes the heart extremely vulnerable to cellular damage, which
in the end leads to a heart attack.
Carnitine, pantethine, and coenzyme Q10 are essential compounds in
the normal metabolism of fat and energy; they are of extreme benefit to
sufferers of angina. These nutrients help avert the accumulation of fatty
acids within the heart muscle by improving the conversion of fatty acids
and other compounds into energy.
Carnitine: Carnitine is a vitamin like compound that stimulates the breakdown
of fats by the mitochondria – the energy producing units in cells. Carnitine is
essential in the transport of fatty acids into the mitochondria, thereby reducing
energy production.
Normal heart function is significantly dependent on adequate concentrations
of carnitine. While the normal heart stores more carnitine than it needs, if the
heart does not have a good supply of oxygen, carnitine levels quickly decrease.
This leads to decreased energy production in the heart and increased risk of
angina and heart disease. Since angina patients have a decreased supply of
oxygen, carnitine supplementation makes a lot of sense.
In several clinical trials carnitine has shown a propensity to relieve angina and
heart disease. Supplementation with carnitine normalizes heart carnitine levels
and allows the heart muscle to utilize its limited oxygen supply more efficiently.
In cases of angina treated with carnitine, improvements have been noted in
exercise tolerance and heart function. The results indicate that carnitine is a
valuable alternative to drugs in the treatment of angina.
In one study of patients with angina, oral administration of 900 mg of
L-carnitine increased mean exercise time and the time necessary for
abnormalities to occur during a stress test (6.4 minutes in the placebo
group, compared to 8.8 minutes in the carnitine treated group).
These results indicate that carnitine may be an effective alternative to
other anti-anginal agents, such as bet blockers, calcium channel
antagonists, and nitrates, especially in patents with chronic angina.
Carnitine, by improving fat metabolism and thereby increasing energy
production in the heart muscle, may also prevent the production of toxic
fatty acid metabolites (products of metabolism). These compounds are
extremely harmful to the heart and are thought to contribute to impaired
heart muscle contractility, increased susceptibility to irregular beats, and
eventual death of heart tissue. Supplemental carnitine increases heart
carnitine levels and prevents the production of toxic fatty acid metabolites.
In a clinical trial, early administration of L-carnitine (40 mg/kg/d) in heart
attack patients was found to significantly reduce heart damage.
Pantethine: Pantethine is the stable form of pantetheine, the active form
of pantothenic acid, which is the fundamental component of coenzyme A
(CoA). CoA is involved in the transport of fatty acids to the mitochondria
and to and from cells. The pathway of synthesis form pantethine to CoA
is much shorter than that from pantothenic acid to CoA, making pantethine
the preferred therapeutic substance. In addition, pantethine has significant
lipid lowering activity, while pantothenic acid has very little (if any) effect in
lowering cholesterol and triglyceride levels.
Pantethine acts by inhibiting cholesterol synthesis and accelerating fatty
acid breakdown in mitochondria. The standard dose of pantethine is 900
mg per day. Like carnitine, it has been shown in clinical trials to significantly
reduce serum triglyceride and cholesterol levels, while increasing HDL-
cholesterol levels, while increasing HDL cholesterol levels. Its lipid lowering
effects are most impressive when its toxicity (virtually none) is compared to
that of conventional lipid lowering drugs.
Pantethine is well indicated for treating angina. Like carnitine, heart
pantethine levels decrease during times of reduced oxygen supply.
Demonstrated effects in animals further indicate that pantethine
would greatly benefit individuals with angina.
Coenzyme Q10: Coenzyme Q10 (CoQ10), also known as ubiquinone, is an
essential component of the mitochondria, where it plays a major in energy
production. Like carnitine and pantethine, CoQ10 can be synthesized within
the body. Nonetheless, deficiency states have been reported. Deficiency can
result from impaired CoQ10 synthesis due to nutritional deficiencies, from a
genetic or acquired defect in CoQ10 synthesis, or from increased tissue
needs. In addition, may of the elderly may have increased CoQ10 requirement;
the decline of CoQ10 levels that occurs with age may be partly responsible for
the age related deterioration of the immune system.
One of the most metabolically active tissues in the body, the heart may be
unusually susceptible to the effects of CoQ10 deficiency. Accordingly,
CoQ10 has shown great promise in the treatment of heart disease.
CoQ10 deficiency is widespread among individuals with heart disease. Heart
tissue biopsies in patients with various heart diseases showed a CoQ10
deficiency in 50 to 70% of cases. Furthermore, cardiovascular disease,
including angina, hypertension, mitral valve prolapse, and congestive
heart failure, require increased tissue levels of CoQ10. In one study,
twelve patients with stable angina pectoris were treated with CoQ10
(150 mg/day for four weeks). The occurrence of anginal attacks was
reduced by 53% compared to the placebo group. In addition, there was a
noteworthy increase in treadmill exercise tolerance (time to onset of chest
pain and time to development of electrocardiogram abnormalities) during
CoQ10 treatment. The results of this study and others imply that CoQ10
is a safe and effective treatment for angina pectoris.
Carnitine, pantethine, and coenzyme Q10 should be considered in all heart
disorders, not just angina.
Magnesium: Magnesium deficiency plays a major role in angina, especially in
Prinzmental’s variant. A magnesium deficiency has been shown to produce
spasms of the coronary arteries, and is though to be a cause of nonocclusive
heart attacks. In addition, it has been observed that men who die suddenly of
heart attacks have appreciably lower levels of heart magnesium, as well as
potassium than matched controls.
It has been suggested that magnesium should become the treatment of choice for
angina caused by coronary artery spasm. Magnesium administration has
also been found to be helpful in the management of arrhythmias and in angina
due to atherosclerosis. Its benefit in all of these situations is presumable by
means of the same mechanisms responsible for its effects in an acute heart
attack (myocardial infarction). It improves the delivery of oxygen to the heart
muscle by relaxing the coronary artery as well as improving the production of
energy within the heart muscle.
Since the mid 1980s, over four thousand patients have been involved in eight
well designed studies that demonstrated the effectiveness of intravenous (IV)
magnesium supplementation. During the first hour of admission to a hospital
for an acute heart attack, administering IV magnesium reduced both immediate
and long term complications as well as death rates.
The beneficial effects of magnesium in an acute heart attack relate to its
ability to: improve energy production within the heart; reduce peripheral vascular
resistance, resulting in reduced demand on the heart; inhibit platelets from
aggregating and forming blood clots; reduce the size of the infarct (blockage);
and improve heart rate and arrhythmias.
Hawthorn: Hawthorne berry and extracts of its flowering tops are extensively
used in Europe for their cardiovascular activity. They exhibit a combination
of effects that are of great value to patients with angina and other heart
problems. Studies have established that hawthorn extracts are effective in
reducing angina attacks as well as in lowering blood pressure and serum
cholesterol levels.
The beneficial effects of hawthorn is the treatment of angina are due to
improvement in the blood and oxygen supply of the heart, resulting from
dilation of the coronary vessels, as well as improvement of the metabolic
processes in the heart.
Hawthorne’s ability to dilate coronary blood vessels has been repeatedly
demonstrated in experimental studies. In addition, hawthorn extracts have
been shown to improve cardiac energy metabolism in human and experimental
studies. The combined effect is extremely important in the treatment of angina,
as it results in improved myocardial function with more efficient use of oxygen.
The improvement in results is not only from increased blood and oxygen supply
to the heart muscle, but is also due to the interaction of hawthorn flavonoids
with key enzymes to enhance the heart muscle’s ability to contract.
Khella: Khella (Ammi visnaga) is an ancient medicinal plant native to the
Mediterranean region, where it has been used in the treatment of angina
and other heart ailments since ancient times, perhaps dating back to the
time of the pharaohs. Several of its components have demonstrated effects
in dilating the coronary arteries. Its mechanism of action appears to be very
similar to the calcium channel blocking drugs – it relaxes the blood vessels
by blocking the entry of calcium through small channels. Calcium influx into
the blood vessels cells leads to constriction. By inhibiting this influx, the
vessel relaxes and the diameter of the vessel increases.
Since the late 1940s, there have been numerous scientific studies on the
clinical effectiveness of khella extracts in the treatment of angina. More
specifically, khellin – a derivative of the plant – was shown to be extremely
effective in relieving angina symptoms, improving exercise tolerance, and
normalizing electrocardiographic tests. This is evident by the concluding
statements in a study published in the New England Journal of Medicine
in 1951:
The high proportion of favorable results, together with the striking degree
of improvement frequently observed, has led us to the conclusion that khellin,
properly used, is a safe and effective drug for the treatment of angina pectoris.
At higher doses (120 to 150 mg per day) pure khellin was associated with mild
side effects such as anorexia, nausea, and dizziness. Even though most clinical
studies used high dosages, several studies show that as little as 30 mg of
khellin per day appears to offer equally good quality results with fewer side
effects.
Rather than using the isolated compound khellin, khella extracts standardized
for khellin content (commonly 12%) are the preferred form as they can deliver
a consistent dosage of these keys compounds. A daily dose of such an extract
would be 250 to 300mg. Khella appears to work very well with hawthorn
extracts.
Intravenous EDTA Chelation Therapy: EDTA chelation therapy is an alternative
to coronary artery bypass surgery and angioplasty that may prove to be more
effective; it is definitely safer and less expensive. While coronary artery bypass
surgery or angioplasty usually costs $40,000 to $100,000, EDTA chelation
therapy is an in office procedure that usually costs less than $2,500 for a
full set of treatments.
EDTA is an amino acid like molecule that, when slowly infused into the
bloodstream, chelates (binds) with minerals such as calcium, iron, copper,
and lead and carries them to the kidneys, where they are excreted. EDTA
chelation has been commonly used for lead poisoning, but in the late fifties
and early sixties it was found to help patients with atherosclerosis.
The discovery that EDTA chelation therapy can be used in the treatment of
angina and other conditions associated with atherosclerosis happened by
accident. In 1956, while Dr. Norman Clark was treating a battery worker for
lead poisoning using EDTA, the patient noticed that his symptoms of angina
disappeared. Dr. Clarke and other began using EDTA chelation therapy in
patients with angina, cerebral vascular insufficiency, and occlusive peripheral
vascular disease.
Between 1956 and 1960, Dr. Clarke and his colleagues treated 283
patients with EDTA chelation therapy; 87% showed improvements in
their symptoms. Heart patients got better, angina disappeared or was
significantly improved, and patients with blocked leg arteries –
particularly those with diabetes – avoided amputation.
It was originally thought that EDTA opened blocked arteries by chelating
out the calcium deposits in the cholesterol plaque. However, it now seems
that the therapeutic effect results from chelating out excess iron and copper –
minerals that, in the presence of oxygen, stimulate free radicals. Free radicals
damage the cells in the artery and are a primary cause of atherosclerosis.
The authors of a review of the progression and regression of atherosclerosis
wrote that the process of atherosclerosis is dependent on the presence of
some metals (copper and iron) and can be completely inhibited by chelating
agents such as EDTA.
In spite of clear benefits to heart patients, EDTA fell into disfavor in the mid
sixties. Advocates of EDTA use believe that this happened for a couple of
different reasons: the lucrative surgical approach to heart and vessel disease
was on the rise, and the patent of EDTA that was held by Abbot Laboratories
expired, so there was no financial motivation for drug companies to fund any
research. Fortunately, a small group of practicing physicians who use EDTA
chelation therapy banded together. In 1972, they founded an organization
that is now called the American College for the Advancement of Medicine to
continue education and research in this important area.
In the early days of EDTA chelation therapy, several serious problems were
discovered. Giving too much of the EDTA or giving it too fast was soon found
to be dangerous. I fact, there were several deaths attributed to kidney failure
caused by toxic reactions to EDTA. Luckily, additional research resulted in
safer protocols, and EDTA chelation therapy as used now is considered very
safe. There have not been any deaths or significant adverse reaction in over
500,000 patients who have undergone EDTA chelation therapy. Because
EDTA chelation improves blood flow through the body, the side effects are
usually favorable and only a few adverse effects are noticed (most often
the only side effect is irritation at the site of injection).
Currently there exists a substantial body of scientific evidence on the use
of EDTA chelation therapy in the treatment of angina, peripheral vascular
disease, and cerebral vascular disease. Since 1987, numerous FDA
approved studies have demonstrated some impressive results. Again,
patients with angina have had symptoms improve or disappear and
patients with blockages in their legs have had blood flow restored or
significantly improved.
Self Treatment
It is becoming increasingly clear that a lifestyle of prudence is central in both
preventing and treating the underlying coronary disease that causes angina.
Especially critical factors are not smoking, getting enough exercise, managing
stress, and eating a low fat diet that is also high in fiber and complex
carbohydrates. Many doctors also recommend a daily aspiring to reduce the
chances of a heart attack, but check with your doctor first; even low dose
aspirin is hazardous for people with uncontrolled high blood pressure, ulcers,
and certain bleeding disorders.
The following are some specific self help strategies for preventing angina:
* Eat four or five small meals, evenly spread out throughout the day, rather
than two or three large ones. After a heavy meal, blood is diverted to the
digestive system, reducing flow to the heart and other muscles. Avoid
exercise at least one hour after eating.
* Beware of alcohol. An occasional drink or two probably is not harmful, but
excessive alcohol intake can damage the heart muscle.
* Avoid going out on cold, windy days. The cold constricts blood vessels and
increases the chance of suffering an attack of angina.
Nutrition Guidelines
Its role in coronary disease is well established. Both alternative and
conventional practitioners now advocate low fat, high fiber diets. The late
Nathan Pritikin developed a very low fat, mostly vegetarian diet for angina
patients that has since been adopted by many mainstream physicians and
nutritionalists. Nutrition therapists may also recommend high doses of
vitamin E, an antioxidant that is believed to lower levels of the harmful
LDL cholesterol. Lecithin is also advocated, but its benefits are not as
well documented as those of vitamin E.
Sources: Merck Manual of Medical Information
Encyclopedia of Natural Health
Smart Medicine for Healthier Living
Helpful Herbal Supplements for Angina
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