Green Tea
The pleasure of a cup of green tea is well accepted, but it appears to accomplish far more than satisfy the palate. Published literature confirms the hypolipidemic nature of green tea, reporting decreases in triglycerides and LDL cholesterol, while increasing the beneficial HDL cholesterol. In addition, green tea suppressed the oxidation of LDL cholesterol, further deterring the atherosclerotic process (Chan et al. 1999).

Some researchers liken green tea to aspirin because of similar therapeutic qualities. Information published in Beyond Aspirin (Newmark et al. 2000), states that green tea contains salicylic acid, a naturally occurring COX-2 inhibitor. Green tea, like aspirin, inhibits thromboxane A2; the inhibition of thromboxane A2 lessens the risks of blood clot formation and the dangers imposed by arterial constriction.

Heart attacks and strokes are less likely to occur if neither fibrinogen levels nor the activity of platelet-activating factor (PAF) become excessive. Green tea lowers fibrinogen levels and is a PAF inhibitor. A 4-year study involving 5910 Japanese women (ages 40 and older) showed twice as many strokes among trial participants who used less green tea (less than 5 cups a day) than in those who used more (greater than or equal to 5 cups daily) (Sato et al. 1989).

A cup of green tea appears to be beneficial to hypertensives through various mechanisms. The loss of arterial elasticity (arteriosclerosis) is one cause of high blood pressure. Youthful arteries expand and contract in compliance with the heartbeat to move blood to peripheral sites. Damaged vessels are unable to participate in this ritual. Green tea (by inhibiting thromboxane) reduces arterial constriction and consequently blood pressure is reduced. Also many antihypertensive drugs are ACE inhibitors, meaning angiotensin pathways are disrupted. Without interruption of this feedback loop, blood vessels vasoconstrict, water is retained, and blood pressure increases. Green tea breaks this sequence, acting as a natural (although mild) ACE inhibitor (Duke Database 1992; Faloon 2000).

The 1st International Symposium on Green Tea (September 22, 1989) reported that green tea reduces blood glucose levels. During the ensuing years, the Life Extension Foundation has frequently informed members that green tea reduces the expected glucose and insulin rise after a carbohydrate load. It should also be noted that green tea contains chemicals regarded as beta-adrenergic receptor blockers, anti-inflammatories, diuretics, and calcium antagonists, proving beneficial in arrhythmias and hypertension (Duke Database 1992).

Green tea, an antioxidant, helps remove excess iron from the liver (Carper 2001). Individuals with hemochromatosis should drink several cups or use two to four 300-mg capsules a day. (Each capsule should provide 95% active polyphenols.) Note: Research suggests that decaffeinated green tea has a different therapeutic disposition than that containing caffeine and may be more effective in reducing iron overload. Caffeine drinks are not appropriate for sympathetic dominant individuals and those taking beta-adrenergic drugs.

As similar as green tea and aspirin are in their defensive mechanisms, it would not be wise for an individual, relying on aspirin as a cardioprotective, to depend only on green tea to the exclusion of aspirin.

Nuts: A Heart Food
According to a report published in the American Journal of Clinical Nutrition, one of the most unexpected and novel findings in nutritional epidemiology in the past 5 years has been that nut consumption protects against ischemic heart disease (IHD) (Sabate 1999). Phytonutrients in nuts, such as luteolin (a flavonoid), tocotrienols, fiber, fatty acids, amino acids, and vitamins and minerals, appear to work synergistically to provide heart protection, lower blood pressure, reduce the risk of stroke, and increase longevity. The protective effect of nuts applies to men and women (both black and Caucasian), all age groups, smokers, and sedentary individuals.

Of the tree nuts, walnuts are unique because they are a rich source of linolenic acid. Almonds are a good source of vitamin E and calcium; peanuts provide folate (important in controlling homocysteine) and resveratrol (inhibits blood clots and the inflammatory process). Nuts are also good sources of arginine and fiber (Kris-Etherton 1999).

The Adventist's Health Study reported that individuals who ate nuts 1-4 times a week reduced their risk of acute myocardial infarction 22% (Fraser et al. 1992). Eating nuts more than 5 times a week resulted in a 51% lower cardiac risk compared to individuals who consumed nuts less than 1 time a week. Persons consuming nuts more than 5 times a week reduced their lifetime IHD risk 12%, and men who developed the disease did so 5.6 years later than men who consumed nuts infrequently.

In 1993, the New England Journal of Medicine published results of a walnut study conducted at Loma Linda University. All trial participants conformed to the National Cholesterol Education Program Step 1 Diet, except that 20% of the calories of one diet were derived from walnuts, offset by lesser amounts of fatty foods. Both diets contained identical foods and macronutrients, except for the addition of walnuts in the test diet.

At the conclusion of the study, participants eating the walnut diet had total cholesterol levels 22.4 mg/dL (12.4%) lower and LDL cholesterol levels 18.2 mg/dL (16.3%) lower than those consuming the control diet. Blood pressure was unaffected on either diet. Researchers noted that subjects on the walnut diet, despite increased energy intake, did not gain weight (Sabate et al. 1993). Comment: Nuts, in general, are healthy foods, but select those not roasted at high temperatures in oils of uncertain quality.

The Journal of the American Medical Association recently expanded the potential benefits of higher nut and peanut butter consumption, showing a significantly reduced risk for Type II diabetes among women who regularly include nuts in their diet (Jiang et al. 2002).

Autonomic Balancing: Right Messages, Good Results
The autonomic nervous system, consisting of the parasympathetic (PNS) and the sympathetic divisions (SNS), play major roles in heart function. For example, when the PNS is active, heartbeat, blood pressure, and respiration rate tend to be decreased, as well as the activity of the adrenal glands. Conversely, when the SNS is dominant, the brain alerts the adrenal glands (small organs located on top of the kidneys) to supply adrenaline, the stress hormone. Adrenaline rushes through the bloodstream to all tissues, organs, and glands, heightening their responsiveness. Subsequently, blood pressure, heart rate, blood glucose levels, respiration, and perspiration increase. It is referred to as the "fight or flight" division because a general state of excitement and preparedness is evidenced.

If the individual is healthy, an adrenaline surge is inconsequential. But, if the heart is diseased or damaged, the sympathetic stimuli can be dangerous, even deadly. Type A individuals often live with chronic stimulation of the SNS, a burdening handicap to long-term survival. Note: Interesting data released from the Stanford University School of Medicine showed that insulin-resistant individuals, with compensatory hyperinsulinemia, have a higher nocturnal heart rate, a finding consistent with the possibility that increased heart rates are secondary to insulin-induced sympathetic activity (Facchini et al. 1996b).

Although each of us is born with a propensity toward a sympathetic, parasympathetic, or balanced response from the autonomic nervous system (ANS), Dr. Nicholas Gonzalez (an authority on autonomic balancing) is finding that chemical pollutants and life-style abuses can shift balance and disrupt the natural tendency of the individual. If either division becomes abrasively dominant, the risks imposed upon the heart can be meaningful. For example, if the PNS becomes overly dominant, the risks are as genuine as if the SNS were overexpressed. A heart receiving its instructions from the PNS may become a bit passive, and cardiac output lethargic. Unable to cope with a one-sided response from the ANS, the heart can make fatal errors.

The SNS and PNS are a two-neuron system, meaning that two sets of nerves interconnect in the ganglion. Minerals play an extremely important role in the message sent to organs and glands from the ANS. For example, Dr. Gonzalez explains that magnesium blocks transmission between the two nerves and the ganglion and is regarded as the very best turn-off for sympathetic arousal. On the other hand, calcium arouses activity in the SNS. Potassium, although not a sympathetic toner, acts directly upon the PNS, encouraging increased responsiveness. Exercise quiets the SNS, burning off sympathetic hormones and making stronger parasympathetic expression.

The pH of a parasympathetic dominant tends to be alkaline; the pH of a sympathetic dominant migrates toward acidity. This principle may best explain the benefit some cardiac patients gain when eating a predominantly fruit and vegetable diet, with protein sources limited to smaller amounts of fish and chicken. The alkalinity of a plant-based diet makes the response from the PNS stronger and the activity in the SNS more subdued. Conversely, red meat turns on the SNS and is beneficial to an individual with an overactive parasympathetic response. In fact, Dr. Gonzalez feels a cholesterol level between 210-220 mg/dL is fitting for a parasympathetic because the cholesterol then assumes the nature of a powerful antioxidant.

A cardiac patient should seek counsel with a physician who can determine metabolic type. A physician who can make this determination will also make cohesive choices regarding supplements, diet, and exercise, eliminating conflicting messages being delivered to the heart. Note: Tapes of Dr. Gonzalez's lectures, addressing the ANS in-depth, may be purchased from Conference Recording Service Inc., (800) 647-1110 or at www.conferencerecording.com. Although the lectures focus on treating cancer, the tapes are extremely interesting and informative.

Beta-Blockers
Since overexpression of the adrenergic system (increasing sympathetic activity) can provoke an irregular heartbeat, scientists have searched for drugs that could block its activity. Propranolol became the granddaddy of the family of beta-blockers and is one of the most prescribed drugs in America for arrhythmias, hypertension, and angina pectoris.

Beta-blockers bind to specific receptors on nerve endings in an effort to control blood pressure, anxiety, and arrhythmias occurring before or after a heart attack. The binding process blocks the effects of impulses transmitted by the adrenergic postganglionic fibers of the SNS. As beta-blockers compete with epinephrine (also known as adrenaline) for receptor sites, the excitory nature of epinephrine is curtailed. Beta-adrenergic receptors are located mainly in the heart, lungs, kidneys, and blood vessels (PDR 1999).

Conventional cardiologists conducting propranolol studies reported satisfaction with beta-blockers, citing fewer second heart attacks among users and a 26% reduction in heart mortality. Many patients were less pleased with beta-blockers, describing clinical depression, erectile dysfunction, and fatigue as compromising factors. Also, beta-blockers have been associated with an increased risk of developing diabetes by impairing insulin sensitivity. Newer beta-blocking drugs such as Toprol are now considered superior to Propranolol.

Calcium Channel Blockers
The heart is controlled by tiny electrical impulses that regulate the heart, not unlike a pacemaker. Calcium plays a key role in regulating the heart's response to these electrical signals. It flows between the heart cells and surrounding fluid through a sort of chemical turnstile, or calcium channel. The more calcium that gets through the turnstile before the electrical signal is received, the more strongly the heart contracts, an effort that increases the heart's workload. Calcium channel blockers do not totally block movement through the turnstile, but they significantly slows it down. For some, this process lessens the labor required of a damaged heart, signaling it to slow down and take it easy. Because calcium channel blockers dilate the arteries and reduce resistance to blood flow, they are also widely used to control hypertension. The FDA first approved calcium channel blockers in 1982 for the purpose of treating arrhythmias.

While most of the literature (cautiously) supports calcium channel blockers, a few clinicians adamantly oppose their usage. According to Gabe Mirkin, M.D., calcium channel blockers are classified as short-, intermediate-, and long-acting. Older studies showed that short- and intermediate-acting calcium channel blockers might increase the risk of heart attacks; a more recent study showed that longer-acting calcium channel blockers might as well (Estacio et al. 1998). Patients were followed for 67 months, at which time the Drug and Safety Monitoring Committee detected a significant difference in the rate of heart attacks among patients treated with nisoldipine (a long-acting calcium channel blocker) compared with those treated with enalapril (an ACE inhibitor). The termination of nisoldipine treatment was recommended, and patients receiving nisoldipine were switched to enalapril.

Professor Bruce Psaty (University of Washington) reported that the risk of a heart attack increased up to 60% among 2655 hypertensive patients taking calcium channel blockers (Psaty et al. 1995). In addition, The Lancet reported that calcium channel blockers, often hailed as an ace in cardiac pharmacology, appear to increase the risk of developing cancer (Pahor et al. 1996). Among 5000 men and women enrolled in a verapamil, diltiazem, and nifedipine study, the risk of cancer increased by about 72% (Atkins 1996c).

Other side effects associated with both calcium channel blockers and beta-blockers are congestive heart failure (CHF), lightheadedness, fatigue, low blood pressure, shortness of breath, and bradycardia (heartbeat less than 60 beats a minute). Although not enough studies exist to prove that calcium channel blockers cause heart attacks or increase the risk of cancer, the research is strong enough for doctors to use calcium channel blockers with the utmost caution (Mirkin 2002b).

Dispersed throughout the Therapeutic section are a few of the herbs (containing one or more chemicals) considered beta-adrenergic receptor blockers or calcium antagonists. The literature also supports magnesium as a SNS inhibitor as well as a calcium antagonist (Whitaker 1995b; Duke 2000; Gonzalez 2000). Researchers state that carnitine may provide independent benefit in ischemia when used as monotherapy or additional benefit when used in combination with conventional beta-blockers or calcium antagonists (Jackson 2001). Never should drug therapy be stopped and a nutraceutical started without counsel with a qualified physician.

Calcium blocking activity
Angelica, garlic, ginger, ginkgo biloba, grape seed, green tea (Camellia sinensis), hawthorn, magnesium, and olive leaf

Beta-blocking activity
Grape seed, green tea, hawthorn, and magnesium

RISK FACTORS ASSOCIATED WITH PRESCRIPTION DRUGS

Many people are unaware that there may be risks associated with taking commonly prescribed prescription medications. In addition, once-daily dosing of certain drugs such as anti-hypertensive agents may not provide 24-hour protection against arterial damage. Individuals who are currently taking any of the medications described in this section are urged to discuss alternative treatment options with their physician.

Nitroglycerin Drugs and Angina
Angina is a sudden intense pain in the chest that is often accompanied by a feeling of suffocation. Angina is caused by a momentary lack of adequate blood supply to the heart muscle. Individuals who have occluded coronary arteries often experience periodic bouts of angina.

Nitroglycerin temporarily dilates blood vessels and reduces workload on the heart. As early as 1879, nitroglycerin was administered to an angina patient (Kipple 1993). Nitroglycerin worked so well that nitroglycerin and other "nitrate" drugs have been used as standard angina therapy ever since. Unfortunately, while these nitrate drugs do provide temporary relief from angina, regular use of nitrate drugs may increase the risk of a future heart attack.

A startling new finding came from a Japanese study that involved 518 patients with suspected coronary artery disease (Murakami et al. 2002). The patients were categorized into groups based on their degree of endothelial dysfunction (a measurement of inner arterial wall damage) and the use of nitrate drugs.

These 518 patients were followed for 45 months to ascertain which patients were more likely to experience major cardiovascular events. As expected, patients with severe endothelial dysfunction had significantly more heart attacks, strokes, bypass surgeries, congestive heart failure, etc. However, the surprising finding was that those who regularly used nitrate drugs were 2.42 times more likely to experience major cardiovascular events. The researchers concluded that the effects of nitrate drugs accelerated atherogenic processes and endothelial dysfunction and that use of nitrate drugs caused future cardiovascular events (Murakami et al. 2002).

Millions of Americans with coronary artery disease have been prescribed nitrate drugs. However, there is now evidence that nitrate drugs actually accelerate arterial wall damage (endothelial dysfunction) and thus contribute to progression of coronary artery disease--the very disorder that the nitrate drugs have been prescribed to alleviate.

Angina patients who rely on nitrate drugs should bring this new information to the attention of their physician. It is important to note that occasional use of a nitrate drug to relieve angina symptoms was not shown to be dangerous in the most recent study. It was the regular use of a nitrate or nitroglycerin drug that increased the risk of heart attack by 2.42 times within a 45-month period (Murakami et al. 2002).

Commonly Prescribed Nitrate Drugs
A 2002 study indicating danger from nitrate drugs referred to regular use rather than occasional use (Murakami et al. 2002). It is highly unlikely that occasional use of a nitrate drug to relieve angina symptoms would cause a problem. However, regular use of a nitrate or nitroglycerin drug more than doubled the risk of heart attack or other pathological vascular event. Commonly prescribed nitrate and nitroglycerin drugs are:
Isosorbide .........................Nitro-Dur Transdermal Infusion
Isosorbide Dinitrate ...........Nitrolingual Pump Spray
Isosorbide Mononitrate .....Nitrostat tablets
Nitroglycerin patches ........Minitran Transdermal Delivery System

For information about an FDA-approved technique that has been shown to safely reduce angina symptoms, refer to "A Non-Invasive Alternative to Coronary Bypass Surgery" in the May 2003 issue of Life Extension magazine (pp. 54-60).

Dietary supplements that have been shown to help protect against endothelial dysfunction include:

Folic acid (Title et al. 2000a; Woo et al. 2002)
Vitamin C (Richartz et al. 2001; Pullin et al. 2002)
Vitamin E (Title et al. 2000b; Raghuveer et al. 2001)
Arginine (Maxwell et al. 2000; Kawano et al. 2002; Lekakis et al. 2002)
Taurine (Wang et al. 1996; Fennessy et al. 2003)
Fish oil (Chin et al. 1994; Morita et al. 2001; Goodfellow et al. 2000)
It should be pointed out that if left untreated, endothelial dysfunction may become so severe that it will not be possible to reverse it with currently available therapies.

The term endothelial dysfunction is increasingly being described in scientific journals as a significant underlying cause of most forms of cardiovascular disease, including hypertension, atherosclerosis, and congestive heart failure.

Class I Anti-Arrhythmic Drugs Kill Thousands
In the June 1995 issue of Life Extension magazine, an article exposed the dangers of a class of anti-arrhythmic drugs the FDA had approved to prevent lethal heart arrhythmias (LEF 1995). In this 1995 article, evidence was introduced that the FDA knew of the risks these drugs posed, but had approved them anyway. When the FDA was confronted with accusations that these drugs had been improperly approved, the reply was that the FDA had a theory that these drugs would save the lives of more people by preventing abnormal heartbeats than the drugs would kill by causing abnormal heartbeats. The problem was that the FDA had no evidence that these drugs would save even a single life.

Even after a large study conducted by the National Heart, Lung and Blood Institute showed that anti-arrhythmic drugs had killed large numbers of Americans, the FDA's response was not to remove the drugs, but to merely suggest changes in the labeling of the drugs (CAST 1989; NHLBI. 2002).

True to its word, the FDA did mandate a change in the labeling of at least one of these anti-arrhythmic drugs (Tambocor®). On page 1889 of the year 2003 Physician's Desk Reference, a large warning box appears containing the following statement:

"An excessive mortality or non-fatal cardiac arrest was seen in patients treated with Tambocor compared with that seen in patients assigned to a carefully matched placebo-treated group. This rate was 16/315 (5.1%) for Tambocor and 7/309 (2.3%) for the matched placebo."

What this warning means is that if you take Tambocor (flecainide), your risk of dying or experiencing a heart attack is more than double compared to taking a placebo.

The sordid history of the FDA's approval of Tambocor and other lethal Class I anti-arrhythmic drugs is chronicled in the book Deadly Medicine by Thomas J. Moore (1995).

Are You Taking the Proper Anti-Hypertensive Medication?
The Life Extension Foundation has repeatedly warned persons with high blood pressure (hypertension) to not depend on one-a-day dosing of anti-hypertensive drugs because many of these drugs do not provide complete 24-hour protection. When an anti-hypertensive drug wears off, the patient is vulnerable to having a stroke. One solution to this problem is to take a lower dose of the anti-hypertensive drug twice a day, even though the FDA claims that one-a-day dosing is adequate.

Failure to keep blood pressure at optimal low levels (below 120/85) dramatically increases mortality risk. The United States government states that blood pressure readings as high as 140/90 are acceptable (CDC 2002), but published results of human studies clearly show that maintaining levels below 120/85 confer longevity and protection against heart attack and stroke (Stamler et al. 1993; Stamler 1999).

The best-selling anti-hypertensive drugs in the United States are not necessarily the most effective. Advertising by drug companies and physician "force-of-habit" prescribing often result in hypertensive individuals taking drugs that do not provide optimal blood pressure-lowering effects.

Life Extension long ago recommended a class of anti-hypertension drugs known as angiotension II receptor blockers. Some of the first drugs approved in this class where Cozaar® and Hyzaar® and Life Extension has suggested them as first line therapy. The only drawback to these drugs was that they did not provide consistent one-a-day protection.

A new drug in this class is called Benicar®. A recent study indicated that Benicar may be the first drug to provide true 24-hour blood pressure reduction (Neutel et al. 2002). A typical starting dose of Benicar is 20 mg a day. For patients requiring further reduction in blood pressure, the dose can be increased to 40 mg a day after 2 weeks.

Optimal control of hypertension requires blood pressure checks throughout the day. This is the only way to be certain an anti-hypertensive drug is not wearing off, endangering the arterial system. Even if you take Benicar, it is still critical to verify that it is actually keeping your blood pressure suppressed during an entire 24-hour period.

INVASIVE VERSUS NONINVASIVE TESTING AND HEART PROCEDURES

Facts to Consider Before a Final Decision Is Made
Invasive heart treatment ranks ninth among the top 10 causes of death. Because of the obvious seriousness of any procedure involving the heart, consenting to invasive testing and surgery should be made rationally rather than emotionally. The intent of this protocol is not to steer the patient in regard to cardiac testing and treatment but rather to enlighten the reader concerning both options and risks. Fortunately, researchers have removed many of the uncertainties from the dilemma.

The detection of a heart problem can be made by several noninvasive tests, medical history, physical examination, electrocardiogram, stress tests, blood tests, and an echocardiogram. An echocardiogram provides a graphic outline of the movements of the heart structures, showing the valves and the action of blood flowing through them, the ability of the left ventricle to pump blood, the walls of the heart (considering thickness), and an assessment of the membrane around the heart (the pericardium). It does not show the coronary arteries well enough to determine blood circulation directly to the heart. For this evaluation, the echocardiogram should be combined with a cardiac stress test. This combination will show the workings of the various parts of the heart during stress compared to rest.

The blood tests are valuable because they confirm or refute uncertainties arising from early-stage diagnosis of a heart attack. Creatine kinase (CK), a small fraction of the CK enzyme (CK-MB), and troponins are heart damage markers or cardiac enzymes measurable in the blood. CK-MB shows an increase above normal about 6 hours after the onset of a heart attack. It typically reaches its peak level within 9-30 hours and usually returns to normal within 48-72 hours (Cardiac Biomarkers 2000).

Blood tests to measure troponins, specifically T (cTnT) and troponin I (cTnI)--cardiac muscle proteins--have been developed. These proteins control the interaction between actin and myosin, muscle proteins that contract or squeeze the heart muscle. Identifying troponins specific to heart muscle allowed for the development of blood assays that can detect heart muscle injury with great sensitivity and specificity. The normally low level of cTnT and cTnI increases substantially within 4-6 hours of heart muscle damage. Peak levels occur at 14-20 hours, usually returning to normal 5-7 days later (American Heart Association 2000; Cardiac Biomarkers 2000; Sobki et al. 2000).

It is now considered possible to use troponin testing to identify individuals at either low or high risk for a coronary event. Even modestly elevated troponin levels are associated with larger numbers of tiny coronary artery blood clots, complex arterial lesions, and impaired blood flow through the vasculature.

Compared to patients with the lowest levels of troponin T, those with the highest troponin T levels are almost 13 times more likely to die over a 37-month period (Lindahl et al. 2000). The type of troponin blood test used by most clinical laboratories is troponin I. If levels exceed 0.4 ng/mL, antiplatelet and antithrombotic therapy should be considered. Nutrients with an antiplatelet and antithrombotic therapeutic profile are highlighted in the Therapeutic section of this protocol.

Researchers at University of Texas Southwestern Medical Center (Dallas) have discovered another impressive cardiac marker, brain natriuretic peptide (BNP), showing remarkable accuracy in regard to predicting cardiac morbidity and mortality. BNP is a neurohormone synthesized in the muscular wall of the left ventricle of the heart that is released into the circulation in response to ventricular dilation and pressure overload. BNP, a counterregulatory hormone, promotes excretion of salt by the kidneys and dilates blood vessels.

To determine the predictive value of BNP, 2525 patients were enrolled in a study (half having experienced a heart attack and the other half displaying unstable angina or chest pains). After a 30-day analysis, the researchers found that levels of BNP were higher among patients who died. Also, it was observed that patients with higher BNP were more likely to have a new or recurrent heart attack, develop heart failure, or experience progression of the disease process. Even in patients who had no detectable heart damage from a previous attack, elevated BNP levels identified individuals at high risk of dying or developing life-threatening cardiac complications (de Lemos et al. 2001).

Angiograms
An angiogram, referred to as cardiac catheterization, is a mechanism in which coronary arteries are luminated by injections of dye, a process that aids in diagnosing blocked arteries. A catheter is introduced through an incision into a large vein, usually of an arm or a leg, and threaded through the circulatory system to the heart. As the dye wends its way through the vasculature, blockages are detected by changes in flow rate at points of occlusion. An angiogram is a popular diagnostic tool, but it is not without risks. It is possible that the catheter will damage the artery or loosen a piece of plaque lining the artery wall. The dislodged plaque can block the flow of blood, causing a stroke. Thrombophlebitis, local infection, and cardiac arrhythmias are other valid concerns.

Data reported in the JAMA debated the relevancy of widespread angiogram usage (Graboys et al. 1987, 1992). A study chronicled 168 patients who were advised to have an angiogram to determine the need for either angioplasty or cardiac surgery: 80%, or 134, of the 168 patients who were evaluated noninvasively were determined not to need catheterization. From the 168 patients, an annual fatal heart attack of 1.1% was observed over a 5-year period compared to a 5-10% mortality rate from coronary bypass surgery and a 1-2% mortality rate from angioplasty. The conclusion of the published report was that noninvasive testing to access the heart's performance is a better and safer determinant of a suitable therapeutic program than searching for blocked arteries. If the patient fails some of the noninvasive tests, an angiogram is warranted to determine the need for surgery (Murray 1999).

Magnetic Resonance Imaging
Up to 70% of heart attacks occur in blood vessels that appear normal on an angiogram. The journal Circulation reported that plaque without any calcium deposits is not detectable by angiograms or CT scans, but it is the most common cause of sudden death from a heart attack. While calcification may lead to a more extensive form of heart disease, it is less likely to lead to a heart attack (Fayad et al. 2000, LEF 2000).

Fatty buildup on arterial walls, although not detectable by an angiogram, can result in a small fraction of plaque breaking free. The circulating particle ultimately increases the risk of a heart attack or stroke.

A special type of MRI, with a sensitive screening technique, is promising in regard to detecting even a slight buildup in coronary arteries, including plaque without calcium deposits. This is especially praiseworthy since coronary arteries are very small and the constant movement of the heart makes a clear image difficult. The newer technique, black blood imaging, blacks out the blood and produces an image of just the artery. Besides being of much greater advantage in diagnosing early-stage heart disease, this process is noninvasive. It is hoped that this newer, more responsible means of assessing the health of coronary arteries will become part of a routine check-up (Fayad et al. 2000).

Coronary Bypass Surgery
Blocked arteries are not always prognosticators of an impending heart attack. The Coronary Artery Surgery Study (CASS) demonstrated that heart patients with healthy hearts, but with one, two, or three of the heart vessels blocked, did amazingly well without heart surgery. The number of blockages did not alter the 1% a year death rate observed in the study groups (Hueb 1989; Alderman et al. 1990).

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These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease