Editor’s Note: Patients with chest pain are routinely not given the opportunity for informed consent. Dr. Wayne’s common sense discussions on heart tests and treatments go a long way to filling that gap. They are scientifically sound and thoroughly researched. Health professionals are invited to access the website of the Noninvasive Heart Center  for references to the  pertinent medical literature. This essay is composed of excerpts from Dr. Wayne’s written works, and is reproduced with permission of the publisher.

Narrowing of arteries correlates poorly with heart function and chest pain symptoms.
In spite of considerable evidence to the contrary, the general emphasis in cardiology today is on the anatomy of coronary artery disease; that is, which coronary arteries are involved, and how much narrowing or obstruction there is. Increasingly it is becoming apparent that the amount of narrowing of the coronary arteries is of only minor importance. Such narrowing does not correlate with the patient's symptoms, the motion of the muscular walls of the heart, the performance of the heart, the blood flow through the coronary arteries, the patient's prognosis, and the results of coronary artery bypass surgery. Importantly, when the angiograms of patients with stable and unstable angina are compared, there are no distinguishing anatomical differences to separate the two groups.

Limitations of the coronary angiogram
There is good reason to believe that the reason for these poor relationships is because the main coronary arteries, the visualization of which is the main objective of coronary angiograms, contain only about 25% of the total coronary blood flow. Indeed, the vast majority of the total coronary circulation cannot even be seen on an angiogram simply because the angiographic technique is unable to visualize vessels smaller than 0.5 mm. An analogy would be looking at a large city from a high altitude. One would be able to see the major freeways but the city streets would be invisible. Thus, if the objective of coronary angiograms is visualize the amount of blood flow to different regions of the heart, it fails miserably.

A single angiogram cannot indicate how long artery is obstructed
Even if a coronary angiogram could determine the approximate amount of blood flow to a given area of the heart, the technique would still have major limitations. Most patients with chest pain due to coronary artery disease (angina pectoris), or with other symptoms such as exertional fatigue or shortness of breath, usually have had some reduction in blood flow to one or more areas of the heart for years without change. Unfortunately, mere reduction in blood flow is not sufficient to establish the cause of someone's chest pain that is of recent onset. What the cardiologist really needs to know is whether there also has been a recent major change in the amount of blood flow to a specific area of the heart. That kind of information cannot be provided by a single angiogram; serial angiograms would be required. Because angiograms are invasive procedures that are costly and not without risk, repetitive tests are impractical. Thus, although a single angiogram will tell us if coronary artery disease has been present, it cannot tell us if that disease has become acutely worse, and is the direct cause of the patient's new symptoms, or alternatively, the presence of coronary artery disease is merely coincidental, and there is some other explanation for the patient's symptoms.

Other causes of chest pain
What might these other causes be? A wide variety of conditions may produce chest pain that may be confused with chest pain due to coronary artery disease. For example, chest wall pain due to muscular or nerve root injury, diseases of the lung or esophagus, particularly gastroesophageal reflux disease (GERD), abdominal diseases such as gallstones, peptic ulcer, and colon disorders with excess amounts of abdominal gas. In addition, a number of conditions may trigger previously existing but silent coronary artery disease. By far the most common is high blood pressure or hypertension. Hypertension is usually a disease of later life while coronary artery disease usually occurs earlier but remains silent. As we age our blood pressure begins to rise. Initially this usually occurs only during periods of stress or physical activities. When this happens it may produce chest pain. Because at rest the blood pressure is still normal, its presence is often overlooked. If angiograms are done, coronary artery disease may be coincidentally present, and the patient's symptoms blamed on it rather than his hypertension. Such a patient is often made to undergo unnecessary angioplasty or coronary artery bypass surgery when simple blood pressure medication will correct the problem. There are still other conditions that may trigger previously silent coronary artery disease such as prostate and kidney disease, thyroid disease and many others. Even certain drugs that cause fluid retention such as the nonsteroidal anti-inflammatory drugs can elevate the blood pressure and cause chest pain.

Because the elimination of all these various causes of chest pain often takes weeks to months, and because of the limitations of the angiographic procedure just described, as well as the costs and risks of angiograms, it seems more rational to direct our attention to the use of other tests that will noninvasively detect any impairment of muscular contraction due to coronary artery disease. Long before the heart muscle becomes permanently damaged due to insufficient blood supply, that muscle fails to perform in a normal manner. It can't, it doesn't have the energy supply.

Other ways to test cardiac function and blood flow to heart muscle
A number of new or relatively new diagnostic tests are available for studying the various phases of the heart's function. These tests continuously image the motion of the muscular walls that surround the heart's chambers as they contract and relax. In effect, the rate and degree to which the chambers empty and fill are revealed. Even events lasting only one-tenth of a second or one-hundreds of a second can be studied. Consequently, the individual functions of every portion of the heart that contributes to the total performance of the heart can be measured and permanently recorded.

The result is a complete picture of the heart's mechanical activities during every phase of the cardiac cycle. If total performance is reduced, that portion of the heart that is responsible not only can be identified, but when its function is impaired as well. This increases the likelihood that the abnormality can be selectively treated with the drug most likely to be beneficial. This is vastly superior to tests, i.e., the electrocardiogram that records only the electrical activity of the heart, or the stress test that measures only total performance, and provide no input as to what part or what phase of the heart's function is impaired, nor insight as to what drug to selectively use to improve the heart's contraction.

Collectively these tests and procedures are called noninvasive tests because they do not invade the body or penetrate the skin. Those noninvasive tests that study the mechanical function of the heart are sometimes referred to as mechanocardiographic tests. Of prime importance is the fact that many of these tests are adaptable for use in the doctor's office. This will have a profound influence on the way heart disease is diagnosed and treated. For the first time, detailed facts about how a patient's heart is functioning will become available on a routine basis.

Value of noninvasive tests and lessons learned
The value of such information can be enormously enhanced by the ease with which it can be updated each time the patient returns for follow up visits. The rewards will be a low cost, safe, easily reproduced group of tests for follow up comparisons that provide early warnings of impairment of any phase of the heart's contraction or relaxation processes.

As a result of the repeated use of these tests in coronary artery disease patients over a period of many years, important new information has come to light about the reasons why patients with stationary disease seemingly become worse. Contrary to today's present held concepts, the development of new symptoms, or the return of old ones, is uncommonly due to progression of the patient's underlying coronary artery disease. The usual cause appears to be some form of functional overload that causes the heart to work beyond its capabilities. Symptoms, when they do appear, do not allow identification of the underlying problem. Thus, it is understandable that the first thought is the patient's disease is getting worse and angioplasty or bypass surgery is recommended.

Noninvasive tests as a guide to treatment and prognosis
In reality, the cause of the temporary functional overload is usually easily correctable with medication. However, because it may exist in silence, it may progress to an advanced state before symptoms appear. By that time it may be too late to treat, and even may remain hidden by its own complications.

Because the precise cause of the functional overload can usually be identified, the specific drug that will be the most effective can be selected to correct the problem, rather than having to use shotgun therapy because the patient's symptoms are nonspecific.

Importantly, as long as there are no changes in the various component functions of the heart that go to make total cardiac performance, the patient will do well. He or she will have little in the way of symptoms, and minimal progression of the disease itself. The changes that eventually do occur appear to be more the result of aging which cannot be avoided. The major problems of heart attacks, premature deaths, unnecessary angioplasty and coronary artery bypass surgery have been drastically reduced or avoided altogether by the above approach. For patients who do not receive the benefits of such diagnosis and treatment because their doctor still employs older methods, that doctor may be more dangerous than their disease.

What you should know about angioplasty and bypass surgery
Many cardiologists try to convince their patients that opening an occluded artery with angioplasty, or bypassing it with coronary artery bypass surgery, will prevent heart attacks or premature death, and that an alternative or alternatives to bypass surgery such as medical treatment with drugs is not an option and will not work. Such decisions against an alternative or alternatives to bypass surgery are usually based solely upon the results of an angiogram that show the presence of coronary artery disease. Unfortunately, no prior angiogram is usually available to determine whether the patient's coronary artery disease is new or old. Without a prior angiogram to compare with, it is impossible to determine whether the patient's coronary artery disease has recently progressed. In other words, any coronary artery disease found has often existed in unchanged form for years. It is, therefore, coincidental, and there is another reason for the patient's chest pain. If so, then it is even more likely there is an alternative or alternatives to angioplasty or bypass surgery. This is particularly likely to be true in patients with recent onset of chest pain.

Only a few studies have shown a survival benefit with surgery, and these were done in the seventies before the availability of modern medication. Even these few studies are suspect as to their reliability because we now know that many reasons exist for the relief of the patient's chest pain after surgery that have nothing to do with the bypass surgery itself. For example, placebo surgery will provide pain relief. In addition, there are no modern studies supporting the claim that angioplasty and bypass surgery are of clinical benefit, and that surgery prevents future heart attacks or death compared to bypass surgery alternatives.

Although symptoms may be relieved in many patients following one of these procedures, such relief is often only temporary, returning within a few months to a few years. Furthermore, from our personal experience over the past 23 years at the Noninvasive Heart Center in dealing with many hundreds of patients with chest pain who have been urged to undergo bypass surgery, most are grossly undertreated with alternative modern medications and other bypass surgery alternatives such as exercise, weight loss, cessation of smoking and stress and blood pressure control. Typically such patients are threatened with medical terrorism tactics such as "You can have a massive heart attack and die at anytime unless you undergo immediate surgery!" Such tactics might be appropriate if they were true, but in the experience of the Noninvasive Heart Center, not once has any patient ever had a heart attack or died because he or she were treated with an alternative or alternatives to bypass surgery. It almost seems that there is a deliberate attempt on the part of the patient's doctor to undertreat because if such patients were treated properly, their symptoms would disappear and the patient would reject surgery.

The efficacy of surgery and angioplasty is not only greatly overrated, but the results of both are unpredictable. Mortality and frequency of complications are much greater than what the patient is led to believe, and many patients are worse off after surgery.

The truth of the matter is that the most recent studies, involving now more than 41,000 patients, and population studies involving more than two million people (see section on comparison studies) have shown that an alternative or alternatives to bypass surgery is associated with a far lower morbidity and mortality. In other words, alternative treatment with modern pharmaceutical agents as well as other alternatives are highly effective, provided the cardiologist you are dealing with knows how to use medication. Sad to say, most do not and prescribe an inadequate number of drugs or too low a dosage. Many cardiologists are still quoting from studies in the late 1970s which showed that bypass surgery provided some protection in patients with poor cardiac function compared to only one bypass surgery alternative treatment with drugs. Obviously, the medical treatment of the 1970s is hardly appropriate compared to that of the early 21st century. Today, there are many available drugs, and a lot more coming down the pike, that make the treatment of obstructive coronary artery disease very safe, and highly effective. When medications are used in appropriate numbers and dosages, the patient is able to live a normal life with a risk of dying or having a heart attack only minimally greater than individuals without coronary artery disease. This is not only my experience, but the experience of other noninvasive cardiologists who do not rush every patient with chest pain in for angiograms and some form of intervention. It also should be pointed out that not only do angioplasty and bypass surgery NOT slow down the progression of the disease and its consequences, but actually accelerate its progression.

Finally, many cardiologist and surgeons will casually dismiss an alternative or alternatives to bypass surgery with modern drugs and other management techniques because these alternatives are unable to eliminate or unclog the obstructed coronary artery. That is true. It is not possible to restore the obstructed coronary artery back to normal by any form of treatment. But we don't have to. What modern drug treatment does is to restore blood flow to the heart muscle in that part of the heart where blood flow is reduced. This is accomplished by dilating other blood vessels in the same area that are not blocked. At the same time other drugs reduce the workload of the heart so that the heart muscle requires less blood. This is like finding another source of income and reducing expenses if you lose your job. Once income to the heart muscle (blood flow) is adequate for the expenses (work load) of the heart, chest pains will disappear, and so will the risk of a heart attack or death..

At this point the body's natural adaptive responses take over with the formation of new blood vessels through angiogenesis (angio = blood vessels, genesis = birth of). The result is the formation of a vast network of small vessels that develop around the obstructed artery allowing blood to flow around the obstructed artery without resistance. In other words, the heart has put in its own bypasses with the help of medical therapy with modern drugs that is an alternative to bypass surgery. Unfortunately, such collateral vessels, as they are called, are not visible on an angiogram because they are too small to be seen by this primitive imaging technique. However, other imaging studies such as an echocardiogram or nuclear imaging will clearly show the heart muscle is functioning and contracting in a perfectly normal manner, even though the artery going to that area of the heart is partially or completely obstructed. How can that be? Obviously, blood is getting through to that heart muscle, even though this can't be seen on the angiogram---an imaging procedures that has been around since 1958 and has obvious limitations. Finally, modern drug therapy is more than just an alternative to bypass surgery and angioplasty. We now recognize that certain drugs such as beta blockers and Ace inhibitors actually slow down and even stop the progression of coronary artery disease, and may even reverse some of the changes that have occurred. Neither bypass surgery nor angioplasty are capable of doing this.

In summary, an alternative or alternatives to bypass surgery or angioplasty with modern drugs and other management techniques has changed the natural history of coronary artery disease. Like so many other diseases of the past that were lethal and are now considered benign because we have effective treatment, it is time to downgrade coronary artery disease from the lethal disease it once was, to a relatively benign disorder which, like arthritis, might bother you once in a while, but should not shorten your life or significantly change its quality.

Alternatives to bypass surgery and angioplasty
In those patients in whom there is significant narrowing of one or more coronary arteries, the heart muscle will remain chronically deprived of blood flow and oxygen. If the reduction in blood flow is large enough, the heart muscle will die and be replaced by a scar. If the reduction in blood flow is not enough to destroy the muscle, then the muscle will be able to survive and function to a limited degree. In the final analysis, both survival and function depend upon two things: blood flow and work load. The situation is very comparable to our daily living. How much money we have at the end of the month depends upon income and expenses. If our income decreases, to maintain the same lifestyle, we have to increase our income from another source. If that cannot be done, we have to cut back on our lifestyle by reducing expenses.

In the case of the heart, income can be equated to blood flow bringing in the necessary oxygen. Drugs are available to increase that blood flow by dilating the coronary arteries. Expenses can be likened to the load the heart has to work against; that is, any physical or emotional strain that causes the heart to labor more. High blood pressure would be an example of an increased work load.

Most drugs used for the treatment of coronary artery disease either reduce the work load on the heart, or they increase the blood supply. How effective one approach is compared to another depends entirely on the clinical situation. As a general rule, work load reducing drugs tend to be more effective than medications that increase the blood flow to the heart muscle.

Work load reducing drugs
There are several classes of drugs which will accomplish this. They include beta blocker drugs, calcium channel blockers, diuretics, and so called ACE inhibitors.

Beta Blockers
The prototype drug in this class is Inderal. This drug has been available for over 25 years and is the most effective of all the beta blockers. It combines with chemical receptors on the surface of the heart known as beta-adrenergic receptors. These receptors are chemically structured in such a way so that they can combine with certain adrenalin-like hormones secreted by the body. These hormones are naturally discharged whenever the heart has to increase its rate, or its force of contraction. This will quickly produce chest pain in individuals with obstructive coronary artery disease.

Beta blockers act by combining with the chemical receptors on the heart's surface, prevent the increase in heart rate caused by adrenaline-line hormones. The final outcome is one in which the heart does not require as much oxygen or blood flow to the heart muscle as it did before the use of beta blockers, and chest pain is prevented.

Beta blockers like Inderal have been shown to protect the heart from future heart attacks, and to reduce mortality in patients after a heart attack, when given on a chronic basis..

Calcium Channel Blockers
An entirely different class of drugs than the beta blockers are the calcium channel blockers. These drugs act by relaxing the muscular walls of all arteries including the coronary vessels. Relaxation of the musculature of a coronary artery will increase its diameter enabling it to carry more blood and oxygen to the heart muscle. In addition, since the arteries throughout the body also are affected, there will be a decrease in the resistance to the flow of blood, and a fall in blood pressure. The final effect will be a reduction in the work the heart must do, and a decrease in its need for oxygen.

Commonly used calcium channel blockers include Cardizem, Procardia, and Norvasc. The advantage of the calcium channel blockers is its dual effect of lowering blood pressure, and increasing coronary blood flow. In general, the calcium channel blocking agents are highly effective, safe, and when used with care, can be depended upon to provide considerable benefit in most patients who are symptomatic.

Drugs which increase blood flow to the heart
Nitroglycerine and Nitrates
Nitroglycerine and nitrates have been used to treat patients with chest pain (angina pectoris) due to coronary artery disease for over 100 years. Two kinds of nitroglycerine drugs are available. One is nitroglycerine available in various forms including sublingual tablets, an ointment, patches and an oral spray. The other preparations are generally referred to as nitrates and consist of tablets that are chewed or swallowed. The most commonly used drug is Isordil or isosorbide dinitrate.

Nitroglycerine and nitrates act by dilating the veins and arteries of the body. Since they preferentially enlarge the caliber of the veins, there is an increase in the blood carrying capacity on the venous side of the circulation. The result is a reduction in the amount of blood returning to the heart, a decrease in the volume of blood within the heart's chambers with each heart beat, and a fall in pressure. In the same way that less air within a balloon brings about less expansion and tension, so is there less pressure and tension within the heart muscle. Accordingly, there is less compression of the microcirculation and an increase in coronary blood flow. Nitroglycerine and nitrates also relax the muscle within the walls of arteries throughout the body including the coronary vessels. Not only does this directly increase coronary blood flow, but it lowers blood pressure and the amount of work that the heart must do.

The most popular form of nitrates besides Isordil are Sorbitrate, Cardilate, Dilatrate, and Peritrate. Various form of nitroglycerine skin patches also are used and include Minitran, Nitro-Dur and Transderm-Nitro.

Diuretics
Most doctors use only beta blockers, calcium channel blockers and nitrates in the treatment of angina pectoris. Few seem to be aware that one of the most effective of drugs in this condition are diuretics. Diuretics are drugs that aid in the elimination of fluid by the kidney. They are essential in the treatment of high blood pressure.

There are sound reasons for using diuretics in the treatment of patients with chest pain or shortness of breath with exertion, even in the absence of high blood pressure. All of the drugs conventionally used for the relief of angina tend to cause fluid retention. Since such fluids are equally distributed throughout the body tissues, this can have a profound influence upon the efficacy of the most useful of the anti-anginal medications, the nitrates. Nitrates act, in part, by dilating the veins of the body. To be absolutely correct, the term venules and small veins should be used since nitrates do not act upon the larger veins. Venules refer to the smallest veins in the circulatory system through which blood flows immediately after it leaves the capillaries. There are a tremendous number of such venules in the body, and they are capable of storing a considerable amount of blood. Such tiny vessels have no protection as do the arteries. There are no muscular fibers within their walls to resist compression or collapse. Consequently, they are quite susceptible to such compression whenever fluid retention causes the tissues of the body to swell. Doctors call such tissue swelling edema.

A great deal of edema must be present before a person is aware it is even there. The best example is in the swelling that occurs in our feet and ankles on long trips. Our shoes feel tighter and our feet swollen. Were it not for prolonged periods of dependency, we would never be aware that such fluid retention was taking place. The tightness we experience reflects the increase in pressure within the tissues. A similar increase in tissue pressure is present whenever there is edema, although we may not be aware of it. Women tend to be more familiar with this feeling than men because of premenstrual fluid retention. The female breast tends to be fuller and more tender in such circumstances.

The increase in tension and pressure within the tissue from fluid retention is sufficient to compress venules and small veins wherever it exists. If enough venules are compressed, the reservoir function of these vessels is eliminated. As previously described, nitroglycerine drugs work as they do because venules capture and store significant amounts of blood, which reduces the volume of blood entering the heart. The fall in pressure that follows, decreases the heart's work, and increases coronary blood flow. Therefore, whenever there is fluid retention, the effectiveness of nitrates is lost. Indeed, this may be one of the mechanisms to account for the development of tolerance to these drugs.

In addition to the fluid retention caused by beta and calcium channel blockers and nitrates, it may develop for other reasons. For example, fluid retention may be seen after stress, during urinary tract infections, and following the use of certain drugs used for pain relief. This latter group of drugs is often referred to as the nonsteroidal, anti-inflammatory drugs or NSAIDS. Fluid retention also may be noted after excessive food or fluid intake.

Such fluid retention is extremely common, and most victims are totally unaware it is present. While the evidence of such fluid retention can be identified by certain noninvasive tests, in most cases it cannot be detected by a doctor, even when the subject is aware that it is present. The signs are recognizable by those familiar with it, and include mild puffiness under the eyes, some difficulty in removing rings from the fingers, a feeling that shoes are tight, and a tightness of snug fitting clothes. Typically these are subjective feelings experienced by the patient and not objective signs that a doctor will notice. Nevertheless, they are important barometers that fluid retention exists.

Diuretics can prevent all this from happening. Usually it is necessary to take them both morning and evening. When this is done, regardless of the cause of the fluid retention, diuretics will eliminate the excess fluid from the body. Because diuretics also help to lower the blood pressure, these drugs, when used with other anti-anginal medications, are extremely effective in relieving symptoms.

ACE Inhibitors
Another group of drugs that may be effective in angina patients is the angiotensin converting enzyme inhibitors, more popularly referred to as the ACE inhibitors. Angiotensin is a hormone produced by the body, and it has the ability to elevate blood pressure. In order for this hormone to work, a converting enzyme is necessary to change its structure. ACE inhibitors prevent this from happening. Strictly speaking these are not anti-anginal drugs. However, they are highly effective in lowering the blood pressure. One of the goals of anti-anginal therapy is to lower pressure to minimize the work of the heart. Unfortunately, many doctors still cling to the old concept that a pressure of 130-140/75-85 is normal, and need not be of concern. Whether these numbers are normal is not the issue---what is overlooked is that a normal blood pressure is too high for someone with heart disease. Experience has shown that the patient with a low blood pressure has less chest pain and fewer heart attacks. Accordingly, the pressure should be reduced to the lowest level possible, as long as it doesn't interfere with the patient's activities. Furthermore, what is usually overlooked by physicians who believe values of 130-140/75-85 are normal, is that these numbers represent resting blood pressures. With stress, blood pressure can easily rise in seconds to 175/100, a value everyone would agree is abnormal. On the other hand, if the pressure is 105/70, and is carefully controlled with medication, stress is not likely to elevate the pressure. Even if it does, it will not be more than 10-15 millimeters of mercury. Clearly, it is less work for the heart if the pressure only rises to 115/80 compared to 175/100.

The prototype ACE inhibitor is Capoten. Vasotec is another useful drug. Unfortunately, both these medications have to be taken twice a day. Newer ACE inhibitors such as Zestril or Prinivil, Lotensin, Altace and Monopril only have to be taken once a day and are extremely effective.

Who Should Be Treated
While the problem of taking anti-anginal drugs to obtain relief of symptoms seems straight forward enough, and is not controversial, it is not so simple as it seems. Some background information is necessary for you to understand what is to follow. The matter involves the question as to whether a reduction in blood supply to the heart muscle always causes symptoms, and if so, how often does this occur, and is it potentially harmful? The medical term for this is ischemia.

When ischemia is mild, there may be no symptoms if it is brief. Even moderate to severe ischemia may not produce chest pain if the duration is only for a few minutes. If it lasts for 15-20 minutes, not only is pain likely to occur, but there probably will be some mild, reversible injury to the cardiac muscle. Ischemia for more than 30 minutes is apt to produce a heart attack---myocardial infarction in medical terminology, with irreversible damage to the muscle.

Up until the early eighties, there was little awareness of how frequently ischemia existed in patients with coronary artery disease, in the absence of chest pain. Studies at that time with the 24 hour EKG monitoring system known as the Holter monitor, demonstrated that cardiac ischemia was far more prevalent than anyone had ever realized. Not only was it more frequent, but 75% of all episodes were silent. Up until this time, the conventional wisdom was to give antianginal drugs only to people to relieve symptoms. If symptoms were abolished, then nothing further had to be done. The fact that many, if not most patients with coronary artery disease were experiencing ischemia without pain, changed the way heart disease had to be treated. The discovery of silent ischemia, as it came to be called, was a major turning point, particularly when it was recognized that silent ischemia might last for many hours every day. Why the ischemia is silent has never been adequately explained, but it will occur in most patients, even in those who also have symptoms.

The question that needs to be answered is whether silent ischemia should be treated, and if so, how intensively? The problem will not be easy to solve. At least when symptoms are present, the doctor can easily determine if the patient's medical program is adequate. If it is, then symptoms will disappear. If it isn't, the patient will continue to have chest pain. In the absence of symptoms, there will have to be other guide lines to determine success or failure. One approach would be to repeat the Holter Monitor at regular intervals; however, this can become costly and is time consuming. Additional ways to determine if the functional status of the heart is improving were discussed in the previous chapter. Whatever approach is used, it is just as important for silent ischemia to be avoided as it is for symptomatic ischemia.

What might be the advantages of treating silent ischemia? Indeed, why is it even necessary, as long as it is not disturbing the patient? Chest pain is not the only symptom, nor even the most frequent indication of coronary artery disease, but it is the one that gets the most attention. Far more prevalent is fatigue of the exertional variety. Typically, patients find that they may be able to do what they always did, but not for as long. They just get tired. After an appropriate rest, the activity can be resumed. Many individuals learn to avoid those efforts that produce fatigue. Except in extreme cases, usually this is not an inconvenience. Unfortunately, this leads to gradual deconditioning of the entire body with a negative impact on cardiovascular function. In fact, ultimately, more patients are limited by their deconditioned state than they are by their cardiovascular disease. Accordingly, any medication that will improve blood flow to the heart, or decrease the heart's work load, will increase exercise tolerance and help prevent the vicious circle of deconditioning.

The second reason why silent ischemia should be treated is to prevent the progression of the complications of chronic cardiac ischemia. Whenever there is damage to a segment of heart muscle, and it is unable to move, the segment on the opposite muscular wall will compensate by contracting more forcefully. In this way the same amount of compression of the heart's chamber takes place, but one wall of the heart may have to move twice the distance as it once did. In time this causes the harder working segment to stretch, and the heart to enlarge. Whenever this happens, the work of the heart increases, stimulating further stretching and enlargement. Eventually, the muscle loses its elasticity, and the heart begins to fail. Once heart failure begins, most patients will die within just a few years.

It would seem logical that prevention of ischemia would prevent this cascade of events from taking place. In fact, that is exactly what occurs. In patients on a full medical program designed to minimize or eliminate ischemia, particularly of the silent variety, there is a dramatic reduction in the complications of chronic ischemic heart disease. Heart failure rarely occurs, the incidence of recurrent heart attacks is very low (1-2% per year), and mortality rate is also extremely low (1-1.5% per year). Because the progression of the disease is extremely slow on such a program, more heroic treatments such as bypass surgery or angioplasty are needed only rarely. A good medical program will allow a patient to be symptom free and enjoy a normal life span. Whether this happens or not depends entirely on the ability of the cardiologist to identify patients with silent ischemia who stand to benefit the most from a medical program similar to the one described in this chapter. Patients who have symptoms will be treated, for they demand attention. It is those without symptoms who have the most to gain, and the most to lose if they are ignored. If you have coronary artery disease, your survival will largely depend upon whom you chose to treat you. So choose well!