The Noninvasive Heart Center
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Point of View---A Life or Death Matter


Howard H. Wayne, M.D., F.A.C.C., F.A.C.P.
The Noninvasive Heart Center of San Diego
San Diego, California, U.S.A.


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.


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. A 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.


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.


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.


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.


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.


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.