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While CAD can be a very dangerous disease, there are many means available to treat it. See and learn more by following the links.

MEDICATIONS. Medications are very useful in the treatment of CAD, and are used in virtually every case. While the ideal medicine, one that would simply quietly and completely "dissolve" the blockages, has not yet been found, some classes of medicines to reduce the blockage to some degree are currently available. Blood thinners, often "simple" aspirin, is indicated in almost every case. Other medicines provide their relief by decreasing the amount of work the heart is asked to do (and subsequently decrease its need for blood) by lowering the pulse rate and blood pressure.

ANGIOPLASTY. There are now several types of procedures which work on the inside of the arteries with catheters introduced from the groin. "Balloon" procedures (PTCA) were the first, and are still the most widely used. "Stents" (small metal cylinders placed with a balloon catheter) remaining in the artery are becoming much more popular. Rotoblators are used to pulverize the plaque into very small fragments which are washed away by the blood. "Athrectomies" use catheters which remove plaque and/or clot procedures. "Lasers" also are used in selected situations, although not very commonly.
[ Perform an angioplasty ]

SURGERY. The major type of surgery available for CAD is bypass surgery. Despite advances in the catheter-based techniques noted above, there are many situations in which bypass is necessary and beneficial. Recent improvements have simplified the procedure in some cases as well.
[ Perform a bypass surgery ]

Regardless of which type of therapy is used initially, it is very important to control those factors which lead to its development in the first place:

My doctor says I can't have balloons or bypass surgery, and medications aren't doing me enough good. Is there anything else for me?

There are several therapies that are being investigated and which show some promise for treatment of "intractable angina".

TRANSMYOCARDIAL LASER REVASCULARIZATION. Lasers have always held a fascination for humans. Previous laser techniques to open arteries in a manner similar to angioplasty are used very uncommonly now. But this new technique, TMR, holds more promise. After opening the chest, lasers are used to create tiny holes from the outside of the heart toward the inside, without causing perforation all the way through if possible. These small channels allow blood to be supplied to the heart muscle in areas where angioplasty or bypass surgery are not feasible. It is possible to combine bypass procedures with TMR as well. Less invasive surgical approaches are being developed, as are catheter-based approaches to TMR.

ENHANCED EXTERNAL COUNTERPULSATION. This technique has been used in China for decades, and is currently being investigated in the United States. In this technique, three sets of inflatable cuffs are placed around the calves, thighs, and buttocks. These are inflated rhythmically in timing with the heart to augment flow. The technique works presumably by enlarging "collateral circulation", that is opening channels for blood to be routed to areas which lack good circulation from areas that do. This has had a surprisingly good long-term benefit in the patients studied to date.

What about chelation therapy?

This subject is about as emotional as any I've ever been associated with in medicine. Chelation is a term describing compounds which bind molecules, typically metal ions, within it. There are numerous chelating agents in the world; the one used in the current context is EDTA. Some have narrow but well-defined uses in mainstream medicine.

EDTA chelation has been advanced for years as a possible agent for reversing atherosclerosis. This was initially felt to be on the basis of removing calcium from atherosclerotic plaques, a concept which is in line with layman's understanding of atherosclerosis as "hardening of the arteries". Time has educated many in the medical community, and shown that calcium in atherosclerotic plaques are not the major issue, and that removing it will leave the majority of the plaque and its active fat and cholesterol intact. More recently, claims of an anti-oxidant effect have been advanced. This likewise has multiple potential flaws in scientific theory, and minimal data.

The emotional issues must be considered in any discussion of this field. Most often, these cannot be overcome to sustain a rational discussion by either "side". Proponents will claim that mainstream medicine has conspired to prevent chelation from becoming accepted to protect the lucrative areas of bypass surgery, angioplasty and the like. Claims of the pharmaceutical industry's inability to make money secondary to a loss of patent rights are often cited as a reason that EDTA is outcast (there are in fact thousands of patents on the uses of EDTA in medicine). One must point out that the chelators also have a very lucrative market, and the question in this instance would simply be is the chelators likewise afraid that his technique will be used less frequently if studied? Claims of conspiracy and greed are neither novel or compelling, only sure to produce an emotional response. I can only say that as a member of the supposed group conspiring, it has been well hidden from me. This issue should be ignored in any rational discussion.

In an era where mainstream medicine has made EVIDENCE its highest standard, there is not sufficient data to support the use of chelation therapy. This in conjunction with its lack of sound scientific theory should simply make one suspicious of its possible merits.

Despite these flaws, one should consider the proof in the pudding however. Even if we don't understand it or the reasons for working may be flawed, it may indeed work. Over the course of 40-50 patients who have told me they have undergone chelation, I have seen one case that I believe improved with the therapy. Others who promote the therapy would claim a 90% improvement rate. I can only say I have seen some of the worst arteries in my experience in patients who have undergone chelation. In its greatest sense, its expense is generally quite high and its benefits questionable. In fairness, if properly administered, the risks of complications are low. The risks of not using more proven therapies may however be quite high. I would consider recommending that a patient consider chelation only in a few very specialized situations.

In the greater context of "alternative therapies", chelation occupies a central position in any "wars" that exist with "traditionalists". The World Wide Web is the hottest of hotbeds supporting chelation and non-traditional therapies. Traditional medicine can hardly be surprised with the popularity of alternative therapies, however: people and patients will continue to be sick, sometimes not improve with therapy, and always eventually succumb to an illness. If this is the case, then traditional medicine cannot claim to have all of the answers, and some patients will therefore look elsewhere. Any arrogance with which patients are treated only serve to accelerate this tendency. As with this area and any other, use as good of judgment as you can muster. There may be alternative techniques that are useful ˝ discuss them with your traditional physician. There are "mainstream" techniques that are clearly proven to be of benefit. Use them and discuss them with your alternative therapist.

Can vitamins help?

There has always been an appeal to the use of "natural" substances, such as vitamins and minerals. In heart disease, attention has been focused most intensely on vitamins with anti-oxidant properties: beta-carotene, vitamin E and vitamin C. Diets high in these naturally occurring substances are associated with increased longevity. It is not as clear whether supplements will be as effective. In other words, the benefits may very well be different for vitamin C taken from, say an orange, as from a vitamin pill.

While I think there is good evidence that certain of these substances can be helpful as outlined below, beta-carotene would seem to be a case pointing out the assumption that "natural" substances necessarily will be effective. Beta-carotene is an anti-oxidant material found naturally in many foods which the body converts to vitamin A. While a diet rich in beta-carotene (spinach, carrots, etc.) does have health benefits, a supplement of beta-carotene given to more than 11,000 male physicians did not reduce the risk of heart attacks. In fact, in this and other studies, there was an increased risk of heart attack in the group taking the beta-carotene supplement. In addition, there are studies showing an increased risk of lung cancer among smokers who take the supplement. It is a long jump between "makes sense" and "it works".

A study published in 1997 showed an increased risk of heart attacks in smokers who took Beta-carotine, and to a less degree, vitamin E. In this case, it may be smarter to "Don't take your vitamins".

On the other hand, vitamin E taken as a supplement of 400-800 units daily has been shown in at least one study to reduce the risk of a second heart attack. Vitamin C (500-1000 mg. daily)is taken by many physicians and others in the hopes that its anti-oxidant properties will be helpful.

What about this other substance I've heard about . . . homocysteine?

Homocysteine is an amino acid, the building blocks of protein, which are in our body. Amino acids aren't "bad" in general, but high levels of homocysteine have been correlated with damage to the walls of arteries and veins, and furthermore cause platelets to become unusually "sticky". Thus, while homocysteine is not deposited in the walls of blood vessels like cholesterol is, it can damage the inside lining of the vessels, and allow the cholesterol to be more easily deposited. Furthermore, it can give patients a "double whammy" by making the platelets more likely to adhere and form a clot, a situation which can lead to heart attacks and strokes. This may be particularly important in the young and in women who do not otherwise seem to have enough risk factors to explain their vascular disease.

Here's some technical aspects of homocysteine metabolism if you’re interested (skip this paragraph if you’re not). Homocysteine is not generally found in high quantities in the food we eat, but is formed from another amino acid which is in our diets, methionine. Homocysteine can be further broken down to cystathionine, and then cysteine which can be broken down and excreted in the urine. In addition, homocysteine can be turned back into methionine. The original hints of homocysteine’s tendency toward causing vascular problems was noted in children who lacked the enzyme to convert homocysteine to cystathionine, and homocysteine eventually overflows into the urine (the name of the disease is therefore "homocystinuria"). This is a rare disease associated with mental retardation and other disorders, but there is also a 50% chance of having a clot involving the arterial or venous system by the age of 30. Some, and it appears this maybe "many", have inefficiencies in the metabolism of homocysteine. Variations in the gene that codes for the enzyme that converts homocysteine to cystathionine have been described, and were recently correlated with vascular risk (Schwartz et.al. Circulation 1997:96:412-417).

Back to the real stuff, this most recent study. Norwegian investigators studied a population of patients with known blockage of the heart vessels (coronary artery disease) and correlated the levels of homocysteine in the blood with mortality at 5 years. 6% of those with levels less than 9 micromoles per liter died, 19% with levels from 9-20 died, and about 32% with levels greater than 20 died. Impressive study. (Nygard, O et al. Plasma homocysteine levels and mortality in patients with coronary artery disease, New England Journal of Medicine 1997;337:230-236).

Fortunately, the metabolism of homocysteine can be helped along by the availability of vitamins that stimulate the pathways favoring its breakdown (vitamin B-6) or reconversion to methionine (B-12 and folic acid [or "folate"]). These vitamins are found in abundance in fish, and dairy products, cereals, and fruits – all of the stuff you were supposed to be eating anyhow! Relatively modest doses of these vitamins have been shown to reduce homocysteine levels significantly:

B-6 (or "pyridoxine") in a dosage of 50-100 mg daily
Folic acid (or "folate") in doses of 400 or more micrograms daily
B-12 probably is important only in those with frank deficiencies

These are comparable to the amounts of these common vitamins that are found in many multivitamin preparations. It is to be stressed that the proper doses of these vitamins has not been determined however, and these are "best estimates" only. It would appear that they are good estimates however – patients in a study from 1997 published in the Journal of the American Medical Association again showed a marked increase in the risk of vascular disease in patients with high homocysteine levels, but that the risk appeared to be lower in those who took multivitamins (Graham et. al., Plasma homocysteine as a risk factor for vascular disease).

You may want to discuss having your homocysteine level determined, or undergoing a "methionine loading test" to see if your levels are high, or whether they are responding to therapy.

Well, is homocysteine something else to worry about? No, worrying won't do a thing about it . . . but I think it is something to take care of. While the authors of the NEJM article recommend further studies, I think there is enough data to act, particularly since the treatment has little in the way of side effects. Eat those green vegetables and fish. If you can't, or this is insufficient, take vitamins as noted above.
ęCOPY 1997 HeartPoint     Updated July 1997

 



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