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Journal of Integrative Medicine 1997;1:7-12

Improved Myocardial Perfusion in Patients with Advanced Ischemic Heart Disease with An Integrative Management Program Including
EDTA Chelation Therapy

Majid Ali, M.D., Omar Ali, M.D., Alfred Fayemi, M.D., Judy Juco, M.D.,
Carol Grieder-Brandenburger, R.N.

From the Departments of Medicine of Capital University of Integrative Medicine, Washington, D.C., and Institute of Preventive Medicine, New York (MA,OA,AF,JJ, CG), the Department of Pathology, College of Physicians and Surgeons, Columbia University, New York (MA), and Department of Pathology, Mount Sinai School of Medicine (AF). Send requests for reprints to MA at Suite 1-H, 140 West End Avenue, New York, N.Y. 10083. This outcome study was presented in part at the 1995 annual meeting of the American Academy of Preventive Medicine in New York.

Objective
    To assess the clinical efficacy of an integrated management program including nutritional and herbal therapies, nongoal-oriented exercise, self- regulation, and EDTA chelation therapy for patients with advanced ischemic heart disease (IHD).

Patients
    Twenty-six consecutive patients who presented with advanced ischemic heart disease and who had fared poorly after one or more coronary bypass operations (5), one or more angioplasty procedures (6), or who failed to respond adequately to multiple drug therapies (15), and who had received a minimum number of 20 EDTA infusions. Duration of follow-up ranged from 15 months to 9 years.

Methods
1. Clinical evaluation of patients before, during and after the integrated program used in this study. 2. Assessment of myocardial perfusion by comparative study of thallium perfusion scans performed before and after the IHD reversal program.

Clinical Outcome Measures
The following clinical outcome criteria were semiquantitatively defined: Excellent outcome, absence of significant symptoms and discontinuance of previously prescribed drug therapies; good, 75%+ relief of symptoms and reduction of drug dose; moderate, 50%+ relief of symptoms and reduction of drug dose; and poor, 25% or less relief of symptoms and reduction of drug dosage. Elements for follow-up included in the clinical outcome sheet were as follows: angina, chest tightness and related discomfort, arrhythmia, other chest symptoms, dyspnea, severity of stress, mood changes, anger, energy level, quality of
sleep, appetite, digestion and frequency of bowel movements (all clinical parameters that determine the degree of AA oxidopathy—a state of chronic and insidious accelerated oxidative molecular injury to all elements of the circulating blood which we consider to be the core pathogenetic mechanism of IHD.1)

Results
Clinical outcome data are as follows: excellent 61%, good 17%, moderate 13%, and poor 9%. Comparative study of pre- and post-chelation myocardial perfusion scans showed clear, objective evidence of significant improvement in myocardial perfusion in five of six patients in whom such studies were performed. No patients during the study period suffered an acute myocardial infarction or underwent angioplasty or coronary bypass operation.

Conclusion
Preliminary and limited outcome data in this study indicate significant potential for reversing IHD in patients with advanced ischemic heart disease by an integrated management plan with global emphasis on reducing oxidative stress on the circulating blood, cardiac myocytes and the conducting system of the heart. The program included nutritional and herbal therapies, self-regulation, nongoal- oriented exercise and EDTA chelation therapy. Additional and larger studies are warranted to fully explore the clinical potential of such an integrated management plan.

INTRODUCTION
    In the United States, advanced IHD is generally managed with one of the following four approaches: (1) pharmacologic regimens comprising multiple drugs; (2) mechanical approaches to segmental coronary arterial lesions, such as angioplasty and coronary bypass surgery; (3) holistic nutritional, herbal, and stress-reduction therapies; and (4) integrative programs that include EDTA chelation infusions in addition to therapies included in the third category. In mainstream cardiology, patients who fail to respond to multiple drug therapies, angioplasty, and bypass surgery generally continue to be managed with ineffective trials of drugs in various combinations. The efficacy of mechanical approaches to segmental coronary lesions in such patients is admittedly poor, even for the staunchest supporters of such therapies. The reason for failure of such therapies is that neither the pharmacologic nor the mechanical coronary approach addresses any of the pathogenetic mechanisms involved in IHD.1,2 Not unexpectedly, there is widespread disillusionment with such therapies.3-11

Patients with failed drug and mechanical therapies sometimes show dramatic improvement when they are managed with integrative, holistic therapies. However, such promising clinical outcomes are rarely, if ever, documented in mainstream literature. There are three reasons for this. First, holistic practitioners are seldom funded to undertake systematic clinical outcome studies. Second, such practitioners have seldom been trained to write papers that meet publication criteria. Finally, on the rare occasions that such reports are submitted by holistic practitioners, the editors of established medical journals readily—and regrettably—reject those reports because of their ingrained prejudice against the outcome being reported. As for the integrative management plans that employ EDTA chelation, several reports show promising results12-25; however, the data for patients with advanced IHD in such reports is often blended with those for patients with milder forms of disease or those without clearly documented IHD.
    In this report, we present outcome data for a series of patients with advanced IHD who received little or no benefit with intensive and extended pharmacologic therapies, angioplasty, or coronary bypass surgery, and who were managed with an integrated management plan that focused on the following issues: adrenergic hypervigilance; optimal hydration and food choices in the kitchen; empirical nutrient and herbal therapies; nongoal-oriented slow, sustained exercise; and a series of intravenous EDTA infusions.

PATIENTS AND CLINICAL OUTCOME RECORDS
    We established the following two criteria for entry of patients in the study: (1) consecutive patients presenting with advanced IHD who were deemed failures of angioplasty, coronary bypass operation, and extended multiple drug therapy; and (2) completion of at least 20 EDTA infusions.

    There were 26 patients (21 males, 5 females) with an average age of 65 years (range 42 to 76). Of those, 6 patients had undergone coronary artery bypass procedures; 5 had undergone angioplasty; six patients had been advised angioplasty or coronary bypass surgery but had declined; and the remaining 9 patients suffered intractable coronary symptoms unrelieved by multiple drug therapies. Duration of treatment ranged from 15 months to 9 years.

INTEGRATIVE PROGRAM FOR ADVANCED IHD
    This study was designed as an open trial and no attempt was made to narrowly define the management plans or to blind any member of the team providing the care. Indeed, attempts to set limits on the integrative therapies that the managing physician may include in the management of a given patient or to establish placebo controls would not only have violated the spirit of integrative medicine, such attempts would have been doomed to failure.

    The integrated program for arresting and reversing advanced IHD employed in this study comprised global strategies for controlling accelerated oxidative stress on the circulating blood and had the following seven major components: (1) education; (2) self-regulation; (3) food choices; (4) limbic exercise; (5) nutritional therapies; (6) herbal protocols; and (7) EDTA infusions.

1. Education

    We recognized a special need to educate patients in the study of three specific areas: (1) philosophy, principles and practice of integrative medicine (focus on the whole person rather than his diagnostic category); (2) the scientific basis of the oxidative phenomena that cause IHD (oxidative coagulopathy and AA oxidopathy occurring in the blood rather than the tissue damage in the coronary arterial walls)1; and (3) the integrative management plans that arrest oxidative coagulopathy and AA oxidopathy, and set the stage for reversal of IHD. As discussed at length in the companion article in this issue of the Journal,1 our concept of the etiology of IHD, and the management approach to advanced IHD based on it, is radically different from the prevailing opinions in mainstream cardiology, to which the patients in the study were exposed before seeking care at the Institute. We recognized that the patients could not give us informed consent for entry into the study unless they were well informed about all such issues. Under ordinary circumstances, this would have been a daunting task of patient education for any institution. However, for over a decade the Institute staff has focused heavily on issues of patient education and has prepared an extensive library of audio and videotapes as well as books discussing at length the issues of health-dis-ease-disease continuum, nutrition, metabolism, and the energetic- molecular basis of degenerative disease. Specifically, books were written, and videotapes and audiotapes were prepared, to explain in simple language scientific concepts of the following: spontaneity of oxidation in nature26-27; molecular duality of oxygen, iron, nitric oxide and other redox-active molecular species28-29; evidence of oxidative damage to circulating blood seen with high-resolution, phase-contrast and darkfield microscopy30,31; electrophysiologic patterns of myocardial activity and pulse pressure in states of adrenergic hypervigilence32-33; changes in such patterns caused by meditative methods including
Limbic Breathing.34-35 Other books and tapes addressed the issues of optimal choices in the kitchen36;proper hydration37; need for avoiding rapid hyperglycemic-hypoglycemic shifts and hyperinsulinemia,38 slow, sustained, noncompetitive and nongoal- directed limbic exercise39,40; and effective methods of self-regulation.41-43 Special lecture-seminars were organized to further facilitate understanding of the principles and practice of integrative medicine as well as reversal of advanced IHD. Additional detailed information was provided in the form of easy-to-read booklets covering subject matters of optimal food choices in the kitchen for reversing IHD,44 limbic exercise, and accelerated oxidative molecular stress.

2. Self-regulation

    The clinical experience at the Institute made it abundantly evident to us that chronic, insidious adrenergic hyperactivity plays a critical role in the cause of clinical syndromes associated with IHD. In a companion article in this issue of the Journal,1 we have discussed at length the effects of anger, stress, and other lifestyle elements on the clinical course of IHD. In recognition of that, our program relied heavily on meditative methods for abating adrenergic hypervigilance, for stress control, and for addressing issues of anger, hostility, fear, and anxiety. In The Cortical Monkey and Healing32 and
What Do Lions Know About Stress?,45 we have described meditative methods, as well as the spiritual work, used in our program. Specifically, we emphasized the practice of Directed Pulses46 and Limbic Breathing34 for slowing the heart and respirations rates and for lowering blood pressure. The training was given in self-regulation seminars held at the Institute and with audiotapes given for use at home.

3. Food Choices

    Detailed discussions of the principles and practice of clinical nutrition as employed in our program have been described in
The Butterfly and Life Span Nutrition .47 Briefly, the essentials of our recommendations for food choices are the following: (1) diligent avoidance of foods that generate sudden hyperglycemic- hypoglycemic shifts and cause rapid surges of insulin and catecholamines; (2) partially-hydrolyzed protein formulations containing 85-90% amino acids used to further relieve stress on glucose-insulin dynamics; (3) ample supplies of essential oils (cold-pressed olive, flaxseed, sesame and pumpkin oils taken cold with salad, uncooked vegetables or other cold foods); (4) avoidance of foods with oxidized, denatured fats; (5) frequent consumption of foods items such as ginger, onions, garlic and others that are empirically known to improve rheologic characteristics of blood; (6) liberal nutrient supplementation of antioxidant vitamins, minerals that support antioxidant enzyme systems and miscellaneous items. Table 1 shows the general range of dosage of nutrient supplementation and herbal protocols employed in the program. It is important to emphasize that nutrient and herbal protocols were prescribed and food choices recommended for individual patients on the basis of evaluation of the specific needs of individual patients, and participating physicians were asked not to limit themselves to any algorithm. Again, this is totally consistent with the principles and practice of integrative medicine. The complete listings of the individual nutrient and herbal protocols have been previously published.48 The advice concerning breakfast focused on issues of: (1) overhydration from morning to early afternoon hours; (2) avoidance of carbohydrate overload (and hence, glucose-insulin-adrenaline roller coasters); and (3) avoidance of oxidized and denatured fats.

4. Limbic Exercise

    According to the Centers for Disease Control of Disease (CDC), lack of physical exercise contributes to more than a third of approximately 500,000 annual cardiac deaths.49 In recognition of such statistics, cardiac rehabilitation programs have sprouted everywhere in the United States. However, almost all such programs emphasize mechanical aspects of exercise with focus on changes in the heart rate, ventilatory parameters, metabolic rates, and duration and intensity of exercise. Extensive empirical experience in the care of severely ill patients led us to challenge this view.39,40
We are convinced that for physical fitness, the Eastern methods of physical fitness that emphasize energy dynamics, fluidity and spontaneity of motion offer far superior results. Thus, our program focused on meditative, slow, sustained, noncompetitive and nongoal-oriented exercise which we designate limbic exercise.39,40 Specifically, our purpose was to help our patients free their bodies from the performance demands of their analytical mind. Training was given using exercise workshops and a specially prepared limbic exercise video. In limbic exercise, frequency of limbic stretching and exercise is considered important and fixation on matters of intensity and duration of exercise is regarded as counterproductive. Once understood and practiced, most of the patients in the study group expressed clear preference for limbic exercise over the traditional cardiac rehabilitation programs. The details of those methods have been published previously in The Ghoraa and Limbic Exercise.39 It is noteworthy that a panel of exercise researchers convened recently by the CDC and the American College of Sports Medicine reported that people need not engage in vigorous exercise to improve their health.49 We also wish to point out that the issue of meditative limbic exercise is especially critical in the management of patients with advanced refractory IHD.

5. Nutrient Therapies

    In accordance with the core principle of integration of safe and empirically-effective therapies, we made no attempt in this study to isolate the clinical benefits of individual nutrient or herbal therapies in our program. Rather, our focus was on integrating as many empirically effective components as could safely be done. Again, the choice of nutrient therapies was made in order to avoid: (1) dehydration; (2)
sugar and simple carbohydrate overload; (3) sugar- insulin-adrenaline roller coasters; (4) food sensitivity reactions; (5) prolonged bowel transit time (desired goal: two to three odorless, effortless bowel movements a day); and (6) avoidance of meals that interfere with sound sleep. The table 1 shows the amounts of the main agents we used. The scientific basis and/or rationale of our use of nutrient and herbal protocols have been described in RDA: Rats, Drugs and Assumptions.50,51

6. Herbal Protocols

    Herbs have been prescribed by herbologists to improve the rheologic characteristics of blood for centuries. They prescribe some herbs for the empirical "blood thinning" effects—the direct prevention of oxidative coagulopathy in the context of AA oxidopathy—while they employ other herbs for the empirical cleansing effects on the colon—the indirect prevention of oxidative coagulopathy by restoring altered states of bowel ecology and correction of increased bowel permeability. For this study, we used the following herbs and plant-derived substances for the former category: hawthorn berry tincture, ginger, garlic, onions, cayenne, turmeric, and some others included in table 1. The elements used in the latter category included the following: echinacea, astragalus, burdock root, goldenseal, pau d'arco, alfalfa, cat's claw, Devil's claw and some others shown in Table 1. The compositions of such protocols have been detailed elsewhere.52

7. EDTA Infusions
    Extensive experience with clinical states characterized by accelerated oxidative stress has convinced us of the value of a series of EDTA infusions for arresting AA oxidopathy and for reversing cellular and tissue damage caused by microclots and microplaques circulating in the bloodstream. As for the clinical efficacy of EDTA therapy for managing and reversing coronary ischemic heart disease, the published studies generally have lacked objective evidence of improved myocardial perfusion. The details of EDTA infusions employed in this study have been published.53

Diagnosis and Management of Ig-E-mediated Disorders
    In the companion article of this issue of the Journal1, we present direct morphologic evidence for the role played by fungemia—and, by implication, mycotoxicosis—in pathogenesis of oxidative coagulopathy and AA oxidopathy. We consider it important to address this issue in the management of patients with advanced IHD when the existence of
yeast overgrowth in the blood can be proven with high-resolution, phase-contrast microscopy.1 For patients with clinical history of allergy, we performed micro-elisa assays for Ig-E antibodies with specificity for mold as described previously.54,55 When high levels of mold- specific IgE was found, patients were administered antigen immunotherapy according to previously published protocols.56,57

Standard Cardiac Care and Reduction and Discontinuance of Drug Therapies
    All patients in the study were required to continue drug regimens begun by their primary care physicians and/or cardiologists since the Institute staff does not provide in-hospital care. Specifically, they were asked not to delay standard cardiac care if symptoms persisted or acute symptoms developed. As their conditions stabilized on our program, their pharmacologic therapies were reviewed and suggestions were made to gradually decrease the drug dosage. Initially, we expected this to pose a problem of how to integrate our cardiac care program with the care of the patients' cardiologists who, with rare exceptions, were evidently hostile to our efforts. In actual experiences the task of decreasing the dose of drugs—and, when safely possible, discontinuing drug use altogether —proved not too difficult. We waited until patients showed clear clinical and laboratory evidence of stabilization of their cardiac status. Only then—and in most cases only after several months of beginning our integrative program when patients could see for themselves evidence of stabilization—did we begin the closely-monitored, slow process of reducing the amounts and frequencies of their drug regimens.

TABLE 1. NUTRIENT AND HERBAL PROTOCOLS

Nutrient & Herbal Protocols Main Components
Antioxidant Vitamins C, 4-6 gm; A 10,000 IU; E, 400-600 IU
Antistress Thiamine, riboflavin and pyridoxine, 30 mg each; Niacinamide, 150 mg; Pantothenic acid, 220 mg; Biotin, 100 mg; Folic acid, 400 mcg; Choline and inositol, 50 mg each; Zinc, 4 mg; and others51
Circulation Magnesium oxide 250 mg; Taurine, 300 mg; Choline bitartrate, 50 mg; Carnitine, 20 mg; Bromelaine, 25 mg; and others51
TPM Taurine, 500 mg; Magnesium sulfate, 300 mg, Potassium citrate, 100 mg
Mineral Chromium, 100 mcg; Selenium, 400 mcg; Molybdenum, 1,000 mcg; Copper, 1 mg; Manganese, 5 mg
Lipid (lipotropic factors and others) Choline, 100 mg; Inositol, 100 mg; Methionine, 100 mg; lecithin, 200 mg
Bowel Ecology51 Echinacea, Astragalus, Burdock root, Goldenseal, Pau d'arco, Artemisia, Alfalfa and others in doses of 350 to 750 mg.
Blood Ecology Butcher's broom, hawthorne, mother's wort, St. John's wort, bilberry, cayenne, turmeric, ginger, dandelion and garlic.
Miscellaneous Herbs52 Ginger, garlic, celery and others.
Medicinal Foods58 Broccoli, burdock, celery, daikon, flaxseed, garlic, ginger, grapefruit, klongi, soybean, squashes and green leafy vegetables.

COMPOSITION AND ADMINISTRATION OF EDTA PROTOCOL
    The composition of ethylenediaminetetraacetic acid (EDTA) infusion protocol used in this study is shown in Table 2. EDTA has a greater affinity for magnesium than for sodium; hence, magnesium readily displaces sodium in the EDTA salt. The components heparin and sodium bicarbonate are used as rheologic agents. The frequency of infusions was weekly except in cases of persistent symptomatology and a high risk of recurrent infarction, in which case EDTA was administered on a twice-weekly basis for the first two to three weeks. The issues of informed consent, clinical and laboratory evaluation, vein access, maintenance of the infusion, protocols for detection of adverse effects during EDTA infusion, and supplemental nutrition have been described previously.
59

TABLE 2. COMPOSITION OF EDTA PROTOCOL

EDTA (sodium salt)

1.5 gm

Magnesium sulfate

2,000 mg

Sodium bicarbonate

2.5 Meq

Multivitamin

*

Heparin

4,000 Units

Normal saline

150-400 ml

Vitamin C

5 gm

Pantothenic acid

500 mg

Pyridoxin

200 mg

Vitamin B12

1,500 mcg

* Multivitamin protocol includes the following: thiamine, 25 mg; riboflavin, 5 mg; niacin, 50 mg; niacinamide, 50 mg, pantothenic acid, 12.5; pyridoxin, 7.5 mg; ascorbic acid, 500 mg; vitamin A, 5,000 IU; vitamin D, 500 IU; vitamin E, 2.5 IU.

RESULTS
    None of the 26 patients in the study underwent angioplasty or coronary bypass during the study period. Two patients required hospitalization for chest symptoms: the admission of the first patient was precipitated by extreme stress resulting from vandalism and violence. No evidence of myocardial ischemia was found after the workup. In the second patient, an electrocardiogram showed evidence of acute myocardial infarction.
    The clinical outcome data are shown in Table 3. The clinical response in seventy-eight percent of patients was deemed excellent according to outcome criteria indicated in the section dealing with clinical outcome measures. Only 9% of patients failed to respond satisfactorily.

TABLE 3. CLINICAL OUTCOME DATA

Excellent

61%

Good

17%

Moderate

13%

Poor

9%

An Illustrative Case History
   
A 67-year-old man underwent coronary bypass surgery in 1987. When first seen at the Institute in 1989, he experienced daily angina attacks and periods of arrhythmia. His symptoms persisted in spite of daily use of Inderal, Vasotec, Ativan, sublingual nitroglycerine, and aspirin. He was homebound due to angina at rest and cardiac arrhythmia. A second coronary bypass was recommended, but prognosis after surgery was considered guarded. The patient refused surgery. The integrated program as outlined above was instituted, including initial weekly EDTA infusions. After 21 months and 45 EDTA infusions, his daily episodes of angina at rest had largely subsided and his clinical condition stabilized enough to permit discontinuance of Inderal and Ativan. About three years after beginning the program, he was walking one mile a day without any chest symptoms. He experienced occasional episodes of chest pain, which he effectively controlled with limbic breathing. All pharmacologic therapies were discontinued at 52 months. The patient declined a repeat thallium scan to assess myocardial perfusion. In 1995, six years after beginning the program, he was hospitalized for chest pain following vandalism of his property and physical violence. A cardiac work-up did not disclose any evidence of myocardial infarction. Now in 1997, he is drug-free and symptom-free.

Comparison of Pre- and Postchelation Myocardial Perfusion Thallium Scans
    Comparative studies of pre- and posttreatment thallium myocardial perfusion scans were conducted by radiologists. They reported objective evidence of improved myocardial perfusion in 5 of 6 patients. The essentials of the radiologist's report in one of those cases are shown in Table 4.
    We quote below excerpts from the radiologists' reports of the comparative study of pre- and posttreatment thallium myocardial perfusion scans for three patients:
    Case 1: 67-year-old male with history of acute myocardial infarction. "Partial redistribution to the inferior wall seen on delayed images of pre-chelation scans not observed on post-chelation study...no inferior wall scarring seen. Triple bypass at 65; 36 chelation infusions. Today's (post-chelation) images demonstrate that the intensity of activity in the inferior wall is greater than noted on the prior (pre-chelation) redistribution images."
    Case 2: 56-year-old woman. Coronary bypass recommended but declined. 29 chelations. Activity increased from walking less than a block to being able to walk three miles. Radiologist's report: "Pre-chelation perfusion scans showed "diminished activity in the inferolateral segment which is fixed on the delayed films and most likely represents infarct." Post-chelation showed "diminished activity without any fixed defects."
    Case 3: 71-year-old male; S/P angioplasty; 34 EDTA infusions. Radiologist's report: "The degree of perfusion deficits in the thallium scans not quantified by the first radiologist. A pattern of increased perfusion in the post-chelation scans recognized by the reviewing radiologist."

Adverse Effects
    Untoward effects were encountered in seven patients. Two patients developed headaches lasting one to five hours. One patient suffered an episode of dizziness lasting less than three hours. Two patients complained of occasional leg cramps, which responded satisfactorily to additional calcium supplementation. Muscular twitching or clinical signs of tetany were not observed in any patient. No evidence of fluid overload, congestive heart failure or phlebitis was encountered in any of the patients.

DISCUSSION
    In a companion article in this issue of the Journal, it is proposed that ischemic heart disease (IHD) is caused by AA oxidopathy. The dysregulation of redox dynamics of plasma and blood corpuscles results in congealing of plasma and agglutination of cells, leading to the formation of microclots and microplaques in the circulating blood, a process designated as oxidative coagulopathy.1 The term microclot refers to loosely formed clots composed of congealed plasma with entrapped damaged erythrocytes, platelets, and leukocytes that are readily discerned in freshly prepared, unstained peripheral blood smears with high-resolution (x 15,000) phase-contrast microscopy. Microclots are sticky and grow in size by a snow-balling effect as they circulate in the bloodstream (illustrated on page 36 of this issue of the Journal). The term microplaque indicates a later stage of microclots when their cellular and plasma components degenerate and they are compacted into plaque- like structures. Such microplaques usually display layers of clotted blood elements and necrotic debris and are also readily observed in freshly prepared peripheral blood smears (see page 37). Such clots and plaques adhere to the arterial intima and initiate atherogenesis.
    According to the AA oxidopathy hypothesis, oxidatively damaged molecules, microclots, and microplaques formed in the circulating blood cause IHD by three principal mechanisms: (1) their accretion on the endothelial surface inflict vascular wall damage and initiate atherogenesis; (2) coronary artery spasms triggered by them result in myocardial ischemia and necrosis without atheromatous occlusion of coronary arteries; and (3) products of oxidative coagulopathy and AA oxidopathy inflict direct oxidative injury to cell and plasma membranes of cardiac myocytes and those of the conducting system of the heart, and lead to cell membrane permeability dysfunctions with consequent membrane depolarization derangements. The term leaky-cell membrane dysfunction has been used to discuss the pathogenesis and clinical implications of such cell and plasma membrane injury.2 The AA oxidopathy hypothesis seeks to establish clotting-unclotting dysequilibrium in the circulating blood as the core pathogenetic element of IHD and regards atherogenic cellular and tissue changes involving the vessel wall as consequential. This hypothesis also calls for a wholly new clinical approach to IHD that is based on global strategies for arresting oxidative coagulopathy and AA oxidopathy and for reducing insidious and accelerated oxidative stress on the circulating blood. It also raises new and serious questions about the appropriateness of
cholesterol-lowering therapies and mechanical coronary interventions in most cases.

Clinical Value and Appropriateness of Coronary Angioplasty
    The growth of invasive cardiology has been staggering, with the number of coronary angioplasty procedures worldwide approaching 900,000 in 1995. Not unexpectedly, U.S. cardiologists took the lion's share.60 This has happened despite the recognition that the pathologic processes involved in IHD are insidious and diffuse while mechanical approaches to coronary artery disease, of necessity, can address only discrete segments of the arteries. The estimated direct cost of coronary angioplasties and coronary bypass procedures is more than $150 billion.60 In addition, there are substantial indirect costs of managing unsuccessful procedures and their complications, which remain unaccounted for and may exceed direct costs. Despite such enormous expenditure, there is little consensus that these procedures prolong life.61-69 We cite one specific example. In a recent report, coronary angioplasty and bypass operations were performed 7.7 and 7.8 times respectively as often for the elderly in the U.S. as in Canada. And yet the clinical outcome was deemed "virtually identical."70 In 1988, two panels of doctors, one in the UK and the other in the U.S.A, judged the appropriateness of the procedure as performed in the two countries.4 That report showed that 17% and 27% of the investigations had been inappropriate by the standards of the U.S.A panel, whereas 42% and 60% were inappropriate by the UK panel ratings.
    Coronary angioplasty, though of some clear short-term benefit in terms of symptom relief, has not been proven to significantly extend life. The incidence of periprocedural death ranges from 1 to 4 percent.60 The incidence of failed angioplasty necessitating repeat angioplasty or coronary bypass operations ranges from 25 to 35 percent. Angiographic restenosis within 6 months occurs in up to 42 percent of cases.60 Some studies report combined rates of repeat angioplasty and coronary bypass operations of over 50 percent.71 The failure rate increases with longer-term follow-up. Stent angioplasty is being hailed as a valid answer to this dilemma. But it also suffers from a severe limitation: Subacute thrombotic occlusion occurs in up to 4 percent of patients within 2 to 14 days and is almost always followed by myocardial infarction or death. Such high rates of poor clinical outcome are not unexpected since angioplasty, even its staunchest supporters concede, addresses none of the underlying causes of IHD. Indeed, angioplasty denudes the endothelium and predictably increases the risk of thrombosis.
    Two large recent studies of registry data cast doubt over the superiority of angioplasty over thrombolytic therapies.72-73 Recent strategies for preventing acute ischemic events during and after coronary angioplasty have been directed at inhibition of platelet surface-membrane glycoprotein Iib/IIIa receptors.74,75 (Epic and Topol 94).The core tenet of AA oxidopathy holds that oxidative injury to blood components can be caused by several non-platelet factors, and would predict that therapies directed at platelet receptors alone are not likely to yield long-term good results. Even in discussions of the atherogenic roles of platelets, we must recognize that the current therapies that seek to modulate platelet dynamics do not address all known platelet dynamics that are involved in IHD. As pointed out by Fuster et al.76 all current antiplatelet and anti-coagulant therapies fail to address all known mechanisms of platelet/coagulation activation. Indeed, those theoretical considerations are validated by extended experience with antiplatelet therapies that failed to show their benefit in reducing the need for subsequent revascularization procedures.77
    Why are the above critical issues not addressed seriously by the cardiology world? Are there viable options to angioplasty and coronary bypass? Why are those options not explored earnestly? We believe those questions cannot be answered without a clear understanding of the financial and political aspects of interventional cardiology.

Clinical Value and Appropriateness of Coronary Bypass Surgery
    Coronary bypass surgery has emerged as one of the most commonly performed surgical procedures in the United States at this time. This is undoubtedly due to proliferation of cardiac surgery centers in community hospitals across the nation. The growth of cardiac surgery is all the more remarkable in view of many reports of its inappropriate use. First, coronary bypass surgery evidently does not address any of the systemic causes of IHD.1 Angiography is used to determine the need for bypass surgery despite well-recognized dissociation between the severity of stenosis and the risk of ischemic complications and infarction.78,79 Angiograms are used as road maps for bypass surgery, and yet such studies are widely unsuitable and inadequate.79,80 It is recognized that angiographically mild lesions not usually targeted for treatment are inherently more likely than severe lesions to cause myocardial infarction.81,82 Gross abuses of this coronary bypass operation have been documented. Specifically, in one survey of coronary bypass surgery, the percentage of appropriate operations was reported to range from 37 to 78% (thus making 63 to 22% of bypasses inappropriate) in some reports.5 We may add here that in the study by Brook et al.4 cited above, 13% of the CBG operations evaluated were deemed inappropriate by the USA and 35% by the UK panel ratings.

Coronary Bypass Surgery for Advanced IHD
    For patients with advanced IHD, the reported perioperative mortality is high (up to 8.4 percent) and long-term survival poor (mortality at three years as high as one-third), and this subject has been reviewed recently by Khan et al.83 Again, this should not come as a surprise since coronary bypass graft (CABG) procedure cannot be expected to address any of the underlying causes of IHD any more than it can in patients with advanced IHD than those with less advanced disease. Lansman et al.84 reported a 30-day mortality after CABG surgery of 4.8% and a perioperative myocardial infarction (MI) rate of 4.8 percent. One- third of their patients did not survive the third anniversary of the operation. A yet higher rate (8.4 percent) of overall hospital mortality was reported in 83 patients who underwent CABG, with a left ventricular ejection fraction of 30% or less by Elefteriades et al.85

Enhanced Quality of Life After Coronary Bypass Surgery
    Most U.S. reports on the clinical usefulness of such interventions seem to be positive and emphasize quality-of-life issues, even when survival advantages of revascularization procedures are meager. This is clearly self-serving since such procedures "generate billions of dollars in revenue."86 We believe a clearer and more reliable picture emerges when data for clinical outcomes in the U.S. is compared with data from other countries. Not unexpectedly, the authors of papers supporting CABG, while recognizing lack of survival benefits for Americans, strived to justify their excess of invasive procedures on the quality-of-life issue. And yet, they neither accounted for the expected perioperative morbidity and mortality of the procedures nor did they address the high incidence of cognitive disorders after bypass surgery. The reported incidence of neuropsychological dysfunction during the perioperative period of coronary bypass surgery varies over a wide range, extending from 25 to 79%.87-91 Even though the incidence of cerebral dysfunction reported from well established cardiac centers with highly experienced staff is often lower, it must be recognized that a growing number of procedures are performed in community hospitals lacking the depth of perspective of university centers, and such data usually goes unreported.
    The justification that the procedures improve the quality of life is not valid in view of the documented high incidence of stroke, recurrent ischemic events, cognitive disorders, and other adverse effects, as well as death caused by procedure-related causes.87-91 As regards angioplasty, the restenosis rate within 6 months of the procedure is reportedly over 40%,56,86 and the mortality of this procedure in some studies is over 8%.85 The generally poor results obtained with mechanical, segmental approaches to coronary artery disease are not unpredictable, since neither angioplasty nor coronary bypass surgery addresses any of the underlying pathogenetic mechanisms of IHD. Those and other considerations have led some investigators to call for innovative research in the cause and management of IHD.92
    The enthusiasts of bypass surgery often report extremely high rates of quality-of-life improvement after CABG. Krumholtz et al.93 claimed that CABG improved the quality of life for 89 percent of their patients (compared with only 44 percent for those on medical therapy alone); however, they deemed the performance of CABG in terms of survival as of borderline significance. How can an absence of any survival advantage of an operation—with mortality and morbidity rates as high as those cited above—be reconciled with claims of improved quality of life? How can the claimed improved quality of life in 89 percent of CABG patients be accepted in view of the reported incidence of neurological and cognitive dysfunctions in CABG patients of 75 percent or more? Perhaps the answer lies in a common observation of clinicians: Patients recovering from any life-threatening surgery may be expected to be thrilled just to recover from anesthesia and relish the attention paid to them by the surgical team. Furthermore, accepting any major surgery is a substantial physical and emotional investment for the patient, and those with life-threatening cardiac procedures are not less likely to be persuaded of the putative gains of their investment than those who undergo other types of surgical operations. Of course, all such benefits are short-lived, as demonstrated by long-term CABG outcome studies.

Physician Practice Versus Patient Outcome Issues
    There are other disturbing aspects of the utilization of angioplasty and coronary bypass operations in the United States. It is well recognized that such procedures have the best chance of yielding a good outcome when performed for the most critically sick persons, i.e., the elderly with left ventricular failure and those with coexisting serious illnesses.94 Predictably, the mortality associated with such cases is also the highest. Regrettably, in our fee-for-service model, the procedural outcomes that assure financial and career rewards for physicians often influence therapeutic decisions made by clinicians. If this were not so, and if financial and personal career issues were not to determine who receives the procedures and who doesn't, cardiologists and cardiac surgeons would favor doing procedures for patients who are most likely to benefit from such procedures (even though those patients are most likely to succumb to such procedures). As shown by Pilote et al.94 critically ill patients who might benefit most are least likely to be offered high-risk procedures.

Care of IHD Within the Context of the Chronically Ill
    It generally goes unrecognized that chronic illness replaced infectious diseases as the dominant public health issue in the 1920s, long before antibiotics appeared on the scene—a global pattern evidently related to nutritional and environmental factors.95 The first National Health Survey conducted in 1935 reported that 22% of Americans lived with a chronic condition.96 In 1987, nearly 30% of the population (90 million Americans) suffered from one or more chronic conditions.97 Based on trends during the preceding decades, nearly 50% of the population (148 million) may be expectedly to become chronically ill. These considerations are evidently pertinent to our discussion of medical options for IHD since it accounts for the major part of the chronically illness population. In the Medicare program, 10% of beneficiaries consumed 70% of medical resources.98
    As the U.S. population ages and the demand for cardiac care by elderly citizens leapfrogs, the issue of the cost of delivering care assumes critical importance. The fact that optimal therapy must focus on utilization of health care resources is becoming increasingly apparent. Consider the following quote from a recent issue of The New England Journal of Medicine:  
    Thirty-seven patients would need to be treated for four years (at a cost of about $438,672 for lovastatin alone) to prevent one patient from undergoing coronary-artery revascularization.99
    For this report, we did not attempt to precisely compare the cost of our entire integrative program for arresting and reversing IHD with the cost of traditional treatment plans that include multiple drug therapies, hospitalizations for angioplasty and coronary bypass surgery, and expensive cardiac rehabilitation programs. However, our estimated cost of the total integrative program for a period of six months is less than $4,000 (including the cost of 20 EDTA infusions [$95.00 per infusion], cost of periodic blood testing, nutrient and herbal supplementation, fees for seminars and the cost of books and tapes). This cost is far less than even the most conservative estimates of mechanical interventional programs in which hospital charges for even one day may exceed the cost of our entire program for a full six months. Cost accounting for in-hospital care is an area a great uncertainty, with estimates of coronary surgery varying over such a broad range as to be worthless. We include another quote from a recent issue of The New England Journal of Medicine to illustrate the magnitude of this problem:

[For complications of coronary artery surgery] True in-hospital costs, including charges for personnel and in-hospital services, if added to the expense of an array of long-term out-of-hospital medical and rehabilitative services, probably result in an additional expenditure ranging from 5 to 10 times the narrowly defined in-hospital costs.100

    In discussions of cost-benefit ratio, a critical issue is how much benefit an integrative program like the one described in this article offers to the patient in terms of prevention of nutritional, autoimmune and degenerative disorders that the patient may suffer concurrently with heart disease or may develop during subsequent years. Evidently, mechanical coronary interventions do not address any of the vascular lesions in other locations such as the brain, limbs, kidneys and other body organs. Nor do drug therapies for IHD offer any preventive advantages to the patient as is done by integrative programs. Indeed, the issue of long-term chemical consequences of pharmacologic regimens employing concurrent use of multiple drugs should loom large in all such discussions.

Proposed and Putative Mechanical and Genetic Advances in Cardiology
    A recent special report on heart disease published in a business magazine advises us that about 1 million Americans die of heart disease each year, including about 300,000 who die of cardiac arrest before reaching a hospital.101 This report was primarily intended for the business and investment community and included the following recent or imminent advances: (1) the use of a gene-spliced version of apo-A-1 Milano gene as a drug to increase blood HDL levels; (2) a "biobypass" approach to coronary artery disease that hopes to use genetically engineered viruses to transfer VEG-F gene to the heart which is projected to promote angiogenesis in the heart; (3) the use of a gene-spliced form of VEG-F gene to be used as a drug with the intended benefit of angiogenesis; (4) the use of total heart replacement implants; (5) the use of an assist pump called "Streamliner," which will whirl like a turbine and pump blood in a continuous stream (the patients will no longer have a pulse); (6) the use of genetically engineered pig hearts, which will carry human immune system proteins; 7) the use of transplantable hearts developed and cloned in animals, following the lead of Dolly, the Scottish covergirl sheep. (How transfer of animal viruses to human recipients will be prevented in such transplants is not obvious); and 8) the use of irradiated filigreed metal stents that will supposedly prevent the formation of occlusive clots in coronary arteries.
    Notwithstanding its value to the business and investment communities, this report prompts us to raise four questions concerning the putative advances in cardiology: (1) How relevant are the proposed advances to patients with advanced IHD at present? (2) How relevant are the proposed advances likely to be for the majority of Americans with advanced IHD in five years? (3) What long- term benefits may be expected from the proposed advances? (4) What costs can we project for such high-tech answers to IHD when the number of potential recipients of such therapies grows into millions in the aging population? The answer to the first question is clear: The proposed advances are of no value. The answer to the second question is also similar: none most likely. As for the third question, we discuss at length in this article as well as in the companion article, AA Oxidopathy, in this issue of the Journal the reasons why mechanical approaches to segmental lesions of the coronary arteries cannot be expected to provide good long-term benefits for a disorder that is essentially an oxidative-metabolic disorder of the circulating blood. The fourth question concerns projected costs of proposed therapies if they were applied to all those who develop IHD. We are unable to answer that question with any precise computer models. However, if the past is any indication—both in terms of frequency of interventional procedures and failure rates—it seems safe to predict that the country simply will not be able to fund such high-tech therapies for all patients with IHD, even if all available health-care dollars were exclusively committed to this disease.

EDTA Chelation for Advanced IHD
    The use of ethylenediaminetetraacetic acid (EDTA) infusions as a chelating agent to "leach" calcium out of atheromatous plaques and so reverse atherosclerosis was first attempted in the 1950s12,13. The early experience, which was reported as promising, was followed by decades of controversy, which regrettably was fueled less by reason and search for effective therapies than by a turf battle among those who favored bypass surgery and those who were branded as "chelating quacks." Clinical outcome reports of a large number of physicians who described positive results were dismissed as unscientific. Even more regrettable was the gross abuse by the powerful bypass industry of medical licensing boards, which revoked or threatened to revoke the licenses of clinicians who used EDTA chelation therapy.
    A critically important element in any discussion of management of cardiovascular disorders is how a given therapy for a segmental lesion in one location affects those in other areas. This is where the clinical benefits of integrated management plans including EDTA chelation far outweigh those of coronary angioplasty and bypass surgery. A systemic and non-segmental approach may be expected to improve tissue perfusion and provide clinical benefit in non-cardiac lesions. This, indeed, happens. We report we our preliminary and positive experience with a similar program including EDTA infusions for arresting or reversing peripheral arterial insufficiency.102 Our data is consistent with that reported by others.103,104 In another report we report our experience in arresting or reversing renal failure with a similar program.105
    This study was conducted as an open clinical outcome trial. In integrative medicine, the emphasis clearly is on the integration of all measures and therapies that can enhance the outcome. Indeed, we hold that the prevailing model of double-blind studies is irrelevant to integrative medicine. There are other important issues. What can be the moral or ethical basis for denying effective therapies to patients with life-threatening advanced IHD? How does one justify giving starch pills to such patients? How can an integrative physician ignore the patient's need for exercise, meditation, choices in the kitchen, and nutrient and herbal therapies? How can he blind himself or his patient to such therapies? Indeed, we believe the double-blind cross-over model of drug research is singularly inappropriate for patients with serious chronic illness. (In our view the use of a placebo group for patients with acute illness is just as inappropriate as it for serious chronic illness.)
    Some adverse effects reported by others but not encountered in the present study are listed in Table 6. Such reactions may be expected and should be looked for in any EDTA chelation program.

SUMMARY
 
  Ischemic heart disease (IHD) is an insidious disorder of redox regulation in which accelerated oxidative molecular injury occurs to all elements of the circulating blood. It is a diffuse disorder that cannot be effectively addressed with mechanical interventional approaches directed at segmental coronary lesions. Nor can the use of pharmacologic therapies that block cell membrane channels or receptors, as essential as such drugs are for controlling acute illness, be expected to yield good long-term results. The growth of interventional cardiology in recent years has been staggering, indisputably fueled by a surfeit of invasive cardiologists and the generation of billions of dollars in revenue for hospitals as well as surgeons. Most physicians know of hospitals, whose very existence was threatened by low occupancy rate, that not only survived but thrived after an invasive cardiology unit was organized. In 1995, almost 900,000 coronary angioplasties were performed, the U.S. being the clear leader in the field. Since over 1.5 million Americans are expected to suffer myocardial infarction annually, it is safe to assume that the use—unwarranted in our view—of angioplasty and coronary bypass will continue to rise unchecked unless serious efforts to educate people about the true state of affairs are undertaken.
    Two simple questions may be asked in this context: First, in the face of such rapid increases in the incidence of chronic illness, how long can the American society sustain the leaping growth in the invasive cardiology industry? Second, how long will the invasive cardiology industry use spurious statistics to sustain itself in the face of growing recognition of its fundamentally flawed "plumbing" approach to a clearly oxidative-metabolic disorder? Our preliminary data are consistent with several previous reports of efficacy of the integrated programs for reversal of IHD employing EDTA chelation therapy, and offer an alternative to ineffective pharmacologic therapies, coronary angioplasty and coronary bypass surgery. In this report, our clinical outcome data shows an extraordinarily safe and effective alternative to the prevailing, and ineffective, therapies for advanced IHD. Our findings of pre- and post-treatment thallium myocardial scans show clear evidence of improved perfusion.

TABLE 4
REVERSAL OF CORONARY DISEASE:
DEFECTS IN BLOOD SUPPLY BEFORE AND
FOUR MONTHS AFTER BEGINNING A HEART DISEASE REVERSAL PROGRAM

Area of Heart Before After
Anterior Wall Present Absent
Posterior Wall Absent Absent
Septal Present *
Inferior Wall Present Absent
Lateral Wall Present Absent
Apex Present Absent

    In Table 5, we list the mechanisms of action of EDTA when administered intravenously.

TABLE 5. EDTA-INDUCED VASODILATATION

* Cardiac:
Coronary vasodilatation with improved myocardial perfusion, relief of ischemic pain, improved contractile and conducting functions of the heart.

* Central Nervous System:
Clarity of thinking, improved memory, warmth, flushing, relief of pain

* Eye:
Improved night vision

* Peripheral Arterial Perfusion:
Improved perfusion with relief of ischemic claudication

* Renal:
Fall in BUN and creatinine levels

* Skin:
Improved perfusion with skin warmth, healing of chronic ischemic ulcers

* Others:
Improvements in other body organ functions

TABLE 6. POTENTIAL ADVERSE EFFECTS OF EDTA
Headache
Lightheadedness
Phlebitis
Hypocalcemia (with or without leg cramps)
Fluid overload
Hypoglycemia
Excessive anticoagulation

Systemic responses in chronic fatigue states
Systemic reactions in chemical sensitivities
Systemic responses in multiple sclerosis and other autoimmune disorders

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İThe Institute of Integrative Medicine İThe Journal of Integrative Medicine

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