Cardiomyopathy

The other MME centers focus on the use of MME in orthopedic and neurological conditions. My background is in Cardiology, and our medical practice, with its heavy involvement in EECP, focuses on the care of individuals with inoperable, recurrent, or treatment refractory cardiovascular disease states. Our MME program began in 9/04 - on this page I will present the outcome of every cardiovascular patient we treat over our 1st two years. We want you to know how we are doing, just as we did eight years ago when we brought EECP to town .

We got involved with MME specifically to help patients too-far-gone for our best current therapies and EECP. We are not utilizing MME as a substitute or replacement for standard cardiovascular care. Our coronary patients either had recurrent disease, no longer amenable to revascularization, or their condition was such that revascularization would be associated with an increased risk - that is why they were treated with MME. Please remember, MME is not FDA approved. MME is considered to be an experimental therapy. Just because one patient gets better doesn't mean that another patient with similar symptoms will get better, and it certainly doesn't mean that all patients will get better. Obviously, our experience with MME in cardiovascular disease is limited. Early on I treated only individuals who had been under my care for years. The out-of-town patients who I am treating now are all well read and nutritionally sophisticated - this is a select group of patients. Thus even if a majority of these patients respond favorably to MME, we can't extrapolate this to the general population of patients with cardiovascular disease. When it comes to the use of MME in cardiovascular disease, you need to understand that we are collecting outcome date on a still experimental therapy. Out goal is to learn how to best integrate MME into a comprehensive approach to the patient with cardiovascular disease, to learn the strengths and the limitations of this technique. As you scroll through the patient list, you will see how we have grown in sophistication in our application of MME, particularly with respect to the use of ancillary and supportive approaches, such as Bioresonance Therapy and Stem Enhance.

While EECP is FDA approved to treat angina, coronary insufficiency, and heart failure, we are utilizing MME under the auspices of an IRB (Institutional Review Board). Scientific openness is important here. I'll divide this page into three sections, Angina and other symptoms due to Coronary Artery Disease, Cardiomyopathy and/or Congestive Heart Failure (CHF), and Other Conditions, acknowledging that there will be some overlap between these categories.

DATE	EVENT
4/00	Initial Heart Attack → Angioplasty with Stent placement to occluded Circumflex; 50% LAD left intact and 70% & 95% distal RCA narrowings not dilatable
7/00	Unstable Angina due to Circumflex 90% in-Stent restenosis → repeat Angioplasty and Stent placement to Circumflex (creating a "Stent Sandwich")
2/01	Recurrent angina with an abnormal 4:44 stress echo study
9/02	Abnormal 2:52 stress echo - Nanobiotic therapy poorly tolerated ® 1/03 angiogram
1/03	LAD 50%, Circumflex stent open, with non-dilatable distal RCA narrowings
12/03	Unstable angina - new 80% LAD narrowing dilated and stented
1/04	Increased angina - both LAD and Circumflex stents open; multiple non-dilatable distal Right Coronary Artery narrowings again noted
9/04	100 hours MME - angina resolved, meds decreased, & diastolic function improved
6/06	Coronary Angiogram - No significant change from 1/04

I've worked hard to control CR's angina, or perhaps we should say that I worked him over hard. Still, CR's symptoms did not come under control until he was treated with MME - here's CR's story:

This 65 year old hypertensive, hyperlipidemic, diabetic man with sleep apnea and several additional coronary risk factors presented with severe chest pain in 4/00. CR was in the midst of a heart attack, due to occlusion of his Circumflex coronary artery, which supplies the side wall of the heart. The Circumflex was dilated open with a balloon catheter, and then stented. High-grade narrowings were seen in the RCA (Right Coronary Artery), but they were located at its distal extent, beyond a bend, and beyond the reach of the angioplasty catheter. The LAD (Left Anterior Descending), which supplies the front wall of the heart, contained a non-flow restrictive 50% narrowing, and was left intact.

CR felt great for three months. Then chest pain recurred, and angiography demonstrated renarrowing within the Circumflex stent, termed in-stent restenosis. The Circumflex narrowing was re-dilated and a 2nd stent was placed within the 1st one, creating a "stent sandwich". CR's angina improved with this procedure, but it did not fully resolve. A stress echo study showed the problem to be insufficient blood flow to the heart muscle supplied by the RCA, which contained 70 & 95% narrowings that could not be angioplastied or stented. CR was put on an extensive nutritional program, diet and drug therapy for sugar control, and as much anti-ischemic drug therapy as he could take, including 200 mg/day of the b-Blocker Metoprolol, but his symptoms did not resolve. Nanobiotic therapy was tried, and helped a little, but CR couldn't tolerate this treatment long-term. Angiography in 1/03 (CR's third) showed the stent sandwich to be open, the LAD to be unchanged, and the same high-grade narrowings in the distal RCA.

11 months later, in 12/03, CR's chest pain flared up - the LAD narrowing now involved 80% of the vessel's flow area; the LAD was dilated and a drug-eluting stent placed. Three weeks later I had to repeat CR's heart cath, due to persistent pain. The LAD stent site was open, but when I injected X-ray dye into this vessel, CR experienced severe angina (The problem here was endothelial dysfunction, an inability of the artery lining endothelial cells to generate Nitric Oxide. Without Nitric Oxide the vessels cannot dilate properly and resist platelet aggregation or vasospasm. Endothelial dysfunction persists for up to 6 months post-procedure in a stented artery.). Multiple pharmacologic and nutritional therapies aimed at endothelial dysfunction were tried, but none got the job done. CR's angina worsened in 1/04, and angiography, CR's 6th, demonstrated a wide open LAD stent site, a moderate, certainly non-critical narrowing of the Circumflex stents, and the high grade RCA narrowings observed on all prior studies. I felt that CR's persistent pain was due to persistent endothelial dysfunction, and to persistent oxygen starvation in the heart muscle supplied by the diseased (and non-dilatable) RCA. A cardiac echo study demonstrated findings of CR's initial heart attack, along with evidence of of diastolic dysfunction (CR's heart was stiff and filled poorly, making him short of breath with effort). CR needed at least two NTG tabs each day and basically felt like hell - as did I, because it was my job to help him, and all I seemed to be able to do was to try different drugs and then carry out heart catheterizations on CR, over and over.

CR has a background in engineering, and he understands electricity and magnetism better than I do. I, on the other hand, understand cardiovascular physiology better than CR. When MME became available in Toledo, we put out heads together and decided that MME might just be able to get the job done, the job that I hadn't completed despite 6 heart caths, three rounds of stenting, and the 8 drugs and 19 different nutritional supplements that I had CR on.

In preparation for MME, CR began sleeping on a 10 Gauss Magnetico negative field sleep pad. At bedtime, every other night, he took DMSA (a metal binding agent). CR did not experience a reduction in angina, but with this simple maneuver his energy level picked up a little, and his long-standing leg aching let up a little. Then we began MME - during the first few sessions, CR noted a strange sensation in his chest - not his angina, not shortness of breath, but more of a tingling sensation. After 45 hours, CR felt he "turned the corner". CR could do more, and he no longer required oxygen during light exercise. CR's improvement continued and we stopped at 100 hours. A post-MME cardiac echo study showed CR's heart to be less stiff (consistent with an improvement in cellular energy generation). Before we started MME, CR would experience angina with daily activities and occasionally at rest. Now CR can work without difficulty; angina has resolved, NTG is no longer needed, and we were able to decrease CR's Metoprolol dose from 200 to 100 mg/day. CR's functional status has thus improved in a meaningful fashion. CR will continue to sleep on the Magnetico sleep pad, and will take DMSA at bedtime 7 days a month.

1/06 Update - CR remains improved, and has not required a hospital stay or invasive study since completing MME in 9/04.

7/06 Update - In 6/606 CR noted recurrent chest tightness and increased shortness of breath with effort; his weight had increased and we couldn't tell whether his symptoms were weight related or due to progressive coronary disease. Angiography revealed a stable situation, to my eye unchanged from CR's 6th heart study in 1/04. CR is going to work on weight and sugar control. CR's Testosterone level is low (a nearly universal finding in male patients with coronary disease). 1400 mg of Testosterone in pellet form was implanted subcutaneously in 7/07. Testosterone dilated coronary vessels, promotes clot dissolution, improves insulin sensitivity, and provides a number of other benefits for the cardiovascular patient, and hopefully will reduce CR's symptoms. The good news is that his coronary disease remains in check.

DATE	EVENT
7/02	Coronary calcium score 891 with a normal 5:00 stress echo
7/03	New onset angina → angio with high-grade, not-dilatable narrowings in the marginal branch of the RCA and in 2 of the 3 marginal branches of the Circumflex.
8/03	35 hours EECP with a full resolution of angina
9/04	Fatigue, palpitations, edema, and shortness of breath with effort → 150 hours MME
11/04	Symptoms improved to resolved, with a negative 5:34 stress echo study

I've been working with WR for 5 years, helping this now 85 year old, incredibly energetic concert violinist with high blood pressure, cardiac arrhythmia (SVT and intermittent atrial fibrillation), edema, and postural dizziness. WR did not tolerate pharmaceutical therapy well, so I had her on only two drugs, but she had been doing well on an incredibly complete and incredibly energetic nutritional program. Mercury overload had been demonstrated and to some degree addressed, and with this her arrhythmia and postural dizziness became easier to control.

A screening coronary artery CT calcium study returned abnormal in 7/02, but WR could complete 5:00 on the treadmill and her stress echo images looked good. Anginal chest tightness developed one year later, and WR's angiographic study demonstrated high-grade narrowings in three major branch vessels, positioned beyond the reach of the angioplasty catheter. EECP was carried out, along with additional anti-atherosclerotic measures. WR did well, and returned to the concert hall and her busy lifestyle.

WR felt herself slowing down, and slowing down fast, in the fall of '04. Shortness of breath was shortening her daily swims and she had no energy. Postural dizziness was more of an issue. I felt that coronary insufficiency was the culprit. We discussed repeat EECP, or a repeat angiogram, looking for a new narrowing that might be the culprit. WR was aware of MME and its potential benefits, and she chose MME over repeat angiography. This turned out to be a good decision.

WR kept a detailed symptom diary during her MME. She noted a gradual improvement in her energy level, and soon she could complete her morning swims without difficulty. Dizziness and palpitations became non-issues. Her 5:34 stress echo study looked great. WR noted a number of non-cardiac benefits. A lipoma on her left arm decreased in size. Pre-MME she was experiencing a tremor when she picked up her violin - this went away and her arthritis also seemed a little better. We treated WR's heart, not her entire body, so its a little difficult to explain her non-cardiac improvements. It may be that by magnetizing the blood as it passes through the heart that we are magnetizing the entire body, or maybe a stronger heart does a better job of supplying energy to the other internal organs. WR doesn't much care that I can't explain why she is better. She's just happy to be better (and by the way, if her concert performance improves, I'm going to take full credit)!

Addendum: Now that WR is doing more, arthritic knee pain is becoming more of an issue. Knee replacement would solve this problem. She might get some relief from the Viox-type drugs (scratch that - bad idea). Our approach, before we resort to drugs or surgery, will be to treat WR's knees with MME.

7/06 Update - WR remains improved; chest pain has not recurred and WR has experienced only a single, brief episode of atrial fibrillation since completing MME in 9/04. She has not required a hospital stay or invasive study.

DATE	EVENT
3/94	LAD angioplasty with restenosis, leading to LIMA to LAD bypass surgery
7/94	Anastomotic lesion, leading to angioplasty of the LAD and diagonal
7/97	Rotablation and stenting of the Circumflex
7/97	Atrial Flutter developed and responded to electrical cardioversion
3/98	Circ restenosis with Class 4 angina despite four drug medical therapy
4/98	35 hours EECP ® Class 1 functional status, 2 drugs dropped, and angina minimal
4/99	20 hour EECP booster for Circ distribution ischemia
8/99	Increased angina - new 80% marginal narrowing that was dilated and stented, LIMA and proximal LAD and diagonal patent, Circ occluded, and distal 90% LAD
11/99	Marginal restenosis, addressed with repeat angioplasty and stent placement
2/00	Class IV angina, resolved with 45 hours EECP
10/00	Angina - Arteries unchanged: Circ 100% with distal LAD 90% - marginal open
11/00	38 hours EECP with again a resolution of angina - 10 hours given in 4/01
11/01	Atypical pain - arteries without change from 10/00 - no disease progression
6/02	EECP booster and EDTA and Nanobiotic therapy ® angina resolved
3/03	EECP booster and again in 8/03
12/03	Angina - arteries unchanged from 10/00 and 11/01
2/04	EECP booster
7/04	Pneumonia, precipitating Atrial Fib-Flutter; drug therapy decreased HR excessively
10/04	Angina with low HR requiring pacemaker implantation Þ Instead 35° EECP - this time with 150 ° MME with DMSA
12/04	Angina resolved, anti-arrhythmic drug stopped and rhythm stable, with an only mildly abnormal 8:00 stress echo study ® sleep pad and cyclic DMSA
2-3/05	EECP booster and 150 hours of MME with DMSA
7/05	Feels great - no angina and rhythm stable

Isn't this a rather long problem and procedure list? JR is one of our favorite patients. Each year the staff invites him to the office Thanksgiving lunch. We should, as JR basically paid for the place. JR's case study has been presented previously on this website (EECP case history #6), as in 4/98 JR did well with EECP, after undergoing 5 heart caths, bypass surgery, and three angioplasty/stent procedures, all in the space of 4 years.

JR did do well with EECP in mid-98; his chest pain resolved and his stress study improved. Angina recurred one year later, and his stress study pointed to ischemia (evidence of insufficient blood flow) in the heart muscle supplied by the occluded Circumflex. I felt his collaterals needed boosting; a booster course of EECP was carried out, and JR again felt well. A new narrowing developed in JR's marginal artery in 8/99. This vessel was dilated and stented, but just as with JR's LAD, the stent closed and a repeat procedure was required 3 months later.

Between late '99 and the present, JR's course has been marked by angina flare-ups every 6 months, each time with a good response to EECP. EECP works not just be augmenting collateral flow. EECP doubles your Nitric Oxide level; this is the angiochemical that dilates your arteries and allows them to resist spasm and platelet clotting. When you take a NTG, what you are really doing is giving your circulation a jolt of Nitric Oxide. JR would do well with EECP, but then the effect would wear off and I'd have to treat him again. My feeling was that some toxin, probably a heavy metal, was producing oxidative stress, basically "chewing up" JR's Nitric Oxide, such that he needed EECP every 6 months to "top up" his Nitric Oxide tank. All along JR had been on a program of antioxidant vitamins and fish oil; we redoubled our efforts and JR began a program of IV EDTA chelation therapy to remove what I thought to the the culprit heavy metals, and JR received several months of Nanobiotic therapy, which also provides EDTA. JR's Mercury amalgam fillings were removed in 2001, but this was not accompanied or followed by any specific medical Mercury detoxification (a big error on my part). These measures have kept JR out of trouble, in that he has never experienced a heart attack, and I think he has had only 2 unplanned cardiac hospital admissions in the last 5 years, but we have not kept JR out of the cath lab, and we have not kept JR pain free.

JR had developed Atrial Flutter in '97; this rapid atrial arrhythmia precipitated angina but fortunately responded to electrical cardioversion. JR was hospitalized with pneumonia in 7/04, and this infection precipitated another episode of atrial arrhythmia. Drug therapy converted JR's rhythm back to normal, but only at a very slow rate. Consequently I had to back off on JR's b-Blocker dose, as this agent works by lowering the heart rate, but then his angina flared up. This was a dilemma. The drug therapy for arrhythmia was working, but slowed JR's heart rate too much, compromising his angina treatment program. The solution was to place a cardiac pacemaker, but a pacemaker would close the door to MME forever - what to do?

I struggled with this one. First I needed to ask: What was I missing? What should I have done to help JR hold on to his Nitric Oxide and remain angina free? What was causing the nerves in his heart to malfunction? We had done everything right. We had done everything we could - except one thing, one very big thing. JR had had his Mercury amalgams removed, but he had never undergone any medical Mercury detoxification. Could Mercury be the toxin chewing up JR's Nitric Oxide? Could Mercury be poisoning JR's cardiac nerves? This hypothesis made sense to me, so I presented JR's case to Dr. Bonlie. JR received a booster course of EECP, to increase the cardiac blood supply and re-generate his Nitric Oxide pool, and he began MME, coupled with oral DMSA Mercury detoxification therapy, aiming to remove Mercury from JR's heart.

JR noticed a "tingle" during his initial MME treatments. At 25 hours he noted a reduction in angina frequency and severity. At 50 hours I began to cut back the dose of JR's anti-arrhythmia drug, and at 100 hours this rhythm control agent was discontinued. Following this EECP booster, coupled with 150 hours of MME, JR feels great, his heart rhythm is normal, and his energy is back. Post-MME JR has experienced only one episode of angina, and that was when I ran him into the ground on a 8:00 stress echo study, which returned only mildly abnormal (his Circumflex is 100% blocked and you can always outstrip the collateral blood supply if you push exercise hard enough, which we did here for diagnostic purposes). JR will sleep on a Magnetico sleep pad and take DMSA on a periodic basis (to keep pulling Mercury and other toxic metals out). Given JR's history, I won't declare victory, not just yet, but he's sure feeling better following MME, and so am I, as I'm the guy who put him through 10 heart catheterizations, bypass surgery, and 5 rounds of angioplasty/stent placement. Let's hope I got it right this time.

JR had the following comments about his MME experience - "My heart is beating stronger than it was before I started MME. Before, my pulse was always low and now it's always in the 60-70's. Even though the 7-days-a-week regimen was at times trying, the ongoing results were encouraging. Now that I'm done and feeling as good as I do, the extra effects and cost make it worthwhile. Overall I'm feeling the best I have felt in several years".

7/05 Update - To be on the safe side, given JR's history of recurrent coronary insufficiency, he received an additional 150 hours of MME with a concomitant EECP booster in 2-3/05. As of 7/05, JR feels great. Angina has not recurred and his rhythm remains normal.

7/06 Update - JR's Atrial Flutter recurred, increasing his heart rate and with this angina recurred. Trans-catheter flutter ablation was carried out, and with this JR's angina resolved. Atrial flutter recurred, and again responded to flutter ablation. A sinus infection put JR back into flutter; cardioversion is planned. I have not repeated JR's coronary angiogram as I feel that the problem is the recurrent atrial arrhythmia, not coronary disease progression. JR tolerates the flutter reasonably well, but it does bring on angina. When in normal rhythm JR is angina free.

DATE	EVENT
2/92	Inferior wall heart attack
2/92	Bypass surgery for Left Main and 3 vessel coronary disease
9/99	Mild angina with an abnormal 9:00 stress echo - medication responsive
11/00	Mildly abnormal 7:35 stress echo
8-12 '01'	Recurrent symptoms ® 4 months of Nanobiotic therapy with a decrease in angina, decrease in coronary artery calcium score from 3240 to 2754, with a still abnormal but improved 8:47 stress echo
4-8 '03	Recurrent angina, responsive to 20 rounds of DeToxMax Plus
9/04	Shocking news ® unstable angina ® All 3 grafts widely patent but the 50% Left Main narrowing was compromising flow to proximal LAD and Circ distributions
10-12 '04	45 hours EECP - symptoms improved but not totally resolved
12/04	104 hours of MME ® Angina fully resolved and meds decreased
6/05	Remains angina free with a normal 7:00 stress echo

MME is a therapy that we had been looking for, a technique that could help patients who were not responding well, or responding completely well, to our prior best therapies. Our best therapies had kept BR's grafts open for 13 years, but hadn't totally resolved his pain, and this man with an upcoming challenge to his non-cardiac health needed something more.

BR Presented in 2/92 with a heart attack involving the back wall of his heart. Angiography demonstrated narrowings within the Left Main and all three of BR's major coronary vessels, leading to three conduit bypass surgery. Angina recurred 7 years later, in association with an abnormal stress echo study, and quieted down nicely with anti-anginal drug therapy. BR's stress echo study 1 year later was a little worse, and angina returned in the fall of '01. BR received 4 months of Nanobiotic therapy; angina lightened up, and BR's stress echo and coronary calcium scores improved. BR's symptoms returned two years later, and quieted down nicely with 20 weeks of DeToxMax Plus. Things went well until the fall of 2004, when BR was broadsided by a confluence of stressful events.

One piece of bad news, or one stressful event, may effect the blood pressure and coronary tone of any patient with coronary artery disease. BR experienced three such stressors, the most important one pertaining to a non-cardiac health issue. His BP soared to 231/114, his arteries clamped down, and I had to admit him to the hospital with troponin positive unstable angina. Angiography demonstrated that all three of his 13-year-old bypass grafts were widely patent, while the 50% Left Main narrowing was compromising flow to the muscle in the LAD and Circumflex distributions proximal to their occlusion and subsequent graft insertion points. I increased BR's drug doses; this helped a little, but not a lot, and also led to fatigue, something BR didn't need.

In thinking about BR, first I was rather pleased with the work that BR and I had done. One in three bypass grafts close the 1st year and 50% of vein grafts close down by 7 years, but all 3 of BR's 13-year-old grafts looked good. However, he still had pain, the meds were causing fatigue, and it was my responsibility to get BR in tip-top shape, to help him deal with an important non-cardiac health challenge.

So, BR underwent EECP, and that helped, but did not totally resolve his angina. EECP was followed by MME, and this did. During MME I was able to cut down on BR's medical regimen, aiming to give him more energy, which he will need in the near future. A stress echo study is planned to serve as a new baseline, and we will continue the treatment programs that have protected BR's grafts over the past 13 years.

7/06 Update - Following completion of EECP and MME in 12/04, BR underwent a medically stressful therapy for a non-cardiac health condition - and he did great. A 7:00 stress echo study carried out in 6/05 looked good. Angina recurred when out in the cold in early '06. A booster course of EECP was carried out, and as of now BR is pain free and feeling well.

DATE	EVENT
6/93	Normal 18:00 stress echo
'94	Atrial fibrillation, responsive to medical/nutritional therapy
11/98	14:42 stress echo with an equivocal fixed inferior wall contraction abnormality
4/04	Shortness of breath with effort - Obviously abnormal 13:00 stress echo with a resting inferior abnormality that worsened with exercise Þ
5-6/04	35 hours EECP
4-8/04	Magnetico negative field sleep pad and oral DMSA
9/04	150 hours MME
10/04	Symptoms - Fully resolved; can play singles tennis without difficulty Stress echo - Contraction abnormality post-exercise worse but treadmill time increased to iiiincreased to 15:00 minutes
12/04	Silver Protein vs. infection, Phosphatidyl Choline for reverse cholesterol transport, with ongoing DMSA/sleep pad therapy ® more MME this winter
3/05	100 hours of MME
4/05	Running again - On no drugs and without a care in the world
4/05	15:00 stress echo with a mild resting abnormality that doesn't worsen post-exercise
9/05	Normal cardiac echo - Inferior wall contraction abnormality no longer present

Coronary disease is not a condition one would expect in RR, but that was the diagnosis facing us last spring, when this 76 year-old semi-retired physician, a former marathon runner, was facing retirement from the tennis court. A life-long athlete, RR's heart rate had always been low, and his EKG was unusual in appearance (related to athleticism). This prompted a stress echo study for insurance purposes in mid-'93. RR burned it up, running for 18:00, just as do high school athletes undergoing sports physicals.

Atrial fibrillation developed in '94. Digoxin, Co-Enzyme Q₁₀, and Carnitine were added to RR's nutritional program; the atrial fib resolved and to this point has not returned. A screening stress echo study in late-'98 demonstrated an equivocal contraction abnormality, at rest and with effort, over the back wall of RR's heart. Given that RR felt great and could complete 14:42 of treadmill stress, I felt that this represented artifact, as opposed to a small inferior wall heart attack (but in retrospect I was probably wrong). RR's risk factor profile looked great: LDL 102, Lp(a) 7, HDL 68, and fasting sugar 86. His homocysteine was a little high at 13.7, but fell with B-vitamin supplementation. RR was maintained on a program of antioxidant, mineral, and essential fatty acid supplementation, and he continued to exercise on a regular basis, and to exercise without difficulty.

RR continued to feel great until the spring of '04, when he began to experience shortness of breath with physical activity. Hunting was a little more difficult; singles tennis was a real strain. A 13:00 stress echo showed an inferior wall contraction abnormality at rest, that definitely worsened with effort. Coronary disease was the obvious culprit - what were we to do next? RR's heart rate and blood pressure remained low, from his athleticism, such that anti-ischemic drug therapy would likely due more harm than good. It didn't make sense to me to subject a 72 year-old who could walk for 13:00 on the treadmill (it is unusual for a 70 year-old to even go 6:00) to angioplasty or bypass surgery, so we decided not to carry out an angiogram. I also needed to come up with an explanation(s) as to why an athletic man with no standard risk factors was being troubled by coronary insufficiency in the first place, so that I could include coverage for those potential culprits into my overall treatment plan for RR.

We are learning that heavy metal overload (probably Mercury more than Arsenic, Lead, and Cadmium), is playing a role in our current rising epidemic of coronary artery disease. These metals poison our antioxidant and reverse cholesterol transport systems, and many other enzyme systems as well. Chronic, smoldering infection, as well as one's life-time "infectious burden" also play key role's (infectious burden correlates with one's CRP level, and with this one's risk of coronary disease and coronary events - the relationship is stronger than the relationship between cholesterol and heart disease). RR's Mercury amalgam fillings were removed in '01; subsequently he had then received 5 IV DMPS (Mercury binder) treatments, decreasing his post-DMPS urine Mercury level from 23 to 8 mcg Hg/G creat. An IV EDTA challenge study had returned abnormal for Lead at 43 mcg/24 hours. These were not particularly alarming levels, so I had not pushed RR into a more aggressive or ongoing metal removal program (another mistake on my part).

Aiming to address these potential culprits as we resolved RR's symptoms, the following program was initiated:

1. RR began to sleep on a 20 Gauss Magnetico negative field sleep pad, taking DMSA 500 mg at bedtime every other evening, aiming for a low-level total body magnetic energizer effect and enhanced metal detoxification.

With these measures RR's symptoms fully resolved. He is back on the tennis court, and he can hunt and fish without any limitation. A follow-up stress echo study was obtained. The exam was stopped at 15:00, not because RR felt poorly, but because he had reached his target HR; he feels he could have gone farther. Post-exercise wall motion, however, looked worse than on RR's pre-treatment study. Viewed out of context, this would suggest that RR was worse. However, given that RR's symptoms had resolved, wall motion may be more abnormal because RR was able to push himself farther. It really doesn't make sense to me that an individual whose symptoms have resolved and whose treadmill time has increased could actually be worse, and again, I couldn't see operating on an asymptomatic 76 year-old who can run for 15:00, so we continued out conservative approach.

4. RR began a program of IV Phosphatidylcholine. This material stimulates LCAT (Lecithin Cholesterol Acyl Transferase), the key HDL-associated enzyme that mediates reverse cholesterol transport (this enzyme is inhibited by heavy metals).

5. RR began MSP (Modified Silver Protein - blocks oxygen utilization in unicellular microbial invaders but leaves multicellular organisms like us alone), aiming to decrease his infectious burden and blunt inflammation.

6. Antioxidants, minerals, essential fatty acids, along with Co-Enzyme Q and carnitine will remain on board, and RR continues to exercise.

7. This winter, when it is too cold outside for RR to go hunting, he will undergo additional MME.

"I undertook 150 hours of MME treatment for coronary artery narrowing. The 12 hour periods during the night were almost enjoyable - four hours of reading and for TV and eight hours of sound sleep. My score on the Bruce Protocol stress challenge increased from 13 to 15 minutes - maximal for my age. More important was my ability to beat my old tennis competitor by playing a full 90 minutes without needing the breathing breaks required before MME.

Happily I never experienced chest pain, just shortness of breath and easy fatigue, before MME corrected that - and I trust will prevent any chest pain angina in the future".

Summer '05 update: RR received an additional 100 hours of MME in March. He has returned to running (no marathons - he leaves those to his kids). RR is not taking a single cardioactive prescription drug. He will keep up with the Magnetico sleep pad, a nutritional program, oral phosphatidylcholine, and periodic oral DMSA.

Fall '05 update: RR feels great - his cardiac echo study is now normal - wall motion is normal, the ejection fraction is normal, and diastolic function is normal - the inferior wall contraction abnormality observed on RR's prior studies has resolved. RR has not undergone angiography, but his clinical presentation, resting echo, and stress echo studies point to coronary artery disease (prior inferior wall heart attack with additional heart muscle at risk) as the culprit. Following RR's initial 150 hours of MME, his symptoms resolved, but RR's stress echo study, obtained as he finished the 150 hours, remained abnormal. Six months later, and following an additional 100 hours of MME, RR's stress echo study was normal - that is, there was no evidence for additional heart muscle at risk - but the resting inferior wall contraction abnormality, reflecting a prior heart attack, was still present. Now, one year out from RR's initial MME, resting wall motion is unequivocally normal.

It means, in my opinion (and I can't be sure of any of this - these are just my thoughts), that cardiac healing brought on by MME occurs slowly, initially at the molecular level, and then at the biochemical level. Later, the blood vessels change, and only late after MME, in RR's case 12 months, do we see a change in the appearance of the heart. Early on, MME is probably generating ATP energy, improving function at the cellular level - RR could do more, early on post-MME, as his cells had more energy. Collateral vessels were likely functioning more efficiently, as static magnetic fields regenerate Nitric Oxide. RR was back on the tennis court, but his stress echo remained abnormal, likely because, in this limited time frame, not enough time had elapsed for the biochemical changes induced by MME to change the diameter of his major coronary arteries. Six months out from MME, RR's stress echo study had normalized. This might be due to the additional 100 hours of MME that he received, or it may simply be that it took 6 months for his original 150 hours to affect the architecture of the arteries. We think that MME stimulates stem cells within an organ to proliferate and migrate. In RR, post-initial MME we saw, at least grossly by echo, no evidence that this phenomena was taking place; the same at 6 months - the dead muscle still looked dead. At 12 months, however, the area appears to have been regenerated. We probably need to be patient - it took our hearts 9 months to form up in the 1st place. Post-MME we probably need to allow the same time frame for the stem cells we stimulate to regenerate the cell population in a damaged region. Again, this is what I think is going on, based on my study of the literature and my analysis of how my patients are responding to MME. Time will tell if we are right - but right now RR is happy with the way his heart looks, and he is happy with his tennis game.

7/06 Update - RR continues to do well; he enjoys hunting, fishing, and hour-long tennis matches and remains asymptomatic.

SD had three otherwise untreatable health problems, so she came to see us for MME and EECP. This 70 year old woman with medically addressed hypertension and diabetes was diagnosed with advanced liver dysfunction in 1993. Her liver was fibrosed and scarred (termed cirrhosis), compromising its ability to clear toxins from the blood and leaving her with an impossible to treat lipid abnormality. Blood draining from the GI tract "damned up" behind the liver, producing esophageal varices. The esophagus is the swallowing tube that connects the throat with the stomach. Think of esophageal varices as varicose veins within the esophageal wall. They don't trouble you - that is until they rupture, producing life-threatening hemorrhage (when I was an intern, I would stay up all night trying to keep esophageal "bleeders" out of shock). The cause of SD's liver dysfunction was never determined. Viral studies returned negative and SD does not consume alcohol; her gastroenterologist could not determine the cause and he had no treatment options to give her.

One year ago, SD began to experience angina, chest pain on the basis of impaired coronary artery blood flow, and shortness of breath with effort, due to impaired cardiac pump function. Given SD's liver problems, her physicians initially tried to treat her with medications, but her symptoms unfortunately progressed. Angiography carried out in the fall of '04 revealed occlusion of two coronary arteries (the Left Anterior Descending and Marginal) and a 90% Right Coronary Artery narrowing. Only one artery, the Circumflex, remained open. Two heart attacks had occurred, compromising heart pump function. Normally a 70 year old with this pattern of blockage would be treated with bypass surgery, but in SD's case, the anesthetic and bleeding risks would be astronomical, and she was turned down for bypass. Despite an extensive drug regimen, SD was experiencing 2 episodes of angina each day, requiring 5-10 NTG tablets per week. SD lives in Southern Ohio but she has family in the Toledo area, so she came up to see us.

To effectively treat SD, I had to effectively treat three problems at once - SD has to be the most complicated patient I have ever taken care of. My plan was to treat SD simultaneously with a program of EECP, MME, nutritional support, and detoxification. EECP was initiated in early 12/04, followed by MME (with oral DMSA), 2 hours each day to the liver and 2 hours each day to the heart, in early 1/05 (our first opening). Her prior medications were continued, and I added N-Acetyl Cysteine, Silymarin, and Lipoic Acid (liver protective nutritional agents).

Angina-wise this program worked; SD's chest pain fully resolved and NTG is no longer required. SD's blood pressure was under great control on medications, with a pre-treatment value of 120/80. Her BP fell further as a result of our treatments (as blood vessels dilated your BP can fall); this led to dizziness, prompting a decrease in her diuretic (water pills) and vasodilator drug doses. This proved to be an error on my part, as off these agents SD's heart failure flared up. We recognized the problem, resumed several of her medication, and with this her heart failure symptoms quieted down. SD's cardiac echo findings did not improve; advanced pump dysfunction and significant regurgitation behind her mitral valve were present before and after our treatments, but perhaps we need to be a little patient here, and not expect anatomic changes in just a few weeks.

In patients with kidney disease, we monitor serum Creatinine as an index of kidney function. Creatinine is generated by our muscles at a constant rate and is cleared from the body via the kidney. If kidney function falters, or if you become dehydrated, the serum creatinine will rise. If kidney function improves, the creatinine level will fall. Clinically we use the serum creatinine to guide our medical treatments for heart failure. The liver also filters the blood, retaining desirable blood products and clearing wastes into the bile. Clinically we use the serum Bilirubin level as a marker of liver function. A normal Bilirubin is < 1.3 mg/dL. SD's pre-treatment Bilirubin was elevated, 2.3 in 9/04 and 3.1 in late 11/04. One week into MME her Bilirubin value was 2.6, suggesting an improvement in liver function, but one week later her Bilirubin was 3.4, above the pre-treatment value. SD didn't feel worse, but this rise in SD's Bilirubin sure had we worried - was I helping her or hurting her? Dr. Bonlie was not worried. He has seen this phenomena before when MME is used to treat advanced liver disease; he sees the Bilirubin rise, and then fall. His theory is that Bilirubin "stuck" within damaged liver cells is released as the cells regain their function. He may cut back on the number of hours each day that the patient is treated with MME, but he never stops, and the Bilirubin always falls back over time. We had the same experience with SD. Advanced heart failure is typically treated with 200 hours of MME, and liver failure requires the same duration of MME treatment, but with SD we stopped after 50 hours to the heart and 50 hours to the liver. We stopped early because SD's primary problem, inoperable angina, had resolved and she needed a break as she had been away from home for nearly two months. Two weeks out from MME SD's labs were repeated and I spoke with both SD and her primary physician. SD was feeling well; angina had not recurred, and her breathing had improved further, and her Bilirubin had fallen to 2.5 - Dr. Bonlie was right. After SD has rested up, our plan will be for her to return to Toledo for further MME to her heart and liver. SD's care is still "a work in progress:, but so far things are certainly going her way.

7/06 - SD had maintained her gain after returning home. She did not required any hospital care or significant change in her program of medications. SD passed away, rather suddenly, from a kidney/urinary tract infection that spread into her blood stream

DATE	EVENT
9/79	Inferior Wall Heart Attack
1/80	Bypass surgery to RCA and Marginal - LAD and Circumflex wide open
'92	Two rounds of angioplasty to the Circumflex
9/92	Open grafts to the RCA and Marginal with LAD 95% and collateral filling of the LAD
'97	Recurrent angina ® 45 IV EDTA treatments
1/02	Effort angina with an abnormal 9:48 stress echo
8/02	Angina improved following 4 months of Nanobiotic therapy
6/04	New CHF - Ejection Fraction 25-30% ® Increased medical therapy
6/04	High grade Left Main and LAD narrowings, 95% narrowing in the SVG to occluded RCA with occlusion of the Circumlex and its graft 100%
7/04	LIMA to LAD and SVG to Diagonal and RCA
9/04	Normal 6:40 stress echo - resting EF 40-45%
12/04	Recurrent angina with a + 13:35 (modified protocol) stress echo - resting EF 30-35% and post-exercise EF 30-35%
1-2/05	45 hours EECP and 100 hours MME
3/05	14:00 (modified protocol) stress echo without angina - resting EF 40-45% and post-exercise EF 50-55%
6/05	Resting EF now normal, with less mitral regurgitation

CM is 25 years out from his original bypass surgery; he is a unique gentleman and I really enjoy working with him. I have one other patient in my practice who is alive 20 years out from bypass surgery, but I've never heard of anyone being physically active 25 years following their bypass. CM has obviously done an excellent job taking care of himself. He's learned a lot and applied these principles to his own health. CM has some strong opinions, and our minds don't always meet; usually he gets his way (should I be arguing with success?), but occasionally I prevail. I pushed CM hard to undergo a second bypass in the summer of '04, and felt bad when it didn't take. Fortunately we were able to rectify the situation with EECP and MME.

CM sustained a small heart attack in '79. The Right Coronary Artery and the Marginal branch of the Circumflex were blocked, and received bypass grafts in '80. The Left Anterior Descending and Circumflex were disease free in '80, but over the years accumulated plaque, such that two rounds of angioplasty to the Circumflex were required in '92. The LAD had a 95% narrowing that could not be addressed with angioplasty, but natural bypasses (collaterals) had developed, such that blood flow in the LAD distribution was not severely impaired. Angina recurred in '97. CM received 45 IV EDTA treatments with excellent results; angina resolved and CM was able to resume an active lifestyle.

I first met CM in 3/99; angina was minimal while a rhythm disturbance, intermittent atrial fibrillation, was noted. Chest discomfort became more of an issue in 1/02, and CM's 9:48 stress echo study returned abnormal. I recommended coronary angiography but CM declined (his last angiogram in '92 was complicated by puncture site occlusion and he was needle shy); instead we treated him with four months of Nanobiotic therapy and with this his symptoms improved.

Two years later CM presented with heart failure and pump dysfunction; his ejection fraction (percentage of blood ejected by the heart with each beat - normal is 50%) was only 25%. CM's kidney chemistries were slightly off, and he was now in fixed atrial fibrillation. Medical therapy for CHF was initiated and I pushed CM into an angiogram. The good news here was that the CHF therapy had worked; CM's ejection fraction had increased to 50%, demonstrating abnormal wall motion only over the back wall (1979 heart attack). The bad news was that only two inflow routes to the heart were open, and only by a thread. The Left Main (serves 2/3rds of the heart) had a 90% narrowing. The RCA was occluded, and its vein graft contained a 95% narrowing - everything else was closed. EECP would not work here and I pushed CM into his second bypass surgery. Three new grafts were placed. Kidney function was sluggish following surgery, but otherwise CM's recovery was uneventful. A stress echo study was carried out in 9/04 to clear CM for a cardiac rehab program; CM's resting ejection fraction was 40-45% and the 6:40 stress study looked good.

Chest pain returned in 12/04, just 6 months out from bypass surgery, and CM's stress echo study returned abnormal. CM's resting ejection fraction was 30-35%, and didn't rise with exercise as it should have; CM experienced angina during the study. One or more of CM's grafts has failed. CM wasn't interested in further angiography or surgery, and this time I wasn't going to push him, especially with the mild kidney dysfunction present. CM was treated with 45 hours of EECP, and 100 hours of MME.

CM tolerated both treatments well. His medications were decreased, and with this his kidney chemistries have normalized. CM still experiences chest pain if he pushed himself, but he can walk on the treadmill at 2.8 MPH for 30², and daily activities can be carried out without major difficulty. His resting ejection fraction is up to 40-45%, and following exercise it rises to 50-55%. MME and EECP didn't give CM a new heart, and the 100 hours of MME did not affect CM's atrial fibrillation, but he got better, allowing us to avoid further invasive treatments - we both agree on this.

6-month update - CM continues to well, exercising at a moderate level on a regular basis. I repeated his echo, and saw further improvement as compared to his 2 month post-MME study done in 3/05. I can still see evidence of two prior heart attacks, but overall pump function has improved a little, and the degree of mitral valve regurgitation has decreased some. As in some of our patients with neurological impairments, I'm seeing an ongoing or "late" further improvement in patients with heart disease treated with MME. I'm getting the idea that the stem cell proliferation or reparative processes that we seem to be generating with MME may take some time to manifest themselves as improved heart function and/or better looking non-invasive studies. And really, should I be surprised? It took 9 months for your heart to develop; shouldn't it take an equal amount of time for freshly stimulated cardiac stem cells to "grow up" and do their thing?

12-month update - CM has improved further. He can go longer on his home treadmill, and he hasn't needed a NTG tab in 6 months. Cardiac echo study shows some lessening in the degree of tricuspid regurgitation since 5/05. The pump function gain that CM experienced with MME has been maintained.

DATE	EVENT
pre '00	Two prior painless heart attacks
9/00	Echo: EF 25% with severe mitral regurgitation Angio: LAD and RCA mid-vessel occlusion, Circumflex distal occlusion, Marginal 70%, with an EF of 15%
1/01	Effort symptoms; resting EF 20-25% with an abnormal 7:00 (modified protocol) stress echo ® 35 hours of EECP
2/01	Symptoms improved, resting EF 20-25%, with a normal 7:00 stress echo
'01	Five months of Nanobiotic therapy
4/03	Recurrent angina, addressed with 35 hours of EECP
1/05	Recurrent symptoms; resting EF 35-45% with mild mitral regurgitation ® 35 hours of EECP and 100 hours of MME - symptoms improved, echo without change

` BV's heart was too far gone in 2000, but this is a concept that we don't believe in. BV, a previously hypertensive smoker with long-standing diabetes, presented with chest tightness and shortness of breath in the fall of '00. Angiography revealed occlusion of all three major coronary arteries, an ejection fraction of only 15%, and severe mitral regurgitation - BV's heart was shot - too far gone for bypass surgery.

I saw BV for the first time in 12/00. BV's meds were adjusted and a cardiac nutritional program was initiated; the next step was 35 hours of EECP. With these measures BV's symptoms improved such that she could carry out desired activities without major difficulty. BV received 5 months of nanobiotic therapy in late '01, and a repeat course of EECP in 4/03 to address recurrent angina. Symptoms recurred in early '05. At this point BV's ejection fraction was in the 35-45% range, with only mild mitral regurgitation. She received 35 hours of EECP, this time coupled with 100 hours of MME. BV's echo picture did not change (and we really didn't expect it to), while effort related chest tightness and shortness of breath did resolve (our goal). BV was too far gone for bypass surgery in 2000, but with a complementary treatment program, EECP, and now MME, her symptoms are minimal and she can carry out all desired activities without difficulty.

7/06 Update - BV remains improved, and has not required a hospital stay or invasive procedure since completing MME in 1/05. Her cardiac echo is unchanged from 1/05; the gain that BV obtained from MME has been maintained. BV is now going to participate in our study of MME in diabetic neuropathy. This is all pretty good for a 72 year old who six years earlier could not undergo bypass surgery because her heart had been too badly damaged by two prior heart attacks.

DATE	EVENT
'99	Normal stress echo
12/00	Abnormal (posterior ischemia) stress echo ® 30 IV EDTA treatments
'01	Normal 15:00 stress echo
8/04	Abnormal 15:00 (posterior ischemia) stress echo
9/04	Lead 18 and Mercury 7.8 by challenge testing - Creatinine abnormal at 1.4
12/04	Atypical pain - 15:00 stress echo produced acute myocardial infarction
12/04	Acute EECP ® Chest pain and ST elevation resolved
12/04	20 Gauss Magnetico sleep pad with topical DMPS-Glutathione begun
1-2/05	35 hours EECP, medical therapy and an extensive nutritional program
3/05	Lead 9.6 and Mercury 1.2 by challenge testing - Creatinine now normal at 1.1
6/05	100 hours MME to the heart - echo now normal

CD is a strong willed man. Six years ago he weighed 360 pounds. After a screening stress echo study returned benign, CD began a program of exercise and dietary modification. CD lost 100 pounds. A repeat stress study in '01 returned mildly abnormal. CD underwent 30 IV EDTA treatments, and a follow-up study one year later looked great.

I began working with CD in 8/04. His stress echo study returned mildly abnormal, but he was able to complete 15:00 of treadmill stress. We discussed angiography, but at that time CD was not experiencing any symptoms of coronary insufficiency. We were also worried about his kidneys, and the potential for the X-Ray contrast dye that we use during angiography to damage his kidneys further. CD's creatinine was elevated at 1.4 mg/dl (creatinine reflects the level of kidney function - normal is £ 1.1 mg/dl). A challenge study returned abnormal for Lead and Mercury (see CD's graphics). CD's work involved welding (source of Lead) and his amalgam fillings (2/3rds of tissue Mercury in Americans comes from past and present amalgam fillings) had only recently been removed. A program of risk factor reduction and nutritional therapy was initiated. At that time I didn't think that we needed to be in a hurry, so I began CD on only a moderate dose oral metal detoxification program. In retrospect, not being in a hurry was an error on my part.

CD came in to see me in late 12/04 with upper abdominal discomfort. This didn't sound at all coronary in nature. CD looked good and otherwise he was feeling well. Just to be on the safe side, I repeated his stress echo study. CD and I chatted about our kids during the exam. The chest discomfort in question was present before, during, and after the study; it worsened only slightly with treadmill stress and CD wasn't feeling at all poorly. The post-exercise echo images, however, revealed impaired motion over the back wall of CD's heart, consistent with an at least partial blockage in the artery serving this region, and his EKG demonstrated ST elevation, consistent with a heart attack. I gave CD a sublingual NTG tablet. The NTG had no effect on his pain, nor the appearance of his EKG or echo. Basically, I had precipitated a heart attack in CD (the 2nd time this had happened in my 20 years of practice). I offered to take CD directly to the hospital catheterization laboratory and carry out an emergency angiogram, but he turned me down. He was worried about the potential for kidney damage from the angiogram, and he just wasn't enthusiastic about stent placement or bypass surgery. As stated above, CD is a strong willed man. I'm smart enough to know that I am not going to win arguments with people who can lose 100 pounds in two years, so I went directly to plan B.

In the US, we use EECP to deal with chronic coronary disease and heart failure, but in China EECP is a first line treatment for acute heart attack. We walked CD from the stress room to the EECP room and treated him for three hours. CD's chest pain resolved, as did his abnormal EKG findings (see CD's graphics). CD received two hours of EECP over each of the next five days; a full course of EECP was completed in January of '05.

Obviously we needed to take a more aggressive approach to the factors underlying CD's coronary disease, and we needed to do it post haste. CD began sleeping on a 20 Gauss Magnetic negative field only sleep pad. Every other evening he rubbed 50 drops of transdermal DMPS-Glutathione into his skin, aiming to mobilize and removed from his system Mercury and Lead. 100 hours of MME was carried out in 6/05. On CD's post-MME resting echo study, I could not see any evidence that he had sustained a heart attack (but the amount of damage done in 12/04 was likely minimal, as we had treated him with instantaneous EECP). A repeat challenge study showed that a great deal of Mercury and Lead had been cleared from CD's system (see CD's graphics).

Our plan is for CD to continue his present pharmacologic and nutritional program. He will continue to sleep on the Magnetico pad, and DMPS-Glutathione will be kept on board at a half dose. A stress echo study will be carried out in several months (we are learning that the peak effect of MME is not obvious for several months after MME is stopped). Oh, and by the way, CD's kidney function is now normal; his creatinine is down to 1.1 mg/dl. While we focused on clearing Mercury and Lead from CD's heart, at the same time we must have cleared Mercury and Lead from his kidneys - after all, the Magnetico sleep pad and the topical DMPS-Glutathione that CD applied have access to every cell in your body. I guess it's a good thing that CD is so strong willed. He argued me out of urgent angiography, an approach to his acute heart disease that could easily have damaged his kidneys, and into a program of EECP and negative field magnetic therapy, an approach that got the job done heart-wise, and at the same time improved the function of his kidneys. I like taking care of patients like CD, and I love this approach to medicine. Click CD's symptoms for a description of how CD felt, in his own words, before and after MME.

	EVENT
'84	Bypass surgery with urgent re-do surgery for acute graft failure
'96	Third coronary artery bypass surgery
'98	Normal 7:00 stress cardiolite perfusion study
10/03	Abnormal 6:00 stress echo study
10/03	Cadmium 9.3, Lead 92, Mercury 11, and Nickel 61 by challenge testing
12/04	Increased symptoms with an abnormal 3:30 stress echo ® Coronary angiography
1/05	LAD 65%, 1st septal 80%, with an occluded LIMA graft, Circumflex 60% with an open vein graft, Marginal 100% with an occluded vein graft, RCA 100% with a patent RIMA graft, inferior hypokinesis with a normal EF
1-3/05	EECP with pharmacologic and nutritional treatment as tolerated
3-5/05	Magnetico sleep pad with topical DMPS-Glutathione
6/05	200 hours of MME: Energy level and exercise tolerance increased, BP control improving, as is DB's tolerance to drug and nutritional therapies

I began working with DB in the fall of "03. Symptoms had recurred, then three years out from her 3rd bypass surgery. DB's BP and lipid values were out of control, and nearly impossible to treat. Multiple BP drugs had been tried; she could tolerate only one - Atenolol. Statin cholesterol lowering agents and Zetia had been prescribed - none were tolerated and CD's LDL was around 200 mg/dl. CD needed help outside the paradigm of more drugs and surgery. It is my observation that patients who just can't tolerate any drugs (and nutritional therapies for that matter) are often metal overloaded. My feeling here is that the enzyme systems involved in drug metabolism and detoxification have been inactivated by the heavy metals. The drugs cannot be broken down and as a result the patient just can't take them - they often can't take anything. I suspected this to be the case with DB. A triple challenge study (low doses of IV EDTA and DMPS alone with oral DMSA and EDTA - followed by a measurement of metals excreted in a 6-hour urine sample) demonstrated spills of Cadmium, Lead, Mercury, and Nickel, supporting my hypothesis. I tried treating DB with an oral preparation containing EDTA and Phosphatidylcholine. DB could tolerate only a low dose (just as she could tolerate only a low dose of anything she could tolerate). With this DB's LDL fell slightly, from 190 to 173 mg/dl.

DB's stress echo study had returned abnormal in 10/03. At that time her symptoms were not marked, and I wasn't enthusiastic about carrying out the angiogram that might lead to her 4th bypass surgery. A repeat stress study carried out in 12/04 looked worse, with an interval decrease in treadmill walking time from 6:00 to 3:30. DB's symptoms were worse too, and thus we proceeded with coronary angiography. This study revealed two open and one closed bypass graft, along with narrowings in the non-bypassed LAD (left anterior descending). Stent placement was not an option here and a 4th surgery risked damage to her two still open grafts. We treated CD with a course of EECP and with this she improved a little. 10 IV EDTA (binds Cadmium, Lead, and Nickel but not Mercury) were administered. Then CD began sleeping on a Magnetico sleep pad, and we switched from IV EDTA to topical DMPS-Glutathione (binds Mercury and to a lesser extent Lead). DB improved further. Her BP became easier to control, and medication intolerance was now less of an issue. After two months of sleep pad/DMPS pre-treatment, DB received 200 hours of MME to her heart. Things are now going DB's way. She will continue to sleep on the Magnetico pad and she will keep up with DMPS based metal detoxification. A stress echo study will be carried out four to six months post-MME, and we will then reassess her treatment plan (please review the following paragraph and then DB's 9/05 update)..

I was trained to think that high cholesterol was the cause of cardiovascular disease. I was trained wrong. Back then we really didn't know what we were dealing with. My thinking is changing. While high cholesterol is clearly an issue, I now feel that heavy metal overload is a more important culprit. It may be that heavy metal overload plays a role not just in the causation of vascular disease, but as a driving force underlying high cholesterol, high blood pressure, and vascular wall inflammation. Heavy metals poison enzyme systems. They can poison the enzymes that carry out reverse cholesterol transport and they can poison the enzymes that make artery dilating substances like Nitric Oxide. Metals poison enzymes and metals poisoned DB. DB's response to MME and metal detoxification supports this new thinking (new to me me anyway). DB's primary problem all along may have been metal overload. We are using EECP, MME, and metal detoxification primarily in patients with end-stage, recurrent, or inoperable patients, patients like DB, but what would have happened had MME and metal detoxification been applied to DB in 1984? Maybe one day, after we prove unequivocally that this approach works (and here we have more work to do), we will be using negative field magnetic therapy/ metal detoxification as a first line therapy - we could call it the DB protocol.

7/05 Update - DB required surgery to address a high-grade carotid artery narrowing; cardiac-wise she did well with the procedure. BP control continues to improve, as does DB's tolerance to prescription medications. In the above paragraph I commented that cholesterol was not the "be all and end all" cause of heart disease as I was taught. In DB's case I might just be right. Her LDL did fall slightly (190 to 173) with an oral chelation program, but in late 8/05, post-MME, and following a total of 5 months of sleep pad/topical DMPS-Glutathione metal chelation, her LDL is down to an all time low of 130 mg/dl - this is in a patient who has never been able to tolerate statin drugs. DB's LDL reduction supports my position that metal overload is playing a role in the progressive, age-related rise in cholesterol that we see in many of our patients. They watch their diet but still their cholesterol keeps rising - because the problem is metal overload - not diet, and not drug deficiency. We will continue to use statin drugs for rapid lipid reduction, but it is only rationale to concomitantly remove toxic metals, and the sleep pad/topical DMPS-Glutathione may be the best approach here.

	EVENT
'93	Lung malignancy ® Resection of 1/2 the right lung
'01	Two vessel bypass surgery
2/04	ed shortness of breath and an abnormal chemical stress perfusion study ®
2/04	RCA only 55%, LIMA arterial graft to occluded LAD open, high-grade Left Main - Circumflex narrowing with occlusion of the Circumflex vein graft ®
2/04	Left Main-Circumflex angioplasty carried out - stent placement not possible
4/04	No improvement and 4:00 stress echo abnormal ® angiography
4/04	Left Main-Circ restenosis - further intervention not possible in Toledo
6/04	Symptoms improved following 35 hours of EECP
9/04	Symptoms recurred ® 35 hours of EECP and 200 hours of MME - no better
4/05	Feeling worse ® Left Main-Circumflex narrowing unchanged to slightly better
5/05	Left Main-Circ narrowing stented in Detroit ® Feels even worse
6/05	Progressive interstitial lung disease diagnosed - heart wasn't the primary problem

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