Subsequent Cardiac and Stroke Events in Patients with Known Vascular Disease Treated with EDTA Chelation Therapy

Dr L. Terry Chappell, Rakesh Shukla, Jun Yang, René Blaha, Tammy Born, Claus Hancke, William Mitchell, Efrain Olszewer, Peter van der Schaar, James Ventresco;

Chappell23 Aug 2012

Context

Myocardial infarction (MI) and strokes are leading causes of death in the US. Surgical and medical treatments can be helpful, but carry risks of morbidity and mortality.

Objective

To evaluate whether cardiac events were reduced for patients with known vascular disease who were treated with intravenous ethylene diamine tetra-acetic acid (EDTA) chelation therapy.

Design

Retrospective study with a 3-year follow-up, compared with similar patient groups by use of meta-analysis.

Population and setting

A total of 220 consecutive patients with known vascular disease were treated with chelation therapy during 1992–2001. Eight outpatient centres were included: five from the US and one each from Denmark, the Netherlands and Brazil. Average patient age was 64 years, 72.3% were males and 18.2% were smokers. Average number of treatments was 58.

Main outcome measures

MI, stroke and death from any cause were primary outcome measures. Secondary measures were resolution of symptoms and need for coronary artery bypass surgery (CABG) and percutaneous transluminal coronary angioplasty.

Results

According to the meta-analysis, expected outcomes in a 3-year follow-up period for 220 patients with coronary artery disease treated only with conventional therapies would be 15 MIs and six deaths. There were no deaths and no MIs in this group of patients who received chelation therapy. Four patients had strokes but recovered well. There were two angioplasties and six CABG procedures. Compared with similar patient populations treated with conventional therapies, patients who also were chelated had a 93.6% lesser need for angioplasty and a 62.5% reduced need for CABG. Of the patients that initiated treatment with symptoms, 68.7% had complete resolution of symptoms.

Conclusions

This study indicates that the administration of intravenous EDTA chelation therapy for patients with vascular disease resulted in fewer subsequent cardiac events than primary treatment with CABG, angioplasty or conventional medical therapy. EDTA chelation therapy for vascular disease is a reasonable, off-label adjunct, especially for patients who refuse or are not eligible for surgery. Clinical trials such as the Trial to Assess Chelation Therapy (TACT) are needed for definitive proof.

For full-text PDF, click here

 

The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction.

by Houston MC

medical-doctor-1236728-639x717Abstract

Mercury, cadmium, and other heavy metals have a high affinity for sulfhydryl (-SH) groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (NAC, ALA, GSH), with subsequent decreased oxidant defense and increased oxidative stress. Both bind to metallothionein and substitute for zinc, copper, and other trace metals reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation; increased oxidative stress is common. Selenium antagonizes mercury toxicity. The overall vascular effects of mercury include oxidative stress, inflammation, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, immune dysfunction, and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, CHD, MI, increased carotid IMT and obstruction, CVA, generalized atherosclerosis, and renal dysfunction with proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury, cadmium, and other heavy metals inactivate COMT, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to heavy metal toxicity. Cadmium concentrates in the kidney, particularly inducing proteinuria and renal dysfunction; it is associated with hypertension, but less so with CHD. Renal cadmium reduces CYP4A11 and PPARs, which may be related to hypertension, sodium retention, glucose intolerance, dyslipidemia, and zinc deficiency. Dietary calcium may mitigate some of the toxicity of cadmium. Heavy metal toxicity, especially mercury and cadmium, should be evaluated in any patient with hypertension, CHD, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, serum, etc. with baseline and provoked evaluation should be done.

http://www.ncbi.nlm.nih.gov/pubmed/17405690