Heart chelation therapy

Tsironi M, Deffereos S, Andriopoulos B et al. Reversal of heart failure in thalassemia major by combined chelation therapy a case report. Eur J Haematol 2005 74(l) 84-85. 

Adverse effects of disodium edetate include hypocalcemia, tetany, convulsions, cardiac dysrhjThmias, respiratory arrest, and renal insufficiency. Other possible symptoms include nausea, vomiting, diarrhea, fever, headache, and urinary urgency. Pain and phlebitis at the site of injection can occur (11). The sodium load in chelation therapy can precipitate heart failure. Renal tubular necrosis can occur (2). 

Chelation therapy using edetic acid has been widely used for the treatment of ischemic heart disease. However, it has been suggested that the therapeutic benefits of this treatment may be due to the changes in lifestyle of the patient rather than the administration of edetic acid (40 mg/kg by infusion over a 3-hour period). ... 

Knudtson ML, Wyse DG, Galbraith PD, et al. Chelation therapy for ischemic heart disease a randomized controlled trial. / Am Med Assoc 2002 287(4) 481 86. 

Some long chain alkyl derivatives of chelating agents have been prepared with the idea of promoting localization in the myocardium (54). This has obvious relevence to iron chelation therapy because of the fatal susceptibility of the heart to iron overload. 

Mossbauer study of B-thalassemia/hemoglobin E heart tissue from patients who had received no transfusion and chelation therapy was carried out in Ref. 120. Preliminary results of normal and lymphoid leukemia chicken liver and spleen tissue study using Mossbauer spectroscopy with a high velocity resolution were obtained in Ref. 132. It was observed that Mossbauer hyperfine parameters of liver and spleen samples demonstrated small changes between the corresponding normal and pathological tissues. 

The main dose-limiting toxicity of all anthracyclines is myelosuppression, with neutropenia more commonly observed than thrombocytopenia. In some cases, mucositis is dose-limiting. Two forms of cardiotoxicity are observed. The acute form occurs within the first 2-3 days and presents as arrhythmias or conduction abnormalities, other electrocardiographic changes, pericarditis, and myocarditis. This form is usually transient and is asymptomatic in most cases. The chronic form results in a dose-dependent, dilated cardiomyopathy associated with heart failure. The chronic cardiac toxicity appears to result from increased production of free radicals within the myocardium. This effect is rarely seen at total doxorubicin dosages below 500-550 mg/m2. Use of lower weekly doses or continuous infusions of doxorubicin appear to reduce the incidence of cardiac toxicity. In addition, treatment with the iron-chelating agent dexrazoxane (ICRF-187) is currently approved to prevent or reduce anthracycline-induced cardiotoxicity in women with metastatic breast cancer who have received a total cumulative dose of doxorubicin of 300 mg/m2. All anthracyclines can produce "radiation recall reaction," with erythema and desquamation of the skin observed at sites of prior radiation therapy. 

In most cases, the reversal of symptomatic myocardiopathy has been achieved without drug toxicity (19,43). Davis and Porter (19) and Tsironi et al. (44) confirmed clinically the laboratory data of Link et al. (45) that DFO therapy reverses cardiac arrhythmias in some patients previously unresponsive to medical treatment. This may be attributed to removal of a toxic labile iron pool. They also mentioned improvement of left ventricular ejection fraction in seven of nine patients. It is important to note that oral chelators are less effective than DFO and are unable to prevent cardiac mortality in patients with established heart disease (46). 

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