Troponin Elevations After Electroconvulsive Therapy: The Need for Caution

BACKGROUND: Electroconvulsive therapy is used to treat patients with severe or resistant depression. Troponin elevations are associated with an adverse prognosis, and it is well known that central nervous system insults can cause biochemical evidence of cardiac injury. No study previously has studied this with electroconvulsive therapy. METHODS: Patients scheduled for electroconvulsive therapy were enrolled. Clinical information, an electrocardiogram, and a baseline sample for cardiac troponin I and T (cTnI and cTnT) were obtained. Electroconvulsive therapy was done with standard techniques. Subsequently, electrocardiograms and additional samples were obtained. cTnT was measured with the Roche assay and cTnI with the Dade Stratus equipment. Values above the 99th percentile were considered abnormal. RESULTS: Seventy patients completed the study. Four patients had elevated levels of cTn before treatment. In 3 patients, the elevations persisted. Four additional patients developed elevated cTn levels during electroconvulsive therapy. Two of the patients with cTn elevations died. No other events occurred during follow-up. CONCLUSIONS: Elevations of cTn occurred in 11.5% of patients treated with electroconvulsive therapy. Some of the elevations preceded therapy and some occurred during treatment. Given the adverse prognostic importance of cTn elevations in general, in addition to additional studies, an increased degree of medical scrutiny may be appropriate for this group of patients and for those receiving electroconvulsive therapy

Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference