Brugada syndrome as a potential cardiac risk factor during electroconvulsive therapy (ECT).

A case of asystole (> 5 s) during electroconvulsive therapy (ECT) is reported in a patient who was subsequently diagnosed to have Brugada syndrome (BS). This hereditary sodium-channelopathy is characterized by typical, though intermittent, ECG abnormalities and carries a high risk of ventricular arrythmia and sudden cardiac death. The general occurence of BS is rare; however, it is more prevalent in men and in southeast Asian populations. As in the reported case, BS carriers may lack a telltale medical history and can present with normal ECG recordings. In these cases, BS can only be unmasked by repeated ECG recordings over time or by specialist cardiological examinations. To our knowledge, BS, which was first characterized in 1992, has not yet been in the focus of cardiac complications during ECT. However, as the presented case illustrates, this syndrome should be considered as a rare but potentially severe cardiac risk factor in the context of ECT.

Clozapine induces oxidative stress and proapoptotic gene expression in neutrophils of schizophrenic patients.

The present study examined cellular effects of the atypical antipsychotic drug clozapine on blood cells of treated patients with and without clozapine-induced agranulocytosis (CA). Blood from one patient who commenced clozapine treatment was examined at weekly intervals for 128 days. Olanzapine-treated (n = 5) and polymedicated (n = 14) schizophrenic patients, as well as healthy subjects (n = 19) and septic shock patients (n = 8), were studied for comparison. We observed dramatically increased numbers of native neutrophils stained for superoxide anion production (P < or = 0.005, n = 10) and significantly elevated expression levels of the proapoptotic genes p53 (P < or = 0.020), bax alpha (P < or = 0.001), and bik (P < or = 0.002) in all tested non-CA patients (n = 19) and CA patients (n = 4). In non-CA patients, the expression of these genes did not correlate to the percentage of apoptotic neutrophils (2.0% +/- 1.3%), but in CA patients about 37% of the neutrophils show morphologic signs of apoptosis (P < or = 0.001). Under G-CSF therapy of CA, the number of apoptotic neutrophils and the expression of the proapoptotic genes decreased significantly. In conclusion, high production of reactive oxygen species in neutrophils of clozapine-treated patients, together with increased expression of proapoptotic genes, suggests that neutrophils are predisposed to apoptosis in schizophrenic patients under clozapine therapy. The correlation between drug and proapoptotic markers was highest for clozapine and bax alpha as well as superoxide anion radicals. This indicates oxidative mitochondrial stress in neutrophils of clozapine-treated patients which probably contributes to the induction of apoptosis and sudden loss of neutrophils and their precursors in CA patients.

Hyperhomocysteinaemia in treated patients with Huntington's disease homocysteine in HD.

Significantly increased plasma total homocysteine levels (t-Hcys) appeared in treated Huntington disease (HD) patients compared to controls and untreated HD subjects. Because the protein Huntingtin interacts with the homocysteine metabolism modulating enzyme cystathionine beta-synthase, we hypothesize that homocysteine promotes neurodegeneration in HD.