For at least the past 30 years it has been known that people with schizophrenia have higher death rates, particularly from cardiovascular causes, than would be expected on the basis of demographics (Allebeck & Wistedt, 1986; Mortensen & Juel, 1990; Newman & Bland, 1991; Walker et al, 1997). Initially, suspicion focused upon lifestyle factors, such as ubiquitous smoking and poor self-care, and perhaps upon a direct effect of the disease. However, some of the suspicion began to shift to the drugs used to treat the disease, fuelled both by the accumulation of case reports among antipsychotic users of serious ventricular arrhythmias and sudden unexpected deaths (Liberatore & Robinson, 1984; Kriwisky et al, 1990; Mehtonen et al, 1991; Donatini et al, 1992; Thomas, 1994; Jackson et al, 1997; Ravin & Levenson, 1997; Zarate et al, 1997; Dickinson, 2000), as well as advancing understanding of the electrophysiological properties of these drugs (Thomas, 1994; Suessbrich et al, 1997; Drici et al, 1998; Rampe et al, 1998; Shader & Greenblatt, 1998; Studenik et al, 1998; Reilly et al, 2000).