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While there is a developing understanding of the influence of sleep on cardiovascular autonomic activity in humans, there remain unresolved issues. In particular, the effect of time within the sleep period, independent of sleep stage, has not been investigated. Further, the influence of sleep on central sympathetic nervous system (SNS) activity is uncertain because results using the major method applicable to humans, the low frequency (LF) component of heart rate variability (HRV), have been contradictory, and because the method itself is open to criticism. Sleep and cardiac activity were measured in 14 young healthy subjects on three nights. Data was analysed in 2‐min epochs. All epochs meeting specified criteria were identified, beginning 2 h before, until 7 h after, sleep onset. Epoch values were allocated to 30‐min bins and during sleep were also classified into stage 2, slow wave sleep (SWS) and rapid eye movement (REM) sleep. The measures of cardiac activity were heart rate (HR), blood pressure (BP), high frequency (HF) and LF components of HRV and pre‐ejection period (PEP). During non‐rapid eye movement (NREM) sleep autonomic balance shifted from sympathetic to parasympathetic dominance, although this appeared to be more because of a shift in parasympathetic nervous system (PNS) activity. Autonomic balance during REM was in general similar to wakefulness. For BP and the HF and LF components the change occurred abruptly at sleep onset and was then constant over time within each stage of sleep, indicating that any change in autonomic balance over the sleep period is a consequence of the changing distribution of sleep stages. Two variables, HR and PEP, did show time effects reflecting a circadian influence over HR and perhaps time asleep affecting PEP. While both the LF component and PEP showed changes consistent with reduced sympathetic tone during sleep, their pattern of change over time differed.

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These data reveal a high incidence of newly diagnosed RHD within an adult urban African community. These data argue strongly for the first episode of RHD to be made a notifiable condition in high burden countries in order to ensure control of the disease through register-based secondary prophylaxis programmes.

Cardiac manifestations of HIV/AIDS identified within this cohort were relatively infrequent. While HIV-related cardiomyopathy and pericardial disease remain important targets for early detection and treatment in this setting, HIV-related cases of CAD remain at historically low levels.

Existing literature on reward motivation pays scant attention to the fact that reward potential of the environment varies dramatically with the light/dark cycle. Evolution, by contrast, treats this fact very seriously: In all species, the circadian system is adapted to optimize the daily rhythm of environmental engagement. We used 3 standard protocols to demonstrate that human reward motivation, as measured in the dynamics of positive affect (PA), is modulated endogenously by the circadian clock. Under naturalistic conditions, 13.0% of PA variance was explained by a 24-hr sinusoid. In a constant routine protocol, 25.0% of PA variance was explained by the unmasked circadian rhythm in core body temperature (CBT). A forced desynchrony study showed PA to align with CBT in exhibiting circadian periodicity independent of a 28-hr sleep/wake cycle. It is concluded that the circadian system modulates reward activation, and implications for models of normal and abnormal mood are discussed.

These unique data suggest that urban Africans in Soweto develop AF at a relatively young age. Conventional strategies used to manage and treat AF need to be carefully evaluated in this setting.

No abstract