After myocardial infarction (MI), monocytes are actively recruited to the brain to augment sleep power and abundance, which in turn helps to limit cardiac inflammation and promotes recovery, according to a study in humans and mice published in Nature. “Our data demonstrate a critical bidirectional relationship between sleep and cardiovascular disease,” says lead investigator Cameron McAlpine.

The investigators found that mice with atherosclerosis, MI or heart failure induced by pressure overload spend more time in slow wave sleep, a stage of sleep also known as deep sleep that is thought to be associated with repair and restorative processes, than healthy mice. In MI, the drive, power and abundance of slow wave sleep increased within 24 h after the infarct. Notably, these sleep changes were driven by active recruitment of monocytes to the brain.