Insomnia, a new Modifiable Risk Factor for Heart Failure?

Mathieu Berger; Geoffroy Solelhac; Frédéric Roche; Raphael Heinzer


Eur Heart J. 2021;42(40):4177-4179. 

In This Article

Underlying Pathophysiological Mechanisms

Underlying mechanisms explaining the association between insomnia and increased incident HF remain largely unknown. Insomnia disorder induces a state of hyperarousal and there may be a bi-directional relationship with unhealthy lifestyle. Indeed, an unbalanced diet and physical inactivity are among the dysfunctional behaviours increasing insomnia symptoms, whereas insomnia may be associated with daytime impairment (e.g. fatigue, attention, and, more specifically, sleepiness) that could favour sedentary behaviour. The underlying pathophysiological mechanisms include: (i) dysregulation of the hypothalamic–pituitary–adrenal axis leading to increased cardiovascular risk along with insulin resistance, diabetes, and depression; (ii) increased sympathetic nervous system activity via activation of hormones implicated in arousal such as cortisol and norepinephrine, leading to increased resting heart rate, elevated blood pressure, and altered heart rate variability; (iii) increased secretion of proinflammatory cytokines involved in atherogenesis such as C-reactive protein, tumour necrosis factor-α, and interleukin-6; and (iv) impaired glucose tolerance and dyslipidaemia (Graphical Abstract).[11] However, insomnia is a heterogeneous condition and its pathophysiological mechanisms may differ from one phenotype to another. One may wonder how difficulty initiating sleep increases the risk of HF. Does it share a common pathway with non-restorative sleep? Are such effects driven by short sleep duration, as proposed by some authors,[12] or rather by sleep fragmentation? Many of the pathophysiological pathways increasing HF risk are probably separately influenced by insomnia and short sleep duration, and the co-occurrence of the two conditions may have synergic effects. Further studies are needed to elucidate these pathophysiological mechanisms in order to determine the best treatment approach.

Graphical Abstract.