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Editor's Correspondence
May 28, 2007

Decreased Sleep in Heart Failure: Are Medications to Blame?

Arch Intern Med. 2007;167(10):1098-1099. doi:10.1001/archinte.167.10.1098-b

In the September 18 issue of the Archives, Arzt and colleagues1 showed that patients with systolic heart failure (HF) only sleep approximately 5 hours per night vs 6.5 hours in a community sample. The authors suggest that the reduced sleep duration in HF could be caused by elevated central noradrenergic activity stimulating alertness. This suggests that pathophysiological factors leading to HF, or the presence of HF itself, may cause shortened sleep. In such a case, optimal therapy for HF may improve sleep, and untreated HF may result in even shorter sleep. Indeed, the accepted approach to the treatment of secondary insomnia is to treat the underlying medical disorder, assuming that the sleep will thereby improve. It would be worthwhile to test this assumption and determine whether sleep improves in a group of patients with HF after instigating therapy. On the other hand, instead of pathophysiological factors related to HF causing shortened sleep, we wonder whether the short sleep in HF is an adverse effect of medication use, since this population was optimally treated.2 For example, in the study by Arzt et al,1 72% of the patients with HF used diuretics that can cause nocturnal polyuria. Thus, adjusting the timing of diuretic use possibly could improve sleep. Furthermore, 81% of their patients with HFused β-blockers, and β1-adrenergic receptor blockers are known to suppress nocturnal plasma melatonin,3 which can result in reduced sleep.4 This hypothesis, that β1-blockers reduce sleep in patients with HF via melatonin suppression, raises the potential for nighttime melatonin supplementation as a therapy to counter an adverse effect of β-blockers and restore normal sleep in this population. Finally, it is established that acute partial sleep loss leads to increased sympathetic activity.5 The authors suggest therefore that sleep loss itself could contribute to the development of HF via its effects on the cardiovascular system.1 Clearly, further studies are needed, but if sleep loss does contribute to the development of HF, then optimizing HF therapy while counteracting any adverse effects of HF medications on sleep duration conceivably could have 2 advantages: improved sleep and improved HF outcome.

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