How sleep helps recovery after a heart attack

Sleep is essential for good cardiovascular health (see here, here and here), and poor quality or insufficient sleep increases the risk of myocardial infarction, regardless of genetics and other risk factors (see here, here and here). Studies have highlighted complex neural circuits by which the brain regulates biological processes underlying cardiovascular disease during sleep. For example, sleep-regulating signals from the hypothalamus modulate the production of immune cells that influence atherosclerosis (see here and here). However, it is unclear whether cardiovascular injury or disease influences sleep and its brain circuits through heart-brain signalling and whether changes in sleep influence neural signals from the brain to the heart.

Recent studies have identified circuits through which the brain senses changes in cardiac physiology. For example, tachycardia (rapid heartbeat) causes anxiety-like behaviours, and sensory neurons in the vagus nerve can cause syncope (sudden, brief loss of consciousness).

To further our understanding of the subject, a team of researchers induced myocardial infarctions (MI) in mice and measured brain waves. These mice spent more time in deep slow-wave sleep, a phase of sleep that has been associated with repair and healing, than control mice that had not suffered MI.

Knowing that after an MI, immune system cells trigger massive inflammation in the heart, the researchers wanted to know if such changes would also affect the brain. They found that after an MI in mice, the microglia rapidly recruits monocytes from the bloodstream to the brain, in the thalamus. The monocytes relocated to the brain are reprogrammed to produce tumour necrosis factor (TNF), an important regulator of inflammation and sleep-promoting factors (see Figure 1).

Figure 1. The role of sleep after a myocardial infarction. Adapted from Rowe, 2024, based on results from Huynh et al., 2024. A. Restorative sleep in mice after myocardial infarction: monocytes recruited to the brain secrete TNF, which acts on sleep-regulating neurons to induce slow-wave sleep, characterized by slow, synchronized electrical oscillations in the brain. This type of sleep inhibits sympathetic nervous signals to the heart, thereby decreasing inflammation to a level that promotes healing. B. When sleep is disrupted, sympathetic nervous signals are no longer inhibited and monocyte recruitment to the brain and heart increases too much, leading to increased inflammation that impairs cardiac function and healing.

Injecting an antagonist into the brain of mice immediately after MI reduced monocyte accumulation and blocked induction of deep slow-wave sleep. To corroborate these results, the researchers used a Ccr2^–/– mouse line (which does not express the Ccr2 receptor located on the surface of monocytes) and observed few monocytes in the brain and no induction of deep slow-wave sleep after provoking MI.

The central role of TNF in sleep induction following MI was confirmed by blocking this cytokine by injection of neutralizing antibodies into the brain of mice immediately after infarction, which resulted in a significant decrease in deep slow-wave sleep. Similar results were observed in a Tnf^–/– mouse line (genetically modified to not express TNF).

In another set of experiments, the researchers disrupted deep slow-wave sleep in mice that had suffered an MI. The sleep disruption impaired heart function, reduced heart rate variability, and caused spontaneous ventricular tachycardia (a severe arrhythmia). After an MI, mice whose sleep was disrupted had poorer cardiovascular health and recovery than mice that had normal, undisturbed sleep.

The findings in mice were validated in humans by examining data from a group of people with acute coronary syndrome (unstable angina or myocardial infarction, conditions in which blood flow from the coronary arteries to the heart is reduced or blocked). Among this group, poor sleep in the weeks following acute coronary syndrome increased susceptibility to further cardiovascular events and reduced recovery of heart function.

This study demonstrates the importance of good, uninterrupted sleep for heart muscle healing after a heart attack. Cardiac rehabilitation programs emphasize appropriate lifestyle changes after a heart attack to improve heart healing and overall health (smoking cessation, diet, physical activity, etc.). Emphasizing the importance of good-quality sleep may be beneficial for the recovery of patients who have suffered a heart attack.