A new study published in the journal Nature has revealed that after a heart attack, the heart communicates with the brain to stimulate increased sleep, aiding in healing and reducing inflammation. The research, conducted at the Icahn School of Medicine at Mount Sinai, demonstrates that the damaged heart sends signals via the immune system to promote restorative sleep as a means of recovery.
Lead investigator Cameron McAlpine, assistant professor of cardiology at the Icahn School of Medicine at Mount Sinai, stated, "Our data show that after a heart attack, the brain undergoes profound changes that increase sleep, and in the following weeks, an increase in the need to sleep is observed," which helps favor the healing of the cardiac muscle and reduce inflammation.
Experiments conducted on mice revealed that deep sleep, or slow-wave sleep, increased threefold after a heart attack, helping to reduce cardiac stress and enhance recovery. Huynh and colleagues observed that injuries to the heart increase slow-wave sleep, which occurred rapidly after the heart attack and lasted for a week. This phenomenon occurred only in the infarcted mice. In contrast, mice with disrupted sleep experienced more serious heart problems, including dangerous heart rhythms and higher mortality rates, and showed poorer cardiovascular health and recovery outcomes than those with undisturbed sleep. Increased inflammation due to disrupted sleep leads to impaired cardiac function and recovery, as the sleep-disrupted mice also exhibited increased inflammation.
The researchers discovered that after a heart attack, monocytes migrate from the blood to the brain and produce a molecule called tumor necrosis factor (TNF), which activates neurons in the thalamus, stimulating increased sleep. Blocking monocyte recruitment or TNF production with pharmacological or genetic interventions eliminated the post-heart-attack increase in sleep. Huynh and colleagues found that TNF acted on sleep-promoting neurons in the brains of mice, activating neurons in the thalamus. "This activation of thalamic neurons promotes 'restorative sleep to aid heart healing after injury' by reducing stress on the heart and limiting inflammation, which is vital for recovery," McAlpine explained.
The findings were validated in humans by examining data from a group of people with acute coronary syndrome. In further tests on post-heart attack patients followed for two years, those who reported good sleep quality in the four weeks after their heart attacks experienced significant improvements in heart function, while those with poorer sleep quality showed double the risk of new cardiovascular events and did not improve or improved very little. Patients who slept well experienced significant improvements in cardiac function and had fewer serious heart-related problems, such as additional heart attacks or hospital visits.
"Health care providers should support their patients in getting sufficient rest after a heart attack," McAlpine said. "Many cardiac management programs do not prioritize sleep as they should." The study supports the idea that good sleep should be an essential part of the post-heart attack treatment plan, especially in intensive care units. Integrating regular sleep evaluations and sleep-hygiene practices into clinical care will be crucial for improving recovery and facilitating healing after a heart attack.
Sleep plays a vital role in recovery by limiting further damage to the heart. During slow-wave sleep, the body undergoes essential repairs and restorative processes. The increase in slow-wave sleep limits the activity of the sympathetic nervous system, lowering heart rate and blood pressure to facilitate healing. The researchers also found that mediators of inflammation, such as signaling proteins called cytokines, influence slow-wave sleep. After a heart attack, monocytes in the brain exhibited a distinct pattern of gene expression that promoted inflammatory signaling through TNF.
While the study revealed new ways the heart and brain communicate to regulate sleep, further research is needed to determine when post-heart-attack inflammation shifts from being beneficial to being harmful. The degree to which inflammation is beneficial after a heart attack is not yet clear. Although questions remain about the balance of inflammation and sex-specific differences in outcomes, the authors' findings strongly support the idea that quality sleep is invaluable for overall recovery. "It's essential to recognize that increased sleep is a healthy response during recovery," McAlpine emphasized.
The study found that many cardiac rehabilitation programs do not incorporate sleep. The researchers indicate that sleep stimulation enhances communication between the brain and heart to reduce inflammation and promote faster recovery. Sleep should be included as part of clinical care for patients after a heart attack. This study provides evidence that the heart and brain interact via the immune system to enhance sleep as a means of healing. The conclusions underline the importance of increasing sleep after a myocardial infarction.
Sources: Nature, El Nuevo Día, 20 minutos, La Repubblica.it, www.theepochtimes.com, Asharq News
This article was written in collaboration with generative AI company Alchemiq