Post Heart Attack Sleep Loss Linked to Depression

Summary
Approximately 15 to 30 percent of heart patients suffer from depression following a myocardial infarction (MI), or heart attack. Depression is commonly associated with disturbances in sleep. The authors of this study used an animal model of a heart attack in order to understand the mechanism of sleep abnormalities and depression following a heart attack. In a rat model, the authors showed that special kinds of brain cells that secrete the neurotransmitter acetylcholine were decreased in the brain stem two weeks after the heart attack. The findings suggest that real anatomic changes may indeed be the cause of depression in patients following a heart attack.

Introduction
Myocardial infarction has increased in incidence over the past decades and even affects younger patients. Following a heart attack, depression that significantly impairs the quality of life and recovery is seen in up to one-third of the patients. Previous studies have demonstrated that sleep abnormalities, especially those involving paradoxical sleep, go hand in hand with depression. Paradoxical sleep is a deep sleep stage with characteristic rapid eye movement, also known as REM sleep. Specific types of brain cells in the brain stem, known as cholinergic neurons, control deep sleep. The authors of this study postulated that sleep abnormalities would be seen in a rat model of a heart attack.

Methodology

  • Researchers used 28 adult male rats in this study.
  • Baseline sleep structure was recorded in 16 rats using surgically implanted electrodes.
  • Artificial heart attack was induced in eight rats and sleep records were again obtained two weeks following the MI.
  • For an anatomic study, 12 rats were used, out of which a heart attack was induced in six. The number of cholinergic neurons was counted in all following the heart attack.
  • Results

  • Before the induced MI, all rats had a similar sleep structure.
  • Rats with the MI showed significant abnormalities in sleep structure, specifically in paradoxical, or REM, sleep, which was shorter than in the control rats that did not undergo MI.
  • The rats with MI had a significantly decreased number of cholinergic neurons in a specific area of the brainstem known as the pedunculopontine tegmentum.
  • Shortcomings/next steps
    The study was conducted on animal models as human studies are likely to be impractical and complicated. Though the results are relevant, anatomic and physiological differences between humans and rats may confound results. Also, the myocardial infarction was artificially induced and may differ in its effects from a myocardial infarction due to disease. Thirdly, the anatomical and sleep studies were conducted two weeks after the heart attack and may have missed early changes. Furthermore, depression was not studied in this model. Future studies can study time-dependent physiological and anatomical changes, to clarify the reasons behind depression and sleep disturbance following a myocardial infarction.

    Conclusion
    Depression is a real and evident complication following a heart attack. This study has shown that a loss of brain cells from the area controlling paradoxical sleep may be responsible for sleep disturbances following an MI. As depression is known to be associated with sleep abnormalities, it is likely that changes in the brain also determine the occurrence of depression. Depression following an heart attack must not, therefore, be attributed to only psychological problems; there is at least some evidence that it could be due to a physical change in the brain. Further research in this area can probably reveal more details in this regard.

    For More Information:
    Loss of Brain Cells Identified as the Cause of Sleep Disturbance Following Myocardial Infarction
    Publication Journal: Sleep, August 2010
    By Thierno Madjou Bah; Francois Laplante, PhD
    From the Centre de biomédecine and the Département de psychiatrie, Université de Montréal, Quebec, Canada, and the Department of Psychiatry, McGill University, Quebec, Canada

    *FYI Living Lab Reports Are Summaries of the Original Research.