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Plasma sphingolipids and depressive symptoms in coronary artery disease
Adam Dinoff1,2, Mahwesh Saleem1,2, Nathan Herrmann1,3
1Neuropsychopharmacology Research Group Hurvitz Brain Sciences Program Sunnybrook Research Institute Toronto ON Canada.
Insights
Higher plasma concentrations of ceramides C16:0 and C18:0, and sphingomyelin SM18:1 are linked to increased depressive symptoms in coronary artery disease (CAD) patients. These findings suggest sphingolipids may play a role in depression within this population.
Area of Science:
- Cardiovascular Medicine
- Neuroscience
- Biochemistry
Background:
- Depression is common in coronary artery disease (CAD) patients, worsening prognosis.
- Sphingolipids are implicated in the biological mechanisms of both CAD and depression.
Purpose of the Study:
- To investigate the association between plasma sphingolipid levels and depressive symptoms in individuals with CAD.
Main Methods:
- 111 CAD patients' depressive symptoms were assessed using the Hospital Anxiety and Depression Scale (HADS).
- Plasma sphingolipid concentrations were quantified using high-performance liquid chromatography-tandem mass spectrometry (LC/MS/MS).
- Linear regression models analyzed the relationship between sphingolipid levels and depression scores.
Main Results:
- Higher plasma concentrations of ceramides C16:0 and C18:0 were significantly associated with increased HADS depression scores.
- Elevated levels of sphingomyelin SM18:1 also correlated with higher depression scores.
- These associations remained significant after adjusting for relevant covariates.
Conclusions:
- Specific sphingolipids, including ceramides C16:0, C18:0, and sphingomyelin SM18:1, may contribute to the pathophysiology of depression in CAD.
- Further research is warranted to explore these sphingolipid-depression links in CAD and other populations.
Background:
Depression is highly prevalent in individuals with coronary artery disease (CAD) and increases the risk of future cardiac events and mortality. Sphingolipids have been implicated in the pathophysiology of both CAD and depression. This study assessed the association between plasma sphingolipid concentrations and depressive symptoms in CAD subjects.
Methods:
Depressive symptoms were measured using the depression subscale of the self-reported Hospital Anxiety and Depression Scale (HADS). Sphingolipid concentrations were measured from fasting plasma samples using high-performance liquid chromatography-coupled electrospray ionization tandem mass spectrometry (LC/MS/MS). Linear regression models were used to assess associations between log-transformed concentrations of plasma sphingolipids and depressive symptoms.
Results:
A total of 111 CAD patients (mean (SD) age = 63.6 ± 6.4, 84.7% male) were included. In linear regression analyses, higher plasma concentrations of ceramides C16:0 (β = 0.204, p = .026) and C18:0 (β = 0.209, p = .023) and sphingomyelin SM18:1 (β = 0.210, p = .024) were significantly associated with higher HADS depression subscale score after adjusting for covariates.
Conclusion:
Sphingolipids, in particular the ceramide species C16:0 and C18:0 and the sphingomyelin species SM18:1, may be implicated in the pathophysiology of depression in CAD. The association between plasma sphingolipid concentrations and depression should be further examined in CAD patients and in other populations.
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