Key result
Higher plasma concentrations of ceramides C16:0 (β=0.204, p=0.026) and C18:0 (β=0.209, p=0.023) and sphingomyelin SM18:1 (β=0.210, p=0.024) were associated with higher depression scores in CAD.
Why the study?
Are plasma sphingolipid concentrations associated with depressive symptoms in patients with coronary artery disease?
Cross-Sectional (n=111)
Are plasma sphingolipid concentrations associated with depressive symptoms in patients with coronary artery disease?
Effect estimate: β 0.204 (C16:0), β 0.209 (C18:0), β 0.210 (SM18:1)
p-value: p=0.026, 0.023, 0.024
Specific plasma sphingolipids, including ceramides C16:0 and C18:0, are associated with greater depressive symptoms in patients with coronary artery disease, suggesting a potential shared pathophysiological pathway.
Sphingolipids were associated with depressive symptoms in CAD; hypothesis-generating for shared pathways and requires prospective validation.
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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Dinoff et al. (2017) conducted a cross-sectional in Coronary artery disease (n=111). Plasma sphingolipid concentrations was evaluated on Depressive symptoms (HADS depression subscale score) (β 0.204 (C16:0), β 0.209 (C18:0), β 0.210 (SM18:1), p=0.026, 0.023, 0.024). Higher plasma concentrations of ceramides C16:0 (β=0.204, p=0.026) and C18:0 (β=0.209, p=0.023) and sphingomyelin SM18:1 (β=0.210, p=0.024) were associated with higher depression scores in CAD.
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