Lower Sphingomyelin SM 42:1 Plasma Level in Coronary Artery Disease—Preliminary Study
Coronary artery atherosclerosis is a common condition characterized by different symptomatology and incidences of risk factors. The disease manifestation may differ; therefore, proper diagnosis is essential. The preventive, diagnostic, and therapeutic arms are still developing to improve patient outcomes. Among diagnostic steps, the non-invasive tools for evaluating non-classical factors related to metabolomic profiles are gaining attention. The aim of this study was to investigate possible metabolic profiling differences between patients with chronic coronary artery disease (CAD) and a control group based on plasma sphingomyelin levels. The study group consisted of 23 patients (72% male, median age of 69 (63–72) years) presenting with chronic coronary syndrome and confirmed epicardial disease in coronary angiography and 15 patients (33% male, median age of 70 (64–72) years) with normal angiographic results. Clinical data were recorded, and blood samples were collected for standard biochemical laboratory assessment and metabolomic profiling. The plasma sphingomyelin levels were evaluated in patients with different degrees of coronary artery atherosclerosis involvement. In addition, the severity of the epicardial disease was estimated by the Gensini Score. The study subgroups did not differ in terms of age (p = 0.765) and co-morbidities, though the male sex was more common in the CAD group (p = 0.007). The analysis revealed significant differences regarding neutrophil count (p = 0.014), neutrophil-to-lymphocyte ratio (NLR) (p = 0.016), and high-density lipoprotein (HDL) (p = 0.003). Among different plasma sphingomyelin species, there was a significant difference in plasma SM42:1 level (16.2 (14.2–19.1) vs. 20.8 (18.9–21.7) (p = 0.044) between the CAD and control groups, respectively. The SM 42:1 plasma level was independent of the number of involved epicardial arteries (p = 0.109). However, Spearman correlations tests were performed between the SM 42:1 plasma level and the number of coronary arteries diagnosed with atherosclerosis disease (rho = −0.356, p = 0.014) and the severity of the disease measured by the Gensini Score (rho = −0.403, p = 0.006). There was no correlation between plasma sphingomyelin levels and NLR (Spearman’s rho = −0.135, p = 0.420), suggesting a lack of inflammatory associations. Further, sphingomyelins showed no relationship with coronary artery disease risk factors such as dyslipidemia and diabetes. Lower plasma SM 42:1 levels were revealed in the CAD group compared with the control group, indicating a possible significance of sphingomyelin 42:1 in coronary artery disease progression.