Aims
Semaphorin 4D (Sema4D) is expressed on platelets and T-cells and known to be involved in inflammation. The aims of this study include comparing Sema4D and N terminal pro brain natriuretic peptide (NT-proBNP) serum levels in heart failure (HF) patients to a control group, evaluating the correlation between Sema4D and NT-proBNP levels, and assessing Sema4D serum levels in HF patients during acute exacerbation and remission.
Conclusions
Sema4D levels in HF patients' serum are significantly higher than in healthy controls. Clinical improvement caused rapid reduction in Sema4D levels, possibly reflecting the inflammatory aspect of HF. These findings might suggest that Sema4D can be used as a diagnostic biomarker of acute HF. Further studies of Sema4D and HF are warranted.
Results
Forty-five patients diagnosed with HF (based on echocardiographic findings, positive NT-proBNP levels, and normal C-reactive protein) and 11 healthy controls (declaring no chronic diseases or medications) comprised the study population. Demographic, clinical, laboratory, and echocardiographic data were used to create the study database. NT-proBNP and Sema4D serum samples were taken on admission and discharge. NT-proBNP levels were significantly higher in the HF group than in controls (P < 0.001). Sema4D levels were significantly higher in HF patients than in healthy controls (2143.04 ± 1253 vs. 762.18 ± 581.6 ng/mL, P < 0.001, respectively). Using linear regression, a higher creatinine level was found to predict both higher levels of NT-proBNP and Sema4D (P = 0.05 and P < 0.014, respectively), while a reduced ejection fraction was found to predict higher NT-proBNP levels only (P < 0.001 and P = 0.87, respectively). Average Sema4D levels reduced significantly at remission (3534.94 ± 1650.55 vs. 2455.67 ± 1424, P = 0.03), while mean NT-proBNP levels did not change significantly. Conclusions: Sema4D levels in HF patients' serum are significantly higher than in healthy controls. Clinical improvement caused rapid reduction in Sema4D levels, possibly reflecting the inflammatory aspect of HF. These findings might suggest that Sema4D can be used as a diagnostic biomarker of acute HF. Further studies of Sema4D and HF are warranted.