BACKGROUND: Ceruloplasmin (Cp) is a serum protein that belongs to the family of α2-globulins and it is increased in patients with after acute myocardial infarction complicated with heart failure. Aim of the study was to investigate levels of serum Cp in patients with acute decompensated heart failure. MATERIALS AND METHODS: The present cross-sectional observational study consists of three groups: Fifty patients with decompensated heart failure (Group 1) and same 50 patients after compensation (Group 2); 50 control patients group with comparable age and sex without heart failure (Group 3). Demographic, echocardiographic and biochemical data of patients were collected. Serum Cp level was determined spectrophotometrically. RESULTS: Serum ceruloplasmin was significantly increased in Groups 1 (820.8 ± 78.5 IU/dL) and 2 (873.5 ± 121.0 IU/dL) compared, to Group 3 (640.6 ± 132.4 IU/dL) (p<0.001). In the sub-group analysis, this difference was due to the difference between Groups 3, Group 1 and 2 (both p=0.0001) whereas no significant difference was present between Group I and Group 2 (p>0.063). A positive correlation was found between Cp and female sex, heart rate, systolic and diastolic blood pressure, acetylsalisilic acid and diuretic use, left ventricular systolic and diastolic diameter, mitral regurgitation, and negative correlation was found between Cp and ejection fraction (p<0.05 for all) whereas none of the parameters were independently associated with serum Cp level (p>0.05). CONCLUSIONS: Findings of the present study suggest that serum Cp level is increased in both decompensated and compensated HF compared to controls. Further large scale studies are needed to elucidate the pathophysiological mechanisms of increased Cp in HF.
BACKGROUND:Ceruloplasmin (Cp) is a serum protein that belongs to the family of α2-globulins and it is increased in patients with after acute myocardial infarction complicated with heart failure. Aim of the study was to investigate levels of serum Cp in patients with acute decompensated heart failure. MATERIALS AND METHODS: The present cross-sectional observational study consists of three groups: Fifty patients with decompensated heart failure (Group 1) and same 50 patients after compensation (Group 2); 50 control patients group with comparable age and sex without heart failure (Group 3). Demographic, echocardiographic and biochemical data of patients were collected. Serum Cp level was determined spectrophotometrically. RESULTS: Serum ceruloplasmin was significantly increased in Groups 1 (820.8 ± 78.5 IU/dL) and 2 (873.5 ± 121.0 IU/dL) compared, to Group 3 (640.6 ± 132.4 IU/dL) (p<0.001). In the sub-group analysis, this difference was due to the difference between Groups 3, Group 1 and 2 (both p=0.0001) whereas no significant difference was present between Group I and Group 2 (p>0.063). A positive correlation was found between Cp and female sex, heart rate, systolic and diastolic blood pressure, acetylsalisilic acid and diuretic use, left ventricular systolic and diastolic diameter, mitral regurgitation, and negative correlation was found between Cp and ejection fraction (p<0.05 for all) whereas none of the parameters were independently associated with serum Cp level (p>0.05). CONCLUSIONS: Findings of the present study suggest that serum Cp level is increased in both decompensated and compensated HF compared to controls. Further large scale studies are needed to elucidate the pathophysiological mechanisms of increased Cp in HF.