క్లినికల్ & ప్రయోగాత్మక కార్డియాలజీ
అందరికి ప్రవేశం

నైరూప్య

Plasma Hemoxygenase-1 and Cardiac Enlargement in Chronic Heart Failure Patients

J. Georgieva, K. Vitlianova

Introduction: Heme oxygenase-1 (HO-1) is a stress protein that is involved in protection of cardiac diaseases from diffrent noxious stimuli. Objective: We investigated whether plasma HO-1 is changed in cronic heart failure (CHF) patients and whether plasma HO-1measurements provide a peripheral biomarker of the disease.
Methods: Plasma HO-1, were measured in 24 normal controls (NEC) and in 53 consecitive patients with CHF admitted to the Clinic of Cardiology over the period May 2010 - January, 2011. Systolic dysfunction was defined at left ventricle ejection fraction (LVEF) < 40%. Standardised protocol was used for colecting information on the investigated variables of interest. Plasma HO-1 and Brain natriuretic peptide (BNP) were measured with immunoassays. Depending on the distribution variables are reported with mean and median. Аssociations of the variables with HO-1 were investigated with linear regression analyses.
Results: Plasma HO-1 concentrations (ng/ml) were significantly lower in CHF patients (median 2.58, range 0.5-7.3) compared with NEC (median 5.2 range 1.2-12.2) (p < 0.01). Circulating BNP levels were not significantly correlated with plasma HO-1 levels. There was a significant negative correlation between HO1 and serum total bilirubin (p<0.05). A negative weak correlations were also observed with functional class (p<0.05) and atrial fibrillation (p<0.05). Plasma levels of HO-1 showed a significant considerable positive correlation with left ventricle (LV) dimensions values. Independent predictive effects on HO-1 levels in multiple regression analysis (F=8.2, p<0.01) were explored for the values of the LV end-diastolic volume and artrial fibrillation.
Conclusion: Plasma HO-1 are decreased in patients with CHF. Levels of HO-1 are independently correlated to the degree of cardiac enlargement. Further studies are needed on the concrete mechanisms of the deranged HO-1 regulation in CHF patients.