Abstract

Chronic heart failure (CHF) is a global term for the physiological state in which cardiac output is insufficient to meet the needs of the body and lungs. While oxidative stress, defined as an excess production of reactive oxygen species relative to antioxidant defence, has been shown to play an important role in the pathophysiology of CHF. However, although high density lipoproteins (HDL) have important cardioprotective properties, inflammation and oxidative stress can induce dramatic changes, which negate their antiatherogenic properties. Thus, such impairment to HDL may provide an important link between inflammation and oxidative stress in the pathogenesis of CHF. This pilot study investigated the antiatherogenic properties of HDL in CHF. Ten control subjects (BNP<100 nM) were matched for age and gender with 22 CHF subjects (BNP>100 nM). HDL 2 and HDL 3 were isolated from serum by rapid ultracentrifugation. SAA was measured by an ELISA procedure, paraoxonase-1 (PON-1) activity, hydroperoxide (HPO) and conjugated diene (CD) concentration were measured by spectrophotometric assays. Results: Compared to the control subjects, BNP was higher in the CHF subjects [50 (11) vs. 2439 (900) nM; p=0.015] and in HDL 2 and HDL 3 , SAA-related inflammation was increased, while the activity of the antioxidant enzyme PON-1 was decreased and CDs, one of the markers of lipid peroxidation, were increased (see table). Conclusion: This pilot study has shown that HDL displayed a proatherogenic phenotype in CHF subjects, which we suggest may be biologically relevant in the pathophysiology of CHF.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call