The relationship between serum lectin-like oxidized LDL receptor-1 levels and systolic heart failure.

OBJECTIVES: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) appears to be involved in atherosclerotic plaque vulnerability and rupture. In this study, we aimed to evaluate the utility of serum LOX-1 levels in the diagnosis and assessment of left ventricular systolic HF and LOX-1's relationship with serum pro-brain natriuretic peptide (NT-proBNP). DESIGN AND SETTINGS: This was a cross-sectional study of all eligible patients admitted to the department of cardiology of the University Hospital between July 2011 and April 2012. METHODS: Fifty-five patients with a diagnosis of systolic heart failure and 25 patients without systolic HF were enrolled in this study. Serum C-reactive protein, NT-proBNP, and LOX-1 were studied. RESULTS: Serum LOX-1 and NT-proBNP levels were significantly higher in the heart failure group and showed a positive correlation with NT-proBNP and negative correlations with left ventricular ejection fraction (EF). In addition, LOX-1 levels in patients with ischaemic cardiomyopathy were significantly higher, while they were similar in patients with dilated cardiomyopathy compared to control subjects. CONCLUSION: Our study demonstrates the utility of the serum LOX-1 levels in the diagnosis of left ventricular systolic heart failure. LOX-1 may have a place in the diagnosis of heart failure, in particular in patients with ischaemic cardiomyopathy.

Evaluation of insulin resistance and plasma levels for visfatin and resistin in obese and non-obese patients with polycystic ovary syndrome.

This study was designed to evaluate insulin resistance and plasma levels of visfatin and resistin in obese and non-obese patients with polycystic ovary syndrome (PCOS). A total of 37 premenopausal PCOS patients with (n = 18, mean (SD) age: 27.5 (5.7 years) or without obesity (n = 19, mean (SD) age: 23.7 (3.1) years) and healthy volunteers (n = 18, mean (SD) age:29.8 (4.1) years) were included in this study. Data on clinical characteristics, glycemic parameters and lipid parameters were recorded for each subject as were plasma visfatin and resistin levels. Mean (SD) HOMA-IR values were significantly higher in obese PCOS patients (3.4 (1.7)) compared with non-obese PCOS patients (2.0 (1.2), p<0.01) and controls (1.6 (0.8), p<0.01). No significant difference was noted between study groups in terms of plasma resistin (ng/mL) or visfatin (ng/mL) levels. There was no correlation between serum plasma visfatin (r = 0.127, p = 0.407) and resistin (r = -0.096, p = 0.544) levels and HOMA-IR. In conclusion, our findings revealed increased likelihood of metabolic and dyslipidemic manifestations in obese compared to non-obese PCOS patients, while no significant difference was noted in visfatin and resistin levels among PCOS patients in terms of co-morbid obesity and in comparison to controls.

Serum fetuin-A levels in patients with systolic heart failure.

OBJECTIVE: Inflammation and dystrophic calcification have been associated with cardiovascular disease (CVD) and chronic heart failure (CHF). The aim of the present study was to investigate the potential usefulness of fetuin-A as a biomarker in CHF. METHODS: Serum fetuin-A was measured in 66 CHF patients with left ventricular function < 50% and in 31 healthy controls at baseline. Fetuin-A was evaluated as a diagnostic marker for systolic heart failure and compared with C-reactive protein (CRP) and pro-brain natriuretic peptide (pro-BNP). RESULTS: The levels of serum fetuin-A were significantly decreased in the CHF patients compared to the control group (P < 0.01). Although there were significant correlations between fetuin-A and certain parameters in patients and controls, none of these were present consistently in either group. It was found that serum fetuin-A levels could identify patients with systolic heart failure with a high degree of sensitivity and specificity. CONCLUSIONS: Serum fetuin-A is decreased in CHF patients, indicating that anti-inflammatory activity is downregulated in CHF and that calcification may be associated with CHF.