Impact of cardiovascular risk factors and inflammatory status on urinary 8-OHdG in essential hypertension.

BACKGROUND: The urinary concentrations of 8-hydroxy-2'-deoxyguanosine (8-OHdG) reflect the oxidation status of hypertensive subjects and it can be used for monitoring oxidative stress changes. However, the influence of cardiovascular risk factors and inflammation on the urinary levels of this marker in hypertension (HT) has never evaluated. The purpose of this study was to analyze the impact of cardiovascular risk factors, and established inflammatory markers on 8-OHdG in essential HT. METHODS: We studied 149 asymptomatic hypertensive patients (61 ± 14 years). A routine physical examination, laboratory analyses, and echo-Doppler study were performed. Urinary 8-OHdG and plasma tumor necrosis factor-α (TNF-α), soluble TNF receptor 1 (sTNF-R1), soluble TNF receptor 2 (sTNF-R2), and interleukin-6 (IL-6) were determined. RESULTS: 8-OHdG/creatinine levels were higher in hypertrophic patients (P = 0.022) and correlated with left ventricular mass index (P < 0.01). When 8-OHdG/creatinine was compared according to obesity and diabetes in our hypertensive subjects, no significant differences were found. 8-OHdG/creatinine was increased in hypertensive smokers (P = 0.032) and women (P = 0.006). Furthermore, 8-OHdG/creatinine correlated with TNF-α, sTNF-R1, sTNF-R2 (P < 0.0001), and with IL-6 (P < 0.05). A multivariate linear regression analysis showed that gender, smoking, and TNF-α were independent factors of 8-OHdG/creatinine. CONCLUSIONS: Urinary 8-OHdG was increased in hypertensive patients with hypertrophy even under medical treatment. The presence of other cardiovascular risk factors on top of HT do not alter the concentrations of this oxidative stress marker, only smoking increasing its levels. TNF-α is an independent factor of 8-OHdG. These data suggest that this urinary marker gives specific additional information, further than blood pressure control alone, when evaluating hypertensive patients.

Variability of NT-proBNP plasma and urine levels in patients with stable heart failure: a 2-year follow-up study.

OBJECTIVES: To examine N-terminal pro-brain natriuretic peptide (NT-proBNP) variability in plasma and urine samples of patients with stable heart failure (HF) during a 24-month follow-up. DESIGN: Prospective study. SETTING: Teaching hospital based study. PATIENTS: 74 clinically and functionally stable patients (NYHA class 2+/-0.5) out of 114 patients diagnosed with HF were followed up, and NT-proBNP plasma and urine levels were measured at baseline, 12 and 24 months. RESULTS: Significant differences in mean urinary levels (p<0.01) were found during follow-up, but no changes were found in plasma. Bland-Altman plots showed few variations in plasma percentages in the three intervals (stage I-basal; stage II-stage I; stage II-basal) with a coefficient of reproducibility (CR) of 22%, 21% and 25%, respectively. Changes in NT-proBNP urinary levels had a CR of 7.1%, 6.8% and 9.4% at the three intervals, respectively. A good correlation was found between plasma and urinary levels of NT-proBNP (p<0.001) and between the different NT-proBNP plasma (p<0.001) and urine measurements (p<0.001). CONCLUSIONS: NT-proBNP plasma and urine levels show good stability in a 24-month follow-up of patients with stable heart failure. Thus, assessment of urinary and plasma NT-proBNP concentrations may be a useful tool for monitoring patients with HF during follow-up. The results suggest that variations in peptide concentrations exceeding 22% in plasma and 7% in urine in a 12-month follow-up and 25% and 9% in a 24-month follow-up may indicate pathophysiological changes.

Left ventricular cavity area reflects N-terminal pro-brain natriuretic peptide plasma levels in heart failure.

AIMS: N-terminal pro-brain natriuretic peptide (NT-proBNP) is useful in the diagnosis of heart failure (HF). LV two-dimensional cavity area from end-diastole (LVEDA) and end-systole (LVESA), and LV fractional area change (LVFAC) reflect changes in LV morphology and function without using geometric assumptions. In a multicenter study, we correlated LVEDA, LVESA and LVFAC with NT-proBNP, comparing patients with dilated and ischemic cardiomyopathy. METHODS AND RESULTS: We studied 106 HF patients. In the dilated group, NT-proBNP correlated with LVEDAI (r=0.6), LVESAI (r=0.7) and LVFAC (r=-0.6), all significant at p<0.001. In patients with ischemic cardiomyopathy we found LVESAI (r=0.3, p<0.05) and LVFAC (r=-0.4, p<0.01). After adjustment for age and BMI, LVFAC and LVESAI were associated in a multiple linear regression analysis with peptide levels (adjusted r(2)=0.5, p<0.001). CONCLUSIONS: In this study we found a good correlation of NT-proBNP with LV cavity areas and LVFAC. Multiple regression analysis showed that when adjusted for age and BMI, LVFAC and LVESAI are independent predictors of NT-proBNP levels in both dilated and ischemic etiologies. Patients with dilated cardiomyopathy showed better results than those with ischemic cardiomyopathy. We think LV areas are a useful and reproducible parameter, do not need geometric assumptions and reflect NT-proBNP plasma levels.

Obese subjects with heart failure have lower N-terminal pro-brain natriuretic peptide plasma levels irrespective of aetiology.

N-terminal pro-brain natriuretic peptide (NT-proBNP) may be useful in the diagnosis of heart failure and ventricular dysfunction. Obesity is an independent cardiovascular risk factor. The purpose of this study was to measure NT-proBNP plasma levels in obese and non-obese subjects with heart failure and to compare levels in subjects with ischaemic and dilated aetiology. In this study, obese subjects had 63% lower NT-proBNP plasma levels than non-obese subjects (p < 0.01). In multivariate analysis, BMI was inversely associated with NT-proBNP plasma levels (p < 0.05) and a 17% decrease in natriuretic peptide levels was attributed to obesity (p < 0.036). When we analyzed data according to the aetiology of heart failure, we found that both groups (ischaemic and dilated) had a 65% decrease in NT-proBNP plasma levels in obese subjects compared to non-obese subjects.