Background: Brain natriuretic peptide (BNP) is a hormone released by the left ventricle (LV) as a consequence of pressure or volume load. BNP increases in left ventricle hypertrophy (LVH), LV dysfunction, and it can also predict cardiovascular mortality in the general population as well as those undergoing hemodialysis (HD). We investigated the association between BNP and volume load in HD patients. Methods: We studied 32 HD patients (60 ± 17.1 years) treated thrice-weekly for at least 6 months. Exclusion criteria were: LV dysfunction, atrial fibrillation, malnutrition. Blood chemistries and BNP were determined on mid-week HD day. Blood pressure (BP) and cardiac diameters were determined on mid-week inter-HD day by using 24-hour ambulatory blood pressure monitoring and echocardiography. Bioimpedance was performed after HD and extracellular water (ECW%), calculated as a percentage of total body water, was considered as the index of volume load. Results: Patients were divided into quartiles of 8 patients depending on the BNP value: 1st qtl BNP ≤45.5 pg/ml (28.4 ± 10.9 pg/ml), 2nd qtl BNP > 45.5 pg/ml and ≤99.1 pg/ml (60.9 ± 15.8 pg/ml), 3rd qtl BNP > 99.1 pg/ml and ≤231.8 pg/ml (160.5 ± 51.8 pg/ml), 4th qtl BNP > 231.8 pg/ml (664.8 ± 576.6 pg/ml). No inter-quartile differences were reported in age, HD age, body mass index spKt/V, or blood chemistries. As expected patients in the 4th BNP quartile showed the highest values of 24-hour pulse pressure (PP) and LV mass index (LVMi). The study of body composition revealed significant differences in ECW%, which was higher in the 4th quartile when compared to the others (4th q: 50 ± 9.6%, vs 1st q. 40.1 ± 2.4%, 2nd q. 41.9 ± 5%, 3rd q. 42.8 ± 6.9%). Using multiple stepwise linear regression where BNP was the dependent variable, and PP and ECW% the independent variables, only ECW% maintained statistical significance as a predictor of BNP levels (PP: Beta = 0.86, p = 0.58; ECW%: Beta = 0.64, p < 0.001 p < 0.001). Conclusions: Few studies have investigated the relationship between plasma BNP and volume load, and direct evidence is lacking. We used bioimpedance and the determination of ECW% to assess volume state in HD patients finding an association between BNP and ECW. The increased synthesis and release of BNP from the LV in HD patients appear to be mainly related to volume stress rather than to pressure load.
These findings support the hypothesis of a continuum among the three conditions studied, or at least between AAMI and DAT, where AAMI seems to be an early, monosymptomatic stage of Alzheimer disease. Accepting this view, it would be questionable to maintain the term "age-associated memory impairment" as a discrete entity.
The role of oxidation injury as an important factor in the pathophysiology of cardiomyopathy (CMP) has recently gained increasing interest. Semiquantitative analysis for isoprostane, 8-epi-prostaglandin F 2a (8-epi-PGF 2a ), and oxidised low-density lipoprotein (ox-LDL) of coronary vascular tissue samples derived from CMP patients revealed an increased extent and intensity of uptake as compared to the respective controls. To evaluate oxidative stress in vivo, we examined plasma, serum, salivary, and urinary 8-epi-PGF 2a in patients with dilated CMP (n = 20) and ischemic CMP (n = 20) with decreased left ventricular ejection fraction (LVEF). Patients with coronary heart disease (CHD) (n = 20) and 20 healthy, age-matched, and sex-matched controls were investigated in parallel. 8-Epi-PGF 2a levels were correlated with the functional severity of heart failure [New York Heart Association (NYHA) classification] and LVEF. 8-Epi-PGF 2a levels were matched according to risk factors (smoking and hypercholesterolemia) and were significantly higher in patients with CMP as compared to healthy controls and patients with CHD in all investigated compartments. A positive correlation between NYHA stages and 8-epi-PGF 2a , as well as a negative correlation to LVEF, could be demonstrated in a subgroup analysis.These findings reflect the enhanced oxidation injury in patients with CMP and, to a lesser extent, in CHD as compared to healthy controls, thus highly indicating the relevance of oxidative stress for the pathogenesis and progression of cardiovascular disease.
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