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Objectives: This study sought to evaluate the relationship between brain natriuretic peptide (BNP), renal function, and the severity of congestive heart failure (CHF)., Background: Both BNP and renal function are prognostic predictors in CHF patients., Methods: We measured the plasma BNP level in the aortic root and coronary sinus in 366 consecutive patients with CHF. Estimated glomerular filtration rate (eGFR) by the Cockcroft-Gault equation was used as an indicator of renal function., Results: By stepwise multivariate analyses, hemodynamic parameters such as left ventricular ejection fraction (LVEF) and left ventricular end-diastolic pressure (LVEDP) but not eGFR were independent predictors of a transcardiac increase (coronary sinus-aortic root) in BNP. Regarding the plasma level of BNP in the aortic root, not only LVEF (p < 0.0001) and LVEDP (p < 0.0001) but also eGFR (p < 0.0001) were independent predictors. Patients were divided into two groups, patients with an eGFR > or =60 ml/min (group 1, n = 229) and patients with an eGFR <60 ml/min (group 2, n = 137). There was no difference in LVEF, LVEDP, or the transcardiac gradient of BNP between the two groups, but the plasma level of BNP in the aortic root was approximately two-fold greater in group 2 than in the group 1., Conclusions: These findings suggest that decreased clearance from the kidney contributes to the elevated BNP in CHF patients with renal dysfunction, especially in patients with an eGFR <60 ml/min.

To evaluate the transcardiac extraction of aldosterone before and after spironolactone administration to patients with congestive heart failure, we measured the plasma aldosterone in the aortic root and the coronary sinus in eight congestive heart failure patients with dilated cardiomyopathy. The plasma aldosterone level was significantly lower in the coronary sinus than in the aortic root before spironolactone administration (87.5 +/- 16 versus 62.2 +/- 11 pg/ml, p = 0.01). After chronic treatment with spironolactone, there was no significant difference in the aldosterone level between the aortic root and the coronary sinus (151 +/- 49 versus 148 +/- 48 pg/ml), and the transcardiac gradient of aldosterone (aortic root to coronary sinus) was significantly decreased (25.3 +/- 7.3 versus 3.1 +/- 4.5 pg/ml, p = 0.046). These results indicate that plasma aldosterone is extracted through the heart in congestive heart failure patients with dilated cardiomyopathy, and that spironolactone inhibits the transcardiac extraction of aldosterone in congestive heart failure patients. This suggests that spironolactone blocks the effects of aldosterone on the failing heart in congestive heart failure patients with dilated cardiomyopathy.

Study Objectives: We evaluated whether interleukin (IL)-6 is produced in the pulmonary circulation and investigated the relationship between IL-6 spillover in the lung and pulmonary vascular resistance (PVR) in patients with congestive heart failure (CHF)., Patients and Interventions: Blood samples were obtained from the main pulmonary artery and pulmonary capillary wedge region in 50 patients with symptomatic left ventricular dysfunction, who had undergone cardiac catheterization, and 9 age-matched control subjects. Plasma IL-6, tumor necrosis factor-alpha, norepinephrine (NE), endothelin-1, atrial and brain natriuretic peptide, and cyclic guanosine monophosphate (cGMP) levels were determined., Measurements and Results: Plasma IL-6 concentrations were significantly higher in the pulmonary capillary wedge region than in the main pulmonary artery in both control subjects and patients with CHF. IL-6 production in the lung increased markedly in patients with severe CHF compared with control subjects and patients with mild CHF. Among hemodynamic variables, neurohumoral factors, and medications, plasma NE levels (p < 0.0001) showed an independent and significant positive relationship with IL-6 production in the lung, and treatment with beta-blockers (p = 0.004) showed an independent and significant negative relationship with IL-6 production in the lung. There was a significant positive correlation between IL-6 production in the lung and both PVR (r = 0.43; p = 0.001) and cGMP production in the lung (r = 0.498; p < 0.0001)., Conclusion: IL-6 production in the pulmonary circulation increases with the severity of CHF and is mainly associated with the activation of the sympathetic nervous system. The local production of IL-6 in the lung may modify PVR in patients with CHF.

Objectives: The aim of this study was to evaluate the relationship between plasma oxidized low-density lipoprotein (oxLDL), a marker of oxidative stress, and the prognosis of patients with chronic congestive heart failure (CHF)., Background: Oxidative stress appears to play a role in the pathophysiology of CHF. We have recently reported the usefulness of plasma oxLDL as a marker of oxidative stress in CHF patients with dilated cardiomyopathy., Methods: We measured the plasma level of oxLDL by sandwich enzyme-linked immunosorbent assay using a specific monoclonal antibody against oxLDL in 18 age-matched normal subjects and in 84 patients with chronic CHF (New York Heart Association functional class II to IV) and monitored them prospectively for a mean follow-up period of 780 days., Results: Plasma oxLDL level was significantly higher in severe CHF patients than in control subjects and mild CHF patients. A significant negative correlation existed between the plasma level of oxLDL and left ventricular ejection fraction (LVEF) and a significant positive correlation between the plasma level of oxLDL and plasma norepinephrine level. Twenty-six patients had cardiac events; 14 had cardiac death and 12 were hospitalized for heart failure or other cardiovascular events. Among 10 variables including LVEF and neurohumoral factors, only high plasma levels of brain natriuretic peptide and oxLDL were shown to be independent predictors of mortality., Conclusions: These results indicate that the plasma level of oxLDL is a useful predictor of mortality in patients with CHF, suggesting that oxidative stress plays an important role in the pathophysiology of CHF.