<b>Relationship Between Exercise Intolerance and Levels of Neurohormonal Factors and Proinflammatory Cytokines in Patients With Stable Chronic Heart Failure</b>

Abstract

SUMMARYWe investigated the correlations between exercise intolerance and the plasma levels of neurohormonal factors and proinflammatory cytokines in chronic heart failure (CHF) patients.Sixty-two CHF patients who underwent cardiopulmonary exercise testing (CPX) were enrolled in this study. Peak oxygen uptake (peak VO 2 ) and the plasma concentrations of noradrenaline (NA), brain natriuretic peptide (BNP), and soluble tumor necrosis factor receptors I and II (TNFR-I and -II) were all measured during the CPX. The patients were divided into three groups according to their peak VO 2 ; a severe exercise intolerance group (severe group; peak VO 2 < 18 mL/min/kg), moderate exercise intolerance group (moderate group; 18 ≤ peak VO 2 ≤ 24), and mild exercise intolerance group (mild group; peak VO 2 > 24).There were no significant differences in left ventricular ejection fraction (EF) among the three groups. NA and BNP both increased gradually in parallel with the worsening of exercise intolerance (NA, 211.5 ± 75.7 pg/mL, 331.8 ± 163.7, 441.9 ± 202.9, respectively; BNP, 37.9 ± 25.4 pg/mL, 148.9 ± 117.1, 247.9 ± 150.0, respectively). TNFR-I and II were significantly higher in the severe group than in the moderate group (1746.1 ± 950.7 versus 1085.2 ± 370.5 pg/mL and 2855.3 ± 1550.9 versus 2047.7 ± 648.7 pg/mL, respectively), while the values in the moderate group were not significantly different from those in the mild group. EF showed no significant correlations with NA, BNP, TNFR-I, or TNFR-II, whereas peak VO 2 exhibited significant negative correlations with NA (r = −0.50, P < 0.0001), BNP (r = −0.53, P < 0.0001), TNFR-I (r = −0.50, P < 0.0001), and TNFR-II (r = −0.45, P < 0.0001).It is concluded that NA and BNP rise in parallel with the degree of exercise intolerance, while TNFR-I and -II rise only when exercise intolerance reaches severe levels. (Int Heart J 2005; 46: 1049-1059

Brain Natriuretic Peptide Levels and Cardiac Functional Capacity in Patients With Dyspnea and Isolated Diastolic Dysfunction

“…Itoh, et al found a relation between BNP levels and worsening exercise tolerance in patients with stable chronic HF. 12) We found similar results (a negative correlation between exercise duration and BNP levels) in a population of patients with isolated diastolic dysfunction. We also detected a negative correlation between BNP levels and AT and MET values.…”

Significance of Sarcopenia Evaluation in Acute Decompensated Heart Failure

“…3,5,6) In patients with chronic HF, the clinical importance of sarcopenia has been recognized in relation to disease severity, reduced exercise capacity, and adverse clinical outcome. [7][8][9][10] Sarcopenia affects approximately 20% of elderly individuals with chronic HF, which exceeds its prevalence in healthy members of the same age group. 11) Nevertheless, the prevalence or impact of sarcopenia on ADHF is still poorly understood.…”

Increase in N-Terminus-Pro-B-Type Natriuretic Peptide During Exercise of Patients With Univentricular Heart After a Total Cavopulmonary Connection

“…It could not be related to any demographic, morphologic, or surgical variables. This result underscores the fact that even during exercise, there is no excessive wall stress to the atrium or single ventricle causing BNP secretion, as seen in patients after several forms of myocardial dysfunction [21,27,29,34,36].…”

“…This holds true for both systolic and diastolic heart failure and is independent of its cause. It also has been shown in many patients with congenital heart defects [5,22,25,35], including those with a univentricular heart and Fontan circulation [23,26].In acquired heart disease, an increase in N-terminus pro-B-type natriuretic peptide (NT-proBNP) during exercise was found related to transient myocardial ischemia [34], the size of a myocardial scar in coronary artery disease [29], and myocardial dysfunction [21,27,36]. However, a more recent report challenged these results because an NTproBNP increase during exercise was related primarily to the level at baseline in a multiple regression analysis [30].…”

“…In acquired heart disease, an increase in N-terminus pro-B-type natriuretic peptide (NT-proBNP) during exercise was found related to transient myocardial ischemia [34], the size of a myocardial scar in coronary artery disease [29], and myocardial dysfunction [21,27,36]. However, a more recent report challenged these results because an NTproBNP increase during exercise was related primarily to the level at baseline in a multiple regression analysis [30].…”