Elevated levels of brain natriuretic peptide in acute hypoxaemic chronic obstructive pulmonary disease

Abstract

1. Studies in vitro have recently shown that both atrial natriuretic peptide and brain natriuretic peptide have pulmonary vasorelaxant activity. The purpose of the present study was to evaluate for the first time whether plasma levels of brain natriuretic peptide are elevated in chronic obstructive pulmonary disease. Plasma levels of brain natriuretic peptide and atrial natriuretic peptide were therefore measured in 12 patients admitted with acute hypoxaemic chronic obstructive pulmonary disease [arterial partial pressure of O2, 6.2 +/- 0.4 kPa; arterial partial pressure of CO2, 6.9 +/- 0.1 kPa; forced expiratory volume in 1 s, 0.6 +/- 0.07 litre (27 +/- 3% of predicted)]. All but three patients had oedema on admission. 2. Plasma levels of both brain natriuretic peptide and atrial natriuretic peptide were elevated in patients with chronic obstructive pulmonary disease (31.4 +/- 4.1 pmol/l and 45.0 +/- 8.1 pmol/l, respectively) compared with healthy control subjects (1.7 +/- 0.8 pmol/l and 8.0 +/- 3.5 pmol/l, respectively). Thus, plasma levels of brain natriuretic peptide and atrial natriuretic peptide in patients with chronic obstructive pulmonary disease were increased by 18.5- and 5.6-fold respectively compared with healthy control subjects. 3. There was a significant inverse correlation between the plasma level of brain natriuretic peptide and the arterial partial pressure of O2 (r = -0.65, r2 = 0.42, P = 0.03), but not between the plasma atrial natriuretic peptide level and the arterial partial pressure of O2 (r2 = 0.07, not significant). The arterial partial pressure of CO2 did not correlate with the plasma level of either brain natriuretic peptide or atrial natriuretic peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

The Effect of Percutaneous Balloon Mitral Valvuloplasty on N-Terminal- Pro B- Type Natriuretic Peptide Plasma Levels in Mitral Stenosis

“…28,29) Furthermore, a study in patients with lone atrial fibrillation demonstrated a significant correlation between BNP levels and left atrial volume index, reflecting the production of BNP in a stretched left atrium. 30) A study by Inoue, et al, supported this hypothesis and suggested that the presence of atrial fibrillation should be taken into consideration when interpreting plasma BNP levels in patients with heart disease. 25) Moreover, Ohta, et al reported that atrial fibrillation raises plasma BNP levels, which is more marked if there is underlying structural heart disease present, and cardioversion reduces plasma BNP levels.…”

“…The patient and control groups did not differ in terms of age (P = 0.722) [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] mm) dimensions were significantly higher in patients with MS (all P < 0.001). No significant difference was detected between the groups regarding left ventricular end-diastolic diameter (P = 0.795), left ventricular end-systolic diameter (P = 0.110), and ejection fraction (P = 0.156).…”

Intraindividual temporal variance of biomarkers and the definition of individualized prognosis in cardiovascular patients

“…BNP will change (generally rise) in response to valvular heart disease, 6 hypertensive heart disease, 7 pericardial disease 8 or pulmonary heart disease; 9 indeed, BNP is reliably not elevated in non-cardiac disease. 10 Hence, its highly attractive and wellchampioned sensitivity sits beside the relative frailty of diagnostic non-specificity, at least for a variety of cardiac conditions or cardiac responses.…”

Comparative effects of angiotensin II on Doppler parameters of left and right heart systolic and diastolic blood flow.

“…However, relatively little is known regarding the effects of angiotensin II on right heart and pulmonary blood flow in humans. The latter may be of relevance in that RAS activation with raised levels of angiotensin II occurs in patients with pulmonary hypertension due to cor pulmonale [4,5,6]. It is therefore interesting to consider whether elevated levels of angiotensin II might in part account for the altered haemodynamic status in cor pulmonale, in terms of producing raised right ventricular after-load and impaired left and right ventricular diastolic filling [7,8].…”