Abstract

Background: Patients with impaired lung function often have systemic inflammation. C-reactive protein (CRP) and N-terminal pro-brain natriuretic peptide (NT-proBNP) are markers for inflammation and cardiac stress, respectively. Objectives: To evaluate the association between both markers and the potential impacts of lung disease on this relationship. Methods: CRP and NT-proBNP were prospectively measured in 697 consecutive outpatients (57.5 ± 16.4 years) with chronic dyspnea. The patients were stratified into quartiles according to CRP levels (quartile 1: median CRP 0.35 mg/l; quartile 2: 1.50 mg/l; quartile 3: 3.62 mg/l; quartile 4: 10.90 mg/l) and classified into 2 categories based on the presence (n = 176) or absence (n = 521) of heart disease. Results: Patients with at least moderately severe airway obstruction and those with interstitial lung disease had higher CRP values than patients without lung disease (median 3.50 vs. 4.34 vs. 1.80 mg/l, respectively; p < 0.01). In patients without heart disease, NT-proBNP values increased from CRP quartiles 1–3 to quartile 4 (median 47.4 vs. 82.1 pg/ml; p < 0.01) after adjusting for important covariates such as age, sex, body mass index, renal function and arterial hypertension. Likewise, the values for NT-proBNP were lower in CRP quartiles 1–3 than in quartile 4 (median 212.0 vs. 647.7 pg/ml; p < 0.01) in patients with heart disease after additional adjustment for the type of cardiac disorder. Lung disease had no direct effect on the relationship between CRP and NT-proBNP. Conclusion: Systemic inflammation that originates in the lung places an excess burden on the heart, which may contribute to the functional impairment of patients with advanced pulmonary disease.

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