Echocardiography, spirometry, and systemic acute-phase inflammatory proteins in smokers with COPD or CHF: an observational study.
Chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF) may coexist in elderly patients with a history of smoking. Low-grade systemic inflammation induced by smoking may represent the link between these 2 conditions. In this study, we investigated left ventricular dysfunction in patients primarily diagnosed with COPD, and nonreversible airflow limitation in patients primarily diagnosed with CHF. The levels of circulating high-sensitive C-reactive protein (Hs-CRP), pentraxin 3 (PTX3), interleukin-1β (IL-1 β), and soluble type II receptor of IL-1 (sIL-1RII) were also measured as markers of systemic inflammation in these 2 cohorts. Patients aged ≥ 50 years and with ≥ 10 pack years of cigarette smoking who presented with a diagnosis of stable COPD (n=70) or stable CHF (n=124) were recruited. All patients underwent echocardiography, N-terminal pro-hormone of brain natriuretic peptide measurements, and post-bronchodilator spirometry. Plasma levels of Hs-CRP, PTX3, IL-1 β, and sIL-1RII were determined by using a sandwich enzyme-linked immuno-sorbent assay in all patients and in 24 healthy smokers (control subjects). Although we were unable to find a single COPD patient with left ventricular dysfunction, we found nonreversible airflow limitation in 34% of patients with CHF. On the other hand, COPD patients had higher plasma levels of Hs-CRP, IL1 β, and sIL-1RII compared with CHF patients and control subjects (p < 0.05). None of the inflammatory biomarkers was different between CHF patients and control subjects. In conclusion, although the COPD patients had no evidence of CHF, up to one third of patients with CHF had airflow limitation, suggesting that routine spirometry is warranted in patients with CHF, whereas echocardiography is not required in well characterized patients with COPD. Only smokers with COPD seem to have evidence of systemic inflammation.
Department of Medical and Surgical Sciences, University of Modena & Reggio Emilia, Modena, Italy.
Bianca
B
Beghé
Alessia
A
Verduri
Barbara
B
Bottazzi
Mariarita
M
Stendardo
Alessandro
A
Fucili
Sara
S
Balduzzi
Chiara
C
Leuzzi
Alberto
A
Papi
Alberto
A
Mantovani
Leonardo M
LM
Fabbri
Claudio
C
Ceconi
Piera
P
Boschetto
D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D002908:Chronic Disease; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000175:diagnosis / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis / Q000000981:diagnostic imaging / Q000503:physiopathology; D053583:Interleukin-1beta / Q000097:blood; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000175:diagnosis / Q000000981:diagnostic imaging / Q000503:physiopathology*; D053574:Receptors, Interleukin-1 Type II / Q000097:blood; D000683:Serum Amyloid P-Component / Q000378:metabolism; D012907:Smoking / Q000503:physiopathology*; D013147:Spirometry; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000097:blood; D000099153:Pentraxins
D015415:Biomarkers; D002097:C-Reactive Protein; D053583:Interleukin-1beta; D020097:Natriuretic Peptide, Brain; D010446:Peptide Fragments; D053574:Receptors, Interleukin-1 Type II; D000683:Serum Amyloid P-Component; D000099153:Pentraxins; C109794:pro-brain natriuretic peptide (1-76)