Background Procalcitonin (PCT) levels have been used to diagnose bacterial infection and sepsis. PCT has also been suggested as a surrogate marker reflecting the response to a clinically relevant bacterial infection and requirement for antibiotic treatment. However, they have never been used to identify bacterial infection co-morbidity in patients with acute heart failure (AHF). Methods The BACH (Biomarkers in Acute Heart failure) trial was a prospective, 15-centre diagnostic and prognostic study of 1641 patients presenting with dyspnoea, 568 of which have been diagnosed with AHF. Patients were included if they had a diagnosis of heart failure, defined by two cardiologists blinded to marker results and reviewing all available data 30 days after enrolment. Here, we evaluate the association between PCT, received antibiotic therapy and all-cause mortality within 90 days, the primary outcome of the trial. Missing covariate data were imputed using the mean. Results PCT was significantly associated with all-cause mortality within 90 days for patients diagnosed with AHF (p=0.025, Cox regression). The proportion of antibiotic treatment during followup was significantly higher in patients with elevated PCT levels (p=0.0008, twofold increase). Finally, after adjusting for covariates such as site, wheezing, history of stroke, creatinine, and neutrophil count to level out group differences, patients with a PCT level .0.205 ng/ml (fifth quintile of PCT in all patients with AHF) have a significantly worse outcome if not treated with antibiotics (p=0.046, fig 1 bottom right). On the other hand, patients with very low PCT values (,0.051 ng/ml, first quintile, fig 1 top right) have a significantly better outcome if not treated with antibiotics (p=0.049). In all patients, as well as in patients with PCT levels between 0.051 and 0.205 ng/ml, the antibiotic treatment effect was not significant (p=0.58 and p=0.36, fig 1 top and bottom left,respectively). Conclusion Our results suggest that in patients with AHF, PCT may act as a surrogate marker reflecting the response to a clinically relevant bacterial infection and requirement for antibiotic treatment. Moreover, results for patients with low PCT levels suggest that patients may be affected by adverse events from the antibiotic therapy. As antibiotic therapy was not a randomised treatment in the BACH trial, results need to be confirmed in a prospective RCT.

PROCALCITONIN IDENTIFIES ACUTE HEART FAILURE BIOMARKERS IN PATIENTS WITH ACUTE HEART FAILURE IN NEED OF ANTIBIOTIC THERAPY: OBSERVATIONAL RESULTS FROM THE BACH (BIOMARKERS IN ACUTE HEART FAILURE) TRIAL / O., Hartmann; J., Landsberg; C., Mueller; R., Nowak; P., Ponikowski; M., Moeckel; C., Hogan; A. H. B., Wu; M., Richards; G. S., Filippatos; DI SOMMA, Salvatore; I. S., Anand; L., Ng; S. X., Neath; R., Christenson; J., Mccord; N. G., Morgenthaler; R., Engineer; A., Bergmann; S. D., Anker; A. S., Maisel; F. W., Peacock. - In: THORAX. - ISSN 0040-6376. - STAMPA. - 64:4(2009), pp. A62-A62. (Intervento presentato al convegno Winter Meeting of the British-Thoracic-Society tenutosi a London, ENGLAND nel DEC 02-04, 2009) [10.1136/thx.2009.127092s].

PROCALCITONIN IDENTIFIES ACUTE HEART FAILURE BIOMARKERS IN PATIENTS WITH ACUTE HEART FAILURE IN NEED OF ANTIBIOTIC THERAPY: OBSERVATIONAL RESULTS FROM THE BACH (BIOMARKERS IN ACUTE HEART FAILURE) TRIAL

DI SOMMA, Salvatore;
2009

Abstract

Background Procalcitonin (PCT) levels have been used to diagnose bacterial infection and sepsis. PCT has also been suggested as a surrogate marker reflecting the response to a clinically relevant bacterial infection and requirement for antibiotic treatment. However, they have never been used to identify bacterial infection co-morbidity in patients with acute heart failure (AHF). Methods The BACH (Biomarkers in Acute Heart failure) trial was a prospective, 15-centre diagnostic and prognostic study of 1641 patients presenting with dyspnoea, 568 of which have been diagnosed with AHF. Patients were included if they had a diagnosis of heart failure, defined by two cardiologists blinded to marker results and reviewing all available data 30 days after enrolment. Here, we evaluate the association between PCT, received antibiotic therapy and all-cause mortality within 90 days, the primary outcome of the trial. Missing covariate data were imputed using the mean. Results PCT was significantly associated with all-cause mortality within 90 days for patients diagnosed with AHF (p=0.025, Cox regression). The proportion of antibiotic treatment during followup was significantly higher in patients with elevated PCT levels (p=0.0008, twofold increase). Finally, after adjusting for covariates such as site, wheezing, history of stroke, creatinine, and neutrophil count to level out group differences, patients with a PCT level .0.205 ng/ml (fifth quintile of PCT in all patients with AHF) have a significantly worse outcome if not treated with antibiotics (p=0.046, fig 1 bottom right). On the other hand, patients with very low PCT values (,0.051 ng/ml, first quintile, fig 1 top right) have a significantly better outcome if not treated with antibiotics (p=0.049). In all patients, as well as in patients with PCT levels between 0.051 and 0.205 ng/ml, the antibiotic treatment effect was not significant (p=0.58 and p=0.36, fig 1 top and bottom left,respectively). Conclusion Our results suggest that in patients with AHF, PCT may act as a surrogate marker reflecting the response to a clinically relevant bacterial infection and requirement for antibiotic treatment. Moreover, results for patients with low PCT levels suggest that patients may be affected by adverse events from the antibiotic therapy. As antibiotic therapy was not a randomised treatment in the BACH trial, results need to be confirmed in a prospective RCT.
2009
01 Pubblicazione su rivista::01a Articolo in rivista
PROCALCITONIN IDENTIFIES ACUTE HEART FAILURE BIOMARKERS IN PATIENTS WITH ACUTE HEART FAILURE IN NEED OF ANTIBIOTIC THERAPY: OBSERVATIONAL RESULTS FROM THE BACH (BIOMARKERS IN ACUTE HEART FAILURE) TRIAL / O., Hartmann; J., Landsberg; C., Mueller; R., Nowak; P., Ponikowski; M., Moeckel; C., Hogan; A. H. B., Wu; M., Richards; G. S., Filippatos; DI SOMMA, Salvatore; I. S., Anand; L., Ng; S. X., Neath; R., Christenson; J., Mccord; N. G., Morgenthaler; R., Engineer; A., Bergmann; S. D., Anker; A. S., Maisel; F. W., Peacock. - In: THORAX. - ISSN 0040-6376. - STAMPA. - 64:4(2009), pp. A62-A62. (Intervento presentato al convegno Winter Meeting of the British-Thoracic-Society tenutosi a London, ENGLAND nel DEC 02-04, 2009) [10.1136/thx.2009.127092s].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/481187
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