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Head-to-head comparison of BNP and IL-6 as markers of clinical and experimental heart failure: Superiority of BNP.
Cytokine. 2007 Nov; 40(2):89-97.C

Abstract

Activation of BNP and IL-6 are hallmarks of left ventricular (LV) dysfunction and congestive heart failure (CHF). To assess the relative activation of BNP and IL-6 in clinical and experimental heart failure, we performed a human study in which plasma N-terminal proBNP (NT-proBNP) and IL-6 were measured in a large group of patients in the chronic phase after myocardial infarction (MI) and an animal study in which LV gene expression of BNP and IL-6 was assessed in rapid ventricular pacing-induced heart failure. In the human study, NT-proBNP and IL-6 were measured by non-extracted, enzyme-linked immunoassay in 845 subjects (n=468 outpatients after MI, MONICA MI register Augsburg; and 377 siblings without MI, control). NT-proBNP (295+/-23pg/mL vs. CTRL 84+/-8, P<0.05) and IL-6 (2.7+/-0.1pg/mL vs. CTRL 2.1+/-0.1, P<0.05) were both elevated in subjects with MI. These increases were particularly pronounced in the presence of concomitant CHF (both P<0.01 vs. CTRL) and LV dysfunction (EF<45%, both P<0.05 vs. CTRL). However, NT-proBNP was significantly correlated with several cardiac structural and functional parameters (EF, LVMI, history of MI, CHF symptoms; all P<0.05) upon regression analysis whereas IL-6 was only correlated with history of MI (P<0.001). Accordingly, MI subjects with symptomatic LV dysfunction were detected by NT-proBNP with a greater sensitivity, specificity, and ROC-area (85%, 88%, and 0.87, respectively) as compared to IL-6 (69%, 53%, and 0.67, respectively). In the animal study, IL-6 and BNP expression were both significantly elevated in CHF (both P<0.05) but with a much greater absolute activation of BNP. In addition, BNP mRNA expression displayed a stronger inverse correlation with LV function (r=-0.74; P<0.001) than IL-6 (r=-0.53; P=0.001) and was a markedly more sensitive and specific molecular marker of LV dysfunction (sensitivity 91%, specificity 100%, ROC-area 0.94) than IL-6 (sensitivity 74%, specificity 83%, ROC-area 0.87). Our animal study provides evidence that IL-6 expression is activated in heart failure but to a significantly lesser degree than that of BNP. Both the stronger expression of BNP and the better correlation with LV function provide the molecular basis for a diagnostic superiority of NT-proBNP in clinical LV dysfunction and heart failure.

Authors+Show Affiliations

Klinik und Poliklinik für Innere Medizin II, Klinikum der Universität Regensburg, 93042 Regensburg, Germany. christoph.birner@klinik.uni-regensburg.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17920926

Citation

Birner, Christoph M., et al. "Head-to-head Comparison of BNP and IL-6 as Markers of Clinical and Experimental Heart Failure: Superiority of BNP." Cytokine, vol. 40, no. 2, 2007, pp. 89-97.
Birner CM, Ulucan C, Fredersdorf S, et al. Head-to-head comparison of BNP and IL-6 as markers of clinical and experimental heart failure: Superiority of BNP. Cytokine. 2007;40(2):89-97.
Birner, C. M., Ulucan, C., Fredersdorf, S., Rihm, M., Löwel, H., Stritzke, J., Schunkert, H., Hengstenberg, C., Holmer, S., Riegger, G., & Luchner, A. (2007). Head-to-head comparison of BNP and IL-6 as markers of clinical and experimental heart failure: Superiority of BNP. Cytokine, 40(2), 89-97.
Birner CM, et al. Head-to-head Comparison of BNP and IL-6 as Markers of Clinical and Experimental Heart Failure: Superiority of BNP. Cytokine. 2007;40(2):89-97. PubMed PMID: 17920926.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Head-to-head comparison of BNP and IL-6 as markers of clinical and experimental heart failure: Superiority of BNP. AU - Birner,Christoph M, AU - Ulucan,Coskun, AU - Fredersdorf,Sabine, AU - Rihm,Munhie, AU - Löwel,Hannelore, AU - Stritzke,Jan, AU - Schunkert,Heribert, AU - Hengstenberg,Christian, AU - Holmer,Stephan, AU - Riegger,Günter, AU - Luchner,Andreas, Y1 - 2007/10/24/ PY - 2007/05/08/received PY - 2007/07/10/revised PY - 2007/08/13/accepted PY - 2007/10/9/pubmed PY - 2008/3/26/medline PY - 2007/10/9/entrez SP - 89 EP - 97 JF - Cytokine JO - Cytokine VL - 40 IS - 2 N2 - Activation of BNP and IL-6 are hallmarks of left ventricular (LV) dysfunction and congestive heart failure (CHF). To assess the relative activation of BNP and IL-6 in clinical and experimental heart failure, we performed a human study in which plasma N-terminal proBNP (NT-proBNP) and IL-6 were measured in a large group of patients in the chronic phase after myocardial infarction (MI) and an animal study in which LV gene expression of BNP and IL-6 was assessed in rapid ventricular pacing-induced heart failure. In the human study, NT-proBNP and IL-6 were measured by non-extracted, enzyme-linked immunoassay in 845 subjects (n=468 outpatients after MI, MONICA MI register Augsburg; and 377 siblings without MI, control). NT-proBNP (295+/-23pg/mL vs. CTRL 84+/-8, P<0.05) and IL-6 (2.7+/-0.1pg/mL vs. CTRL 2.1+/-0.1, P<0.05) were both elevated in subjects with MI. These increases were particularly pronounced in the presence of concomitant CHF (both P<0.01 vs. CTRL) and LV dysfunction (EF<45%, both P<0.05 vs. CTRL). However, NT-proBNP was significantly correlated with several cardiac structural and functional parameters (EF, LVMI, history of MI, CHF symptoms; all P<0.05) upon regression analysis whereas IL-6 was only correlated with history of MI (P<0.001). Accordingly, MI subjects with symptomatic LV dysfunction were detected by NT-proBNP with a greater sensitivity, specificity, and ROC-area (85%, 88%, and 0.87, respectively) as compared to IL-6 (69%, 53%, and 0.67, respectively). In the animal study, IL-6 and BNP expression were both significantly elevated in CHF (both P<0.05) but with a much greater absolute activation of BNP. In addition, BNP mRNA expression displayed a stronger inverse correlation with LV function (r=-0.74; P<0.001) than IL-6 (r=-0.53; P=0.001) and was a markedly more sensitive and specific molecular marker of LV dysfunction (sensitivity 91%, specificity 100%, ROC-area 0.94) than IL-6 (sensitivity 74%, specificity 83%, ROC-area 0.87). Our animal study provides evidence that IL-6 expression is activated in heart failure but to a significantly lesser degree than that of BNP. Both the stronger expression of BNP and the better correlation with LV function provide the molecular basis for a diagnostic superiority of NT-proBNP in clinical LV dysfunction and heart failure. SN - 1096-0023 UR - https://www.unboundmedicine.com/medline/citation/17920926/Head_to_head_comparison_of_BNP_and_IL_6_as_markers_of_clinical_and_experimental_heart_failure:_Superiority_of_BNP_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1043-4666(07)00379-1 DB - PRIME DP - Unbound Medicine ER -