Biologically active adrenomedullin: prognostic value in patients with acute chest pain

Janet-Jacqueline Olic (Regensburg)1, M. Schlossbauer (Regensburg)1, U. Hubauer (Regensburg)1, J. Hupf (Regensburg)1, L. S. Maier (Regensburg)1, C. G. Jungbauer (Regensburg)1

1Universitätsklinikum Regensburg Klinik und Poliklinik für Innere Med. II, Kardiologie Regensburg, Deutschland


Aims: It is already known that N-terminal pro B-type natriuretic peptide (NT-proBNP) measured in acute coronary syndrome (ACS) independently predicts mortality and adverse cardiac events. The goal of this study was to evaluate the prognostic value of biologically active adrenomedullin (bio-ADM) compared to NT-proBNP in patients presenting with acute chest pain as well as in the subgroup of patients with ACS in the emergency department.

Methods and results: Bio-ADM and NT-proBNP were measured at admission in 341 patients with acute chest pain. In the current analysis, 197 patients suffered from ACS. A follow-up (median of 55 months) was performed in regard to all-cause mortality as well as combined endpoint of major adverse cardiac events (all-cause mortality, ACS with the necessity of a coronary intervention, congestive heart failure, and stroke/transient ischaemic attack; MACE). 60 patients died during follow-up and 108 reached the combined endpoint. Bio-ADM and NT-proBNP correlated positively and significantly (r = 0.465, p < 0.05). Additionally, the concentrations of both biomarkers were significantly elevated in patients with troponin positive ACS as well as unstable angina pectoris compared to patients with chest wall syndrome (each p < 0.05). Moreover, deceased patients as well as patients with MACE showed significant higher concentrations of bio-ADM and NT-proBNP. Regarding ROC analysis, both markers showed very satisfying area under the curve (AUC) values for all-cause mortality and MACE (all-cause mortality: AUCbio-ADM 0.76, AUCNT-proBNP 0.82; MACE: AUCbio-ADM 0.72, AUCNT-proBNP 0.76). Both biomarkers presented still satisfying AUC values for all-cause mortality and MACE in the ACS cohort. There were no significant differences between the AUCs for bio-ADM and NT-proBNP in each case (p = n. s.). Regarding Kaplan-Meier analysis, bio-ADM and NT-proBNP were each a significant predictor for all-cause mortality and MACE in the overall study cohort as well as in the subgroup of patients with ACS (each p < 0.05). In accordance with Cox regression analysis, bio-ADM and NT-proBNP were significant and independent predictors for all-cause mortality in total study cohort and ACS subgroup (each p < 0.05). With a combination of the two biomarkers the event rate for both endpoints increased in comparison to NT-proBNP or bio-ADM alone (each p < 0.05).

Conclusions: In addition to NT-proBNP, bio-ADM seems to provide a significant predictive value in a long-term follow-up in patients with acute chest pain and patients with ACS regarding the endpoints all-cause mortality and major adverse cardiac events.

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