Clin Res Cardiol 100, Suppl 1, April 2011

V884 - Plasma soluble Fms-like tyrosine kinase-1 (sFlt) and placental growth factor (PlGF) in pulmonary hypertension: Results from the BioSPHERE-I Study
 
H. M. Nef1, H. Tiede2, H. Möllmann1, R. Voswinckel2, A. M. Zeiher3, S. Dimmeler4, R. Schermuly5, A. Rolf1, C. Liebetrau1, C. Troidl6, W. Seeger2, A. Ghofrani2, C. W. Hamm1
 
1Abt. Kardiologie, Kerckhoff Klinik GmbH, Bad Nauheim; 2Medizinische Klinik II, Pneumologie, Universitätsklinikum Giessen und Marburg GmbH, Giessen; 3Zentrum Innere Medizin III, Schwerpunkt Kardiologie, Universitätsklinikum Frankfurt am Main, Frankfurt am Main; 4Zentrum für Molekulare Medizin, Goethe Universität, Institut für Kardiovaskuläre Regeneration, Frankfurt am Main; 5Herz- und Lungenforschung, Max-Planck-Institut für, Bad Nauheim; 6Experimentelle Kardiologie, Grödelhaus, Kerckhoff Klinik GmbH, Bad Nauheim;
 
Background: Pulmonary arterial hypertension (PAH) is more prevalent than previously believed and a severe pathologic condition leading to increased mortality. A major shortcoming in assessing PAH is the lack of non-invasive parameters that function as biomarker. Plasma soluble Fms-like tyrosine kinase-1 (sFlt) and placental growth factor (PlGF) indicative of hypoxia might be valuable predictors of PAH.
Methods: In the BioSPHERE-I study 229 patients with different types of PAH (idiopathic PAH, IPAH [29.2%]; PAH and lung diseases [17.5%], LDPAH; chronic thrombembolic PH, CTEPH [27.5%]; PAH of other causes, APAH [25.8%]) were included. Manifest PAH was diagnosed by right heart catherization. Plasma samples from pulmonary artery were collected at baseline and sFlt and PlGF was measured by sandwich enzyme immunoassay (Quantikine, R&D Systems, MN, USA). A follow up visit was scheduled 12 months after baseline assessment. All cause mortality, clinical worsening, and hospitalization were considered as endpoints. 80 patients with exclusion of an increased pulmonary pressure served as control group.
Results: Plasma level for sFLT (Control: 98.3±3.9; IPAH: 5178±460.2; LDPAH: 5300±409.9; APAH: 6896±658.3, CTEPH: 3653.9±333.0) and PlGF (Control: 13.9±0.4; IPAH: 47.1±3.7; LDPAH: 52.8±3.5; APAH: 56.5±3.7, CTEPH: 38.6±2.9) were significantly increased in all  different subtypes of pulmonary hypertension. In the multivariate regression analysis,  the NYHA class correlated with the level of sFlt and PlGF. Hemodynamic parameters and PlGF or sFLT did not correlate. The area under the curve of the receiver operating characteristics curve for optimized cut-off points for sFlt and PlGF was 0.861 (95% CI 0.832-0.899) and 0.787 (95% CI 0.755-0.819), respectively. For the clinical endpoints death, clinical worsening or hospitalization, no predictive value for sFlt and PlGF was documented.
Conclusion: sFlt and PlGF are potent diagnostic biomarkers in patients with various forms of PAH. Moreover, severity of PAH as indicated by clinical symptoms like dyspnea correlate to the plasma level of sFLT and PlGF. However, a predictive value of sFlt and PlGF regarding survival could not be documented.
 
Clin Res Cardiol 100, Suppl 1, April 2011
Zitierung mit Vortrags- oder Posternummer s.o.
DOI 10.1007/s00392-011-1100-y

http://www.abstractserver.de/dgk2011/ft/abstracts/V884.htm