Increased circulating placental growth factor during percutaneous coronary intervention is associated with applied radiocontrast agent.
OBJECTIVE
Recent studies have suggested placental growth factor (PlGF) and vascular endothelial growth factor (VEGF) as promising new biomarkers for risk stratification in acute coronary syndromes (ACS). However, little is known about the influence of percutaneous coronary intervention (PCI) on circulating PlGF and VEGF levels.


METHODS
Thirty-five patients with ACS, 27 patients with stable coronary artery disease (sCAD), and nine healthy controls were enrolled in the study. Although all patients with ACS and 14 patients with stable angina pectoris underwent PCI, 13 patients with coronary artery disease required no revascularization (sCAD). PlGF and VEGF plasma concentrations were measured by immunoassay during and at the end of PCI and coronary angiography.


RESULTS
Plasma PlGF levels were comparable in patients with ACS and sCAD on admission. Although coronary angiography or heparin alone did not alter PlGF and VEGF levels, immediately after PCI a dramatic increase was seen in circulating PlGF and a decrease in VEGF, which was independent of the clinical presentation of the patients, heparin administration, or the angiographic procedure itself, but was associated with the extent of coronary artery disease and the amount of the injected contrast media. In-vitro experiments revealed that radiocontrast agents induced the release of PlGF from endothelial cells without altering PlGF mRNA expression.


CONCLUSIONS
Patients undergoing PCI exhibit an increase in circulating PlGF, probably caused by posttranslational modifications of radiocontrast agents in endothelial cells. Therefore, analysis of plasma PlGF and VEGF levels may consider the timing of blood sampling with respect to PCI and contrast media exposure.
Steppich
Birgit Annette
BA
Medizinische Klinik und Deutsches Herzzentrum der Technischen Universität München, München, Germany.
Kaufmann
Jan
J
Sepp
Dominik
D
Kunert
Katharina
K
Rutz
Tobias
T
Stratz
Christian
C
Ott
Ilka
I
D000787:Angina Pectoris / Q000097:blood / Q000209:etiology / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D000925:Anticoagulants / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002478:Cells, Cultured; D003287:Contrast Media / Q000009:adverse effects*; D017023:Coronary Angiography; D023921:Coronary Stenosis / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging / Q000628:therapy*; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D007479:Iopamidol / Q000009:adverse effects / Q000031:analogs & derivatives; D009203:Myocardial Infarction / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology / Q000628:therapy*; D000072483:Placenta Growth Factor; D011257:Pregnancy Proteins / Q000097:blood*; D012720:Severity of Illness Index; D013997:Time Factors; D016896:Treatment Outcome; D014283:Triiodobenzoic Acids / Q000009:adverse effects; D015854:Up-Regulation; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
D000925:Anticoagulants; D015415:Biomarkers; D003287:Contrast Media; C508600:IL6 protein, human; D015850:Interleukin-6; C000608036:PGF protein, human; D011257:Pregnancy Proteins; D014283:Triiodobenzoic Acids; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000072483:Placenta Growth Factor; C057937:iomeprol; D006493:Heparin; C044834:iodixanol; D007479:Iopamidol