Open AccessDynamics and implications of circulating anti-angiogenic VEGF-A165b isoform in patients with ST-elevation myocardial infarction
Author(s) -
Luisa Hueso,
César RíosNavarro,
Amparo RuizSaurí,
Francisco J. Chorro,
Julio Núñez,
María-Jesús Sanz,
Vicente Bodı́,
Laura Piqueras
Publication year - 2017
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/s41598-017-10505-9
Subject(s) - myocardial infarction , cardiology , ejection fraction , medicine , percutaneous coronary intervention , conventional pci , angiogenesis , infarction , vascular endothelial growth factor , ex vivo , in vivo , heart failure , vegf receptors , biology , microbiology and biotechnology
Angiogenesis is crucial to restore microvascular perfusion in the jeopardized myocardium in the weeks following reperfused ST-segment elevation myocardial infarction (STEMI). (VEGF)-A 165 b, an anti-angiogenic factor, has been identified as a regulator of vascularization; however, it has not been previously implicated in acute myocardial infarction. We sought to investigate the dynamics of circulating VEGF-A 165 b and its association with cardiac magnetic resonance-derived infarct size and left ventricular ejection fraction (LVEF). 50 STEMI patients and 23 controls were included. Compared with control individuals, serum VEGF-A 165 b was elevated in STEMI patients prior to primary percutaneous coronary intervention (PCI). Following PCI, serum VEGF-A 165 b increased further, reaching a maximum level at 24 h and decreased one month after reperfusion. VEGF-A 165 b levels at 24 h were associated with a large infarct size and inversely related to LVEF. VEGF-A 165 b expression was increased in myocardial infarct areas from patients with previous history of AMI. An ex vivo assay using serum from STEMI patients showed that neutralization of VEGF-A 165 b increased tubulogenesis. Overall, the study suggests that VEGF-A 165 b might play a deleterious role after AMI as an inhibitor of angiogenesis in the myocardium. Accordingly, neutralization of VEGF-A 165 b could represent a novel pro-angiogenic therapy for reperfusion of myocardium in STEMI.