Journal
SCIENTIFIC REPORTS
Volume 7, Issue -, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41598-017-10505-9
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Funding
- Carlos III Health Institute [CPII13/00025, PI15/00082, PI14/00271, PIE15/00013, CB16/11/00486, SAF2014-57845-R]
- Spanish Ministry of Health
- Spanish Ministry of Economy and Competiveness
- European Regional Development Fund (FEDER)
- Cardiology Spanish Society and Generalitat Valenciana [PROMETEO/2013/007]
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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.
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