Key result
HFpEF is linked to ~130% higher sVEGFR-1 levels compared to healthy controls.
Why the study?
The clinical significance of VEGF and sVEGFR-1 in patients with HFpEF and the effects of different treatments on angiogenesis were not well understood.
Case-Control (n=72)
Should not change HFpEF management; leaves open sVEGFR-1 as hypothesis-generating biomarker or target.
Objective In this study, our aim was to investigate the clinical significance of VEGF, sVEGFR-1 in HFpEF patients. Materials and methods Seventy-two participants enrolled in this cross-sectional case-control study including HFpEF patients (n=41) and healthy (n=31) subjects. Blood samples were collected and serum VEGF, sVEGFR-1 analysis, and transthoracic echocardiography were performed. Results and discussion The average sVEGFR-1 level of HFpEF patient group was significantly higher than the control group (respectively 0.136 ng/L (0.04–0.34), 0.06 ng/L (0.01–0.25); p<0.001). The average VEGF level of HFpEF patients using beta blocker was significantly higher than the HFpEF patients not using it (respectively 0.585±0.194 ng/L; 0.349±0.269 ng/L; p=0.025). The average VEGF level of HFpEF patients using statins was significantly higher than the HFpEF patients without a medication (respectively 0.607±0.099 ng/L; 0.359±0.273 ng/L; p=0.038). Conclusion Our study is the first study demonstrating the relations among HFpEF, accompanying morbidities, VEGF and sVEGFR-1 levels. Statins and beta blockers may have positive effects on angiogenesis in HFrEF patients via increasing VEGF levels.
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Ertürk et al. (2018) conducted a case-control in Heart failure with preserved ejection fraction (HFpEF) (n=72). Heart failure with preserved ejection fraction (HFpEF) vs. Healthy subjects was evaluated on sVEGFR-1 level (p=<0.001). HFpEF was associated with significantly higher sVEGFR-1 levels compared to healthy controls (0.136 vs 0.06 ng/L; p<0.001), while beta blocker and statin use increased VEGF levels in HFpEF patients.
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