scholarly journals Vascular Endothelial Growth Factor Is Associated with the Morphologic and Functional Parameters in Patients with Hypertrophic Cardiomyopathy

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Radek Pudil ◽  
Martina Vasatova ◽  
Alena Fucikova ◽  
Helena Rehulkova ◽  
Pavel Rehulka ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Hypertrophic Cardiomyopathy ◽  
Growth Factor ◽  
Vena Cava ◽  
Left Ventricular ◽  
Diagnostic Process ◽  
Vascular Endothelial ◽  
Functional Changes ◽  
Functional Parameters ◽  
Endothelial Growth Factor

Background. Hypertrophic cardiomyopathy (HCM) is mostly autosomal dominant disease of the myocardium, which is characterized by myocardial hypertrophy. Vascular endothelial growth factor (VEGF) is involved in myocyte function, growth, and survival. The aim of study was to analyze the clinical significance of VEGF in structural and functional changes in patient with HCM. Methods. In a group of 21 patients with nonobstructive HCM, we assessed serum VEGF and analyzed its association with morphological and functional parameters. Compared to healthy controls, serum VEGF was increased: 199 (IQR: 120.4–260.8) ng/L versus 20 (IQR: 14.8–37.7) ng/L, P<0.001. VEGF levels were associated with left atrium diameter (r=0.51, P=0.01), left ventricle ejection fraction (r=-0.56, P=0.01), fractional shortening (r=-0.54, P=0.02), left ventricular mass (r=0.61, P=0.03), LV mass index (r=0.46, P=0.04), vena cava inferior diameter (r=0.65, P=0.01), and peak gradient of tricuspid regurgitation (r=0.46, P=0.03). Conclusions. Increased VEGF level is associated with structural and functional parameters in patients with HCM and serves as a potential tool for diagnostic process of these patients.

Vascular endothelial growth factor, left ventricular dysfunction and mortality in hemodialysis patients

2008 ◽  
Vol 26 (9) ◽  
pp. 1875-1882 ◽  
Author(s):  
Francesca Mallamaci ◽  
Francesco A Benedetto ◽  
Giovanni Tripepi ◽  
Sebastiano Cutrupi ◽  
Patrizia Pizzini ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Hemodialysis Patients ◽  
Left Ventricular ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Vascular Endothelial Growth Factor Receptor Inhibitors Impair Left Ventricular Diastolic Functions

2021 ◽  
Vol 62 (6) ◽  
pp. 1297-1304
Author(s):  
Haruka Yokoyama ◽  
Wataru Shioyama ◽  
Takuya Shintani ◽  
Shinichiro Maeda ◽  
Sachiko Hirobe ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Left Ventricular ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Diastolic Functions

scholarly journals Χαμηλής συχνότητας νευρομυϊκή ηλεκτρική διέγερση των σκελετικών μυών των κάτω άκρων και νεοαγγειογένεση σε ασθενείς με χρόνια καρδιακή ανεπάρκεια με χαμηλό κλάσμα εξώθησης

2018 ◽  
Author(s):  
Νικόλαος Μαγκούτης
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Walking Distance ◽  
Left Ventricular Ejection ◽  
Vascular Endothelial ◽  
Ventricular Ejection Fraction ◽  
Endothelial Growth Factor

Εισαγωγή: Η χαμηλής συχνότητας νευρομυική ηλεκτρική διέγερση (ΝΜΗΔ) των σκελετικών μυών των κάτω άκρων, μία εναλλακτική μορφή άσκησης σε ασθενείς που δεν είναι σε θέση ή δεν θέλουν να ασκηθούν φυσικά, βελτιώνει την κλινική εικόνα και αγγειοδιασταλτική ικανότητα των ασθενών με καρδιακή ανεπάρκεια (ΚΑ). Προσπαθήσαμε, λοιπόν, να εκτιμήσουμε την επίδραση της ΝΜΗΔ στα επίπεδα του αυξητικού παράγοντα Α του αγγειακού ενδοθηλίου (Vascular Endothelial Growth Factor-A, VEGF-A), των ενδοθηλιακών προγονικών κυττάρων (Endothelial Progenitor Cells, EPCs), και των CD34+ κυττάρων σε ασθενείς με ΚΑ με χαμηλό κλάσμα εξώθησης της αριστερής κοιλίας (Left Ventricular Ejection Fraction, LVEF) (<40%).Μέθοδοι: Τυχαιοποιήσαμε 27 αθενείς με ΚΑ με χαμηλό κλάσμα εξώθησης, ηλικίας 72 ετών, με συμπτώματα κατηγορίας ΙΙ/ΙΙΙ κατά ΝΥΗΑ σε πρόγραμμα FES ή sham διέγερσης 6 εβδομάδων. Μετρήσαμε τα επίπεδα των VEGF-A, EPCs και CD34+ κυττάρων αρχικά και μετά την θεραπεία σε συνδυασμό με κλινικούς, λειτουργικούς και βιοχημικούς δείκτες.Αποτελέσματα: Τα αρχικά δημογραφικά, οι μετρήσεις σοβαρότητας της ΚΑ (κατηγοριοποίηση κατά NYHA, LVEF, BNP, λόγος Ε/Ε΄) και οι επιλεγμένοι δείκτες αγγειογένεσης (VEGF-A, CD34+ κύτταρα) δεν διέφεραν σημαντικά μεταξύ των δύο ομάδων, εκτός από τα EPCs, τα οποία ήταν λιγότερα στην ομάδα FES (p=0.003).H FES προκάλεσε σημαντικά μεγαλύτερη αύξηση στα επίπεδα των VEGF-A [∆-VEGF-A, 98.7pg/mL (21.6), στην ομάδα FES έναντι 3.1pg/mL (12.5), στην ομάδα της sham διέγερσης, p=0.002], ενώ υπήρξε μια τάση μεγαλύτερης αύξησης των EPCs στην ομάδα FES σε σχέση με την ομάδα sham [5.3% of CD34+ (1.4) έναντι 0.1 (0.8), p=0.092] και των CD34+ κυττάρων στην ομάδα FES [2572.7 cells/mL (1119.70] σε σχέση με μια σημαντική πτώση των αντίστοιχων επιπέδων στην ομάδα sham [-852.9 (1278.6), p=0.060]. Εξάλλου, η FES βελτίωσε σημαντική την κατηγοριοποίηση κατά NYHA (p<0.001), την διανυθείσα απόσταση κατά την δοκιμασία βάδισης των 6 λεπτών (6-minute walking distance, p<0.001), τα επίπεδα του BNP (p<0.001), ενώ μείωσε σημαντικά και τον λόγο Ε/Ε΄(p<0.001). Οι μεταβολές των VEGF-A και των EPCs συσχετίστηκαν με στατιστικά σημαντικό τρόπο με την 6-MWD (rho=0.549, p=0.003 and rho=0.684, p<0.001, αντίστοιχα) καθώς και η μεταβολή των CD34+ κυττάρων τόσο με τη μεταβολή της 6MWD (rho=0.648, p<0.001) όσο και με τη μεταβολή του λόγου Ε/Ε΄(rho=-0.597, p=0.001). Συμπέρασμα: Η FES φαίνεται ότι επάγει την έκφραση των VEGF-A και κινητοποιεί τα CD34+ κύτταρα και τα EPCs σε συνδυασμό με βελτίωση της λειτουργικής ικανότητας και αιμοδυναμικών παραμέτρων σε ασθενείς με ΚΑ με χαμηλό LVEF.

Abstract 419: Cytokine-Mediated Release of Vascular Endothelial Growth Factor and Stromal-Derived Factor 1 Induces Neovascularization and Prevents Left Ventricular Remodeling in a Porcine Model of Ischemia Reperfusion.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Franca S Angeli ◽  
Sarah Jahn ◽  
Nicolas Amabile ◽  
Gina Orcino ◽  
Mia Shapiro ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Treatment Group ◽  
Left Ventricular ◽  
Control Group ◽  
Lv Function ◽  
Vascular Density ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
The Impact

Cytokine therapy has been suggested to improve left ventricle (LV) function after myocardial infarction (MI). The mechanisms for this benefit remain debatable. We investigated the impact of a prolonged combined therapy with Darbepoetin alfa (DARB) and Granulocyte Colony-Stimulating Factor (G-CSF) on LV function and vascular density after MI, correlating it with circulating progenitor cells (CPC), Vascular Endothelial Growth Factor (VEGF) and Stromal-Derived Factor 1 (SDF-1) release. Methods and Results : MI was induced in swine by a 90 minutes balloon occlusion of the left anterior descending artery. Animals were divided between treatment group with DARB-GCSF combination therapy (bolus of DARB 0.9 and GCSF 10ug/kg IV at time of reperfusion, followed by 5 doses of GCSF 5ug/kg SC from day 5 to 9, and four doses of 0.45ug/kg DARB SC once per week starting at day 1, n = 8) or control group (saline injections, n = 8). White blood cells (WBC), CPC, defined by CD45, CD31, CD90 and SLA-1 expression, and circulating levels of VEGF and SDF-1 were assessed at baseline (T0), 1 (T1), 2 (T2), and 3 (T3) weeks post-MI. LV function was assessed by echocardiography at T0, T1 and T6 (6 weeks post-MI), and vascular density by histology at T6. MI size was the same in both groups by post-MI CPK peak and LV ejection fraction (EF) at T1 (41+/−1 vs. 40+/−2%). In the treatment group only, from T0 to T1, there was an increase in WBC (16 ± 2 to 42 ± 2 x 10 6 /ml, p <0.01) and CPC (5 ± 1 to 9 ± 1 x 10 5 /ml, p = 0.01) and SDF-1 levels peaked from T0 to T2 (1345+/−60 to 1554 +/− 60 pg/ml; p<0.01) and stabilized at T3. All these values remained unchanged in the control group. VEGF levels (pg/ml) peaked at T2 in both groups (14+/−1 vs. 12+/−1), but remained increased at T3 in DARB-GCSF group only (13+/−1 vs. 9+/−1; p<0.01). LVEF (41+/−1 vs. 33+/−1, p<0.01) and arteriole density at the infarct zone (44+/−14 vs. 27+/−12/mm 2 , p = 0.02) and remote zone (18 +/−8 vs.11+/−5, p = 0.055) were higher compared to the control at T6. Conclusion : Our data suggest that prolonged therapy with DARB-GCSF combination after MI modulates angiogenesis and promotes stabilization of LV function by increasing CPC, and releasing SDF-1 and VEGF. This therapy provides a novel strategy to prevent post-MI LV remodeling and potentially improve outcome.

Abstract 13712: Association Between Soluble Vascular Endothelial Growth Factor Receptor-2 and Prognosis in Patients With Chronic Heart Failure: The PREHOSP-CHF Study

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Moritake Iguchi ◽  
Hiromichi Wada ◽  
Tsuyoshi Shinozaki ◽  
masahiro suzuki ◽  
Yoichi Ajiro ◽  
...  
Keyword(s):  
Heart Failure ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Left Ventricular ◽  
The Body ◽  
Left Ventricular Ejection ◽  
Vascular Endothelial ◽  
Ventricular Ejection Fraction ◽  
Endothelial Growth Factor

Introduction: Soluble vascular endothelial growth factor receptor-2 (sVEGFR-2) acts as an endogenous inhibitor of VEGF, a key regulator of angiogenesis and lymphoangiogenesis. However, little is known about the critical role of sVEGFR-2 in heart failure (HF). Methods: We performed a multicenter prospective cohort study (PREHOSP-CHF Study) to determine the predictive value of sVEGFR-2 for major adverse cardiovascular (CV) events (MACE) among patients with chronic HF (CHF). A total of 1,021 patients were included in the analyses. The mean age (SD) was 75.5 (12.6) years. 59.6% were male. The primary outcome was MACE defined as a composite of CV death or HF hospitalization. The secondary outcomes were all-cause death and CV death. Serum levels of sVEGFR-2 were determined employing specific enzyme-linked immunosorbent assays. Results: The patients with lower sVEGFR-2 concentrations were older, and had higher rates of female sex, atrial fibrillation and anemia. The baseline sVEGFR-2 level was inversely correlated with left ventricular ejection fraction, and was positively correlated with the body mass index. During the median follow-up of 730 days, a total of 210 (20.6%) all-cause deaths, 99 (9.7%) CV deaths and 308 (30.2%) HF hospitalizations occurred. Unadjusted Cox proportional hazard analyses revealed that the patients with the lowest quartile (Q1) of sVEGFR-2 did not show a significantly higher risk of MACE (p=0.7), but showed the greatest risks of CV death (p=0.003) and all-cause death (p=0.007). Even after adjusting for established risk factors and CV biomarkers (N-terminal pro-brain natriuretic peptide, contemporary sensitive cardiac troponin-I, and high-sensitivity C-reactive protein), those with the Q1 of sVEGFR-2 exhibited the greatest risk of CV death (p=0.02; hazard ratio [HR], 2.05; 95% confidence interval [CI], 1.17-3.66 [vs. Q2]; HR, 2.42; 95%CI, 1.30-4.68 [vs. Q3]; HR, 1.52; 95%CI, 0.80-2.99 [vs. Q4]), but not that of all-cause death. The sex-stratified analyses revealed that the association between sVEGFR-2 and CV death was still significant in men, but not in women (p for interaction, 0.07). Conclusions: A low sVEGFR-2 value was not associated with MACE, but was independently associated with CV mortality among patients with CHF.

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