Heparin strongly induces soluble fms-like tyrosine kinase 1 release in vivo and in vitro--brief report.

OBJECTIVE: Soluble fms-like tyrosine kinase 1 (sFlt1) is involved in the pathophysiology of preeclampsia and coronary artery disease. Because sFlt1 has a heparin-binding site, we investigated whether or not heparin releases sFlt1 from the extracellular matrix. METHODS AND RESULTS: We measured sFlt1 before and after heparin administration in 135 patients undergoing coronary angiography, percutanous coronary intervention, or both. sFlt1 was increased directly after heparin administration (from 254 to 13,440 pg/mL) and returned to baseline within 10 hours. Umbilical veins and endothelial cells treated with heparin released sFlt1. Heparinase I and III also increased sFlt1. Mice treated with heparin had elevated sFlt1 serum levels. Their serum inhibited endothelial tube formation. CONCLUSIONS: Heparin releases sFlt1 by displacing the sFlt1 heparin-binding site from heparan sulfate proteoglycans. Heparin could induce an antiangiogenic state.

Soluble fms-like tyrosine kinase-1 (sFLT-1) predicts post-percutaneous coronary intervention (PCI) myocardial infarction (MI type 4a).

CONTEXT: Acute myocardial infarction (AMI) related to percutaneous coronary intervention (PCI) (MI type 4a) occurs in up to 26% of elective patients. OBJECTIVE: To evaluate if sFLT-1 helps to predict MI type 4a in troponin negative patients with elective PCI. MATERIALS AND METHODS: We enrolled 135 patients, 106 had a PCI. sFLT-1 levels were assessed at five time points before and after PCI. RESULTS: MI type 4a occurred in 22.1% of patients. sFLT-1 levels at admission above 251 pg/mL indicated a significant relative risk for MI type 4a of 2.83. CONCLUSION AND DISCUSSION: Increased sFLT-1 levels at baseline might indicate unstable atherosclerosis and risk for microembolization and thus be predictive of MI type 4a.

Tea-induced improvement of endothelial function in humans: No role for epigallocatechin gallate (EGCG).

Consumption of tea is inversely associated with cardiovascular diseases. However, the active compound(s) responsible for the protective effects of tea are unknown. Although many favorable cardiovascular effects in vitro are mediated by epigallocatechin gallate (EGCG), its contribution to the beneficial effects of tea in vivo remains unresolved. In a randomised crossover study, a single dose of 200 mg EGCG was applied in three different formulas (as green tea beverage, green tea extract (GTE), and isolated EGCG) to 50 healthy men. Flow-mediated dilation (FMD) and endothelial-independent nitro-mediated dilation (NMD) was measured before and two hours after ingestion. Plasma levels of tea compounds were determined after each intervention and correlated with FMD. FMD significantly improved after consumption of green tea containing 200 mg EGCG (p < 0.01). However, GTE and EGCG had no significant effect on FMD. NMD did not significantly differ between interventions. EGCG plasma levels were highest after administration of EGCG and lowest after consumption of green tea. Plasma levels of caffeine increased after green tea consumption. The results show that EGCG is most likely not involved in improvement of flow-mediated dilation by green tea. Instead, other tea compounds, metabolites or combinations thereof may play a role.