The long-term success of coronary stent implantation is limited by in-stent restenosis (ISR). In spite of a broad variety of animal models available, an ideal high-throughput model of ISR has been lacking. Apolipoprotein E (apoE) deficient rats enable the evaluation of human-sized coronary stents while at the same time providing an atherogenic phenotype. Whereas apoE deficient rats have been proposed as animal model of atherosclerosis, to date it is unknown whether they also develop pronounced ISR. We sought to assess ISR after abdominal aorta stent implantation in apoE deficient rats. A total of 42 rats (16 wildtype, 13 homozygous apoE−/− and 13 heterozygous apoE+/− rats) underwent abdominal aorta stent implantation. After 28 days blood samples were analyzed to characterize lipid profiles. ISR was assessed by histomorphometric means. Homozygous apoE−/− rats exhibited significantly higher total cholesterol and low-density cholesterol levels than wildtype apoE+/+ and heterozygous apoE+/− rats. ISR was significantly pronounced in homozygous apoE−/− rats as compared to wildtype apoE+/+ (p = <0.0001) and heterozygous apoE+/− rats (p = 0.0102) on western diet. Abdominal aorta stenting of apoE−/− rats is a reliable model to investigate ISR after stent implantation and thus can be used for the evaluation of novel stent concepts. Apolipoprotein E (apoE) deficient rats have been proposed as animal model of atherosclerosis. We investigated the development of restenosis 28 days after stent implantation into the abdominal aorta of wildtype apoE+/+, homozygous apoE−/− and heterozygous apoE+/− rats, respectively. Homozygous apoE−/− rats exhibited significantly higher LDL and significantly lower HDL cholesterol levels compared to wildtype apoE+/+ and heterozygous apoE+/− rats. Restenosis after stent implantation was significantly pronounced in western-diet-fed homozygous apoE−/− rats, accompanied by a significantly increased neointimal thickness. Thus, apoE knockout rats exhibit elevated restenosis and might provide a novel tool for testing of innovative stent concepts.

Elevated fibroblast growth factor 23 (FGF23) levels are associated with adverse outcome in populations with cardiovascular disease and chronic kidney failure. It is unclear if FGF23 has significance in prognosis estimation in patients with acute heart failure (HF) when compared to traditional risk estimation tools. Serum levels of intact FGF23 were assessed in 139 patients admitted to the Intermediate Care Unit of a tertiary hospital for acute HF. Patients were followed-up for one year. After exclusion of patients who were lost to follow-up, data outliers, and patients with sampling errors, the final study cohort comprised 133 patients. The Seattle Heart Failure (SHF) Model was used to estimate one-year survival. FGF23 levels correlated with HF severity and were strongly associated with one-year mortality. Associations between one-year outcome and FGF23, assessed on day 1 after admission, were still evident after multivariable adjustment (OR 15.07; 95%CI 1.75–129.79; p = 0.014). FGF23 levels predicted the one-year outcome with similar accuracy as the SHF Model, both if assessed on day 1 and on day 2 after admission (FGF23d1: AUC 0.784; 95%CI 0.669–0.899; FGF23d2: AUC 0.766; 95%CI 0.631–0.901; SHF: AUC 0.771; 95%CI 0.651–0.891). The assessment of FGF23 in patients with acute HF might help identify high-risk patients that are more prone to complications, need a closer follow-up and more aggressive treatment.

(1) Background: Fibroblast growth factor 23 (FGF23) is associated with mortality in patients with heart failure (HF); however, less is known about mortality associations in patients with myocardial infarction (MI). (2) Methods: FGF23 was assessed in 180 patients with acute MI, 99 of whom presented with concomitant acute HF. Patients were followed up for one year, and outcome estimates by FGF23 were compared to GRACE score estimates. (3) Results: Log-transformed serum levels of intact FGF23 (logFGF23) did not differ between MI patients with and without HF, and no difference in logFGF23 was observed between 14 MI patients who died and those who survived. However, when only MI patients with concomitant HF were considered, logFGF23 was significantly higher among non-survivors compared to that in survivors. While logFGF23 was not associated with the outcome in the entire cohort, logFGF23 was fairly predictive for one-year mortality in patients with concomitant HF (AUC 0.78; 95%CI 0.61–0.95), where it outperformed GRACE score estimates (AUC 0.70; 95%CI 0.46–0.94). (4) Conclusions: FGF23 was associated with one-year mortality only in MI patients who concomitantly presented with HF, surpassing the predictive ability of GRACE score estimates. No associations were observed in patients without HF despite similar FGF23 levels at admission. Further studies are warranted to investigate whether FGF23 is causal for dismal outcome of HF.