Objectives
This study sought to test 2 hypotheses: 1) fibroblast growth factor (FGF)-23 identifies patients with stable ischemic heart disease (SIHD) at high risk of cardiovascular events independent of clinical factors, renal function, and established cardiovascular biomarkers; and 2) FGF-23 identifies patients who derive greater clinical benefit from angiotensin-converting enzyme inhibitor therapy.
Background
FGF-23 is an endocrine regulator of mineral metabolism and markedly elevated levels are associated with cardiovascular events in patients with chronic kidney disease. Data in patients with SIHD are more sparse.
Methods
FGF-23 levels were measured in 3,627 patients with SIHD randomly assigned to trandolapril or placebo within the PEACE (Prevention of Events With Angiotensin-Converting Enzyme) trial and followed up for a median of 5.1 years.
Results
After adjustment for clinical risk predictors, left ventricular ejection fraction, markers of renal function, and established cardiovascular biomarkers, FGF-23 concentration was independently associated with an increased risk of cardiovascular death or heart failure among patients allocated to placebo (quartile 4 hazard ratio: 1.73; 95% confidence interval, 1.09 to 2.74; p = 0.02) and significantly improved metrics of discrimination. Furthermore, among patients in the top quartile of FGF-23 levels, trandolapril significantly reduced cardiovascular death or incident heart failure (hazard ratio: 0.45; 95% confidence interval: 0.28 to 0.72), whereas there was no clinical benefit in the remaining patients (hazard ratio: 1.07; 95% confidence interval: 0.75 to 1.52; p interaction = 0.0039). This interaction was independent of and additive to stratification based on renal function.
Conclusions
Elevated levels of FGF-23 are associated with cardiovascular death and incident heart failure in patients with SIHD and identify patients who derive significant clinical benefit from angiotensin-converting enzyme inhibitor therapy regardless of renal function.
Background: The early survival advantage of endovascular aneurysm repair (EVAR) compared with open repair reverses over time, possibly because of higher rates of reintervention related to endoleaks and aneurysm sac expansion. Therefore, we sought to examine the association between sac behavior, endoleaks, reintervention, and long-term survival.Methods: We reviewed all patients undergoing EVAR in the Vascular Quality Initiative between 2003 and 2017 with an imaging study at 1 year postoperatively (66 months). We defined aneurysm sac changes by Society for Vascular Surgery guidelines (change $5 mm) and determined independent predictors of sac behavior, new endoleak, and reintervention using hierarchical logistic regression. We employed Cox regression to examine the association between sac behavior and long-term survival. We performed propensity matching between patients with sac regression and those with failure to regress as a secondary analysis.Results: Of 30,074 EVAR patients, 14,817 (49%) had a 1-year imaging study and were included in this study. At 1 year, 40% of sacs regressed, 35% remained stable, and 25% expanded. Factors independently associated with sac expansion were age
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