eart failure (HF) is a major and growing public health problem in developed countries. 1 In the United States, approximately 5 million individuals have HF, and more than 550,000 new cases are diagnosed annually. 1 To our knowledge, only a few reports have focused on this issue in Japan. 2,3 The purpose of this study was to estimate the impact of population aging on the number of outpatients with left ventricular dysfunction (LVD) over the next 5 decades in Japan. All study participants provided informed consent and the study design was approved by the ethics review board of Niigata University Graduate School of Medical and Dental sciences.We applied estimated age-, gender-, and conditionspecific prevalences to the projected Japanese population in each age group and gender for the future until 2055, to provide a prospective estimate of the number of these patients. The primary data source was the Sado Heart Failure Study, a hospital-based research project primarily designed to count the number of patients with LVD by total enumeration in all hospitals on the island of Sado. The proportion of echocardiographically diagnosed systolic (SD) and isolated diastolic dysfunction (IDD) patients (together referred to as LVD) in the general population in 2003 4,5 was used as a substitute for the prevalence of LVD in the present study

No abstract

Background Follistatin-like 1 (FSTL1) is an extracellular glycoprotein that is found in human serum. Recent work suggests that FSTL1 is secreted in response to ischemic injuries and that its overexpression is protective in the heart and vasculature. Methods and Results Here, we examined serum FSTL1 levels in patients with chronic heart failure with left ventricular (LV) ejection fraction <40% (n=86). The distribution of the sample, from these chronic heart failure patients, was separated into three tertiles of low, medium and high FSTL1 levels. Serum FSTL1 levels were increased 56% above age- and gender-matched, healthy controls. Diabetes mellitus, brain natriuretic peptide level, left atrial size, LV posterior wall thickness, LV end-diastolic diameter and LV mass were significant determinants of FSTL1 serum levels by bivariate analysis. After controlling for significant covariates, FSTL1 levels predicted LV hypertrophy (as measured by LV mass index) by multivariate linear regression analysis (P<0.001). Unadjusted survival analysis demonstrated increased mortality in patients with increasing FSTL1 levels (P=0.09). After adjusting for significant parameters, patients with increased FSTL1 remained at the highest risk of death [hazard ratio (95% confidence limits) 1.028, (0.98 and 1.78)]; (P=0.26). To determine whether elevated FSTL1 may be derived from the myocardium, FSTL1 protein expression was measured in samples from explanted, failing (n=18) and non-failing human hearts (n=7). LV failing hearts showed 2.5-fold higher FSTL1 protein levels than non-failing control hearts (P<0.05). Conclusions Elevated serum FSTL1 in human heart failure patients was associated with LV hypertrophy. Further studies on the role of FSTL1 as a biomarker in chronic systolic heart failure are warranted.