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Purpose: The aim of this study was to investigate real-world patient characteristics, medication use, and health care resource utilization (HCRU) and costs among patients with clinical atherosclerotic cardiovascular disease (ASCVD) as defined by 2013 American College of Cardiology/American Heart Association (ACC/AHA) guidelines, to examine burden of disease and unmet needs, such as potential undertreatment., Patients and Methods: This retrospective cohort study utilized a nationally representative managed care database to identify newly diagnosed ASCVD patients between January 1, 2007, and November 30, 2012 (index = first ASCVD diagnosis date) in the USA. Patients had ≥12-month pre-index (baseline) and ≥12-month post-index (follow-up) health plan enrollment and no baseline lipid-lowering medication (LLM). Patient characteristics, LLM utilization patterns, HCRU, and costs were examined for all patients and by subgroups based on LLM use pattern and/or follow-up low-density lipoprotein cholesterol (LDL-C) levels., Results: A total of 128,017 ASCVD patients were identified with a mean (SD) age of 59 (13) years, 43.1% female, and 48.8% with ≥36-month follow-up. Within 12-month follow-up, 10.6% had high-intensity statins and 56.9% had no LLM fills. Baseline mean (SD) all-cause costs were $8,852 ($25,608). At 12-month follow-up, mean (SD) all-cause and ASCVD-related costs were $31,443 ($54,040) and $20,289 ($45,159), respectively. The 36-month analyses showed similar distributions. Multivariable analyses showed that age, gender, region, health insurance type, baseline comorbidities, baseline use of specific medications, baseline lipid profiles, and index ASCVD type were significantly associated with all-cause and ASCVD-related health care costs., Conclusion: Patients have nonoptimal treatment for ASCVD and substantial HCRU and costs associated with residual risk. Unmet needs and cost burdens of ASCVD patients merit additional investigation., Competing Interests: Disclosure Thomas P Power is an employee of AIM Specialty Health, a wholly owned subsidiary of Anthem, Inc. Xuehua Ke, Mark J Cziraky, Michael Grabner, John J Barron, and Ralph Quimbo are employees of HealthCore, Inc., a wholly owned subsidiary of Anthem, Inc., under contract with Eli Lilly and Company for the conduct of this study. Nicole Gidaya Bonine was an employee of HealthCore, Inc., under contract with Eli Lilly and Company for the conduct of this study at the time of the study. Zhenxiang Zhao and Burkhard Vangerow are employees and stock/shareholders of Eli Lilly and Company. Peter P Toth is an employee of CGH Medical Center and an adjunct associate professor at Johns Hopkins University School of Medicine, under contract with HealthCore, Inc.; has relationships for the following: speakers bureau – Amarin Corporation, AstraZeneca Plc, Genzyme Corporation, GlaxoSmithKline Plc, Kowa Pharmaceuticals America, Inc., and Merck & Co., Inc.; consultant – Amgen, AstraZeneca Plc, Atherotech Diagnostics Lab, Kowa Pharmaceuticals America, Inc., Liposcience, Inc., Merck & Co., Inc., and Novartis Pharmaceuticals Corporation. The authors report no other conflicts of interest in this work.

Aim: To assess the prevalence of high-risk atherosclerotic cardiovascular disease (ASCVD, defined as history of acute coronary syndrome [hACS], cerebrovascular atherosclerotic disease [CeVAD], peripheral artery disease [PAD], or coronary artery disease w/diabetes [CADD]) and associated costs and cardiovascular (CV) events in Japan., Methods: A retrospective analysis was conducted using the Japan Medical Data Center (JMDC) database (2006-2011). ASCVD prevalence was estimated on the basis of diagnoses for CeVAD, PAD, CADD, and hACS (ACS claim ＞ 30-≤ 365 days after ACS-related hospitalization) during 1/1/ 2008-12/31/2009. Population denominators used in the prevalence estimations were provided by JMDC. A subcohort with an insurance coverage for ≥ 12 months before and ≥ 24 months after first/index ASCVD claim during 1/1/2008-12/31/2009 were analyzed on the basis of costs (in 2012 US dollars) and events., Results: ASCVD prevalence was 1,869/100,000 population. In total, 8,112 patients met inclusion criteria for the cost and CV event analyses. Among these patients, 4.0% experienced any event (myocardial infarction, stroke, coronary revascularization, hospitalization for unstable angina) in the year after ASCVD diagnosis, which decreased to 2.2% in year 2. First-year event rates were highest (22%) in patients with hACS. Mean [SD] all-cause costs per patient in year 1 were $7,031 [$14,359] for all patients with ASCVD combined. Extrapolated to the entire employed population, total first-year costs were estimated at $8.2 billion., Conclusions: ASCVD is not rare in Japan, even within a relatively young population of employed persons. Further, the total direct first-year cost burden of ASCVD in the employed Japanese population is high. These data may inform future economic assessments of new ASCVD treatments.

The antioxidant activity of genistein is associated with preventing atherosclerosis; however, the underlying mechanisms are not fully understood. In this study, human umbilical vein endothelial cells (HUVECs) were pretreated with genistein at different concentrations (10 nM, 100 nM and 1000 nM) for 6 h and then exposed to ox-LDL (50 mg/L) for another 24 h. Results showed that genistein restrained reactive oxygen species (ROS) and malondialdehyde (MDA) production, and ameliorated the inhibitory effect on superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (GPx) activity elicited by ox-LDL stimulation. The effects of genistein were correlated with the upregulation of sirtuin-1 via inhibiting miR-34a, and were abolished by sirtuin-1 siRNA or miR-34a mimic. Moreover, the antioxidation of genistein was associated with miR-34a/sirtuin-1-mediated nuclear translocation and deacetylation of foxo3a, accompanying with the enhanced expressions of MnSOD and CAT. The present study suggests that miR-34a/sirtuin-1/foxo3a might play an important role in genistein reversing ox-LDL-induced oxidative damage in HUVECs. [ABSTRACT FROM AUTHOR]