The U.S. Department of Veterans Affairs (VA) is the nation's largest care provider for hepatitis C virus (HCV)-infected patients and is uniquely suited to inform national efforts to eliminate HCV. An extensive array of delivery of services, policy guidance, outreach efforts, and funding has broadened the reach and capacity of the VA to deliver direct-acting antiviral (DAA) HCV therapy, supported by an infrastructure to effectively implement change and informed by extensive population health data analysis. The VA has treated more than 92 000 HCV-infected veterans since all-oral DAAs became available in January 2014, with cure rates exceeding 90%; only 51 000 veterans in VA care are known to remain potentially eligible for treatment. Key actions advancing the VA's aggressive treatment of HCV infection that are germane to non-VA settings include expansion of treatment capacity through the use of nonphysician providers, video telehealth, and electronic technologies; expansion of integrated care to address psychiatric and substance use comorbidities; and electronic data tools for patient tracking and outreach. A critical component of effective implementation has been building infrastructure through the creation of regional multidisciplinary HCV Innovation Teams, whose system redesign efforts have produced innovative HCV practice models addressing gaps in care while providing more efficient and effective HCV management for the populations they serve. Financing for HCV treatment and infrastructure resources coupled with reduced drug prices has been paramount to the VA's success in curing HCV infection. The VA is poised to share and extend best practices to other health care organizations and providers delivering HCV care, contributing to a concerted effort to reduce the overall burden of HCV infection.
Abstract-The serum lipoprotein(a) [Lp(a)] level is a known risk factor for arteriosclerotic coronary artery disease.However, its association with restenosis after percutaneous transluminal coronary angioplasty (PTCA) is controversial. We hypothesized that the Lp(a) level is a significant risk factor for restenosis after angioplasty through a pathophysiological mechanism leading to excess thrombin generation or inhibition of fibrinolysis. We designed a prospective study of the relation of Lp(a) to outcome after PTCA, in which we measured selected laboratory variables at entry and collected clinical, procedural, lesion-related, and outcome data pertaining to restenosis. Restenosis was defined as Ͼ50% stenosis of the target lesion by angiography or as ischemia in the target vessel distribution by radionuclide-perfusion scan. Before the patients underwent PTCA, blood was obtained by venipuncture for measurement of Lp(a), total cholesterol, thrombin-antithrombin (TAT) complex, ␣ 2 -antiplasmin-plasmin (APP) complex, and plasminogen activator inhibitor-1 (PAI-1). Evaluable outcome data were obtained on 162 subjects, who form the basis of this report. Restenosis occurred in 61 subjects (38%). The Lp(a) level was not correlated significantly with TAT, APP, PAI-1, or the TAT-APP ratio. Levels of TAT, APP, and PAI-1 were not statistically different in the patients with versus those without restenosis. The median ratio of TAT to APP was 2-fold higher in the restenosis group, and this difference approached statistical significance (Pϭ0.07). Univariate analysis was performed for the association of clinical, lesion-related, and procedural risk factors with restenosis. Lp(a) levels did not differ significantly in the restenosis versus no-restenosis group, whether assessed categorically (Ͼ25 mg/dL versus Ͻ25 mg/dL) or as a continuous variable by Mann-Whitney U test. The number of lesions dilated and the lack of family history of premature heart disease were significantly associated with restenosis (Pϭ0.002 and Pϭ0.008, respectively). A history of diabetes mellitus was of borderline significance (Pϭ0.055). By multiple logistic regression analysis, the number of lesions dilated was the only variable significantly associated with restenosis (Pϭ0.03). We conclude that the number of lesions dilated during PTCA is a significant risk factor for restenosis, whereas the serum Lp(a) level was not a significant risk factor for restenosis in our patient population. The TAT to APP ratio merits further study as a possible risk factor for restenosis. (Arterioscler Thromb Vasc Biol. 1998;18:1281-1286.)Key Words: lipoprotein(a) Ⅲ angioplasty Ⅲ thrombin Ⅲ plasmin Ⅲ antiplasmin P ercutaneous transluminal coronary angioplasty (PTCA) has become a standard procedure for the treatment of coronary artery disease. However, in spite of advances in techniques, restenosis after PTCA remains a common complication, at a rate of 30% to 40% in the absence of stent placement.1-4 Various risk factors predictive of restenosis have been identified, and these can ...
The current study evaluates changes in access as a result of the MyVA Access program-a system-wide effort to improve patient access in the Veterans Health Administration. Data on 20 different measures were collected, and changes were analyzed using t tests and Chow tests. Additionally, organizational health-how able a system is to create health care practice change-was evaluated for a sample of medical centers (n = 36) via phone interviews and surveys conducted with facility staff and technical assistance providers. An organizational health variable was created and correlated with the access measures. Results showed that, nationally, average wait times for urgent consults, new patient wait times for mental health and specialty care, and slot utilization for primary and specialty care patients improved. Patient satisfaction measures also improved, and patient complaints decreased. Better organizational health was associated with improvements in patient access.
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