Finance modeling in the delivery of medical care in tertiary-care hospitals in the Department of Veterans Affairs

BACKGROUND: In the mid-1990s, the Department of Veterans Affairs (DVA) implemented the Veterans Equitable Resource Allocation (VERA), a new financial model developed to attempt to better distribute the approximately $18 billion annual budget among roughly 170 Veterans Administration Medical Centers (VAMCs). VERA is based on a Health Maintenance Organization (HMO) model. VERA provides reimbursement to each of the 22 regional Veterans Integrated Service Networks (VISNs), and subsequent VISN distribution to individual VAMCs is based on an individual medical center's enrollment of unique social security numbers (uniques). In HMO vocabulary these are individual "covered lives." METHODS: Currently available demographic and staffing information regarding the DVA's 23 tertiary hospital systems (Category 7 hospitals) on the KLF database (DVA Austin Data Base) and published information on the DVA website were reviewed. The following was obtained: (1) staffing information-physician and nurse full-time employment equivalent (FTEE) staffing; (2) patient demographics and hospital workload-facility uniques (u), outpatient facility uniques, average daily census (ADC), discharges, and outpatient clinic visits. The following staffing ratios were calculated for both physician and nursing: FTEE/(u/1000), FTEE/(discharges/1000), FTEE/(clinic visits/1000), FTEE/ADC. For all categories the means +/- SD were calculated and correlation coefficients were calculated on pertinent pairings. RESULTS: Although categorized as similar tertiary care facilities, the 23 "Group 7" VA hospitals are anything but equivalent when reviewed using the VERA financing model with respect to physician staffing, nurse staffing, and facility uniques. Using VERA methodology, average physician FTEE and total nursing FTEE staffing/(u/1000) are 3.67 +/- 0.89 and 15.53 +/- 3.77, respectively. Correlation statistics of staffing versus unique SSNs demonstrated correlation coefficients of 0.46 and 0.59 with respect to physician and nurse staffing, respectively. On the other hand, when physician FTEE and nursing FTEE staffing were compared with VAMC workload parameters (total ADC, discharges, and outpatient visits), correlation coefficients were more consistent, ranging from 0.62 to 0.86. CONCLUSIONS: In the VERA model, the reward of a larger annual budget for an individual VAMC or the regional VISN is realized when staffing of VAMCs is minimized, overall provided medical services (especially costly tertiary services) are limited, and the number of covered lives is maximized. A VAMC staffing system that equates medical services delivered in a tertiary VAMC setting based on an HMO model like VERA (where the user population is skewed toward the sicker, older patient) shows decreased correlation when compared with VAMC workload model parameters.     

Association of beta-adrenergic receptor polymorphisms and progression to heart failure in patients with idiopathic dilated cardiomyopathy

PURPOSE: Increased sympathetic nervous system activation via the beta-adrenergic pathway influences the evolution of idiopathic dilated cardiomyopathy. We assessed the effects of beta-adrenergic receptor variants on heart failure in idiopathic dilated cardiomyopathy. METHODS: We prospectively analyzed 171 consecutive patients (mean [+/- SD] age, 49 +/- 14 years; 129 men) with idiopathic dilated cardiomyopathy who were receiving conventional treatment. All were characterized by polymerase chain reaction-restriction fragment length polymorphism analysis for Ser49Gly and Arg389Gly in the beta1-adrenergic receptor; the 5' leader cistron (LC) Arg19Cys, Arg16Gly, Gln27Glu, and Thr164Ile in the beta2-adrenergic receptor; and Arg64Trp in the beta3-adrenergic receptor. The endpoint was heart failure, defined as a worsening of clinical condition leading to hospitalization for heart failure, cardiac transplantation, or death from heart failure. RESULTS: During a median follow-up of 33 months, 24 patients had heart failure. In a Cox univariate analysis, the beta1Gly49 and beta2 5'LC-Cys19, Arg16, and Gln27 alleles were associated with a lower risk of heart failure. In a multivariate analysis that considered age, functional class, left ventricular ejection fraction, and beta-blocker use, three beta2-adrenergic receptor alleles were associated with lower risk: 5'LC-Cys19 (hazard ratio [HR]: 0.15; 95% confidence interval [CI]: 0.05 to 0.42), Arg16 (HR: 0.12; 95% CI: 0.04 to 0.35), and Gln27 (HR: 0.15; 95% CI: 0.05 to 0.42). CONCLUSION: The Gly49 allele in the beta1-adrenergic receptor and the 5' LC-Cys19, Arg16, and Gln27 alleles in the beta2-adrenergic receptor were associated with a lower risk of heart failure in idiopathic dilated cardiomyopathy, suggesting that the beta1- and beta2-adrenergic receptor genes are modifier genes.     

The 212A variant of the APJ receptor gene for the endogenous inotrope apelin is associated with slower heart failure progression in idiopathic dilated cardiomyopathy

BackgroundIdiopathic dilated cardiomyopathy (IDC) has multiple genetic and acquired causes. Apelin is an endogenous peptide that increases cardiac inotropism through his APJ receptor. No data are available concerning the APJ gene mutations responsible for IDC or on the role of APJ receptor gene variants in predicting heart failure (HF) progression.Methods and ResultsWe prospectively evaluated 202 consecutive patients with IDC and 202 matched controls: 90 were screened for APJ gene mutations and all 202 were genotyped for G212A and A445C APJ receptor polymorphisms. No mutations were found within the coding or untranslated regions of the APJ receptor, and no differences in allelic or genotype frequencies were observed comparing patients with a healthy control population. The correlations between APJ receptor polymorphisms and HF progression were assessed. During a median follow-up of 37 months, 35 patients experienced HF progression. Univariate analysis showed that patients carrying at least 1 copy of 212A had a significantly lower risk for HF-related events than those who were homozygous for the G212 variant, and multivariate analysis confirmed that it was significantly related to a more favorable prognosis.ConclusionsAPJ is unlikely to be a gene causing IDC, but the independent correlation between the 212A allele and a better prognosis suggests that it might act as a modifier gene.     

Ventricular asynchrony predicts a better outcome in patients with chronic heart failure receiving cardiac resynchronization therapy

OBJECTIVES: The aim of this study was to evaluate whether the clinical benefit of cardiac resynchronization therapy (CRT) can be prospectively predicted by means of the baseline evaluation of left ventricular asynchrony. BACKGROUND: The reverse remodeling associated with CRT is more evident in patients with severe heart failure (HF) and left bundle branch block (LBBB) who have left ventricular asynchrony. METHODS: Baseline left ventricular asynchrony was assessed in 60 patients with severe HF and LBBB by calculating the electrocardiographic duration of QRS and the echocardiographic septal-to-posterior wall motion delay (SPWMD). Left ventricular size and left ventricular ejection fraction (LVEF), mitral valve regurgitation, and functional capacity were also evaluated. The progression toward HF (defined as a worsening clinical condition leading to a sustained increase in conventional therapies, hospitalization, cardiac transplantation, and death) was assessed during follow-up, as were the changes in LVEF after six months. RESULTS: During the median follow-up of 14 months, 16 patients experienced HF progression. Univariate analysis showed that ischemic cardiomyopathy, changes in the QRS duration after implantation, and SPWMD significantly correlated with events. At multivariate analysis, a long SPWMD remained significantly associated with a reduced risk of HF progression (hazard ratio: 0.91; 95% confidence interval: 0.83 to 0.99; p <0.05). An improvement in LVEF was observed in 79% of the patients with a baseline SPWMD of > or =130 ms and in 9% of those with an SPWMD of <130 ms (p <0.0001). CONCLUSIONS: Baseline SPWMD is a strong predictor of long-term clinical improvement after CRT in patients with severe HF and LBBB.     

Influence of gender and family history of hypertension on autonomic control of heart rate, diastolic function and brain natriuretic peptide

OBJECTIVE: To verify in a unitary view whether autonomic control of heart rate and cardiac structure and function are modified early in offspring of hypertensive families. METHODS AND RESULTS: We selected 87 age- and sex-matched young normotensive subjects with (n = 45) and without (n = 42) a family history of hypertension who underwent evaluations of arterial pressure, time-domain parameters of autonomic heart rate control (24-h ECG monitoring), spectral baroreflex sensitivity, left ventricular geometry and function (echo-Doppler) and plasma brain natriuretic peptide levels (BNP). The group with a family history of hypertension significantly differed from their counterparts for systolic pressure (119 +/- 11 versus 114 +/- 9 mmHg, P< 0.05), heart rate (RR interval, 766 +/- 64 versus 810 +/- 93 ms, P< 0.05), heart rate variability [the standard deviation of normal RR intervals (SDNN), 147 +/- 29 versus 171 +/- 33 ms, P < 0.051, diastolic function (isovolumetric relaxation time, 65 +/- 9 versus 60 +/- 8 ms, P< 0.05) and BNP (23 +/- 13 versus 37 +/- 10 pg/ml, P< 0.05). Baroreflex sensitivity values did not differ between the two groups. When gender was considered, all the above-mentioned measures, as well as baroreflex sensitivity, were significantly different between males with and without a family history of hypertension but not between females, except for BNP, which was lower in males and females with a history of hypertension (males, 24 +/- 11 versus 38 +/- 8 pg/ml, P< 0.01; females 21 +/- 14 versus 36 +/- 13 pg/ml, P < 0.05). CONCLUSIONS: Male, but not female, hypertensive offspring have modified diastolic function and autonomic control of heart rate; BNP is the only parameter able to characterize hypertensive offspring independently from the influence of gender. This provides the hypothesis that the impaired production of this hormone could play a primary role in the pre-hypertensive state.     

Post-absorptive and insulin-mediated muscle protein metabolism in liver-transplanted patients

Cirrhotic patients after liver transplantation show a near-normal glucose homeostasis when in stable condition. In contrast, the basal and insulin-mediated whole-body protein metabolism remain altered several years after the graft. To examine whether the persisting defect of protein metabolism was due to the muscle, 7 non-diabetic livertransplanted patients in stable condition were studied by means of the catheterization of the brachial artery and the deep forearm vein (to measure the balance across the forearm) and the infusion of labelled leucine and phenylalanine associated with indirect calorimetry. Whole-body proteolysis (as determined by endogenous leucine flux, ELF), protein synthesis (from non-oxidative leucine disposal, NOLD) and leucine oxidation (LO) were reduced in comparison to previously obtained values in a normal population. Insulin infusion (while maintaining euglycemia) induced a not significant variation of forearm phenylalanine Ra (24.4→16.5 μmol/100 ml forearm min⁻¹; proteolysis) and Rd (18.5→19.7; protein synthesis). In contrast, the whole-body insulin-dependent inhibitions of ELF (31.5→21.8 μmol/m² min) and NOLD (27.3→18.4) were impaired with respect to a normal population. On the basis of the present results, we conclude that skeletal muscle is not responsible for the alterations of leucine metabolism persisting after liver transplantation. By exclusion, this points to the liver as the major determinant of the leucine metabolism defect. Received: 12 July 2001 / Accepted in revised form: 13 February 2002 Correspondence to L. Luzi