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There is a well-established, strong association between socioeconomic position and mortality. Public health mortality analyses thus routinely consider the confounding effect of socioeconomic position when possible. Particularly in the absence of personally reported data, researchers often use area-based measures to estimate the effects of socioeconomic position. Data are limited regarding the relative merits of measures based on US Census tract versus ZIP code (postal code). ZIP-code measures have more within-unit variation but are also more easily obtained. The current study reports on 293,138 middle-aged men screened in 14 states in 1973-1975 for the Multiple Risk Factor Intervention Trial and having 25-year mortality follow-up. In risk-adjusted proportional hazards models containing either ZIP-code-based or tract-based median household income, all-cause mortality hazard ratios were 1.16 (95% confidence interval: 1.14, 1.17) per Dollars 10,000 less ZIP-code-based income and 1.15 (95% confidence interval: 1.13, 1.16) per Dollars 10,000 less tract-based income; adding either income variable to a risk-adjusted model improved model fit substantially. Both were significant independent predictors in a combined model; tract-based income was a slightly stronger mortality predictor (hazard ratios = 1.05 and 1.11 for ZIP-code-based and tract-based income, respectively). These patterns held across various causes of death, for both Blacks and non-Blacks, and with or without adjustment for ZIP-code-based income diversity or tract-based proportion below poverty.

Latinos are now the largest minority in the United States, but their distinctive health needs and mortality patterns remain poorly understood. Proportional hazards regressions were used to compare Latino versus White risk- and income-adjusted mortality over 25 years' follow-up from 5,846 Latino and 300,647 White men screened for the Multiple Risk Factor Intervention Trial. Men were aged 35-57 years and residing in 14 states when screened in 1973-1975. Data on coronary heart disease risk factors, self-reported race/ethnicity, and home addresses were obtained at baseline; income was estimated by linking addresses to census data. Mortality follow-up through 1999 was obtained using the National Death Index. The fully adjusted Latino/White hazard ratio for all-cause mortality was 0.82 (95% confidence interval (CI): 0.77, 0.87), based on 1,085 Latino and 73,807 White deaths; this pattern prevailed over time and across states (thus, likely across Latino subgroups). Hazard ratios were significantly greater than one for stroke (hazard ratio = 1.30, 95% CI: 1.01, 1.68), liver cancer (hazard ratio = 2.02, 95% CI: 1.21, 3.37), and infection (hazard ratio = 1.69, 95% CI: 1.24, 2.32). A substudy found only minor racial/ethnic differences in the quality of Social Security numbers, birth dates, soundex-adjusted names, and National Death Index searches. Results were not likely an artifact of return migration or incomplete mortality data.

Abstract Background Although highly active antiretroviral therapy (HAART) has improved HIV survival, some patients receiving therapy are still dying. This analysis was conducted to identify factors associated with increased risk of post-HAART mortality. Methods We evaluated baseline (prior to HAART initiation) clinical, demographic and laboratory factors (including CD4+ count and HIV RNA level) for associations with subsequent mortality in 1,600 patients who began HAART in a prospective observational cohort of HIV-infected U.S. military personnel. Results Cumulative mortality was 5%, 10% and 18% at 4, 8 and 12 years post-HAART. Mortality was highest (6.23 deaths/100 person-years [PY]) in those with ≤ 50 CD4+ cells/mm3 before HAART initiation, and became progressively lower as CD4+ counts increased (0.70/100 PY with ≥ 500 CD4+ cells/mm3). In multivariate analysis, factors significantly (p < 0.05) associated with post-HAART mortality included: increasing age among those ≥ 40 years (Hazard ratio [HR] = 1.32 per 5 year increase), clinical AIDS events before HAART (HR = 1.93), ≤ 50 CD4+ cells/mm3 (vs. CD4+ ≥ 500, HR = 2.97), greater HIV RNA level (HR = 1.36 per one log10 increase), hepatitis C antibody or chronic hepatitis B (HR = 1.96), and HIV diagnosis before 1996 (HR = 2.44). Baseline CD4+ = 51-200 cells (HR = 1.74, p = 0.06), and hemoglobin < 12 gm/dL for women or < 13.5 for men (HR = 1.36, p = 0.07) were borderline significant. Conclusions Although treatment has improved HIV survival, defining those at greatest risk for death after HAART initiation, including demographic, clinical and laboratory correlates of poorer prognoses, can help identify a subset of patients for whom more intensive monitoring, counseling, and care interventions may improve clinical outcomes and post-HAART survival.

Background: Research on the relationship between orthopaedic volume and outcomes has focused almost exclusively on elective arthroplasty procedures. Geriatric patients who have sustained an intertrochanteric hip fracture are older and have a heavier comorbidity burden in comparison with patients undergoing elective arthroplasty; therefore, any advantage of provider volume in terms of mortality could be overwhelmed by the severity of the hip fracture condition itself. This study examined the association between surgeon and hospital volumes of procedures performed for the treatment of intertrochanteric hip fractures in Medicare beneficiaries and inpatient through ninety-day postoperative mortality. Methods: The Medicare 100% files of hospital and physician claims plus the beneficiary enrollment files for 2000 through 2002 identified beneficiaries who were sixty-five years of age or older and who underwent inpatient surgery for the treatment of an intertrochanteric hip fracture with internal fixation. Provider volumes of intertrochanteric hip fracture cases were calculated with use of unique surgeon and hospital provider numbers in the claims. Fixed effects regression analysis using generalized estimating equations was used to model the association between hospital and surgeon intertrochanteric hip fracture volume and inpatient through ninety-day mortality, controlling for age, sex, race, Charison comorbidity score, subtrochanteric fracture, prefracture nursing home residence, Medicaid-administered assistance, surgical device, and year. The unadjusted inpatient, thirty, sixty, and ninety-day mortality rates and adjusted relative risks are reported. Results: Between March 1, 2000, and December 31, 2002, 192,365 claims met inclusion criteria and matched with provider information. The unadjusted inpatient, thirty-day, sixty-day, and ninety-day mortality rates were 2.91%, 7.92%, 12.34%, and 15.19%, respectively. Patients managed at lower-volume hospitals had significantly higher (10% to 20%) adjusted risks of inpatient mortality than those managed at the highest-volume hospitals. By sixty days postoperatively, the increased mortality risk persisted only among patients managed at the lowest-volume hospitals (six cases per year or fewer). Patients who were managed by surgeons who treated an average of two or three cases per year had the highest mortality risks when compared with patients managed by the highest-volume surgeons. Conclusions: Only the highest-volume hospitals showed an inpatient mortality benefit for Medicare patients with intertrochanteric hip fractures. Unlike the situation with elective arthroplasty procedures, our findings do not indicate a need to direct patients with routine hip fractures exclusively to high-volume centers, although the higher mortality rates found in the lowest-volume hospitals warrant further investigation. [ABSTRACT FROM AUTHOR]

OBJECTIVE -- To examine the long-term association of metabolic syndrome with mortality among those at high risk for cardiovascular disease (CVD). RESEARCH DESIGN AND METHODS -- A total of 10,950 Multiple Risk Factor Intervention Trial (MRFIT) survivors were followed for mortality an additional median 18.4 years (1980-1999). Proportional hazards models examined multivariate-adjusted risks associated with Adult Treatment Panel III--defined metabolic syndrome conditions, with BMI substituted for waist circumference. RESULTS -- At MRFIT annual visit 6, 4,588 (41.9%) men, mean age (±SD) 53.0 ± 5.9 years, had metabolic syndrome and 6,362 did not. Comparing men with metabolic syndrome to men without, adjusted hazard ratios (HRs) were 1.21 (95% C1 1.13-1.29), 1.49 (1.35-1.64), and 1.51 (1.34-1.70) for 18-year total, CVD, and coronary heart disease mortality, respectively. Among men with metabolic syndrome, elevated glucose (1.54 [1.34-1.78]) and low HDL cholesterol (1.45 [1.17-1.54]) were most predictive of CVD mortality, followed by elevated BMI (1.34 [1.17-1.54]), elevated blood pressure (1.25 [0.98-1.58]), and elevated triglycerides (1.06 [0.86-1.30]). In contrast, for men without metabolic syndrome, the HR for low HDL cholesterol was 1.02 (0.86-1.22). Among metabolic syndrome men with no nonfatal CVD event, smokers with elevated LDL cholesterol showed higher CVD mortality (1.79 [1.22-2.631) compared with nonsmokers without elevated LDL cholesterol; this additional risk was even greater for metabolic syndrome men with a nonfatal CVD event (2.11 [1.32-3.38]). CONCLUSIONS -- Metabolic syndrome is associated with an increased risk of mortality. Among those with metabolic syndrome, risk is further increased by having more metabolic syndrome conditions, by cigarette smoking, and by elevated LDL cholesterol. Primary prevention of each metabolic syndrome condition should be emphasized, and presence of each condition should be treated in accordance with current guidelines. [ABSTRACT FROM AUTHOR]

Objectives. We explored differences between Black and White men for cardiovascular disease (CVD) mortality across major risk factor levels. Methods. Major CVD risk factors were measured among 300647 White and 20223 Black men aged 35 to 57 years who were screened for the Multiple Risk Factor Intervention Trial (MRFIT). Hazard ratios for CVD deaths for Black and White men over 25 years of follow-up were calculated for subgroups stratified according to risk factor levels. Results. CVD was responsible for 2518 deaths among Black men and 30772 deaths among White men. The age-adjusted Black-to-White CVD hazard ratio was 1.35 (95% confidence interval [CI] = 1.29, 1.40); the risk- and income-adjusted ratio was 1.05 (95% CI = 1.01, 1.10). CVD mortality rates were dramatically lower in cases of favorable risk profiles. However, fully adjusted Black-to-White CVD hazard ratios within groups at low, intermediate, high, and very high levels of overall risk were 1.76, 1.20, 1.10, and 0.94, respectively. Similar gradients were evident for individual risk factors. Conclusions. Higher CVD mortality rates among Black men were largely mediated by risk factors and income. These data underscore the need for sustained primordial risk factor prevention among Black men. [ABSTRACT FROM AUTHOR]

Background The magnitude of coronary mortality risk associated with diabetes or prior myocardial infarction (MI) is debatable. Modulating effects of age, risk factors, and duration of follow-up may explain discrepancies in previous research. Associations with noncardiovascular mortality are little explored. Objectives To compare mortality patterns in men with a history of diabetes or MI and to assess modulating effects on mortality of age, cardiovascular risk factors, and follow-up duration. Methods We compared the 25-year mortality of 4809 men with diabetes only and 4625 men with MI only (all men aged 35-57 years). Results The adjusted hazard ratio (HR) for all-cause mortality for those with MI only vs those with diabetes only was 0.97 (95% confidence interval, 0.92-1.03; P = .32). The pattern of deaths was different: higher coronary mortality (HR = 1.37; P<.001) and lower mortality from noncardiovascular causes (HR = 0.66; P<.001) in those with MI only compared with those with diabetes only. This finding prevailed across all ages and levels of cardiovascular risk factors. Hazard ratios for coronary mortality significantly declined over follow-up (2.7, 1.7, 1.2, 1.1, and 1.0 for ≤5, 6-10, 11-15, 16-20, and >20 years of follow-up, respectively), whereas HRs for noncardiovascular mortality remained relatively constant. Conclusions Overall, diabetes and MI were similarly strong predictors of total mortality. Higher mortality from noncardiovascular causes was observed in those with diabetes only, whereas prior MI was more strongly predictive of coronary mortality than diabetes at any age and level of cardiovascular risk factors. The difference in coronary mortality between the 2 groups was most evident in the first 10 years of follow-up. [ABSTRACT FROM AUTHOR]

Background: During the design phase of a clinical trial, sample size estimates should take into account medical screening criteria, the 'healthy volunteer' effect, consequences of run-in phases, and secular trends in the event rate of interest. All of these have been shown to relate to subsequent event rates, and hence trial power to detect intervention effects. The Multiple Risk Factor Intervention Trial (MRFIT) used three successive screenings of 361 662 men to enroll 12 866; observed coronary heart disease (CHD) mortality after a mean of 6.9 years was substantially lower than projected during design. We explore factors which may have contributed to these mortality differences and whether they persisted throughout follow-up. Methods: Proportional hazards models were used to compare 25-year mortality according to trial eligibility, self-exclusions, medical exclusions, and participation. Results: After adjustment for baseline risk factors and age, there was higher mortality among men excluded for presence of disease [hazard ratio (HR) 1.52, 95% confidence interval (CI) 1.43 – 1.61, for total; HR 1.92, CI 1.75 – 2.11, for CHD] compared to those not excluded which persisted throughout follow-up. Volunteers had lower total (HR 0.82, CI 0.76 – 0.87) and CHD (HR 0.79, CI 0.70 – 0.88) mortality than those discontinuing participation. Men excluded with characteristics deemed likely to interfere with adherence had higher total (HR 1.19, CI 1.07 – 1.33) and noncardiovascular disease (CVD) (HR 1.32, CI 1.14 – 1.53) mortality but no higher CVD (HR 1.04, CI 0.88 – 1.23) or CHD (HR 0.98, CI 0.80 –1.20) mortality compared to those not excluded. Differences in mortality were stronger during the first five years, but declined only slightly over 25 years. Conclusions 25-year mortality was significantly higher for non-volunteers and exclusions. Differences between observed and predicted six-year total mortality for trial participants were largely attributable to volunteers and exclusions, but there were additional differences for CHD mortality, which were likely due to downward secular trends. These results emphasize the importance of anticipating these factors during clinical trial design, even for trials of short duration. Clinical Trials 2004;1: 148 – 161. [ABSTRACT FROM AUTHOR]