Predictors of injury‐related and non‐injury‐related mortality among veterans with alcohol use disorders

Aims To describe the association between alcohol use disorders (AUDs) and mortality and to examine risk factors for and all‐cause, injury‐related and non‐injury‐related mortality among those diagnosed with an AUD. Setting Department of Veterans Affairs, Veterans Health Administration (VHA). Participants A cohort of individuals who received health care in VHA during the fiscal year (FY) 2001 (n = 3 944 778), followed from the beginning of FY02 through the end of FY06. Measurements Demographics and medical diagnoses were obtained from VHA records. Data on mortality were obtained from the National Death Index. Findings Controlling for age, gender and race and compared to those without AUDs, individuals with AUDs were more likely to die by all causes [hazard ratio (HR) = 2.30], by injury‐related (HR = 3.29) and by non‐injury‐related causes (HR = 2.21). Patients with AUDs died 15 years earlier than individuals without AUDs on average. Among those with AUDs, Caucasian ethnicity and all mental illness diagnoses that were assessed were associated more strongly with injury‐related than non‐injury‐related mortality. Also among those with AUDs, individuals with medical comorbidity and older age were at higher risk for non‐injury related compared to injury‐related mortality. Conclusions In users of a large health‐care system, a diagnosis of an AUD is associated significantly with increased likelihood of dying by injury and non‐injury causes. Patients with a diagnosis of an AUD who die from injury differ significantly from those who die from other medical conditions. Prevention and intervention programs could focus separately upon selected groups with increased risk for injury or non‐injury‐related death.     

Effects of Alcohol Taxes on Alcohol‐Related Mortality in Florida: Time‐Series Analyses From 1969 to 2004

Background: Over a hundred studies have established the effects of beverage alcohol taxes and prices on sales and drinking behaviors. Yet, relatively few studies have examined effects of alcohol taxes on alcohol‐related mortality. We evaluated effects of multiple changes in alcohol tax rates in the state of Florida from 1969 to 2004 on disease (not injury) mortality. Methods: A time‐series quasi‐experimental research design was used, including nonalcohol deaths within Florida and other states’ rates of alcohol‐related mortality for comparison. A total of 432 monthly observations of mortality in Florida were examined over the 36‐year period. Analyses included ARIMA, fixed‐effects, and random‐effects models, including a noise model, tax independent variables, and structural covariates. Results: We found significant reductions in mortality related to chronic heavy alcohol consumption following legislatively induced increases in alcohol taxes in Florida. The frequency of deaths (t = ?2.73, p = 0.007) and the rate per population (t = ?2.06, p = 0.04) declined significantly. The elasticity effect estimate is ?0.22 (t = ?1.88, p = 0.06), indicating a 10% increase in tax is associated with a 2.2% decline in deaths. Conclusions: Increased alcohol taxes are associated with significant and sizable reductions in alcohol‐attributable mortality in Florida. Results indicate that 600 to 800 lives per year could be saved if real tax rates were returned to 1983 levels (when the last tax increase occurred). Findings highlight the role of tax policy as an effective means for reducing deaths associated with chronic heavy alcohol use.     

Impulsivity and socio‐economic status interact to increase the risk of gambling onset among youth

Aims To determine if impulsivity and socio‐economic status (SES) interact to influence gambling onset in youth. Design Longitudinal study of grade 7 students followed for 8 years. Setting Montréal, Canada. Participants A total of 628 adult students aged 12.6 years on average at cohort inception. Measurements Impulsivity and SES (parent education, area deprivation) were collected during secondary school. Age of gambling onset was collected retrospectively when participants were aged 20.3 years. Cox proportional hazards regression was used to model the association between time to first report of gambling and interaction terms for each of impulsivity and parent education, and impulsivity and area deprivation accounting for sex and ethnicity. Findings Median (interquartile range) age of gambling onset was 17.0 (4.0) years. Impulsivity independently increased the risk of gambling onset among participants with no university‐educated parent [hazard ratio (HR) 1.3; 95% confidence interval 1.1–1.5] and those living in highly deprived areas (HR 1.7; 1.5–2.0). Impulsivity was not associated with gambling onset among high SES youth. Among participants with high impulsivity, risks were elevated for those with no university‐educated parent relative to one or more university‐educated parent (HR 1.7; 1.1–2.7), and for participants living in deprived relative to advantaged areas (HR 5.0; 2.6–9.6). SES was not associated with gambling onset among participants with low impulsivity. Conclusions Impulsivity is a risk factor for gambling onset among low but not high SES youth, and low SES influences gambling onset primarily among impulsive youth. Gambling prevention programmes may need to consider potential interaction between impulsivity and SES.     

Estimating the number of alcohol‐attributable deaths: methodological issues and illustration with French data for 2006

Aims Computing the number of alcohol‐attributable deaths requires a series of hypotheses. Using French data for 2006, the potential biases are reviewed and the sensitivity of estimates to various hypotheses evaluated. Methods Self‐reported alcohol consumption data were derived from large population‐based surveys. The risks of occurrence of diseases associated with alcohol consumption and relative risks for all‐cause mortality were obtained through literature searches. All‐cause and cause‐specific population alcohol‐attributable fractions (PAAFs) were calculated. In order to account for potential under‐reporting, the impact of adjustment on sales data was tested. The 2006 mortality data were restricted to people aged between 15 and 75 years. Results When alcohol consumption distribution was adjusted for sales data, the estimated number of alcohol‐attributable deaths, the sum of the cause‐specific estimates, was 20 255. Without adjustment, the estimate fell to 7158. Using an all‐cause mortality approach, the adjusted number of alcohol‐attributable deaths was 15 950, while the non‐adjusted estimate was a negative number. Other methodological issues, such as computation based on risk estimates for all causes for ‘all countries’ or only ‘European countries’, also influenced the results, but to a lesser extent. Discussion The estimates of the number of alcohol‐attributable deaths varied greatly, depending upon the hypothesis used. The most realistic and evidence‐based estimate seems to be obtained by adjusting the consumption data for national alcohol sales, and by summing the cause‐specific estimates. However, interpretation of the estimates must be cautious in view of their potentially large imprecision.     

Lower life expectancy among people with an HCV notification: a population‐based linkage study

Among people with hepatitis C virus (HCV) infection, liver disease‐related deaths have risen over the last 20 years. Life expectancy has not been estimated in this population. HCV notifications (mandatory notification of anti‐HCV‐positive serology since 1991) reported to the New South Wales Health Department from 1992 to 2006 were linked to cause of death data. Abridged life tables were constructed from age‐specific mortality rates. Life expectancy from ages 18–70 years for non‐drug‐related mortality causes was estimated using competing risk methods and compared to the general population of Australia. The cohort comprised 81 644 individuals with an HCV notification, with median follow‐up of 7.6 years. Median age at notification was 34 years [interquartile range (IQR) 28–42] and 63% were male. Between 1992 and 2006, 4607 deaths occurred. Median age at liver‐ and drug‐related death among males was 51 (IQR 45–66) and 36 (IQR 31–42) years, respectively, and among females was 63 (IQR 49–74) and 36 (IQR 30–41) years, respectively. In each year of follow‐up before 2000, 15–21% of deaths were liver‐ and 30–39% were drug‐related. After 2000, liver‐related deaths increased to 20–26% of deaths in each year and drug‐related deaths decreased to 13–19%. Excluding drug‐related causes of death, life expectancy was lowered by an average of 4.2 (SD ± 1.0) and 5.4 (SD ± 0.7) years for males and females, respectively. Among people with an HCV notification, an increasing proportion of deaths are liver‐related. Following removal of drug‐related mortality, life expectancy in this population remained considerably lower, compared with the general population.     

Sex‐related Disparity in Surgical Mortality among Pediatric Patients

Background. It has been reported that gender differences in cardiovascular outcomes found in adults also are present in children who undergo surgical repair for congenital heart disease. Methods. California statewide hospital discharge data 1989–99 were used to study outcomes in children <18 years undergoing cardiac surgery. Hospital discharge data were linked to death registry data to study postdischarge death within 30 days of discharge. We used logistic regression to evaluate the effect of gender on mortality controlling for age, race and ethnicity, type of insurance, household income, date and month of surgery, type of admission, hospital case volume, and various types of procedures. Results. There were 25 402 cardiac surgery cases with 1505 in‐hospital deaths (mortality rate of 5.92%). An additional 37 deaths occurred within 30 days after hospital discharge. Crude mortality rates for males (5.99%) and females (5.84%) were not significantly different. However, fewer neonates were female and females underwent a higher proportion of low‐risk procedures than males. Logistic regression revealed that females, compared with males, had a significantly higher odds ratio (OR) for in‐hospital mortality (OR = 1.18, P < .01) and overall (up to 30 days post discharge) mortality (OR = 1.18, P < .01). The risk‐adjusted length of hospital stay was similar between females and males while charges per hospital day were slightly higher in females than males. The prevalence of Down syndrome, pulmonary hypertension, and failure to thrive were higher in females. Conclusions. Female gender is associated with an 18% higher in‐hospital and 30‐day postdischarge mortality as compared with male gender. There was no difference in length of hospital stay between males and females. The mechanism by which female gender acts as a risk factor requires further investigation.     

Association of IFNL3 and IFNL4 polymorphisms with liver‐related mortality in a multiracial cohort of HIV/HCV‐coinfected women

African Americans coinfected with HIV and hepatitis C virus (HCV) have lower liver‐related mortality than Caucasians and Hispanics. While genetic polymorphisms near the IFNL3 and IFNL4 genes explain a significant fraction of racial differences in several HCV‐related outcomes, the impact of these variants on liver‐related mortality has not been investigated. We conducted a cohort study of HIV/HCV‐coinfected women followed in the multicentre, NIH‐funded Women's Interagency HIV Study (WIHS) to investigate whether 10 polymorphisms spanning the IFN‐λ region were associated with liver‐related mortality by dominant, recessive or additive genetic models. We also considered whether these polymorphisms contributed to previously reported differences in liver‐related death by race/ethnicity (ascertained by self‐report and ancestry informative markers). Among 794 coinfected women, there were 471 deaths including 55 liver‐related deaths during up to 18 years of follow‐up. On adjusted analysis, rs12980275 GG genotype compared to AG+AA hazards ratios [(HR) 0.36, 95% CI 0.14–0.90, P = 0.029] and rs8109886 AA genotype compared to CC+AC (HR 0.67, 95% CI 0.45–0.99, P = 0.047) were most strongly associated with liver‐related death although these associations were no longer significant after adjusting for race/ethnicity (HR 0.41, 95% CI 0.16–1.04, P = 0.060 and HR 0.78, 95% CI 0.51–1.19, P = 0.25, respectively). African American women had persistently lower liver‐related death independent of IFN‐λ variants (HRs ≤ 0.44, P values ≤ 0.04). The lower risk of death among African American HIV/HCV‐coinfected women is not explained by genetic variation in the IFN‐λ region suggesting, that other genetic, behavioural and/or environmental factors may contribute to racial/ethnic differences in liver‐related mortality.     

Moderate-Vigorous Physical Activity in Older People in Northern Ireland: Levels, Demographic Patterns and Types of Moderate-Vigorous Physical Activity Undertaken

Work on the health benefits of physical activity currently recommends participation in 2.5 h of moderate-vigorous physical activity/week, and advocates consideration of the physical activity gained from activities of daily living in this total. Using the inclusion of activities of daily living, this analysis aimed to investigate the physical activity undertaken by a representative sample of older people living in Northern Ireland (NI). Using a telephone questionnaire, 426 individuals (representative of the NI older population) reported participating in a mean 4.1?±?6.3 h of moderate–vigorous physical activity/week, but 225 (53 %) of these individuals reported participation in less than 2.5 h of moderate-vigorous activity/week, and 126 of these individuals reported none. Regression analyses revealed greater participation by males, younger individuals and those living in less deprived areas (smallest B?=??0.11, p?=?0.03). Males were also found to participate in more Do-It-Yourself, cycling, heavy gardening and exercise/sport in summer and less heavy housework, than females (smallest B?=??0.03, p?=?0.05), but no differences were found dependent on age or deprivation of residential area. These findings suggest a need to increase participation in moderate-vigorous physical activity in this population, with specific emphasis on females, older individuals and those living in more deprived areas. Analysis of the types of moderate-vigorous physical activity undertaken suggests that females may benefit particularly from increased opportunity or promotion of exercise/sport as a leisure activity.     

Elevated overdose mortality rates among First Nations individuals in a Canadian setting: a population‐based analysis

Aims To determine the total burden of illicit drug overdose mortality over the study period in the province of British Columbia and investigate possible population‐level determinants by estimating rates among subgroups including First Nations individuals. Design Review of coroner case files. Setting The province of British Columbia, Canada. Participants Individuals dying from an illicit drug overdose between 2001 and 2005. Measurements Age‐adjusted mortality rates, standardized mortality ratios (SMR) and years of potential life lost (YPLL), stratified by major population groups. Findings Over the study period, 909 individuals died from illicit drug overdoses, including 104 (11.4%) First Nations individuals. Compared to the general population, First Nations males and females suffered from substantially elevated SMR and YPLL. In a multivariate logistic regression analysis, First Nations deaths were significantly more likely to be among women, related to injection drug use and to have occurred in the Downtown Eastside area of Vancouver, the local epicentre of human immunodeficiency virus infection and open drug use (all P < 0.05). Conclusions This report found highly elevated overdose death rates and levels of premature mortality among First Nations Canadians in British Columbia compared to the general population. While previously unidentified, these findings are consistent with the poorer population health profile of First Nations Canadians. Although further research is needed to identify the causes of the elevated death rates, our findings support increased availability of evidence‐based overdose prevention measures.     

Adult deaths and the future: a cause‐specific analysis of adult deaths from a longitudinal study in rural Tanzania 2003–2007

Objectives To determine patterns and risk factors for cause‐specific adult mortality in rural southern Tanzania. Methods The study was a longitudinal open cohort and focused on adults aged 15–59 years between 2003 and 2007. Causes of deaths were ascertained by verbal autopsy (VA). Cox proportion hazards regression model was used to determine factors associated with cause‐specific mortality over the 5‐year period. Results Thousand three hundred and fifty‐two of 65 548 adults died, representing a crude adult mortality rate (AMR) of 7.3 per 1000 person years of observation (PYO). VA was performed for 1132 (84%) deaths. HIV/AIDS [231 (20.4%)] was the leading cause of death followed by malaria [150 (13.2%)]. AMR for communicable disease (CD) causes was 2.49 per 1000 PYO, 1.21 per 1000 PYO for non‐communicable diseases (NCD) and 0.53 per 1000 PYO for accidents/injury causes. NCD deaths increased from 16% in 2003 to 24% in 2007. High level of education was associated with a reduction in the risk of dying from NCDs. Those with primary education (HR = 0.67, 95% CI: 0.49, 0.92) and with education beyond primary school (HR = 0.11, 95% CI: 0.02, 0.40) had lower mortality than those who had no formal education. Compared with local residents, in‐migrants were 1.7 (95% CI: 1.37, 2.11) times more likely to die from communicable disease causes. Conclusion NCDs are increasing as a result of demographic and epidemiological transitions taking place in most African countries including Tanzania and require attention to prevent increased triple disease burden of CD, NCD and accident/injuries.     

Area‐Level Poverty Is Associated with Greater Risk of Ambulatory–Care–Sensitive Hospitalizations in Older Breast Cancer Survivors

OBJECTIVES: To estimate the frequency of ambulatory care–sensitive hospitalizations (ACSHs) and to compare the risk of ACSH in breast cancer survivors living in high‐poverty with that of those in low‐poverty areas. DESIGN: Prospective, multilevel study. SETTING: National, population‐based 1991 to 1999 National Cancer Institute Surveillance, Epidemiology, and End Results Program data linked with Medicare claims data throughout the United States. PARTICIPANTS: Breast cancer survivors aged 66 and older. MEASUREMENTS: ACSH was classified according to diagnosis at hospitalization. The percentage of the population living below the U.S. federal poverty line was calculated at the census‐tract level. Potential confounders included demographic characteristics, comorbidity, tumor and treatment factors, and availability of medical care. RESULTS: Of 47,643 women, 13.3% had at least one ACSH. Women who lived in high‐poverty census tracts (≥30% poverty rate) were 1.5 times (95% confidence interval (CI)=1.34–1.72) as likely to have at least one ACSH after diagnosis as women who lived in low‐poverty census tracts (<10% poverty rate). After adjusting for most confounders, results remained unchanged. After adjustment for comorbidity, the hazard ratio (HR) was reduced to 1.34 (95% CI=1.18–1.52), but adjusting for all variables did not further reduce the risk of ACSH associated with poverty rate beyond adjustment for comorbidity (HR=1.37, 95% CI=1.19–1.58). CONCLUSION: Elderly breast cancer survivors who lived in high‐poverty census tracts may be at increased risk of reduced posttreatment follow‐up care, preventive care, or symptom management as a result of not having adequate, timely, and high‐quality ambulatory primary care as suggested by ACSH.     

Inverse relationship between body mass index and mortality in older nursing home residents: a meta‐analysis of 19,538 elderly subjects

Body mass index (BMI) and mortality in old adults from the general population have been related in a U‐shaped or J‐shaped curve. However, limited information is available for elderly nursing home populations, particularly about specific cause of death. A systematic PubMed/EMBASE/CINAHL/SCOPUS search until 31 May 2014 without language restrictions was conducted. As no published study reported mortality in standard BMI groups (<18.5, 18.5–24.9, 25–29.9, ≥30 kg/m²), the most adjusted hazard ratios (HRs) according to a pre‐defined list of covariates were obtained from authors and pooled by random‐effect model across each BMI category. Out of 342 hits, 20 studies including 19,538 older nursing home residents with 5,223 deaths during a median of 2 years of follow‐up were meta‐analysed. Compared with normal weight, all‐cause mortality HRs were 1.41 (95% CI = 1.26–1.58) for underweight, 0.85 (95% CI = 0.73–0.99) for overweight and 0.74 (95% CI = 0.57–0.96) for obesity. Underweight was a risk factor for higher mortality caused by infections (HR = 1.65 [95% CI = 1.13–2.40]). RR results corroborated primary HR results, with additionally lower infection‐related mortality in overweight and obese than in normal‐weight individuals. Like in the general population, underweight is a risk factor for mortality in old nursing home residents. However, uniquely, not only overweight but also obesity is protective, which has relevant nutritional goal implications in this population/setting.     

Case-mix adjustment for evaluation of mortality in cystic fibrosis.

Comparison of patient mortality rates in cystic fibrosis (CF) obtained from different institutions requires the use of case-mix adjustment methods to account for baseline differences in patient and disease characteristics. There is no current professional consensus on the use of case-mix adjustment methods for use in comparing mortality rates in CF. Characteristics used for this case-mix adjustment should include those that are different across institutions and are associated with patient survival. They should not include characteristics of disease severity that may be a consequence of effectiveness of treatment. The goal of these analyses was to identify a set of these characteristics of patients or disease that would be useful for case-mix adjustment of CF mortality rates. Data from the Cystic Fibrosis Foundation Patient Registry and from the United States Census of the Population (1990) were used in these analyses. Kaplan-Meier techniques, the log-rank test, and Cox proportional hazards regression were used to estimate survivorship, calculate hazard ratios (HR), 95% confidence intervals (CI(95%)), and to conduct tests of statistical significance. The data set included all 30,469 CF patients seen at CF Care Centers from 1982-1998. There were 5,906 deaths during 508,721 person-years of follow-up. In multivariate analyses, female gender (HR 1.30, CI(95%) (1.16, 1,47), P < 0.001), nonwhite race (HR 1.48, CI(95%) (1.07, 2.04), P = 0.018), Hispanic ethnicity (HR 1.85, CI(95%) (1.42, 2.43), P < 0.001), and symptomatic presentation (respiratory, gastrointestinal, respiratory and gastrointestinal, meconium ileus, and other symptomatic presentations; HRs 1.38-1.83; P values, 0.028 to < 0.001) were associated with higher risk of death. The homozygous Delta F508 genotype (HR 1.36, CI(95%) (1.19, 1.55), P < 0.001) and neither mutation being Delta F508 (HR 1.40, CI(95%) (1.15, 1.71), P = 0.001) were also associated with higher risk of death. Patients diagnosed after 36 months of age had almost 50% reduction in risk of death compared to those diagnosed before 6 months of age (HR 0.52 CI(95%) (0.44, 0.61), P < 0.001). When patients living in zip codes with a median household income > $50,000/year (corrected for the 1999 consumer price index) were compared with those living in areas with a median household income < $20,000/year, it was apparent that those in the wealthier areas had a 40% reduced risk of death (HR 0.60, CI(95%) (0.44, 0.82), P = 0.001). All of these characteristics were independently significant predictors of death, and all of these characteristics differed significantly across the CF Care Centers. This case-mix adjustment model uses patient and disease characteristics available at the time of diagnosis of CF, and is not believed to be influenced by subsequent treatment to predict the risk of death. If these case-mix adjustment methods are adopted broadly, they will make it possible to study treatment effects and differences in mortality outcomes, while adjusting for baseline differences in patient and disease characteristics.     

QT Interval and Long‐Term Mortality Risk in the Framingham Heart Study

Background : The association between QT interval and mortality has been demonstrated in large, prospective population‐based studies, but the strength of the association varies considerably based on the method of heart rate correction. We examined the QT‐mortality relationship in the Framingham Heart Study (FHS). Methods : Participants in the first (original cohort, n = 2,365) and second generation (offspring cohort, n = 4,530) cohorts were included in this study with a mean follow up of 27.5 years. QT interval measurements were obtained manually using a reproducible digital caliper technique. Results : Using Cox proportional hazards regression adjusting for age and sex, a 20 millisecond increase in QTc (using Bazett's correction; QT/RR^1/2 interval) was associated with a modest increase in risk of all‐cause mortality (HR 1.14, 95% CI 1.10–1.18, P < 0.0001), coronary heart disease (CHD) mortality (HR 1.15, 95% CI 1.05–1.26, P = 0.003), and sudden cardiac death (SCD, HR 1.19, 95% CI 1.03–1.37, P = 0.02). However, adjustment for heart rate using RR interval in linear regression attenuated this association. The association of QT interval with all‐cause mortality persisted after adjustment for cardiovascular risk factors, but associations with CHD mortality and SCD were no longer significant. Conclusion : In FHS, there is evidence of a graded relation between QTc and all‐cause mortality, CHD death, and SCD; however, this association is attenuated by adjustment for RR interval. These data confirm that using Bazett's heart rate correction, QTc, overestimates the association with mortality. An association with all‐cause mortality persists despite a more complete adjustment for heart rate and known cardiovascular risk factors.     

Insulin use and increased risk of mortality in type 2 diabetes: a cohort study

Aim: To compare population‐based rates of all‐cause and cardiovascular (CV) mortality in newly treated patients with type 2 diabetes according to levels of insulin exposure. Methods: Using the administrative databases of Saskatchewan Health, 12272 new users of oral antidiabetic therapy were identified between 1991 and 1996 and grouped according to cumulative insulin exposure based on total insulin dispensations per year: no exposure (reference group); low exposure (0 to <3); moderate exposure (3 to <12) and high exposure (≥12). Time‐varying multivariable Cox proportional hazards models were used to examine the relationship between insulin exposure and all‐cause, CV‐related and non‐vascular mortality after adjustment for demographics, medications and comorbidities. Results: Average age was 65 (s.d. 13.9) years, 45% were female, and mean follow‐up was 5.1 (s.d. 2.2) years. In total, 1443 (12%) subjects started insulin, and 2681 (22%) deaths occurred. The highest mortality rates were in the high exposure group; 95 deaths/1000 person‐years compared with 40 deaths/1000 person‐years in the no exposure group [unadjusted hazard ratio (HR): 2.32; 95% confidence interval (CI): 1.96–2.73]. After adjustment, we observed a graded risk of mortality associated with increasing exposure to insulin: low exposure [adjusted HR (aHR): 1.75; 95% CI: 1.24–2.47], moderate exposure (aHR: 2.18; 1.82–2.60) and high exposure (aHR: 2.79; 2.36–3.30); p = 0.005 for trend. Analyses restricted to CV‐related (p = 0.042 for trend) and non‐vascular (p = 0.004 for trend) mortality showed virtually identical results. Conclusions: We observed a significant and graded association between mortality risk and insulin exposure level in an inception cohort of patients with type 2 diabetes that persisted despite multivariable adjustment.     

Long‐term morbidity and mortality in a Canadian post‐transfusion hepatitis C cohort: Over 15 years of follow‐up

The Federal Government of Canada established a $1.1 billion compensation programme in 1999 to support individuals who acquired hepatitis C virus (HCV) through blood products between January 1986 and July 1990. We aimed to describe the morbidity and mortality of this unique post‐transfusion cohort (n = 4550) followed for over 15 years from 2000 to 2016. The age‐standardized mortality rates were compared with that of the Canadian general population and HCV cohorts from other countries. We evaluated all‐cause mortality using Kaplan‐Meier survival curves and HCV‐related and unrelated mortality using competing risk models. The age‐standardized all‐cause and HCV‐related mortality rates per 10 000 person‐years were 127 (95% CI: 117‐138) and 76 (95% CI: 69‐85) for males, and 77 (95% CI: 69‐87) and 43 (95% CI: 37‐51) for females, respectively. The risk of death of the post‐transfusion cohort was almost twice as high as the Canadian general population (rate ratio = 1.8; 95% CI: 1.7‐1.9). All‐cause, HCV‐related and HCV‐unrelated mortality were 20%, 12% and 8%, respectively at 15 years of follow‐up. By comparison, HCV‐related mortality rates per 10 000 person‐years for population‐based HCV cohorts varied from 18 and 11 in Australia to 65 and 43 in Scotland for males and females, respectively. We reported long‐term follow‐up data for the largest post‐transfusion cohort in the literature. The all‐cause mortality rates were markedly higher than that of the Canadian general population. We also showed that HCV‐related mortality were greater compared to other HCV cohorts. This suggests that continued efforts to identify and treat post‐transfusion HCV are warranted.     

Neighbourhood deprivation and excess coronary heart disease mortality and hospital admissions in Plymouth, UK: an ecological study

BACKGROUND: Among primary coronary heart disease (CHD) risk factors, certain socioeconomic characteristics of individuals and living environments appear to play a central role.The objective of this study was to assess the burden of neighbourhood deprivation-associated excess in mortality and hospital admission from CHD in Plymouth. METHODS: A small area ecological study using indices of neighbourhood deprivation and coronary heart disease mortality and hospital admission data aggregated for 1991-2003 for CHD mortality and for 1997-2004 for CHD hospital admission. Locally defined community areas (n = 43) were classified according to the Townsend index, measuring material deprivation. RESULTS: CHD mortality and hospital admission increased with Townsend deprivation score in all ages and gender groups.The age-adjusted deprivation-associated excess CHD hospital admission was 15.4% in men and 27.9% in women higher for most compared to the least deprived group.The age-adjusted deprivation-associated excess CHD mortality was 31.5% and 18.9% for men and women, respectively. Excess mortality in the 13-year period studied accounted for more than 1380 and 670 deaths for men and women. Excess hospital admissions in the 7-year period studied accounted for more than 966 and 769 hospital admissions for men and women. A larger proportion of excess CHD deaths were found among men while excess CHD hospital admissions were found among women. The most deprived areas showed the highest mortality and hospital admission risk. CONCLUSION: Despite the existence of a system of universal health care, inequalities in CHD mortality and hospital admission persist and need to be taken into account when implementing intervention programmes.     

Alcohol consumption and mortality and hospital admissions in men from the Midspan Collaborative cohort study

Aims To investigate the relationships between alcohol consumption and mortality and morbidity risk by specific causes. Design Prospective cohort study. Setting Twenty‐seven work‐places in West and Central Scotland. Participants A total of 6000 men aged 21–64 years at screening in 1970–1973, median follow‐up 29 years. Measurements Relative rates, using Cox's proportional hazard models, by weekly reported units of alcohol consumption for all cause, coronary heart disease (CHD), stroke, respiratory, digestive, liver disease and alcohol‐related causes of mortality and for specific causes of acute hospital admissions. Findings Mortality risk was increased for men drinking 15–21 or more units per week for all causes, stroke, liver disease and alcohol‐related causes. For respiratory mortality, drinkers of 35 or more units had double the risk compared to non‐drinkers. CHD mortality showed increasing trends with consumption when adjusted for age and after full adjustment showed no clear patterns, although the 8–14 units group had a lower risk than non‐drinkers [relative rate 0.81 (0.68–0.97)]. Hospital admissions had similar patterns to mortality for stroke and liver disease. Increased risk began at 8–14 units for alcohol‐related admissions, and at 15–21 units for respiratory admissions. Non‐drinkers had higher risks of having a CHD admission than drinkers and there were decreasing trends with increasing consumption (P = 0.019). Conclusions Consumption of 15–21 units per week and over was associated with increased mortality from most causes and increased risk of hospital admissions from stroke, liver disease and respiratory diseases. Alcohol‐related admissions were raised from 8 to 14 units. Alcohol use may have been under‐reported in our study, but it was similar to other studies of the time. The apparent protective effect of alcohol with CHD admissions could be due partly to detrimental effects of heavy drinking causing sudden deaths. The associations, including that with respiratory disease, may arise from inadequate adjustment for confounding by other factors such as smoking.