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Objective: To estimate the incremental effects on cost and quality of life of cardiac rehabilitation after an acute coronary syndrome. Design: Open randomised controlled trial with 1 year's follow‐up. Analysis was on an intention‐to‐treat basis. Setting: Two tertiary hospitals in Sydney. Intervention: 18 sessions of comprehensive exercise‐based outpatient cardiac rehabilitation or conventional care as provided by the treating doctor. Participants: 113 patients aged 41–75 years who were self‐caring and literate in English. Patients with uncompensated heart failure, uncontrolled arrhythmias, severe and symptomatic aortic stenosis or physical impairment were excluded. Main outcome measures: Costs (hospitalisations, medication use, outpatient visits, investigations, and personal expenses); and measures of quality of life. Incremental cost per quality‐adjusted life year (QALY) saved at 1 year (this estimate combines within‐study utility effects with reported 1‐year risk of survival and treatment effects of rehabilitation on mortality). Sensitivity analyses around a base case estimate included alternative assumptions of no treatment effect on survival, 3 years of treatment effect on survival and variations in utility. Results: The estimated incremental cost per QALY saved for rehabilitation relative to standard care was $42 535 when modelling included the reported treatment effect on survival. This increased to $70 580 per QALY saved if treatment effect on survival was not included. The results were sensitive to variations in utility and ranged from $19 685 per QALY saved to rehabilitation not being cost‐effective. Conclusions: The effects on quality of life tend to reinforce treatment advantages on survival for patients having postdischarge rehabilitation after an acute coronary syndrome. The estimated base case incremental cost per QALY saved is consistent with those historically accepted by decision making authorities such as the Pharmaceutical Benefits Advisory Committee.

ObjectiveTo help determine whether midlife obesity is a cause of dementia and whether low body mass index (BMI), low caloric intake, and physical inactivity are causes or merely consequences of the gradual onset of dementia by recording these factors early in a large 20-year prospective study and relating them to dementia detection rates separately during follow-up periods of <5, 5 to 9, 10 to 14, and 15+ years.MethodsA total of 1,136,846 UK women, mean age 56 (SD 5) years, were recruited in 1996 to 2001 and asked about height, weight, caloric intake, and inactivity. They were followed up until 2017 by electronic linkage to National Health Service records, detecting hospital admissions with mention of dementia. Cox regression yielded adjusted rate ratios (RRs) for first dementia detection during particular follow-up periods.ResultsFifteen years after the baseline survey, only 1% were lost to follow-up, and 89% remained alive with no detected dementia, of whom 18,695 had dementia detected later, at a mean age of 77 (SD 4) years. Dementia detection during years 15+ was associated with baseline obesity (BMI 30+ vs 20–24 kg/m2: RR 1.21, 95% confidence interval 1.16–1.26, p < 0.0001) but not clearly with low BMI, low caloric intake, or inactivity at baseline. The latter 3 factors were associated with increased dementia rates during the first decade, but these associations weakened substantially over time, approaching null after 15 years.ConclusionsMidlife obesity may well be a cause of dementia. In contrast, behavioral changes due to preclinical disease could largely or wholly account for associations of low BMI, low caloric intake, and inactivity with dementia detection during the first decade of follow-up.