Effectiveness of a National Transitional Care Program in Reducing Acute Care Use

This study evaluated the effectiveness of a national transitional care program for elderly adults with complex care needs and limited social support. The Aged Care Transition (ACTION) Program was designed to improve coordination and continuity of care and reduce rehospitalizations and visits to emergency departments (EDs). Dedicated care coordinators provided coaching to help individuals and families understand the individuals' conditions, effectively articulate their preferences, and enable self‐management and care planning. Participants were individuals aged 65 and older hospitalized and enrolled from five public general hospitals in Singapore between February 2009 and July 2010 (N = 4,132). The coordinators worked with participants during hospitalization and followed up with telephone calls and home visits for 1 to 2 months after discharge and coordinated placements with appropriate community service providers. Unplanned rehospitalization and ED visit (up to 6 months after discharge) rates were compared with those of a comparator group of individuals who did not receive care coordination using propensity score‐based weighting. Participant and caregiver surveys on quality of life and self‐rated health were also administered. Recipients of the ACTION program had fewer unplanned rehospitalizations and ED visits after discharge. Propensity score–adjusted odds ratios of participants versus control for number of unplanned rehospitalization and ED visits were 0.5 (95% confidence interval (CI) = 0.5–0.6) and 0.81 (95% CI = 0.72–0.90) 30 days after discharge and 0.6 (95% CI = 0.6–0.7) and 0.90 (95% CI = 0.82–0.99) 180 days after discharge. Quality of life and self‐rated health were better 4 to 6 weeks after discharge than 1 week after discharge. These findings confirm the effectiveness of the ACTION program in improving the transition of vulnerable older adults from hospital to community. Such transitional care should be considered as an integral part of care integration.     

Amiodarone-associated optic neuropathy: a critical review

Although amiodarone is the most commonly prescribed anti-arrhythmic drug, its use is limited by serious toxicities, including optic neuropathy. Current reports of amiodarone-associated optic neuropathy identified from the Food and Drug Administration's Adverse Event Reporting System and published case reports were reviewed. A total of 296 reports were identified: 214 from the Adverse Event Reporting System, 59 from published case reports, and 23 from adverse events reports for patients enrolled in clinical trials. Mean duration of amiodarone therapy before vision loss was 9 months (range 1-84 months). Insidious onset of amiodarone-associated optic neuropathy (44%) was the most common presentation, and nearly one third were asymptomatic. Optic disk edema was present in 85% of cases. Following drug cessation, 58% had improved visual acuity, 21% were unchanged, and 21% had further decreased visual acuity. Legal blindness (<20/200) was noted in at least one eye in 20% of cases. Close ophthalmologic surveillance of patients during the tenure of amiodarone administration is warranted.     

Reduced memory in fat mass and obesity‐associated allele carriers among older adults with cardiovascular disease

Background: Much attention has been paid to the prevalence and predisposition of the fat mass and obesity‐associated (FTO) gene to obesity, although only a few studies have characterized the extent to which this affects cognitive function. This study examined differences between risk allele carriers (i.e. FTO‐AC/AA) and non‐carriers (i.e. FTO‐CC) on indices of attention/executive function/psychomotor speed, memory, language, and visual‐spatial ability in a sample of older patients with cardiovascular disease. Methods: We recruited 120 older adults from an outpatient cardiology clinic who underwent blood draw and completed neuropsychological testing. Participants were classified into two groups: one for those who were homozygous for the non‐risk‐conferring allele (i.e. FTO‐CC) (n= 49) and the other for those who had at least one copy of the obesity risk‐conferring A allele (i.e. FTO‐AC/AA) (n= 71). Results: Mancova analyses adjusting for age and years of education revealed the FTO‐AC/AA group performed significantly worse on indices of memory (λ= 0.94, F(2, 115) = 3.58, P= 0.03, partial η²= 0.06). Follow‐up tests revealed a significant effect for the FTO‐AC/AA group, relative to the non‐carrier group, on encoding (i.e. California Verbal Learning Test Total Learning) and California Verbal Learning Test long‐delay free recall (P < 0.05). No such differences between FTO carriers and non‐carriers emerged on tests of attention/executive function/psychomotor speed, language, or visual‐spatial ability (P > 0.05 for all). Conclusions: These findings suggest that the FTO risk allele is associated with reduced memory performance, particularly on aspects of memory encoding and delayed recall. To elucidate underlying mechanisms, these findings will need to be replicated in larger samples that utilize neuroimaging.     

Impairments in hippocampal synaptic plasticity following prenatal ethanol exposure are dependent on glutathione levels

Previous studies from our laboratory have shown that prenatal ethanol exposure (PNEE) causes a significant deficit in synaptic plasticity, namely long‐term potentiation (LTP), in the dentate gyrus (DG) region of the hippocampus of male rats. PNEE has also been shown to induce an increase in oxidative stress and a reduction in antioxidant capacity in the brains of both male and female animals. In this study the interaction between LTP and the major antioxidant in the brain, glutathione (GSH), is examined. We show that depletion of the intracellular reserves of GSH with diethyl maleate (DEM) reduces LTP in control male, but not female animals, mirroring the effects of PNEE. Furthermore, treatment of PNEE animals with N‐acetyl cysteine (NAC), a cysteine donor for the synthesis of GSH, increases GSH levels in the hippocampus and completely restores the deficits in LTP in PNEE males. These results indicate that in males GSH plays a major role in regulating LTP, and that PNEE may cause reductions in LTP by reducing the intracellular pool of this endogenous antioxidant. © 2013 Wiley Periodicals, Inc.