Hearing Loss Treatment in Older Adults With Cognitive Impairment: A Systematic Review.

Purpose: The purpose of this systematic review was to assess studies of treating hearing loss in older adults with cognitive impairment. Of interest to this review is identifying clinical adaptations that may be used to tailor hearing loss treatment to older adults with cognitive impairment in order to better serve this vulnerable population. Method: A systematic search with controlled vocabulary and key word terms was applied to PubMed, the Cochrane Library, Embase, CINAHL, and PsycINFO. Search concepts included terms related to hearing loss and cognitive impairment. The overall search resulted in 4,945 unique references, 50 of which were eligible for full-text review and 13 of which were included in the final review. Included manuscripts were categorized according to the American Speech-Language-Hearing Association's levels of evidence and the National Institutes of Health Quality Assessment Tools. Results: Only 1 study implemented a randomized controlled trial design to assess cognitive function and behavioral symptoms after treatment with hearing aids. Other quasiexperimental studies evaluated dementia-related symptoms and/or auditory function after treating hearing loss in pre/post research designs. Finally, evidence from case studies suggested that hearing loss treatment is feasible, reduces stressful communication for caregivers, and improves dementia-related behavior problems. Conclusion: Based on the systematic review, evidence suggests that treating hearing loss in persons with cognitive impairment can have benefits to communication and quality of life. Because of the quasi- and nonexperimental nature of most of the evidence found in this review, further studies are necessary to understand the effect of treatment in the context of a variable and progressive disease.

Physiological roles of the transient outward current Ito in normal and diseased hearts.

The Ca(2+)-independent transient outward K(+) current (I(to)) plays a critical role in underlying phase 1 of repolarization of the cardiac action potential and, as a result, is central to modulating excitation-contraction coupling and propensity for arrhythmia. Additionally, I(to) and its molecular constituents are consistently reduced in cardiac hypertrophy and heart failure. In this review, we discuss the physiological role of I(to) as well as the molecular basis of this current in human and canine hearts, in which I(to) has been thoroughly studied. In particular, we discuss the role of Ito; in the action potential and the mechanisms by which I(to) modulates excitation-contraction coupling. We also describe the effects of mutations in the subunits constituting the Ito channel as well as the role of I(to) in the failing myocardium. Finally, we review pharmacological modulation of I(to) and discuss the evidence supporting the hypothesis that restoration of I(to) in the setting of heart failure may be therapeutically beneficial by enhancing excitation-contraction coupling and cardiac function.

Loss of K+ currents in heart failure is accentuated in KChIP2 deficient mice.

INTRODUCTION: KV 4 together with KV Channel-Interacting Protein 2 (KChIP2) mediate the fast recovering transient outward potassium current (I(to,f)) in the heart. KChIP2 is downregulated in human heart failure (HF), potentially underlying the loss of I(to,f). We investigated remodeling associated with HF hypothesizing that KChIP2 plays a central role in the modulation of outward K(+) currents in HF. METHODS AND RESULTS: HF was induced by aortic banding in wild-type (WT) and KChIP2 deficient (KChIP2(-/-)) mice, evaluated by echocardiography. Action potentials were measured by floating microelectrodes in intact hearts. Ventricular cardiomyocytes were isolated and whole-cell currents were recorded by patch clamp. Left ventricular action potentials in KChIP2(-/-) mice were prolonged in a rate dependent manner, consistent with patch-clamp data showing loss of a fast recovering outward K(+) current and upregulation of the slow recovering I(to,s) and I(Kur). HF decreased all outward K(+) currents in WT mice and did not change the relative contribution of I(to,f) in WT mice. Compared to WT HF, KChIP2(-/-) HF had a larger reduction of K(+) -current density. However, the relative APD prolongation caused by HF was shorter for KChIP2(-/-) compared with WT, and the APs of the 2 HF mouse types were indistinguishable. CONCLUSION: I(to,f) is just one of many K(+) currents being downregulated in murine HF. The downregulation of repolarizing currents in HF is accentuated in KChIP2(-/-) mice. However, the prolongation of APs associated with HF is less in KChIP2(-/-) compared to WT, suggesting other compensatory mechanism(s) in the KChIP2(-/-) mouse.