Driving Habits and Reaction Times on a Driving Simulation in Older Drivers With Chronic Heart Failure.

BACKGROUND: Judgement and reaction times during complex tasks like driving may be impaired in older adults with chronic heart failure (HF). This study sought to report the driving habits and reaction times of older patients with HF in a specially designed urban driving simulation. METHODS AND RESULTS: We conducted a prospective observational study in HF patients and controls. Patients in both groups underwent cognitive testing and screening for depression. Current drivers undertook a questionnaire regarding driving habits followed by an urban road driving simulation consisting of 3 laps. Five separate hazards appeared in the third lap without warning. Reaction times and stopping distances to the hazards were calculated. Of 247 patients with HF approached for the study, 124 had already voluntarily stopped driving owing to HF (n = 92) or other medical conditions (n = 32), 60 had never had a license, and 32 declined to participate. Of the 74 controls approached, 1 was not currently driving owing to a medical condition and 46 declined to participate. Patients in both groups had similar levels of cognitive function, mood and driving habits. 30 patients with HF (mean age, 74 ± 5 years; median NT-proBNP 1510 pg/mL [interquartile range (IQR), 546-3084 pg/L]) and 26 controls (mean age, 73 ± 5 years; median NT-proBNP 135 pg/mL [IQR, 73-182 pg/L]) completed the simulation. During lap 3, there was no difference in the driving speed between patients (mean 22.0 ± 4.5 mph) and controls (mean 21.7 ± 3.3 mph; P = .80). Patients had longer reaction times (median, 1.10 seconds; IQR, 0.98-1.30 seconds) than controls (median, 0.96 seconds; IQR, 0.83-1.10 seconds; P = .02), but there was no difference in stopping distances (patients: median, 43.9 m [IQR, 32.2-49.5 m]; controls: median, 38.1 m [IQR, 32.3-48.8 m]; P = .31). CONCLUSIONS: Many older adults with HF no longer drive. Those who continue to drive seem to be safe to drive on simulated urban roads.

Randomised controlled trial of video clips and interactive games to improve vision in children with amblyopia using the I-BiT system.

BACKGROUND: Traditional treatment of amblyopia involves either wearing a patch or atropine penalisation of the better eye. A new treatment is being developed on the basis of virtual reality technology allowing either DVD footage or computer games which present a common background to both eyes and the foreground, containing the imagery of interest, only to the amblyopic eye. METHODS: A randomised control trial was performed on patients with amblyopia aged 4-8 years with three arms. All three arms had dichoptic stimulation using shutter glass technology. One arm had DVD footage shown to the amblyopic eye and common background to both, the second used a modified shooter game, Nux, with sprite and targets presented to the amblyopic eye (and background to both) while the third arm had both background and foreground presented to both eyes (non-interactive binocular treatment (non-I-BiT) games). RESULTS: Seventy-five patients were randomised; 67 were residual amblyopes and 70 had an associated strabismus. The visual acuity improved in all three arms by approximately 0.07 logMAR in the amblyopic eye at 6 weeks. There was no difference between I-BiT DVD and non-I-BiT games compared with I-BiT games (stated primary outcome) in terms of gain in vision. CONCLUSIONS: There was a modest vision improvement in all three arms. Treatment was well tolerated and safe. There was no difference between the three treatments in terms of primary stated outcomes but treatment duration was short and the high proportion of previously treated amblyopia and strabismic amblyopia disadvantaged dichoptic stimulation treatment. TRIAL REGISTRATION NUMBER: NCT01702727, results.

Systemic arterial pressure wave reflections during acute hemorrhage.

OBJECTIVE: To determine the effects of hemorrhage on wave-reflection-induced systolic pressure augmentation in the aorta. DESIGN: Randomized, controlled laboratory experiment. SETTING: University research laboratory. SUBJECTS: Twenty-five anesthetized pigs randomized to surgical controls (n = 7), hemorrhage (n = 9, H), and hemorrhage with reinfusion (n = 9, HR). INTERVENTIONS: Hemorrhage of 1 mL/kg/min over 20 mins followed by observation (H) or reinfusion (HR) of shed blood. MEASUREMENTS AND MAIN RESULTS: High-fidelity systemic arterial pressure waveforms, from ascending aorta to femoral artery, were transduced and archived digitally using intravascular semiconductor catheter-tipped pressure transducers. Wave-reflection-induced systolic pressure augmentation was determined using the augmentation index in the ascending aorta (AIaa) and distal descending aorta (AIda). Pulse wave velocity, wave travel times, and lumped pressure wave reflection sites were also calculated. AI values were positive at baseline with greater decreases in AIda compared with AIaa observed following hemorrhage, with negative values achieved for AIda alone. AI returned to control values following reinfusion. Lumped reflection site positions and pressure contour maps suggested that a single lumped reflection site (lower abdomen/pelvis) at baseline was replaced by two discrete sites (upper abdomen and pelvis) following hemorrhage, which only recovered following reinfusion. Hemorrhage was associated with hemodynamic conditions that favored late return of wave reflection from the trunk and with the absence of significant changes in systemic vascular resistance. CONCLUSIONS: Hemorrhage-induced early return of pressure wave reflection from the abdominal vasculature is associated with systolic pressure augmentation in the ascending aorta and has the potential to worsen afterload conditions and decrease coronary artery perfusion and cardiac performance. Hemorrhage-induced splanchnic vasoconstriction causing pressure wave reflection may explain these loading conditions in the ascending aorta, and systolic pressure augmentation may be a more useful guide to left ventricular afterload than systemic vascular resistance.