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Introduction: The Zio® XT continuous ambulatory electrocardiographic monitor (Zio) contains an accelerometer that can help quantify an individual's physical activity in the free-living environment. Purpose: (1) To estimate activity cut-points to estimate daily time spent performing very light, light, or moderate to vigorous physical activity (VLIPA, LIPA, MVPA) for the Zio accelerometer. (2) To describe how Zio's 24-h wear protocol affects estimates of daily MVPA relative to a waist-worn accelerometer's waking-wear protocol. Methods: Three hundred eighty one participants from the Atherosclerosis Risk in Communities (ARIC) study wore a waist-mounted ActiGraph GT3X (except while sleeping or water-based activities) and a Zio (24-h) simultaneously for three to seven days. For each person-minute, physical activity was summarized as the Mean Amplitude Deviation (MAD) for the Zio and Vector Magnitude Counts (VMC) for the GT3X. Cut points previously used in ARIC were mapped from GT3X VMC to Zio MAD using a conditional two-sample quantile–quantile approach. Results: Evenson VMC cut-points for the GT3X (VLIPA≥76, LIPA≥903, MVPA≥2075 counts/min) were mapped to MAD for Zio (9.04, 28.2, and 58.1 mili-g). Daily hours spent in each intensity category were each strongly correlated (ICC > 0.7) between summaries produced by Zio and GT3X when restricting estimates to overlapping wear time. Zio and GT3X-estimated MVPA had high agreement (ICC = 0.77) when using device-specific wear time, but Zio measured one hour more of daily LIPA and VLIPA (95% CI = 0.83, 1.07 hrs/day). Conclusions: We recommend the use of our cut-points for clinical research with Zio accelerometry in populations of older adults. [ABSTRACT FROM AUTHOR]

Joint models linking longitudinal biomarkers or recurrent event processes with a terminal event, for example, mortality, have been studied extensively. Motivated by studies of recurrent delirium events in patients receiving care in an intensive care unit (ICU), we devise a joint model for a recurrent event process and multiple terminal events. Being discharged alive from the ICU or experiencing mortality may be associated with a patient's hazard of delirium, violating the assumption of independent censoring. Moreover, the direction of the association between the hazards of delirium and mortality may be opposite of the direction of association between the hazards of delirium and ICU discharge. Hence treating either terminal event as independent censoring may bias inferences. We propose a competing joint model that uses a latent frailty to link a patient's recurrent and competing terminal event processes. We fit our model to data from a completed placebo‐controlled clinical trial, which studied whether Haloperidol could prevent death and delirium among ICU patients. The clinical trial served as a foundation for a simulation study, in which we evaluate the properties, for example, bias and confidence interval coverage, of the competing joint model. As part of the simulation study, we demonstrate the shortcomings of using a joint model with a recurrent delirium process and a single terminal event to study delirium in the ICU. Lastly, we discuss limitations and possible extensions for the competing joint model. The competing joint model has been added to frailtypack, an R package for fitting an assortment of joint models. [ABSTRACT FROM AUTHOR]

Background: People living with human immunodeficiency virus (HIV+) have greater risk for sudden arrhythmic death than HIV-uninfected (HIV-) individuals. HIV-associated abnormal cardiac repolarization may contribute to this risk. We investigated whether HIV serostatus is associated with ventricular repolarization lability by using the QT variability index (QTVI), defined as a log measure of QT-interval variance indexed to heart rate variance.Methods: We studied 1123 men (589 HIV+ and 534 HIV-) from MACS (Multicenter AIDS Cohort Study), using the ZioXT ambulatory electrocardiography patch. Beat-to-beat analysis of up to 4 full days of electrocardiographic data per participant was performed using an automated algorithm (median analyzed duration [quartile 1-quartile 3]: 78.3 [66.3-83.0] hours/person). QTVI was modeled using linear mixed-effects models adjusted for demographics, cardiac risk factors, and HIV-related and inflammatory biomarkers.Results: Mean (SD) age was 60.1 (11.9) years among HIV- and 54.2 (11.2) years among HIV+ participants (P<0.001), 83% of whom had undetectable (<20 copies/mL) HIV-1 viral load (VL). In comparison with HIV- men, HIV+ men had higher QTVI (adjusted difference of +0.077 [95% CI, +0.032 to +0.123]). The magnitude of this association depended on the degree of viremia, such that in HIV+ men with undetectable VL, adjusted QTVI was +0.064 (95% CI, +0.017 to +0.111) higher than in HIV- men, whereas, in HIV+ men with detectable VL, adjusted QTVI was higher by +0.150 (95% CI, 0.072-0.228) than in HIV- referents. Analysis of QTVI subcomponents showed that HIV+ men had: (1) lower heart rate variability irrespective of VL status, and (2) higher QT variability if they had detectable, but not with undetectable, VL, in comparison with HIV- men. Higher levels of C-reactive protein, interleukin-6, intercellular adhesion molecule-1, soluble tumor necrosis factor receptor 2, and soluble cluster of differentiation-163 (borderline), were associated with higher QTVI and partially attenuated the association with HIV serostatus.Conclusions: HIV+ men have greater beat-to-beat variability in QT interval (QTVI) than HIV- men, especially in the setting of HIV viremia and heightened inflammation. Among HIV+ men, higher QTVI suggests ventricular repolarization lability, which can increase susceptibility to arrhythmias, whereas lower heart rate variability signals a component of autonomic dysfunction. [ABSTRACT FROM AUTHOR]