👤 Auris Browne

To investigate the moderating role of physical activity intensity and sedentary break patterns on the association between sedentary time (ST) and cardiometabolic risk in older adults. This cross-sectional study included 248 community-dwelling older adults without major cardiovascular diseases (66.0 ± 4.6 years; 78% female). Physical activity and ST were measured using a hip-worn accelerometer over seven consecutive days. Cardiometabolic disease risk was assessed using a sex-specific continuous metabolic syndrome score (cMetS). ST was entered as the explanatory variable for cMetS, while moderate-to-vigorous physical activity (MVPA), light physical activity (LPA), and the number of short (1-5 min) and long (>5 min) sedentary breaks were tested as moderators. All analyses were adjusted for traditional cardiometabolic risk factors and accelerometer wear time. MVPA (β = -0.005, p = 0.046), LPA (β = -0.030, p = 0.050), short (β = -0.003, p = 0.070) and long (β = -0.010, p = 0.011) sedentary breaks moderated the association between ST and cMetS. The Johnson-Neyman technique revealed that the association between ST and cMetS became non-significant (p ≥ 0.05) at thresholds of MVPA ≥ 19 min/day, LPA ≥ 5.9 h/day, short breaks ≥ 87/day, and long breaks ≥ 10/day. Our findings suggest that specific thresholds of MVPA and LPA, as well as short and long sedentary breaks may offset the deleterious association between ST and cardiometabolic risk in older adults. Show less

The roles of lipoprotein(a) [Lp(a)] and related oxidized phospholipids (OxPLs) in the development and progression of coronary disease is known, but their influence on extracoronary vascular disease is not well-established. We sought to evaluate associations between Lp(a), OxPL apolipoprotein B (OxPL-apoB), and apolipoprotein(a) (OxPL-apo(a)) with angiographic extracoronary vascular disease and incident major adverse limb events (MALEs). Four hundred forty-six participants who underwent coronary and/or peripheral angiography were followed up for a median of 3.7 years. Lp(a) and OxPLs were measured before angiography. Elevated Lp(a) was defined as ≥150 nmol/L. Elevated OxPL-apoB and OxPL-apo(a) were defined as greater than or equal to the 75th percentile (OxPL-apoB ≥8.2 nmol/L and OxPL-apo(a) ≥35.8 nmol/L, respectively). Elevated Lp(a) had a stronger association with the presence of extracoronary vascular disease compared to OxPLs and was minimally improved with the addition of OxPLs in multivariable models. Compared to participants with normal Lp(a) and OxPL concentrations, participants with elevated Lp(a) levels were twice as likely to experience a MALE (odds ratio: 2.14, 95% confidence interval: 1.03, 4.44), and the strength of the association as well as the C statistic of 0.82 was largely unchanged with the addition of OxPL-apoB and OxPL-apo(a). Elevated Lp(a) and OxPLs are risk factors for progression and complications of extracoronary vascular disease. However, the addition of OxPLs to Lp(a) does not provide additional information about risk of extracoronary vascular disease. Therefore, Lp(a) alone captures the risk profile of Lp(a), OxPL-apoB, and OxPL-apo(a) in the development and progression of atherosclerotic plaque in peripheral arteries. Show less