No abstract

Research suggests stress is a risk factor for cardiovascular disease (CVD), 1-4 but the underlying mechanisms remain unclear. Mental stress activates the sympathetic nervous system, 5 causing a constellation of adverse cardiovascular effects, including increased blood pressure, heart rate, and endothelial dysfunction. 6 One potential pathway through which chronic exposure to psychosocial stressors are hypothesized to influence CVD risk is through injury to the endothelial lining of blood vessels due to sustained and repeated activation of the sympathetic nervous system. 7 Endothelial dysfunction plays a critical role in the initiation and progression of atherosclerosis, 8 and thus, may be a major pathway linking chronic stress and CVD.Studies have shown that acute exposure to a mental stressor is significantly associated with prolonged endothelial dysfunction, 6,9 but few studies have examined the impact of chronic stress and these studies have been in ethnically homogeneous populations. A national study of non-Hispanic Whites found that chronic exposure to discrimination predicted higher levels of circulating endothelial-leukocyte adhesion molecule-1 (E-selectin), an indicator of endothelial dysfunction, in men but not women. 10 Two studies of caregivers (>80% non-Hispanic White) found that global stress and caregiver stress were each associated with lower brachial artery flow-mediated dilation (FMD). 11,12 In this study, we examined associations of chronic stress with 3 markers of endothelial dysfunction in a multiethnic population of middle-and older-age adults. Brachial artery FMD is a noninvasive, commonly used method to assess endothelial function of the peripheral conduit artery. With this method, reduced artery dilation is suggestive of poorer endothelial function. We also included 2 serological biomarkers of endothelial dysfunction: intercellular adhesion molecule-1 (ICAM-1) and E-selectin. These cellular adhesion molecules are expressed on the surfaces of endothelial cells as part of the inflammatory response to endothelial damage. We hypothesized that higher chronic stress would be associated with lower FMD, higher ICAM-1, and higher E-selectin levels. Given previous heterogeneous findings by gender, 10 and the dearth of studies in multiethnic populations, we also examined whether associations varied by race/ ethnicity or gender. Chronic Stress and Endothelial BACKGROUNDEndothelial dysfunction may represent an important link between chronic stress and cardiovascular disease (CVD) risk. However, few studies have examined the impact of chronic stress on endothelial dysfunction. The purpose of this study was to examine whether chronic stress was associated with flow-mediated dilation (FMD) and 2 biomarkers of endothelial dysfunction (intercellular adhesion molecule-1 (ICAM-1) and E-selectin) in a multiethnic sample of adults (ages 45-84 years).

Central arterial stiffness is associated with incident hypertension and negative cardiovascular outcomes. Obese individuals have higher central blood pressure (BP) and central arterial stiffness than their normal‐weight counterparts, but it is unclear whether obesity also affects hemodynamics and central arterial stiffness after maximal exercise. We evaluated central hemodynamics and arterial stiffness during recovery from acute maximal aerobic exercise in obese and normal‐weight individuals. Forty‐six normal‐weight and twenty‐one obese individuals underwent measurements of central BP and central arterial stiffness at rest and 15 and 30 min following acute maximal exercise. Central BP and normalized augmentation index (AIx@75) were derived from radial artery applanation tonometry, and central arterial stiffness was obtained via carotid‐femoral pulse wave velocity (cPWV) and corrected for central mean arterial pressure (cPWV/cMAP). Central arterial stiffness increased in obese individuals but decreased in normal‐weight individuals following acute maximal exercise, after adjusting for fitness. Obese individuals also exhibited an overall higher central BP (P < 0.05), with no exercise effect. The increase in heart rate was greater in obese versus normal‐weight individuals following exercise (P < 0.05), but there was no group differences or exercise effect for AIx@75. In conclusion, obese (but not normal‐weight) individuals increased central arterial stiffness following acute maximal exercise. An assessment of arterial stiffness response to acute exercise may serve a useful detection tool for subclinical vascular dysfunction.

Inflammation is associated with greater risk of cardiovascular events and reduced vascular function with ageing. Higher cardiorespiratory fitness is associated with lower risk of cardiovascular events and better vascular function. We evaluated the role of fitness in the vascular response to acute inflammation in 26 younger adults (YA) and 62 older adults (OA). We used an influenza vaccine to induce acute inflammation. Blood pressure, flow-mediated dilatation (FMD), augmentation index, carotid elastic modulus and inflammatory markers were measured before and 24 h after vaccination. Peak oxygen uptake was measured via a treadmill test. 'Fit' was defined as a peak oxygen uptake greater than the age- and sex-determined 50th percentile according to the American College of Sports Medicine. An interaction effect existed for the FMD response during acute inflammation (P < 0.05). The YA (low fit, from 11.5 ± 1.8 to 9.2 ± 1.3%; moderately fit, from 11.9 ± 0.8 to 9.0 ± 0.8%) and moderately fit OA (from 7.5 ± 1.0 to 3.9 ± 0.8%) had similar reductions in FMD at 24 h (P < 0.05). Low-fit OA did not reduce FMD at 24 h (from 5.5 ± 0.4 to 5.2 ± 0.5%, P > 0.05). The reduction in FMD in YA was similar between fitness groups (P > 0.05). All groups had similar reductions in mean arterial pressure and increases in inflammatory markers. The augmentation index and carotid elastic modulus did not change during acute inflammation. In conclusion, in OA, higher fitness is associated with a greater decrease in endothelial function during acute inflammation, and this response is similar to that of young adults. This suggests that moderately fit OA may maintain vascular reactivity in response to stress, indicating preserved vascular function in moderately fit versus low-fit OA.