Opioid prescription and risk of atrial fibrillation in younger veterans.

BACKGROUND: Opioids may play a part in the development of atrial fibrillation (AF). Understanding the relationship between opioid exposure and AF can help providers better assess the risk and benefits of prescribing opioids. OBJECTIVE: To assess the incidence of AF as a function of prescribed opioids and opioid type. DESIGN: We performed unadjusted and adjusted time-updated Cox regressions to assess the association between opioid exposure and incident AF. PARTICIPANTS: The national study sample was comprised of Veterans enrolled in the Veterans Health Administration (VHA) who served in support of post-9/11 operations. MAIN MEASURES: The main predictor of interest was prescription opioid exposure, which was treated as a time-dependent variable. The first was any opioid exposure (yes/no). Secondary was opioid type. The outcome, incident AF, was identified through ICD-9-CM diagnostic codes at any primary care visit after the baseline period. KEY RESULTS: A total of 609,763 veterans (mean age: 34 years and 13.24% female) were included in our study. Median follow-up time was 4.8 years. Within this cohort, 124,395 veterans (20.40%) were prescribed an opioid. A total of 1,455 Veterans (0.24%) were diagnosed with AF. In adjusted time-updated Cox regressions, the risk of incident AF was higher in the veterans prescribed opioids (hazard ratio [HR]: 1.47; 95% confidence interval [CI]: 1.38-1.57). In adjusted time-updated Cox regressions, both immunomodulating and nonimmunomodulating opioid type was associated with increased risk of incident AF (HR: 1.40; 95% CI: 1.25-1.57 and HR: 1.49; 95% CI: 1.39-1.60), compared to no opioid use, respectively. CONCLUSIONS: Our findings suggest opioid prescription may be a modifiable risk factor for the development of AF.

Ecologically Assessed Sleep Duration and Arterial Stiffness in Healthy Men and Women.

OBJECTIVE: Among younger adults, to determine the associations of actigraph- and self-reported sleep duration with arterial stiffness (AS) assessed in clinic and in ecologically valid contexts, and to examine sex-specific associations. METHODS: Healthy adults (n = 282, median age = 29, 67% women) completed a state-of-the-art assessment of AS at rest (SphygmoCor; carotid femoral pulse wave velocity [cfPWV]; central augmentation index [cAIx]) and 7 days of actigraphy-assessed sleep with concurrent, momentary cAIx assessment for 36 hours (Oscar-2). Multivariable regressions were conducted on the full sample, and sex-stratified, to examine cross-sectional linear and quadratic associations of average sleep duration with resting PWV and cAIx, average cAIx while awake and asleep, and nocturnal cAIx dipping, adjusted for demographic and health covariates. Exploratory analyses included self-reported sleep duration with AS, and of actigraphy and self-reported sleep duration with the ambulatory arterial stiffness index (AASI; Oscar-2). RESULTS: Overall and by sex, associations of average sleep duration with resting cfPWV, resting cAIs, and awake cAIx were not significant. Sleep duration showed a positive, linear association with sleep cAIx in women (95% CI:1.07,5.86, ΔR2 = 0.021). Among women, sleep duration was also inversely associated with cAIx dipping (95% CI:-4.48,-0.95, ΔR2 = 0.020). Analyses with self-reported sleep duration and AASI as alternate predictors and outcomes were not significant. CONCLUSIONS: Certain sleep duration-AS associations may be sex-specific. Assessing sleep and momentary AS in ecologically valid conditions outside the research laboratory is valuable to understand these relations. While this investigation should be replicated, findings raise the question of whether interventions to target sleep duration also reduce AS.

Use of a Single-Item Ecological Momentary Assessment to Measure Daily Exercise: Agreement with Accelerometer-Measured Exercise.

Accelerometers have been used to objectively quantify physical activity, but they can pose a high burden. This study was conducted to determine the feasibility of using a single-item smartphone-based ecological momentary assessment (EMA) in lieu of accelerometers in long-term assessment of daily exercise. Data were collected from a randomized controlled trial of intermittently exercising, otherwise healthy adults (N = 79; 57% female, mean age: 31.9 ± 9.5 years) over 365 days. Smartphone-based EMA self-reports of exercise entailed daily end-of-day responses about physical activity; the participants also wore a Fitbit device to measure physical activity. The Kappa statistic was used to quantify the agreement between accelerometer-determined (24 min of moderate-to-vigorous physical activity [MVPA] within 30 min) and self-reported exercise. Possible demographic predictors of agreement were assessed. Participants provided an average of 164 ± 87 days of complete data. The average within-person Kappa was κ = 0.30 ± 0.22 (range: -0.15-0.73). Mean Kappa ranged from 0.16 to 0.30 when the accelerometer-based definition of an exercise bout varied in duration from 15 to 30 min of MVPA within any 30 min period. Among the correlates examined, sex was significantly associated with agreement; mean agreement was higher among women (κ = 0.37) than men (κ = 0.20). Agreement between EMA self-reported and accelerometer-measured exercise was fair, suggesting that long-term exercise monitoring through a single-item EMA may be acceptable.

Association of depression and anxiety disorders with outcomes after revascularization in chronic limb-threatening ischemia hospitalizations nationwide.

OBJECTIVE: Patients with chronic limb-threatening ischemia (CLTI), the end stage of peripheral artery disease, often present with comorbid depression and anxiety disorders. The prevalence of these comorbidities in the inpatient context over time, and their association with outcomes after revascularization and resource usage is unknown. METHODS: Using the 2011 to 2017 National Inpatient Sample, two cohorts were created-CLTI hospitalizations with endovascular revascularization and CLTI hospitalizations with surgical revascularization. Within each cohort, the annual prevalence of depression and anxiety disorder diagnoses was determined, and temporal trends were evaluated using the Cochran-Mantel-Haenszel test. Hierarchical multivariable logistic and linear regression analyses were used to examine the association of depression and anxiety disorder diagnoses with inpatient major amputation, mortality, length of stay (LOS), and cost, adjusting for illness severity, comorbidities, and potential bias in the documentation of depression and anxiety disorder diagnoses stratified by patient sociodemographic data. RESULTS: Across the study period were a total of 245,507 CLTI-related hospitalizations with endovascular revascularization and 138,922 with surgical revascularization. Hospitalizations with a depression or anxiety disorder diagnosis increased from 10.8% in 2011 to 15.3% in 2017 in the endovascular revascularization cohort and from 11.7% in 2011 to 14.4% in 2017 in the surgical revascularization cohort (Ptrend < .001). In the endovascular revascularization cohort, depression was associated with higher odds of major amputation (odds ratio, 1.15; 95% confidence interval, 1.03-1.30). In addition, depression (9 vs 8 days [P < .001]; $105,754 vs $102,481 [P = .018]) and anxiety disorder (9 vs 8 days [P < .001]; $109,496 vs $102,324 [P < .001]) diagnoses were associated with a longer median LOS and higher median costs. In the surgical revascularization cohort, depression was associated with a higher odds of major amputation (odds ratio, 1.33; 95% confidence interval, 1.13-1.58) and a longer LOS (median, 9 vs 9 days; P = .004). CONCLUSIONS: Depression and anxiety disorder diagnoses have become increasingly prevalent among CLTI hospitalizations including revascularizations. When present, these psychiatric comorbidities are associated with an increased risk of amputation and greater resource usage.

The Perceived Stress Scale as a Measure of Stress: Decomposing Score Variance in Longitudinal Behavioral Medicine Studies.

BACKGROUND: The Perceived Stress Scale (PSS) is a widely used measure designed to assess perceptions of recent stress. However, it is unclear to what extent the construct assessed by the PSS represents factors that are stable versus variable within individuals, and how these components might vary over time. PURPOSE: Determine the degree to which variability in repeated PSS assessments is attributable to between-person versus within-person variance in two different studies and populations. METHODS: Secondary analyses utilized data from two studies with up to 13 PSS assessments: An observational study of 127 patients with heart failure followed over 39 months (Study 1), and an experimental study of 73 younger, healthy adults followed over 12 months (Study 2). Multilevel linear mixed modeling was used to estimate sources of variance in the PSS total and subscale scores across assessments. RESULTS: Between-person variance accounted for a large proportion of the total variance in PSS total scores in Study 1 (42.3%) and Study 2 (51.1%); within-person variance comprised the remainder. Between-person variance was higher for shorter assessment periods (e.g., 1 week), and was comparable when examining only the first 12 months of assessments in each study (52.9% vs. 51.1%). CONCLUSIONS: Within two samples differing in age and health status, between-person variance accounted for approximately half of the total variation in PSS scores over time. While within-person variance was observed, the construct assessed by the PSS may substantially reflect a more stable characteristic of how an individual perceives stressful life circumstances than previously appreciated.

The Perceived Stress Scale (PSS) is a widely used questionnaire designed to assess how an individual perceives recent stress in their life. It is unclear, however, the degree to which the PSS is measuring factors that are consistent within individuals versus those that fluctuate, and how these components might change when the PSS is administered repeatedly over time. To address this knowledge gap, data from two studies were used­a study of 137 patients with heart failure followed for 39 months and a study of 73 younger, healthy adults followed for 12 months. In each, participants completed up to 13 PSS assessments, with 2,880 total PSS assessments completed across the studies. Multilevel linear mixed modeling was used to examine sources of score variance across assessments. Between-person variance (i.e., score variability that is relatively stable over time but differs between individuals) accounted for approximately half of the total variation in PSS scores over time, and was higher over shorter assessment periods. While within-person variance was observed (i.e., score variability that fluctuates within the same individual over time), these results suggest that the PSS may assess a substantially more stable characteristic of how an individual perceives stressful life circumstances than previously appreciated.

Anhedonic Depression Is Not Associated With Risk of Recurrent Major Adverse Cardiac Events and All-Cause Mortality in Acute Coronary Syndrome Patients.

BACKGROUND: Depression after acute coronary syndrome (ACS) is common and increases risks of adverse outcomes, but it remains unclear which depression features are most associated with major adverse cardiac events (MACE) and all-cause mortality (ACM). PURPOSE: To examine whether a subtype of depression characterized by anhedonia and major depressive disorder (MDD) predicts 1-year MACE/ACM occurrence in ACS patients compared to no MDD history. We also consider other depression features in the literature as predictors. METHODS: Patients (N = 1,087) presenting to a hospital with ACS completed a self-report measure of current depressive symptoms in-hospital and a diagnostic interview assessing MDD within 1 week post-hospitalization. MACE/ACM events were assessed at 1-, 6-, and 12-month follow-ups. Cox regression models were used to examine the association of the anhedonic depression subtype and MDD without anhedonia with time to MACE/ACM, adjusting for sociodemographic and clinical covariates. RESULTS: There were 142 MACE/ACM events over the 12-month follow-up. The 1-year MACE/ACM in patients with anhedonic depression, compared to those with no MDD, was somewhat higher in an age-adjusted model (hazard ratio [HR] = 1.63, p = .08), but was not significant after further covariate adjustment (HR = 1.24, p = .47). Of the additional depression features, moderate-to-severe self-reported depressive symptoms significantly predicted the risk of MACE/ACM, even in covariate-adjusted models (HR = 1.72, p = .04), but the continuous measure of self-reported depressive symptoms did not. CONCLUSION: The anhedonic depression subtype did not uniquely predict MACE/ACM as hypothesized. Moderate-to-severe levels of total self-reported depressive symptoms, however, may be associated with increased MACE/ACM risk, even after accounting for potential sociodemographic and clinical confounders.

Immediate and long-term effects of the COVID-19 pandemic and lockdown on physical activity in patients with implanted cardiac devices.

BACKGROUND: Physical activity (PA) is an important determinant of cardiovascular health that may be affected the COVID-19 pandemic. Therefore, we examined the immediate and long-term effects of the pandemic and lockdown on PA in patients with established cardiovascular risk. METHODS: Objectively-measured daily PA data was obtained from cardiovascular implantable electronic devices (CIEDs) from 3453 U.S patients (mean and standard deviations [SD] age, 72.65 [13.24] years; 42% women). Adjusted mixed-effects models stratified by device type were used to compare daily PA from periods in 2020: pre-lockdown (March 1-14), lockdown (March 15 to May 8), and the reopening phase of the pandemic (May 9 to December 31) versus 2019. Patient characteristics and events associated with inactivity during lockdown and the proportion of patients who returned to their 2019 PA-level by the end of reopening phase (December 31, 2020) were examined. RESULTS: Daily PA was significantly lower during the lockdown compared to the same period in 2019 (-15%; p < .0001), especially for pacemaker patients, adults aged <65, and patients more active prior to lockdown. Non-COVID hospitalization and ICD shock were similarly associated with low PA during lockdown (p = .0001). In the reopening phase of the pandemic, PA remained 14.4% lower in the overall sample and only 23% of patients returned to their 2019 PA level by the end of follow-up. CONCLUSIONS: In this large cohort of patients with CIEDs, PA was markedly lower during the lockdown and remained lower for months after restrictions were lifted. Strategies to maintain PA during a national emergency are urgently needed.

Posttraumatic Stress Disorder, Antidepressant Use, and Hemorrhagic Stroke in Young Men and Women: A 13-Year Cohort Study.

BACKGROUND AND PURPOSE: Antidepressants are commonly prescribed for posttraumatic stress disorder (PTSD) and may increase the risk of bleeding, including hemorrhagic stroke. METHODS: We prospectively examined independent effects of PTSD, selective serotonin and norepinephrine reuptake inhibitors (SSRI and SNRI) on the risk of incident hemorrhagic stroke in a nationwide sample of 1.1 million young and middle-aged veterans. Time-varying multivariate Cox models were used to examine hemorrhagic stroke risk by PTSD status and use of SSRI or SNRI while adjusting for demographics, lifestyle factors, stroke, and psychiatric comorbidities. Sensitivity analyses controlled for health care utilization. RESULTS: During 13 years of follow-up (2.14 years on average), 507 patients (12% women) suffered a hemorrhagic stroke. The overall incidence rate was 1.70 events per 10 000-person years. In unadjusted models, PTSD was associated with an 82% greater risk of new-onset hemorrhagic stroke (hazard ratio [HR], 1.82 [95% CI, 1.48-2.24]), SSRI use was associated with a >2-fold risk (HR, 2.02 [95% CI, 1.66-2.57]), and SNRI use was associated with a 52% greater risk (HR, 1.52 [95% CI, 1.08-2.16]). In fully adjusted models, effects of PTSD and SNRI were attenuated (adjusted HR, 1.03 [95% CI, 0.81-1.34]; adjusted HR, 1.19 [95% CI, 0.83-1.71]), but SSRI use remained associated with a 45% greater risk of hemorrhagic stroke (adjusted HR, 1.45 [95% CI, 1.13-1.85]). Hypertension, drug abuse, and alcohol abuse were also associated with increased stroke risk. Nonobesity and being non-Hispanic were protective factors. In sensitivity analyses, health care utilization was a small but significant predictor of stroke. CONCLUSIONS: In the largest known investigation of PTSD and antidepressant-associated risk for hemorrhagic stroke in young adults, use of SSRIs, but neither PTSD nor SNRIs were independently associated with incident stroke. SNRIs may be preferable for treating PTSD and comorbid conditions, although pursuing other modifiable risk factors and non-pharmacological treatments for PTSD also remains essential.

Psychological stress in heart failure: a potentially actionable disease modifier.

Psychological stress is common in patients with heart failure, due in part to the complexities of effective disease self-management and progressively worsening functional limitations, including frequent symptom exacerbations and hospitalizations. Emerging evidence suggests that heart failure patients who experience higher levels of stress may have a more burdensome disease course, with diminished quality of life and increased risk for adverse events, and that multiple behavioral and pathophysiological pathways are involved. Furthermore, the reduced quality of life associated with heart failure can serve as a life stressor for many patients. The purpose of this review is to summarize the current state of the science concerning psychological stress in patients with heart failure and to discuss potential pathways responsible for the observed effects. Key knowledge gaps are also outlined, including the need to understand patterns of exposure to various heart failure-related and daily life stressors and their associated effects on heart failure symptoms and pathophysiology, to identify patient subgroups at increased risk for stress exposure and disease-related consequences, and the effect of stress specifically for patients who have heart failure with preserved ejection fraction. Stress is a potentially modifiable factor, and addressing these gaps and advancing the science of stress in heart failure is likely to yield important insights about actionable pathways for improving patient quality of life and outcomes.

Impact of Mental Stress and Anger on Indices of Diastolic Function in Patients With Heart Failure.

BACKGROUND: Under controlled conditions, mental stress can provoke decrements in ventricular function, yet little is known about the effect of mental stress on diastolic function in patients with heart failure (HF). METHODS AND RESULTS: Twenty-four patients with HF with ischemic cardiomyopathy and reduced ejection fraction (n = 23 men; mean left ventricular [LV] ejection fraction 27 ± 9%; n = 13 with baseline elevated E/e') completed daily assessment of perceived stress, anger, and negative emotion for 7 days, followed by a laboratory mental stress protocol. Two-dimensional Doppler echocardiography was performed at rest and during sequential anger recall and mental arithmetic tasks to assess indices of diastolic function (E, e', and E/e'). Fourteen patients (63.6%) experienced stress-induced increases in E/e', with an average baseline to stress change of 6.5 ± 9.3, driven primarily by decreases in early LV relaxation (e'). Age-adjusted linear regression revealed an association between 7-day anger and baseline E/e'; patients reporting greater anger in the week before mental stress exhibited higher resting LV diastolic pressure. CONCLUSIONS: In patients with HF with reduced ejection fraction, mental stress can provoke acute worsening of LV diastolic pressure, and recent anger is associated with worse resting LV diastolic pressure. In patients vulnerable to these effects, repeated stress exposures or experiences of anger may have implications for long-term outcomes.

Association of prescription opioids and incident cardiovascular risk factors among post-9/11 Veterans.

Reports indicate that long-term opioid therapy is associated with cardiovascular disease (CVD). Using VA electronic health record data, we measured the impact of opioid use on the incidence of modifiable CVD risk factors. We included Veterans whose encounter was between October 2001 to November 2014. We identified Veterans without CVD risk factors during our baseline period, defined as the date of first primary care visit plus 365 days. The main exposure was opioid prescriptions (yes/no, long-term (i.e. ≥90 days) vs no opioid, and long-term vs short-term (i.e. <90 days)), which was time-updated yearly from the end of the baseline period to February 2015. The main outcome measures were incident CVD risk factors (hypertension, dyslipidemia, diabetes, obesity, and current smoking). After excluding prevalent CVD risk factors, we identified 308,015 Veterans. During the first year of observation, 12,725 (4.1%) Veterans were prescribed opioids, including 2028 (0.6%) with long-term exposure. Compared to patients without opioid use, Veterans with opioid use were more likely to have CVD risk factors. Those with long-term exposure were at higher risk of having hypertension (adjusted average hazards ratio [HR] 1.45, 99% confidence interval [CI] 1.33-1.59), dyslipidemia (HR 1.45, 99% CI 1.35-156), diabetes (HR 1.30, 99% CI 1.07-1.57), current smoking status (HR 1.34, 99% CI 1.24-1.46), and obesity (HR 1.22, 99% CI 1.12-1.32). Compared to short-term exposure, long-term had higher risk of current smoking status (HR 1.12, 99% CI 1.01-1.24). These findings suggest potential benefit to screening and surveillance of CVD risk factors for patients prescribed opioids, especially long-term opioid therapy.

The Foundational Role of Cardiovascular Imaging in the Characterization of Mental Stress-Induced Myocardial Ischemia in Patients with Coronary Artery Disease.

PURPOSE OF REVIEW: Mental stress-provoked myocardial ischemia (MSIMI) is an ischemic phenomenon provoked by the experience of psychologically stressful circumstances. While MSIMI was initially identified 50 years ago during activities of daily living through the use of wearable Holter monitor, subsequent research utilized the technologies of cardiac imaging-ventriculography and myocardial perfusion-under controlled conditions to pursue an understanding of pathophysiology and prognosis. This work revealed that MSIMI occurs in almost half of patients with stable coronary artery disease (CAD) and is associated with cardiac events and early mortality. We provide a focused review of the instrumental role that cardiac imaging has played in elucidating how stress affects cardiac physiology and how emerging diagnostic techniques will allow for further research on stress-mediated changes in the coronary macro- and microvasculature. RECENT FINDINGS: Observations about the cardiac response to mental stress diverge from underlying cornerstones of the traditional CAD paradigm which is based upon myocardial oxygen demand and the degree of epicardial coronary stenosis. Evidence from studies utilizing non-invasive and invasive studies of coronary perfusion indicates perturbations in the microvascular compartment in response to mental stress. Cardiovascular imaging enjoined with mental stress provocation may be a commanding tool to advance our understanding of non-obstructive CAD and the coronary microvasculature. This further understanding will facilitate incorporation of mental stress testing in the clinical care of patients with discrepant diagnostic work-up of CAD and in patients who experience anginal symptoms due to non-exertional and/or emotional triggers. Such algorithms will be crucial to identify treatment targets to modify the risk associated with mental stress-associated ischemia and adverse prognosis.

Effects of Psychological Stress on Vascular Physiology: Beyond the Current Imaging Signal.

PURPOSE OF REVIEW: This review describes the effects of psychological stress on the physiology of the entire vascular system, from individual cellular components to macrovascular and microvascular responses, and highlights the importance of the vascular system in the context of current limitations in cardiac imaging for evaluation of the cardiovascular response to mental stress. RECENT FINDINGS: The physiological responses that mediate vascular changes are based on evolutionary needs, but there is increasing evidence that the long-term consequences of psychological stress can precipitate the development and progression of cardiovascular disease (CVD). While there is an extensive body of literature describing localized physiological responses or overt cardiovascular manifestations, often framed within the organ-specific scope of cardiovascular imaging, there has not been a comprehensive description of the global vascular effects of psychological stress. Given the global nature of these processes, targeted cardiovascular imaging modalities may be insufficient. Here we approach the vascular response to mental stress systematically, describing the effects on the endothelium, vascular smooth muscle, and adventitia. We then address the mental stress effects on large vessels and the microvascular compartment, with a discussion of the role of microvascular resistance in the pathophysiology of mental stress-induced myocardial ischemia. Vascular responses to psychological stress involve complex physiological processes that are not fully characterized by routine cardiovascular imaging assessments. Future research incorporating standardized psychological assessments targeted toward vascular mechanisms of stress responses is required to guide the development of behavioral and therapeutic interventions.

Posttraumatic Stress Disorder and Risk for Stroke in Young and Middle-Aged Adults: A 13-Year Cohort Study.

Background and Purpose- In older populations, transient ischemic attack (TIA) and ischemic stroke have been linked to psychological factors, including posttraumatic stress disorder (PTSD). Whether PTSD also increases risk for early incident stroke in young adults is unknown. Methods- We prospectively assessed the incidence of TIA and ischemic stroke in a cohort of 987 855 young and middle-aged Veterans (mean age of 30.29±9.19 years; 87.8% men, 64.4% white) who first accessed care through the Veterans Health Administration from October 2001 to November 2014 and were free of TIA and ischemic stroke at baseline. For each outcome, time-varying multivariate Cox models were constructed to examine the effect of PTSD on incident stroke. We also assessed for effect modification by sex. Additional sensitivity analyses controlled for healthcare utilization. Results- Over a 13-year period, TIA and ischemic stroke were diagnosed in 766 and 1877 patients, respectively. PTSD was diagnosed in 28.6% of the sample during follow-up. In unadjusted analyses, PTSD was significantly associated with new-onset TIA (hazard ratio [HR], 2.02; 95% CI, 1.62-2.52) and ischemic stroke (HR, 1.62; 95% CI, 1.47-1.79). In fully adjusted models, the association between PTSD and incident TIA (HR, 1.61; 95% CI, 1.27-2.04) and ischemic stroke (HR, 1.36; 95% CI, 1.22-1.52) remained significant. The effect of PTSD on ischemic stroke risk was stronger in men than in women (HR, 0.63; 95% CI, 0.47-0.86; P=0.003), but no effect of sex was found for TIA. Conclusions- PTSD is associated with a significant increase in risk of early incident TIA and ischemic stroke independent of established stroke risk factors, coexisting psychiatric disorders, and healthcare utilization. Sex moderated the relationship for adults with ischemic stroke but not TIA. These findings suggest that psychological factors, including PTSD, may be important targets for future age-specific prevention strategies for young adults.

The Association of Posttraumatic Stress Disorder With Clinic and Ambulatory Blood Pressure in Healthy Adults.

OBJECTIVE: Posttraumatic stress disorder (PTSD) is associated with incident cardiovascular risk. We tested the association of PTSD with clinic and ambulatory blood pressure (ABP) in a sample of healthy participants and tested ABP reactivity to anxiety as a mechanism by which PTSD may influence blood pressure (BP). METHODS: Participants were originally enrolled during workplace BP screenings at three sites; approximately 6 years (standard deviation = 1.0) later, they completed nine clinic BP assessments within three visits, 1 week apart. Before the third visit, participants were screened for PTSD (≥33 on the PTSD Checklist-Civilian) and depression (Beck Depression Inventory) and then completed 24-hour ABP monitoring with electronic diary assessment of anxiety (0-100) at each awake reading. RESULTS: Of 440 participants, 92 (21%) screened positive for PTSD. In regression models adjusted for depression and demographic and clinical variables, PTSD was associated with greater mean systolic BP (3.8 mm Hg clinic [95% confidence interval {CI}] = 1.1-6.5, p = .006), 3.0 mm Hg awake ABP [95% CI = 0.1-5.9, p = .04], and a nonsignificant 2.1 mm Hg ABP during sleep [95% CI = -1.0 to 5.1, p = .18]). PTSD was associated with greater 24-hour median anxiety (p < .001), and changes in anxiety were positively associated with concurrent systolic ABP (p < .001). ABP reactivity to anxiety was greater in participants with PTSD, which partially explained the association of PTSD with ABP. CONCLUSIONS: PTSD is associated with greater systolic BP, partly because of greater anxiety, and systolic BP reactivity to anxiety throughout the day. Daily anxiety and related BP reactivity may be targets for interventions to reduce the cardiovascular risk associated with PTSD.

The Influence of Daily Stress on Sedentary Behavior: Group and Person (N of 1) Level Results of a 1-Year Observational Study.

OBJECTIVE: The purpose of this study, which used mobile technologies to continuously collect data for 1 year, was to examine the association of psychological stress with objectively measured sedentary behavior in adults at both the group (e.g., nomothetic approach) and individual (e.g., idiographic approach) level. METHODS: Data were collected in an observational study of healthy adults (n = 79) residing in the New York City metro area who were studied for 365 days from 2014 to 2015. Sedentary behavior was objectively measured via accelerometry. A smartphone-based electronic diary was used to assess level of stress ("Overall, how stressful was your day?" 0-10 scale) and sources of stress. RESULTS: The end-of-day stress rating was not associated with total sedentary time (B = -1.34, p = .767) at the group level. When specific sources of stress were evaluated at the group level, argument-related stress was associated with increased sedentariness, whereas running late- and work-related stress were associated with decreased sedentariness. There was a substantial degree of interindividual variability in the relationship of stress with sedentary behavior. Both the level and sources of stress were associated with increased sedentariness for some, decreased sedentariness for others, and had no effect for many (within-person variance p < .001). CONCLUSIONS: These findings suggest that the influence of stress on sedentary behavior varies by source of stress and from person to person. A precision medicine approach may be warranted to target reductions in sedentary time, although further studies are needed to confirm the observed findings in light of study limitations including a small sample size and enrollment of participants from a single, urban metropolitan area.

Clinic Blood Pressure Underestimates Ambulatory Blood Pressure in an Untreated Employer-Based US Population: Results From the Masked Hypertension Study.

BACKGROUND: Ambulatory blood pressure (ABP) is consistently superior to clinic blood pressure (CBP) as a predictor of cardiovascular morbidity and mortality risk. A common perception is that ABP is usually lower than CBP. The relationship of the CBP minus ABP difference to age has not been examined in the United States. METHODS: Between 2005 and 2012, 888 healthy, employed, middle-aged (mean±SD age, 45±10.4 years) individuals (59% female, 7.4% black, 12% Hispanic) with screening BP <160/105 mm Hg and not taking antihypertensive medication completed 3 separate clinic BP assessments and a 24-hour ABP recording for the Masked Hypertension Study. The distributions of CBP, mean awake ABP (aABP), and the CBP-aABP difference in the full sample and by demographic characteristics were compared. Locally weighted scatterplot smoothing was used to model the relationship of the BP measures to age and body mass index. The prevalence of discrepancies in ABP- versus CBP-defined hypertension status-white-coat hypertension and masked hypertension-were also examined. RESULTS: Average systolic/diastolic aABP (123.0/77.4±10.3/7.4 mm Hg) was significantly higher than the average of 9 CBP readings over 3 visits (116.0/75.4±11.6/7.7 mm Hg). aABP exceeded CBP by >10 mm Hg much more frequently than CBP exceeded aABP. The difference (aABP>CBP) was most pronounced in young adults and those with normal body mass index. The systolic difference progressively diminished, but did not disappear, at older ages and higher body mass indexes. The diastolic difference vanished around age 65 and reversed (CBP>aABP) for body mass index >32.5 kg/m2. Whereas 5.3% of participants were hypertensive by CBP, 19.2% were hypertensive by aABP; 15.7% of those with nonelevated CBP had masked hypertension. CONCLUSIONS: Contrary to a widely held belief, based primarily on cohort studies of patients with elevated CBP, ABP is not usually lower than CBP, at least not among healthy, employed individuals. Furthermore, a substantial proportion of otherwise healthy individuals with nonelevated CBP have masked hypertension. Demonstrated CBP-aABP gradients, if confirmed in representative samples (eg, NHANES [National Health and Nutrition Examination Survey]), could provide guidance for primary care physicians as to when, for a given CBP, 24-hour ABP would be useful to identify or rule out masked hypertension.

Risk for Incident Hypertension Associated With Posttraumatic Stress Disorder in Military Veterans and the Effect of Posttraumatic Stress Disorder Treatment.

OBJECTIVE: Posttraumatic stress disorder (PTSD) increases cardiovascular disease and cardiovascular mortality risk. Neither the prospective relationship of PTSD to incident hypertension risk nor the effect of PTSD treatment on hypertension risk has been established. METHODS: Data from a nationally representative sample of 194,319 veterans were drawn from the Veterans Administration (VA) roster of United States service men and women. This included veterans whose end of last deployment was from September 2001 to July 2010 and whose first VA medical visit was from October 1, 2001 to January 1, 2009. Incident hypertension was modeled as 3 events: (1) a new diagnosis of hypertension and/or (2) a new prescription for antihypertensive medication, and/or (3) a clinic blood pressure reading in the hypertensive range (≥140/90 mm Hg, systolic/diastolic). Posttraumatic stress disorder diagnosis was the main predictor. Posttraumatic stress disorder treatment was defined as (1) at least 8 individual psychotherapy sessions of 50 minutes or longer during any consecutive 6 months and/or (2) a prescription for selective serotonin reuptake inhibitor medication. RESULTS: Over a median 2.4-year follow-up, the incident hypertension risk independently associated with PTSD ranged from hazard ratio (HR), 1.12 (95% confidence interval [CI], 1.08-1.17; p < .0001) to HR, 1.30 (95% CI, 1.26-1.34; p < .0001). The interaction of PTSD and treatment revealed that treatment reduced the PTSD-associated hypertension risk (e.g., from HR, 1.44 [95% CI, 1.38-1.50; p < .0001] for those untreated, to HR, 1.20 [95% CI, 1.15-1.25; p < .0001] for those treated). CONCLUSIONS: These results indicate that reducing the long-term health impact of PTSD and the associated costs may require very early surveillance and treatment.

Does Stress Result in You Exercising Less? Or Does Exercising Result in You Being Less Stressed? Or Is It Both? Testing the Bi-directional Stress-Exercise Association at the Group and Person (N of 1) Level.

BACKGROUND: Psychosocial stress contributes to heart disease in part by adversely affecting maintenance of health behaviors, while exercise can reduce stress. Assessing the bi-directional relationship between stress and exercise has been limited by lack of real-time data and theoretical and statistical models. This lack may hinder efforts to promote exercise maintenance. PURPOSE: We test the bi-directional relationship between stress and exercise using real-time data for the average person and the variability-individual differences-in this relationship. METHODS: An observational study was conducted within a single cohort randomized controlled experiment. Healthy young adults, (n = 79) who reported only intermittent exercise, completed 12 months of stress monitoring by ecological momentary assessment (at the beginning of, end of, and during the day) and continuous activity monitoring by Fitbit. A random coefficients linear mixed model was used to predict end-of-day stress from the occurrence/non-occurrence of exercise that day; a logistic mixed model was used to predict the occurrence/non-occurrence of exercise from ratings of anticipated stress. Separate regression analyses were also performed for each participant. Sensitivity analysis tested all models, restricted to the first 180 days of observation (prior to randomization). RESULTS: We found a significant average inverse (i.e., negative) effect of exercise on stress and of stress on exercise. There was significant between-person variability. Of N = 69, exercise was associated with a stress reduction for 15, a stress increase for 2, and no change for the remainder. We also found that an increase in anticipated stress reported the previous night or that morning was associated with a significant 20-22% decrease (OR = 0.78-0.80) in the odds of exercising that day. Of N = 69, this increase in stress reduced the likelihood of exercise for 17, increased the odds for 1, and had no effect for the remainder. We were unable to identify psychosocial factors that moderate the individual differences in these effects. CONCLUSIONS: The relationship of stress to exercise can be uni- or bi-directional and varies from person to person. A precision medicine approach may improve exercise uptake.