Posttraumatic Stress Disorder Is Associated With Worse Endothelial Function Among Veterans

Grenon, S. Marlene; Owens, Christopher D.; Alley, Hugh; Pérez, Sandra; Whooley, Mary A.; Neylan, Thomas C.; Aschbacher, Kirstin; Gasper, Warren J.; Hilton, Joan F.; Cohen, Beth E.

doi:10.1161/jaha.115.003010

Cited by 47 publications

(45 citation statements)

References 47 publications

(73 reference statements)

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“…It is now well-established that PTSD is independently associated with increased risk for coronary artery disease and related mortality (Edmondson & Cohen 2013, Edmondson et al 2013). Moreover, among veterans treated in an outpatient clinic, those with PTSD had worse indicators of endothelial function (Grenon et al 2016), which might have contributed to the early onset and progression of CVD in this population. Similarly, PTSD within the Danish general population was associated with higher rates of myocardial infarction, ischaemic stroke and venous thromboembolism, irrespective of gender (Gradus et al 2015).…”

Section: Posttraumatic Stress Disorder: Emerging Risk Factors For Carmentioning

confidence: 99%

Cardiovascular Disease Risk Factors in Patients With Posttraumatic Stress Disorder (Ptsd): A Narrative Review

et al. 2017

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Section: Posttraumatic Stress Disorder: Emerging Risk Factors For Carmentioning

confidence: 99%

Cardiovascular Disease Risk Factors in Patients With Posttraumatic Stress Disorder (Ptsd): A Narrative Review

et al. 2017

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“…The general pattern of results across that line of research provides support for associations between PTSD and C-reactive protein [74, 75, 76•], TNFα [76•, 77], IL-6 [77], and IL-1β [77]. Additionally, a growing body of evidence suggests that PTSD is cross-sectionally associated with impaired endothelial functioning as measured by circulating markers of endothelial cell integrity [76•], and direct observation of nitric oxide-related vascular reactivity in the brachial artery [78]. There is also preliminary evidence that PTSD predicts increasing endothelial cell dysfunction over time [76•].…”

Section: Traumatic Stress and Inflammation And Immune Responsementioning

confidence: 99%

“…Specifically, robust associations between estimated white blood cell counts and accelerated DNAm age have emerged across studies, such as a negative relationship between CD4 T-cell counts and accelerated Hannum DNAm [55, 60••, 61–62]. There is also preliminary evidence for an association between Horvath epigenetic age acceleration (adjusted for white blood cell counts) and increased C-reactive protein as well as between Hannum epigenetic age acceleration (in an index combined with white blood cell counts, see below) and increased C-reactive protein [78]. However, the interpretation of these associations is not yet clear.…”

Section: Potential Mechanisms Linking Traumatic Stress To Acceleratedmentioning

confidence: 99%

Traumatic Stress and Accelerated Cellular Aging: From Epigenetics to Cardiometabolic Disease

Wolf

Morrison

2017

Curr Psychiatry Rep

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Purpose of review The aim of this paper is to review the recent literature on traumatic stress-related accelerated aging, including a focus on cellular mechanisms and biomarkers of cellular aging and on the clinical manifestations of accelerated biological aging. Recent findings Multiple lines of research converge to suggest that PTSD is associated with accelerated aging in the epigenome, and the immune and inflammation systems, and this may be reflected in premature onset of cardiometabolic and cardiovascular disease. Summary The current state of research paves the way for future work focused on identifying the peripheral and central biological mechanisms linking traumatic stress to accelerated biological aging and medical morbidity, with an emphasis on processes involved in inflammation, immune functioning, oxidative stress, autonomic arousal, and stress responding. Ultimately, such work could help reduce the pace of biological aging and improve health and wellness.

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“…Multiple large epidemiological studies have demonstrated that PTSD is independently associated with a significantly greater risk for developing hypertension, other cardiovascular diseases such as coronary artery disease, and mortality (8,32). Although the mechanisms leading to increased cardiovascular disease risk are not fully understood, recent evidence suggests chronically heightened sympathetic nervous system (SNS) activity and reactivity (24,44) in patients with PTSD that is mediated by altered arterial baroreflex sensitivity (BRS) (44). SNS overactivity has a major role in causing and sustaining hypertension (21) and contributes to the development of heart failure (31), arrhythmias (22), and atherogenesis (17).…”

Section: Introductionmentioning

confidence: 99%

Acute effects of device-guided slow breathing on sympathetic nerve activity and baroreflex sensitivity in posttraumatic stress disorder

Fonkoue

Marvar

Norrholm

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

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Patients with posttraumatic stress disorder (PTSD) have elevated sympathetic nervous system reactivity and impaired sympathetic and cardiovagal baroreflex sensitivity (BRS). Device-guided slow breathing (DGB) has been shown to lower blood pressure (BP) and sympathetic activity in other patient populations. We hypothesized that DGB acutely lowers BP, heart rate (HR), and improves BRS in PTSD. In 23 prehypertensive veterans with PTSD, we measured continuous BP, ECG, and muscle sympathetic nerve activity (MSNA) at rest and during 15 min of DGB at 5 breaths/min ( n = 13) or identical sham device breathing at normal rates of 14 breaths/min (sham; n = 10). Sympathetic and cardiovagal BRS was quantified using pharmacological manipulation of BP via the modified Oxford technique at baseline and during the last 5 min of DGB or sham. There was a significant reduction in systolic BP (by -9 ± 2 mmHg, P < 0.001), diastolic BP (by -3 ± 1 mmHg, P = 0.019), mean arterial pressure (by -4 ± 1 mmHg, P = 0.002), and MSNA burst frequency (by -7.8 ± 2.1 bursts/min, P = 0.004) with DGB but no significant change in HR ( P > 0.05). Within the sham group, there was no significant change in diastolic BP, mean arterial pressure, HR, or MSNA burst frequency, but there was a small but significant decrease in systolic BP ( P = 0.034) and MSNA burst incidence ( P = 0.033). Sympathetic BRS increased significantly in the DGB group (-1.08 ± 0.25 to -2.29 ± 0.24 bursts·100 heart beats·mmHg, P = 0.014) but decreased in the sham group (-1.58 ± 0.34 to -0.82 ± 0.28 bursts·100 heart beats·mmHg, P = 0.025) (time × device, P = 0.001). There was no significant difference in the change in cardiovagal BRS between the groups (time × device, P = 0.496). DGB acutely lowers BP and MSNA and improves sympathetic but not cardiovagal BRS in prehypertensive veterans with PTSD. NEW & NOTEWORTHY Posttraumatic stress disorder is characterized by augmented sympathetic reactivity, impaired baroreflex sensitivity, and an increased risk for developing hypertension and cardiovascular disease. This is the first study to examine the potential beneficial effects of device-guided slow breathing on hemodynamics, sympathetic activity, and arterial baroreflex sensitivity in prehypertensive veterans with posttraumatic stress disorder.

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Posttraumatic Stress Disorder Is Associated With Worse Endothelial Function Among Veterans

Cited by 47 publications

References 47 publications

Cardiovascular Disease Risk Factors in Patients With Posttraumatic Stress Disorder (Ptsd): A Narrative Review

Cardiovascular Disease Risk Factors in Patients With Posttraumatic Stress Disorder (Ptsd): A Narrative Review

Traumatic Stress and Accelerated Cellular Aging: From Epigenetics to Cardiometabolic Disease

Acute effects of device-guided slow breathing on sympathetic nerve activity and baroreflex sensitivity in posttraumatic stress disorder

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