scholarly journals Posttraumatic Stress Disorder and Cardiovascular Disease

2015 ◽  
pp. 227-236
Author(s):  
Donald Edmondson ◽  
David Hiti ◽  
Ian Kronish
Keyword(s):  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Disorder

scholarly journals Early onset neurocirculatory response to static handgrip is associated with greater blood pressure variability in women with posttraumatic stress disorder

2020 ◽  
Vol 318 (1) ◽  
pp. H49-H58 ◽  
Author(s):  
Jeung-Ki Yoo ◽  
Mark B. Badrov ◽  
Rosemary S. Parker ◽  
Elizabeth H. Anderson ◽  
Jessica L. Wiblin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
Muscle Contraction ◽  
Posttraumatic Stress ◽  
Early Onset ◽  
Stress Disorder ◽  
Muscle Sympathetic Nerve Activity ◽  
Pressor Responses ◽  
Increased Risk

Posttraumatic stress disorder (PTSD) is a psychiatric illness that is more prevalent in women, and accumulating evidence suggests a link between PTSD and future development of cardiovascular disease. The underlying mechanisms are unclear, but augmented sympathetic reactivity to daily stressors may be involved. We measured muscle sympathetic nerve activity (MSNA), blood pressure (BP), and heart rate responses in 14 women with PTSD and 14 healthy women (controls) during static handgrip (SHG) exercise to fatigue at 40% of maximal voluntary contraction (MVC). Two minutes of postexercise circulatory arrest (PECA) was followed immediately after SHG to fatigue. MVC and the time to fatigue during SHG did not differ between groups (both P > 0.05). At the first 30 s of SHG, women with PTSD showed augmented sympathetic neural [mean ± SD, ∆MSNA burst frequency (BF): 5 ± 4 vs. 2 ± 3 bursts/30 s, P = 0.02 and ∆MSNA total activity (TA): 82 ± 58 vs. 25 ± 38 arbitrary units/30 s, P = 0.004] and pressor (∆systolic BP: 10 ± 5 vs. 4 ± 3 mmHg, P = 0.003) responses compared with controls. However, MSNA and BP responses at fatigue and during PECA were not different between groups. More interestingly, the augmented initial neural and pressor responses to SHG were associated with greater awake systolic BP variability during ambulation in women with PTSD (MSNA BF: r = 0.55, MSNA TA: r = 0.62, and SBP: r = 0.69, all P < 0.05). These results suggest that early onset exercise pressor response in women with PTSD may be attributed to enhanced mechano- rather than metaboreflexes, which might contribute to the mechanisms underlying the link between PTSD and cardiovascular risk. NEW & NOTEWORTHY The novel findings of the current study are that women with posttraumatic stress disorder (PTSD) exhibited augmented sympathetic neural and pressor responses at the first 30 s of submaximal isometric muscle contraction. More interestingly, exaggerated neurocirculatory responses at the onset of muscle contraction were associated with greater ambulatory awake systolic blood pressure fluctuations in women with PTSD. Our findings expand the knowledge on the physiological mechanisms that perhaps contribute to increased risk of cardiovascular disease in such a population.

scholarly journals Autonomic and inflammatory consequences of posttraumatic stress disorder and the link to cardiovascular disease

2015 ◽  
Vol 309 (4) ◽  
pp. R315-R321 ◽  
Author(s):  
Chevelle Brudey ◽  
Jeanie Park ◽  
Jan Wiaderkiewicz ◽  
Ihori Kobayashi ◽  
Thomas A. Mellman ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Autonomic Dysfunction ◽  
Stress Disorder ◽  
Renin Angiotensin System ◽  
Multiple Organ ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Organ Systems

Stress- and anxiety-related disorders are on the rise in both military and general populations. Over the next decade, it is predicted that treatment of these conditions, in particular, posttraumatic stress disorder (PTSD), along with its associated long-term comorbidities, will challenge the health care system. Multiple organ systems are adversely affected by PTSD, and PTSD is linked to cancer, arthritis, digestive disease, and cardiovascular disease. Evidence for a strong link between PTSD and cardiovascular disease is compelling, and this review describes current clinical data linking PTSD to cardiovascular disease, via inflammation, autonomic dysfunction, and the renin-angiotensin system. Recent clinical and preclinical evidence regarding the role of the renin-angiotensin system in the extinction of fear memory and relevance in PTSD-related immune and autonomic dysfunction is also addressed.

scholarly journals Combined effect of posttraumatic stress disorder and prescription opioid use on risk of cardiovascular disease

2019 ◽  
Vol 27 (13) ◽  
pp. 1412-1422 ◽  
Author(s):  
Jeffrey F Scherrer ◽  
Joanne Salas ◽  
Patrick Lustman ◽  
Peter Tuerk ◽  
Sarah Gebauer ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Disorder ◽  
Opioid Analgesic ◽  
Hazard Ratio ◽  
Prescription Opioid ◽  
Opioid Use ◽  
Increased Risk ◽  
Exposure Variable

Aim Prescription opioid analgesic use (OAU) is associated with increased risk of cardiovascular disease (CVD). OAU is more common in patients with than without posttraumatic stress disorder (PTSD), and PTSD is associated with higher CVD risk. We determined whether PTSD and OAU have an additive or multiplicative association with incident CVD. Methods and results Veterans Health Affairs patient medical record data from 2008 to 2015 was used to identify 2861 patients 30–70 years of age, free of cancer, CVD and OAU for 12 months before index date. We defined a four-level exposure variable: 1) no PTSD/no OAU, 2) OAU alone, 3) PTSD alone and 4) PTSD+OAU. Cox proportional hazard models estimated the association between the exposure variable and incident CVD. The mean age was 49.0 (±11.0), 85.7% were male and 58.3% were White, 34.4% had no PTSD/no OAU, 32.9% had PTSD alone, 10.6% had OAU alone, and 22.1% had PTSD+OAU. Compared with patients with no PTSD/no OAU, those with PTSD alone were not at increased risk of incident CVD (hazard ratio = 0.82; 95% confidence interval (CI): 0.63–1.17); however, OAU alone and PTSD+OAU were both significantly associated with incident CVD (hazard ratio = 1.99; 95% CI:1.36–2.92 and hazard ratio = 2.20; 95% CI: 1.61–3.02). There was no significant additive or multiplicative PTSD and OAU association with incident CVD. Conclusion OAU is associated with nearly a two-fold increased risk of CVD in patients with and without PTSD. Despite no additive or multiplicative interaction effects, the high prevalence of OAU in PTSD may represent a novel contributor to the elevated CVD burden among patients with PTSD.

scholarly journals Increased vascular α1-adrenergic receptor sensitivity in older adults with posttraumatic stress disorder

2020 ◽  
Vol 319 (6) ◽  
pp. R611-R616
Author(s):  
Cortnie L. Hartwig ◽  
Justin D. Sprick ◽  
Jinhee Jeong ◽  
Yingtian Hu ◽  
Doree G. Morison ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Sympathetic Nerve ◽  
Stress Disorder ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Blood Pressure Reactivity ◽  
Pressure Reactivity

Posttraumatic stress disorder (PTSD) is an independent risk factor for the development of hypertension and cardiovascular disease. Patients with PTSD have heightened blood pressure and sympathetic nervous system reactivity; however, it is unclear if patients with PTSD have exaggerated vasoconstriction in response to sympathetic nerve activation that could also contribute to increased blood pressure reactivity. Therefore, we hypothesized that patients with PTSD have increased sensitivity of vascular α1-adrenergic receptors (α1ARs), the major mediators of vasoconstriction in response to release of norepinephrine at sympathetic nerve terminals. To assess vascular α1AR sensitivity, we measured the degree of venoconstriction in a dorsal hand vein in response to exponentially increasing doses of the selective α1AR agonist, phenylephrine (PE), in 9 patients with PTSD (age = 59 ± 2 yr) and 10 age-matched controls (age = 60 ± 1 yr). Individual dose-response curves were generated to determine the dose of PE that induces 50% of maximal venoconstriction (i.e., PE ED50) reflective of vascular α1AR sensitivity. In support of our hypothesis, PE ED50 values were lower in PTSD compared with controls (245 ± 54 ng/min vs. 1,995 ± 459 ng/min, P = 0.012), indicating increased vascular α1AR sensitivity in PTSD. The PTSD group also had an increase in slope of rise in venoconstriction, indicative of an altered venoconstrictive reactivity to PE compared with controls (19.8% ± 1.2% vs. 15.1% ± 1.2%, P = 0.009). Heightened vascular α1AR sensitivity in PTSD may contribute to augmented vasoconstriction and blood pressure reactivity to sympathoexcitation and to increased cardiovascular disease risk in this patient population.

Posttraumatic Stress Disorder and Cardiovascular Disease

2021 ◽  
Author(s):  
Christopher J. O’Donnell ◽  
Lisa Schwartz Longacre ◽  
Beth E. Cohen ◽  
Zahi A. Fayad ◽  
Charles F. Gillespie ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Disorder
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