Posttraumatic stress disorder (PTSD), sleep, and cardiovascular disease risk: A mechanism-focused narrative review.

2022 ◽  
Author(s):  
Corinne Meinhausen ◽  
Aric A. Prather ◽  
Jennifer A. Sumner
2020 ◽  
Vol 319 (6) ◽  
pp. R611-R616
Author(s):  
Cortnie L. Hartwig ◽  
Justin D. Sprick ◽  
Jinhee Jeong ◽  
Yingtian Hu ◽  
Doree G. Morison ◽  
...  

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.


1992 ◽  
Vol 57 (4) ◽  
pp. 164-171 ◽  
Author(s):  
Paul R.J. Falger ◽  
Wybrand Op den Velde ◽  
Johannes E. Hovens ◽  
Erik G.W. Schouten ◽  
Johannes H.M. De Groen ◽  
...  

2021 ◽  
Vol 9 (2) ◽  
pp. e000741
Author(s):  
Hazem A Sayed Ahmed ◽  
Eric Merrell ◽  
Mansoura Ismail ◽  
Anwar I Joudeh ◽  
Jeffrey B Riley ◽  
...  

ObjectivesTo review the pathophysiology of COVID-19 disease, potential aspirin targets on this pathogenesis and the potential role of aspirin in patients with COVID-19.DesignNarrative review.SettingThe online databases PubMed, OVID Medline and Cochrane Library were searched using relevant headlines from 1 January 2016 to 1 January 2021. International guidelines from relevant societies, journals and forums were also assessed for relevance.ParticipantsNot applicable.ResultsA review of the selected literature revealed that clinical deterioration in COVID-19 is attributed to the interplay between endothelial dysfunction, coagulopathy and dysregulated inflammation. Aspirin has anti-inflammatory effects, antiplatelet aggregation, anticoagulant properties as well as pleiotropic effects on endothelial function. During the COVID-19 pandemic, low-dose aspirin is used effectively in secondary prevention of atherosclerotic cardiovascular disease, prevention of venous thromboembolism after total hip or knee replacement, prevention of pre-eclampsia and postdischarge treatment for multisystem inflammatory syndrome in children. Prehospital low-dose aspirin therapy may reduce the risk of intensive care unit admission and mechanical ventilation in hospitalised patients with COVID-19, whereas aspirin association with mortality is still debatable.ConclusionThe authors recommend a low-dose aspirin regimen for primary prevention of arterial thromboembolism in patients aged 40–70 years who are at high atherosclerotic cardiovascular disease risk, or an intermediate risk with a risk-enhancer and have a low risk of bleeding. Aspirin’s protective roles in COVID-19 associated with acute lung injury, vascular thrombosis without previous cardiovascular disease and mortality need further randomised controlled trials to establish causal conclusions.


2020 ◽  
Vol 318 (1) ◽  
pp. H49-H58 ◽  
Author(s):  
Jeung-Ki Yoo ◽  
Mark B. Badrov ◽  
Rosemary S. Parker ◽  
Elizabeth H. Anderson ◽  
Jessica L. Wiblin ◽  
...  

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.


2015 ◽  
Vol 309 (4) ◽  
pp. R315-R321 ◽  
Author(s):  
Chevelle Brudey ◽  
Jeanie Park ◽  
Jan Wiaderkiewicz ◽  
Ihori Kobayashi ◽  
Thomas A. Mellman ◽  
...  

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.


2021 ◽  
Vol 16 ◽  
Author(s):  
Esmee ME Bovee ◽  
Martha Gulati ◽  
Angela HEM Maas

Evidence has shown that women with a history of preeclampsia or haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome have an increased risk of cardiovascular disease later in life. Recommendations for screening, prevention and management after such pregnancies are not yet defined. The identification of promising non-traditional cardiovascular biomarkers might be useful to predict which women are at greatest risk. Many studies are inconsistent and an overview of the most promising biomarkers is currently lacking. This narrative review provides an update of the current literature on circulating cardiovascular biomarkers that may be associated with an increased cardiovascular disease risk in women after previous preeclampsia/HELLP syndrome. Fifty-six studies on 53 biomarkers were included. From the summary of evidence, soluble fms-like tyrosine kinase-1, placental growth factor, interleukin (IL)-6, IL-6/IL-10 ratio, high-sensitivity cardiac troponin I, activin A, soluble human leukocyte antigen G, pregnancy-associated plasma protein A and norepinephrine show potential and are interesting candidate biomarkers to further explore. These biomarkers might be potentially eligible for cardiovascular risk stratification after preeclampsia/HELLP syndrome and may contribute to the development of adequate strategies for prevention of hypertension and adverse events in this population.


2019 ◽  
Vol 13 (4) ◽  
pp. 270-283 ◽  
Author(s):  
Ian G. Barron ◽  
Caitlin Bourgaize ◽  
Daniela Lempertz ◽  
Colleen Swinden ◽  
Susan Darker-Smith

There is currently a limited number of studies into the efficacy of eye movement desensitization reprocessing (EMDR) therapy with children and adolescents with posttraumatic stress disorder (PTSD). The current study utilizes a systematic narrative review of methodologies and findings of previous literature reviews and meta-analyses as well as analyzing randomized control trials (RCTs) conducted from 2002 to 2018. Following initial scoping of the extent of studies, two systematic literature searches were conducted, firstly for literature reviews and secondly for recent RCTs. Nine databases were utilized. Eight reviews and seven RCTs were identified and analyzed for quality of methodology and outcome as measured by impact on PTSD symptoms. EMDR was found to be efficacious in reducing children's PTSD symptoms compared to waitlist conditions, with similar outcomes to cognitive behavior therapy (CBT). EMDR was effective with both single-event trauma as well as cumulative trauma such as sexual abuse. EMDR was equally effective with girls and boys as well as children from different cultures. EMDR achieved medium to large effect sizes. Reductions in PTSD were maintained at 2-, 3-, 6-, and 12-month follow-up. In conclusion, EMDR was consistently found to be an efficacious treatment for children with PTSD. Recommendations are made for future practice and research.


2019 ◽  
Vol 27 (13) ◽  
pp. 1412-1422 ◽  
Author(s):  
Jeffrey F Scherrer ◽  
Joanne Salas ◽  
Patrick Lustman ◽  
Peter Tuerk ◽  
Sarah Gebauer ◽  
...  

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.


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