Publications by authors named "Michael T Osborne"

The heart and brain have a complex interplay wherein disease or injury to either organ may adversely affect the other. The mechanisms underlying this connection remain incompletely characterized. However, nuclear molecular imaging is uniquely suited to investigate these pathways by facilitating the simultaneous assessment of both organs using targeted radiotracers.

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Lower socioeconomic status (SES) and higher neuroticism polygenic risk score (NEU-PGS) associate with cardiovascular disease (CVD). Chronic stress increases CVD risk via activation of neural, autonomic, and immune pathways. We evaluated whether 1) higher NEU-PGS accentuates the association between lower SES and major adverse cardiovascular events (MACE); and 2) higher stress-associated neural activity and C-reactive protein and lower heart rate variability contribute to the SES-MACE link among those with higher NEU-PGS.

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Background: Imaging markers of atherosclerotic inflammation are needed to enhance cardiovascular risk assessment and evaluate the impact of therapies. We sought to test the hypothesis that treatments impacting arterial inflammation can be evaluated using a simplified measure of periaortic fat attenuation (FA) assessed on noncontrast, nongated computed tomography of the descending thoracic aorta.

Methods: Measurements were performed on F-fluorodeoxyglucose positron emission tomography/computed tomography images from a double-blind, randomized trial conducted between 2008 and 2009 that assessed the impact of statin therapy on arterial inflammation.

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Objective: Individuals with bipolar disorder are at greater risk of developing cardiovascular disease. However, the mechanisms underlying this association remain poorly understood. This study aimed to (1) determine the risk of major adverse cardiovascular events (MACE) after adjusting for important confounders and (2) evaluate the neural, autonomic, and immune mechanisms underlying the link between bipolar disorder and cardiovascular disease.

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Background: Individuals with posttraumatic stress disorder (PTSD) have high rates of cardiovascular disease (CVD) and increased cardiometabolic CVD risk factors (CVDRFs, e.g., hypertension, hyperlipidemia, or diabetes mellitus).

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Background: Noise exposure and lower socioeconomic status (SES) are both independently linked to increased cardiovascular disease (CVD) risk. Although these factors frequently coexist, their combined impact and the underlying pathophysiological mechanisms remain poorly understood.

Objectives: This study aimed to evaluate the joint effects of high transportation noise exposure and lower SES on major adverse cardiovascular events (MACE) and the role of the neural-arterial axis in mediating this relationship.

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Article Synopsis
  • Large vessel vasculitides (LVV) are inflammatory disorders that primarily affect large arteries like the aorta, often linked to conditions such as giant cell arteritis and Takayasu arteritis, with age and gender influencing prevalence.
  • Giant cell arteritis commonly occurs in individuals over 50, especially women, while Takayasu arteritis typically affects younger women; both require urgent diagnosis to prevent serious complications like blindness or artery damage.
  • Noninvasive imaging techniques, such as ultrasound and MRI, have revolutionized the diagnosis and management of LVV, reducing the need for invasive procedures and aiding in monitoring treatment response and disease progression.
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  • Prior research was limited in understanding how cardiometabolic risk factors (CVDRFs), like hypertension and diabetes, mediate the link between anxiety/depression and cardiovascular disease (CVD).
  • The study followed over 71,000 participants for a decade to assess the impact of anxiety/depression on the development of CVDRFs and the role of neuro-immune mechanisms, with findings showing a clear association and effect differences based on age and sex.
  • Results indicated that anxiety/depression significantly increases the risk of developing CVDRFs, especially in younger women, and this relationship may be influenced by neuro-immune pathways.
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Article Synopsis
  • Depression and anxiety are linked to an increased risk of deep venous thrombosis (DVT), particularly in women with posttraumatic stress disorder (PTSD).
  • A study involving over 106,000 participants found that PTSD significantly increases DVT risk, with a strong association in women compared to men.
  • The relationship between PTSD and DVT appears to be influenced by changes in stress-related neural activity and heart rate variability, indicating potential areas for preventive treatments in at-risk individuals, especially women.
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Controversy exists as to whether anxiety and depression increase deep vein thrombosis (DVT) risk, and the mechanisms mediating potential links remain unknown. We aimed to evaluate the association between anxiety and depression and DVT risk and determine whether upregulated stress-related neural activity (SNA), which promotes chronic inflammation, contributes to this link. Our retrospective study included adults (N = 118 871) enrolled in Mass General Brigham Biobank.

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Background And Aims: Chronic stress associates with cardiovascular disease, but mechanisms remain incompletely defined. Advanced imaging was used to identify stress-related neural imaging phenotypes associated with atherosclerosis.

Methods: Twenty-seven individuals with post-traumatic stress disorder (PTSD), 45 trauma-exposed controls without PTSD, and 22 healthy controls underwent 18F-fluorodeoxyglucose positron emission tomography/magnetic resonance imaging (18F-FDG PET/MRI).

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Despite decades of research, the heart-brain axis continues to challenge investigators seeking to unravel its complex pathobiology. Strong epidemiologic evidence supports a link by which insult or injury to one of the organs increases the risk of pathology in the other. The putative pathways have important differences between sexes and include alterations in autonomic function, metabolism, inflammation, and neurohormonal mechanisms that participate in crosstalk between the heart and brain and contribute to vascular changes, the development of shared risk factors, and oxidative stress.

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  • This study investigates how physical activity (PA) affects cardiovascular disease (CVD) and psychological health, particularly focusing on stress-related brain activity.
  • It found that increased PA is linked to lower stress-related neural activity and a reduction in CVD events, with these effects being more pronounced in individuals with depression.
  • The results suggest that engaging in PA may help decrease CVD risk partly by reducing stress impacts on the brain, especially for those suffering from depression.
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Article Synopsis
  • PTSD is linked to a higher risk of major adverse cardiovascular events (MACE), but the exact reasons for this connection are not well understood.
  • Recent research indicates that neuro-immune mechanisms—such as increased stress-related neural activity, autonomic nervous system function, and inflammation—may be responsible for this link.
  • The study found that these neuro-immune mechanisms (specifically stress-associated neural activity, heart rate variability, and inflammation markers) mediate the relationship between PTSD and MACE, suggesting that targeting these mechanisms could improve treatment for PTSD and reduce MACE risk.
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Transportation noise is a ubiquitous urban exposure. In 2018, the World Health Organization concluded that chronic exposure to road traffic noise is a risk factor for ischemic heart disease. In contrast, they concluded that the quality of evidence for a link to other diseases was very low to moderate.

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Background: Body mass index (BMI) is a controversial marker of cardiovascular prognosis, especially in women. Coronary microvascular dysfunction (CMD) is prevalent in obese patients and a better discriminator of risk than BMI, but its association with body composition is unknown.

Objectives: The authors used a deep learning model for body composition analysis to investigate the relationship between CMD, skeletal muscle (SM), subcutaneous adipose tissue (SAT), and visceral adipose tissue (VAT), and their contribution to adverse outcomes in patients referred for evaluation of coronary artery disease.

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Importance: The mechanisms underlying the association between chronic stress and higher mortality among individuals with cancer remain incompletely understood.

Objective: To test the hypotheses that among individuals with active head and neck cancer, that higher stress-associated neural activity (ie. metabolic amygdalar activity [AmygA]) at cancer staging associates with survival.

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Background: Chronic stress associates with major adverse cardiovascular events (MACE) via increased stress-related neural network activity (SNA). Light/moderate alcohol consumption (AC) has been linked to lower MACE risk, but the mechanisms are unclear.

Objectives: The purpose of this study was to evaluate whether the association between AC and MACE is mediated by decreased SNA.

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The heart and brain have a complex interplay wherein disease or injury to either organ may adversely affect the other. The mechanisms underlying this connection remain incompletely characterized. However, nuclear molecular imaging is uniquely suited to investigate these pathways by facilitating the simultaneous assessment of both organs using targeted radiotracers.

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