Publications by authors named "Aaron Trammell"

Evaluation for right ventricular (RV) dysfunction is an important part of risk assessment in care of patients with pulmonary hypertension (PH) as it is associated with morbidity and mortality. Echocardiography provides a widely available and acceptable method to assess RV function. RV global longitudinal strain (RVGLS), a measure of longitudinal shortening of RV deep muscle fibers obtained by two-dimensional echocardiography, was previously shown to predict short-term mortality in patients with PH.

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Purpose: Pulmonary hypertension (PH) is a heterogenous, often progressive disorder leading to right heart failure and death. Previous analyses show stable PH mortality rates from 1980 to 2001 but increasing from 2001 to 2010 especially among women and non-Hispanic (NH) Black. This study seeks to identify recent trends in PH mortality in the United States from 1999 to 2019.

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Pulmonary hypertension (PH) comprises a diverse group of disorders that share a common pathway of pulmonary vascular remodeling leading to right ventricular failure. Development of anti-remodeling strategies is an emerging frontier in PH therapeutics that requires a greater understanding of the interactions between vascular wall cells and their extracellular matrices. The ubiquitous matrix glycan, hyaluronan (HA), is markedly elevated in lungs from patients and experimental models with PH.

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Pulmonary hypertension affects about one in four patients with advanced chronic kidney disease and significantly increases the risk of death. Kidney transplantation is the recommended management option for patients with progressive or end-stage kidney disease. However, the resource-limited nature of kidney transplantation and its intensive peri-operative and posttransplantation management motivates careful consideration of potential candidates' medical conditions to optimally utilize available graft organs.

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Background: Sepsis is one of the leading causes of hospital mortality, and diabetes is a risk factor for the development of infections. Although strong evidence has shown an association between metformin and reduced risk of infections, the risk of developing infections with newer classes of oral anti-diabetic drugs (OADs) has been less certain. Our study aims to examine the association between outpatient OAD use and hospital admissions for infections.

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Pulmonary hypertension (PH) is a complex condition that arises due to pulmonary vascular disease, heart disease, lung disease, chronic thromboembolism, or several rare causes. Regardless of underlying cause, PH increases mortality, yet there are no directed treatments for the most common forms of PH due to left heart or lung disease. Because metabolic factors have been implicated in the pathogenesis of PH, we used a large administrative cohort to assess diabetes and weight, potentially modifiable risk factors, on PH outcome.

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Pulmonary hypertension (PH) occurs when the pulmonary vasculature is itself diseased or becomes affected secondarily by comorbid conditions, commonly left heart or lung disease. The high prevalence of chronic cardiopulmonary conditions among patients served by Veterans Health Administration (VHA) suggests this population may be particularly susceptible to PH. We sought to identify clinical features and outcomes in veterans diagnosed with PH.

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Pulmonary arterial hypertension (PAH) is associated with metabolic derangements including insulin resistance, although their effects on the cardiopulmonary disease are unclear. We hypothesized that insulin resistance promotes pulmonary hypertension (PH) development and mutations in type 2 bone morphogenetic protein receptor (BMPR2) cause cellular insulin resistance. Using a BMPR2 transgenic murine model of PAH and two models of inducible diabetes mellitus, we explored the impact of hyperglycemia and/or hyperinsulinemia on development and severity of PH.

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Background: Pulmonary arterial hypertension (PAH) is a proliferative disease of the pulmonary vasculature that preferentially affects women. Estrogens such as the metabolite 16α-hydroxyestrone (16αOHE) may contribute to PAH pathogenesis, and alterations in cellular energy metabolism associate with PAH. We hypothesized that 16αOHE promotes heritable PAH (HPAH) via microRNA-29 (miR-29) family upregulation and that antagonism of miR-29 would attenuate pulmonary hypertension in transgenic mouse models of Bmpr2 mutation.

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Pulmonary hypertension (PH) is a frequent complication of left heart disease and parenchymal lung disease, and it portends increased mortality. A growing number of medications are approved for the treatment of World Health Organization (WHO) group 1 pulmonary arterial hypertension (PAH). However, they are not well studied in PH of other etiologies (WHO groups 2-5).

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Despite consensus guidelines for right heart catheterization (RHC) in the diagnosis of pulmonary arterial hypertension (PAH), considerable differences exist in the performance of RHC, interpretation of hemodynamic data, and frequency of RHC performance in patients with established disease. These differences may lead to variability in diagnosis or treatment of PAH. We sought to gather information on the standard practice of RHC for the diagnosis and management of PAH from experienced pulmonary vascular disease specialists.

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Background: Heterogeneity in response to treatment of pulmonary arterial hypertension (PAH) is a major challenge to improving outcome in this disease. Although vasodilator-responsive PAH (VR-PAH) accounts for a minority of cases, VR-PAH has a pronounced response to calcium channel blockers and better survival than vasodilator-nonresponsive PAH (VN-PAH). We hypothesized that VR-PAH has a different molecular cause from VN-PAH that can be detected in the peripheral blood.

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Rationale: Shorter survival in heritable pulmonary arterial hypertension (HPAH), often due to BMPR2 mutation, has been described in association with impaired right ventricle (RV) compensation. HPAH animal models are insulin resistant, and cells with BMPR2 mutation have impaired fatty acid oxidation, but whether these findings affect the RV in HPAH is unknown.

Objectives: To test the hypothesis that BMPR2 mutation impairs RV hypertrophic responses in association with lipid deposition.

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