Obesity and Pulmonary Hypertension

Ayinapudi, Karnika; Singh, Twinkle; Motwani, Ayush; Jemtel, Thierry H. Le; Oparil, Suzanne

doi:10.1007/s11906-018-0899-2

Cited by 42 publications

(24 citation statements)

References 100 publications

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“…Obesity and its comorbidities such as obstructive sleep apnea-hypopnea syndrome and metabolic syndrome directly increase the prevalence of PAH [12,46]. Patients with higher BMI are often susceptible to inflammation, insulin resistance and; plausibly, these factors exacerbate vascular remodeling in PAH [47]. In addition, sex hormones play a decisive role in determining etiology and management of PAH; as such, it has been well established that female patients have higher morbidity and lower mortality, which intriguingly suggest that estrogen influences this disease in a differential manner [48].…”

Section: Discussionmentioning

confidence: 99%

Differential serum lipid distribution in IPAH and CHD-PAH patients

Chen

Rathinasabapathy

Luo

et al. 2022

Respiratory Medicine

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Lipid homeostasis is dysregulated in pulmonary arterial hypertension (PAH). A decrease in serum high-and lowdensity lipoprotein cholesterol (HDL-C and LDL-C) is significantly associated with the worse prognosis of PAH. However, no study has investigated the differential distribution of lipids in various PAH subtypes. We enrolled 190 patients in this retrospective study, which includes 20 patients with congenital heart disease without PAH (CHD-nonPAH), 101 patients with PAH associated with congenital heart disease (CHD-PAH), 69 patients with idiopathic PAH (IPAH) and 81 healthy controls. Laboratory parameters such as liver and renal function, serum lipids, C-reactive protein, N-terminal pro-brain natriuretic peptide (NT-proBNP), echocardiography, right heart catheterization and 6-min walk distance (6MWD) were performed. All types of cholesterol including HDL-C, LDL-C and total cholesterol (CHOL) were significantly lower in IPAH patients in association with right heart function. Although LDL-C and CHOL were lower in CHD-PAH, they were not associated with disease severity or heart failure. Thus, we conclude that IPAH and CHD-PAH patients exhibited a differential distribution pattern of serum lipids.

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Section: Discussionmentioning

confidence: 99%

Differential serum lipid distribution in IPAH and CHD-PAH patients

Chen

Rathinasabapathy

Luo

et al. 2022

Respiratory Medicine

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“…This has implications in enhanced leukocyte recruitment, cytokine production, microvascular permeability, airway obstruction, and damaged endothelial cells [200] causing a highly increased risk for several respiratory systemic diseases [201]. Third, in combination with systemic inflammation, insulin resistance, and oxidative stress, expansion of AT surrounding the pulmonary artery contributes to the pathobiology of pulmonary arterial hypertension [202], impairing the structure and function of the lung. Fourth, as discussed, patients with obesity may lose their functional lung MSCs, vulnerable to the development of pulmonary fibrosis, a severe complication observed in COVID-19 patients [89].…”

Section: Obesity and Its Connection To Hypertension And Respiratory Dmentioning

confidence: 99%

Obesity and COVID-19: Molecular Mechanisms Linking Both Pandemics

Ritter

Kreis

Louwen

et al. 2020

IJMS

111

122

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The coronavirus disease 2019 COVID-19 pandemic is rapidly spreading worldwide and is becoming a major public health crisis. Increasing evidence demonstrates a strong correlation between obesity and the COVID-19 disease. We have summarized recent studies and addressed the impact of obesity on COVID-19 in terms of hospitalization, severity, mortality, and patient outcome. We discuss the potential molecular mechanisms whereby obesity contributes to the pathogenesis of COVID-19. In addition to obesity-related deregulated immune response, chronic inflammation, endothelium imbalance, metabolic dysfunction, and its associated comorbidities, dysfunctional mesenchymal stem cells/adipose-derived mesenchymal stem cells may also play crucial roles in fueling systemic inflammation contributing to the cytokine storm and promoting pulmonary fibrosis causing lung functional failure, characteristic of severe COVID-19. Moreover, obesity may also compromise motile cilia on airway epithelial cells and impair functioning of the mucociliary escalators, reducing the clearance of severe acute respiratory syndrome coronavirus (SARS-CoV-2). Obese diseased adipose tissues overexpress the receptors and proteases for the SARS-CoV-2 entry, implicating its possible roles as virus reservoir and accelerator reinforcing violent systemic inflammation and immune response. Finally, anti-inflammatory cytokines like anti-interleukin 6 and administration of mesenchymal stromal/stem cells may serve as potential immune modulatory therapies for supportively combating COVID-19. Obesity is conversely related to the development of COVID-19 through numerous molecular mechanisms and individuals with obesity belong to the COVID-19-susceptible population requiring more protective measures.

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“…In an animal model study, greater susceptibility to acute lung injury was found in obese rats [11]. In addition, there seems to be a higher prevalence of pulmonary hypertension in obese individuals, probably due to inflammatory responses in obesity [12].…”

Section: Introductionmentioning

confidence: 93%

Metaborreflexo inspiratório eleva a pressão arterial em indivíduos obesos e eutróficos

et al. 2019

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Resumo Introdução: O metaborreflexo, ativado pelo acúmulo de metabólitos durante o exercício, ocasiona vasoconstrição periférica, resultando em elevação da pressão arterial. Indivíduos obesos apresentam redução da endurance muscular inspiratória, sugerindo um acúmulo precoce de metabólitos e, consequentemente, alterações no metaborreflexo inspiratório. Objetivo: Comparar as respostas hemodinâmicas mediadas pelo metaborreflexo inspiratório em indivíduos obesos e em eutróficos. Método: Participaram do estudo vinte indivíduos obesos (31 ± 6 anos, dez homens, 37,5 ± 4,7 kg/m 2 ) e vinte eutróficos (29 ± 8 anos, dez homens, 23,2 ± 1,5 kg/m 2 ) submetidos a avaliação da força muscular respiratória através de manovacuometria. O metaborreflexo inspiratório foi induzido através de exercício resistido a 60% da pressão inspiratória máxima mantido até a exaustão. O protocolo controle consistiu na respiração sem resistência inspiratória (zero cmH 2 O) mantida durante 30 minutos. A pressão arterial e a frequência cardíaca foram mensuradas ao longo dos protocolos, realizados em dias distintos e em ordem randomizada. Resultados: O protocolo de indução do metaborreflexo inspiratório induziu aumento das pressões arteriais sistólica, diastólica e média, bem como da frequência cardíaca semelhante em indivíduos obesos e eutróficos. Conforme esperado, no protocolo controle as variáveis hemodinâmicas permaneceram inalteradas. Conclusão: A força muscular inspiratória não variou (p = 0,814) entre indivíduos obesos e eutróficos. Este estudo sugere que indivíduos obesos apresentam respostas hemodinâmicas, induzidas pelo metaborreflexo inspiratório, semelhantes aos indivíduos eutróficos.

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Obesity and Pulmonary Hypertension

Cited by 42 publications

References 100 publications

Differential serum lipid distribution in IPAH and CHD-PAH patients

Differential serum lipid distribution in IPAH and CHD-PAH patients

Obesity and COVID-19: Molecular Mechanisms Linking Both Pandemics

Metaborreflexo inspiratório eleva a pressão arterial em indivíduos obesos e eutróficos

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