Association Between Body Mass Index and Perioperative Mortality After Repair of Ruptured Abdominal Aortic Aneurysms

Liang, Tiffany W.; Wang, S. Keisin; DiMusto, Paul D.; McAninch, Christopher M.; Acher, Charles W.; Timsina, Lava; Dalsing, Michael C.; Motaganahalli, Raghu L.

doi:10.1177/1538574420939356

Cited by 6 publications

(3 citation statements)

References 25 publications

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“…We used a ubiquitously used model, relevant to clinical findings that obesity and hypertension increase the risk of mortality in AA and AAD. 58,59 The results (Figures 1, 2 and Figure S1) confirmed that AngII/AT1R interaction in the context of ApoE −/− genotype and high-fat diet together create the AA and AAD disease state. Therefore, TRV027 and OLM were tested in this model for efficacy to prevent the disease.…”

Section: Discussionsupporting

confidence: 58%

Distinct Mechanisms of β-Arrestin–Biased Agonist and Blocker of AT1R in Preventing Aortic Aneurysm and Associated Mortality

et al. 2023

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BACKGROUND: Aortic aneurysm (AA) is a “silent killer” human disease with no effective treatment. Although the therapeutic potential of various pharmacological agents have been evaluated, there are no reports of β-arrestin–biased AT1R agonist (TRV027) used to prevent the progression of AA. METHODS: We tested the hypothesis that TRV027 infusion in AngII-induced mouse model of AA prevents AA. High–fat-diet–fed ApoE-null mice were infused with AngII to induce AA and co-infused with TRV027 and a clinically used AT1R blocker Olmesartan to prevent AA. Aortas explanted from different ligand infusion groups were compared with assess different grades of AA or lack of AA. RESULTS: AngII produced AA in ≈67% male mice with significant mortality associated with AA rupture. We observed ≈13% mortality due to aortic arch dissection without aneurysm in male mice. AngII-induced AA and mortality was prevented by co-infusion of TRV027 or Olmesartan, but through different mechanisms. In TRV027 co-infused mice aortic wall thickness, elastin content, new DNA, and protein synthesis were higher than untreated and Olmesartan co-infused mice. Co-infusion with both TRV027 and Olmesartan prevented endoplasmic reticulum stress, fibrosis, and vasomotor hyper responsiveness. CONCLUSIONS: TRV027-engaged AT1R prevented AA and associated mortality by distinct molecular mechanisms compared with the AT1R blocker, Olmesartan. Developing novel β-arrestin–biased AT1R ligands may yield promising drugs to combat AA.

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Section: Discussionsupporting

confidence: 58%

Distinct Mechanisms of β-Arrestin–Biased Agonist and Blocker of AT1R in Preventing Aortic Aneurysm and Associated Mortality

et al. 2023

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“…There were 28 studies 70,96,107,109,150,156,160–181 (29 cohorts; 2,068,365 participants) with surgical populations (Table S3): 17 cohorts in North America, 6 were in Europe, 4 in East Asia, and 1 each in South Asian and the Pacific. Mean age of participants ranged from 46 to 83 years.…”

Section: Resultsmentioning

confidence: 99%

Associations between body mass index and all‐cause mortality: A systematic review and meta‐analysis

2023

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SummaryFasting insulin and c‐reactive protein confound the association between mortality and body mass index. An increase in fat mass may mediate the associations between hyperinsulinemia, hyperinflammation, and mortality. The objective of this study was to describe the “average” associations between body mass index and the risk of mortality and to explore how adjusting for fasting insulin and markers of inflammation might modify the association of BMI with mortality. MEDLINE and EMBASE were searched for studies published in 2020. Studies with adult participants where BMI and vital status was assessed were included. BMI was required to be categorized into groups or parametrized as non‐first order polynomials or splines. All‐cause mortality was regressed against mean BMI squared within seven broad clinical populations. Study was modeled as a random intercept. β coefficients and 95% confidence intervals are reported along with estimates of mortality risk by BMIs of 20, 30, and 40 kg/m2. Bubble plots with regression lines are drawn, showing the associations between mortality and BMI. Splines results were summarized. There were 154 included studies with 6,685,979 participants. Only five (3.2%) studies adjusted for a marker of inflammation, and no studies adjusted for fasting insulin. There were significant associations between higher BMIs and lower mortality risk in cardiovascular (unadjusted β −0.829 [95% CI −1.313, −0.345] and adjusted β −0.746 [95% CI −1.471, −0.021]), Covid‐19 (unadjusted β −0.333 [95% CI −0.650, −0.015]), critically ill (adjusted β −0.550 [95% CI −1.091, −0.010]), and surgical (unadjusted β −0.415 [95% CI −0.824, −0.006]) populations. The associations for general, cancer, and non‐communicable disease populations were not significant. Heterogeneity was very large (I2 ≥ 97%). The role of obesity as a driver of excess mortality should be critically re‐examined, in parallel with increased efforts to determine the harms of hyperinsulinemia and chronic inflammation.

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“…A retrospective study involving 5,455 AAA patients revealed that morbidly obese individuals (BMI>34 kg/m 2 ) exhibited higher 30-day mortality rates in both open aneurysm repair (OAR) and endovascular aneurysm repair (EVAR) procedures compared to non-obese patients, including those with milder obesity ( 24 ). Additionally, for every 1 kg/m2 increase in BMI, the risk of 30-day death in hospitalized patients undergoing repair for ruptured abdominal aortic aneurysm was significantly elevated by 1.08 (95% CI,1.01-1.17; P=0.04) ( 23 ).…”

Section: Obesity To Aaa: Foe or Friend?mentioning

confidence: 99%

Obesity and the obesity paradox in abdominal aortic aneurysm

Lu,

Lin,

Zhou

et al. 2024

Front. Endocrinol.

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Obesity, characterized by its complexity and heterogeneity, has emerged as a significant public health concern. Its association with increased incidence and mortality of cardiovascular diseases stems not only from its complications and comorbidities but also from the endocrine effects of adipose tissue. Abdominal aortic aneurysm (AAA), a chronic inflammatory condition, has been closely linked to obesity. Intriguingly, mild obesity appears to confer a protective effect against AAA mortality, whereas severe obesity and being underweight do not, giving rise to the concept of the “obesity paradox”. This review aims to provide an overview of obesity and its paradoxical relationship with AAA, elucidate its underlying mechanisms, and discuss the importance of preoperative weight loss in severely obese patients with AAA.

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Association Between Body Mass Index and Perioperative Mortality After Repair of Ruptured Abdominal Aortic Aneurysms

Cited by 6 publications

References 25 publications

Distinct Mechanisms of β-Arrestin–Biased Agonist and Blocker of AT1R in Preventing Aortic Aneurysm and Associated Mortality

Distinct Mechanisms of β-Arrestin–Biased Agonist and Blocker of AT1R in Preventing Aortic Aneurysm and Associated Mortality

Associations between body mass index and all‐cause mortality: A systematic review and meta‐analysis

Obesity and the obesity paradox in abdominal aortic aneurysm

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