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Peer-reviewedCC BY-NC-ND 4.0Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Social Determinants of Health and Polygenic Susceptibility in Nonsyndromic Ascending Aortic Aneurysm

  • Navraj S. Sagoo1,2,3
  • Rajveer Sagoo1,2
  • Jaden F. LeGate1
  • Isabela A. Maluli1
  • Charlene N. Radler1
  • Tianci Wang1
  • Mohanakrishnan Sathyamoorthy1,2,3,4,5
5 affiliations
  1. 1Sathyamoorthy Lab, Department of Internal Medicine Burnett School of Medicine at Texas Christian University Fort Worth TX USA
  2. 2College of Science and Engineering Texas Christian University Fort Worth TX USA
  3. 3University of Tennessee‐Chattanooga Chattanooga TN USA
  4. 4Consultants in Cardiovascular Medicine and Science Fort Worth TX USA
  5. 5Fort Worth Institute for Molecular Medicine and Genomics Research Fort Worth TX USA
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Abstract

Background: Nonsyndromic ascending aortic aneurysm (AsAA) may remain clinically silent until dissection or rupture. The contributions of multidomain social determinants of health (SDOH) and polygenic susceptibility to AsAA risk are not well defined.

Methods: In a cross‐sectional analysis of 124 180 participants in the National Institutes of Health All of Us Research Program, 14 SDOH measures were summarized as a standardized composite score, and an ascending aortic diameter polygenic risk score (PRS; polygenic score, 004927) was standardized within ancestry strata. Associations were tested using Firth‐penalized logistic regression adjusted for clinical risk factors; discrimination was assessed by area under the receiver operating characteristic curve.

Results: Among 124 180 participants, 346 had AsAA. Compared with controls, cases were older (mean age, 70.7±9.0 versus 57.1±16.4 years) and more often men (60.4% versus 37.1%). Each 1‐SD increase in the SDOH composite was associated with AsAA after clinical adjustment (odds ratio, 1.21 [95% CI, 1.04–1.40]) and in joint models including PRS (odds ratio, 1.28 [95% CI, 1.11–1.48]). The PRS was associated with AsAA after clinical adjustment (odds ratio per SD, 1.94 [95% CI, 1.74–2.16]); AsAA prevalence increased from 0.08% (lowest PRS decile) to 0.77% (highest). SDOH and PRS were minimally correlated (r=−0.002), with no evidence of interaction (interaction odds ratio, 1.03; P=0.62). Discrimination improved from basic covariates (area under the receiver operating characteristic curve, 0.774) to clinical covariates (area under the receiver operating characteristic curve, 0.841) and to the full model including SDOH and PRS (area under the receiver operating characteristic curve, 0.870 [95% CI, 0.851–0.889]).

Conclusions: Social adversity and higher polygenic susceptibility were associated with nonsyndromic AsAA, supporting further study of integrated social and genetic risk stratification.

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Cite

BibTeXRIS
BibTeX
@article{sagoo2026social,
  title = {{Social Determinants of Health and Polygenic Susceptibility in Nonsyndromic Ascending Aortic Aneurysm}},
  author = {Navraj S. Sagoo and Rajveer Sagoo and Jaden F. LeGate and Isabela A. Maluli and Charlene N. Radler and Tianci Wang and Mohanakrishnan Sathyamoorthy},
  journal = {Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease},
  year = {2026},
  month = aug,
  doi = {10.1161/jaha.126.050179},
  url = {https://doi.org/10.1161/jaha.126.050179},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Social Determinants of Health and Polygenic Susceptibility in Nonsyndromic Ascending Aortic Aneurysm
AU  - Navraj S. Sagoo
AU  - Rajveer Sagoo
AU  - Jaden F. LeGate
AU  - Isabela A. Maluli
AU  - Charlene N. Radler
AU  - Tianci Wang
AU  - Mohanakrishnan Sathyamoorthy
PY  - 2026
DA  - 2026/08/30
JO  - Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
DO  - 10.1161/jaha.126.050179
UR  - https://doi.org/10.1161/jaha.126.050179
AB  - Background: Nonsyndromic ascending aortic aneurysm (AsAA) may remain clinically silent until dissection or rupture. The contributions of multidomain social determinants of health (SDOH) and polygenic susceptibility to AsAA risk are not well defined.  Methods: In a cross‐sectional analysis of 124 180 participants in the National Institutes of Health All of Us Research Program, 14 SDOH measures were summarized as a standardized composite score, and an ascending aortic diameter polygenic risk score (PRS; polygenic score, 004927) was standardized within ancestry strata. Associations were tested using Firth‐penalized logistic regression adjusted for clinical risk factors; discrimination was assessed by area under the receiver operating characteristic curve.  Results: Among 124 180 participants, 346 had AsAA. Compared with controls, cases were older (mean age, 70.7±9.0 versus 57.1±16.4 years) and more often men (60.4% versus 37.1%). Each 1‐SD increase in the SDOH composite was associated with AsAA after clinical adjustment (odds ratio, 1.21 [95% CI, 1.04–1.40]) and in joint models including PRS (odds ratio, 1.28 [95% CI, 1.11–1.48]). The PRS was associated with AsAA after clinical adjustment (odds ratio per SD, 1.94 [95% CI, 1.74–2.16]); AsAA prevalence increased from 0.08% (lowest PRS decile) to 0.77% (highest). SDOH and PRS were minimally correlated (r=−0.002), with no evidence of interaction (interaction odds ratio, 1.03; P=0.62). Discrimination improved from basic covariates (area under the receiver operating characteristic curve, 0.774) to clinical covariates (area under the receiver operating characteristic curve, 0.841) and to the full model including SDOH and PRS (area under the receiver operating characteristic curve, 0.870 [95% CI, 0.851–0.889]).  Conclusions: Social adversity and higher polygenic susceptibility were associated with nonsyndromic AsAA, supporting further study of integrated social and genetic risk stratification.
SN  - 2047-9980
ER  -