Loss of Chromosome Y and Risk of Abdominal Aortic Aneurysm

Taylor Nordan; Tiffany R Bellomo; Md Mesba Uddin; Liying Xue; So Mi Jemma Cho; Kaavya Paruchuri; Marie Billaud; Peter Libby; Pradeep Natarajan; Tetsushi Nakao

doi:10.1001/jamacardio.2026.3981

. 2026 Sep 30:e263981. Online ahead of print. doi: 10.1001/jamacardio.2026.3981

Loss of Chromosome Y and Risk of Abdominal Aortic Aneurysm

Taylor Nordan ¹, Tiffany R Bellomo ^2,³, Md Mesba Uddin ^2,³, Liying Xue ^2,³, So Mi Jemma Cho ^2,³, Kaavya Paruchuri ^2,³, Marie Billaud ^1,⁴, Peter Libby ^1,⁴, Pradeep Natarajan ^2,^3,⁴, Tetsushi Nakao ^1,^2,^4,^✉

¹Heart and Vascular Institute, Mass General Brigham, Boston, Massachusetts

²Medical and Population Genetics Program and Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, Massachusetts

³Cardiovascular Research Center and Center for Genomic Medicine, Massachusetts General Hospital, Boston

⁴Harvard Medical School, Boston, Massachusetts

Accepted for Publication: August 17, 2026.

Published Online: September 30, 2026. doi:10.1001/jamacardio.2026.3981

Open Access: This is an open access article distributed under the terms of the CC-BY-NC-ND License, which does not permit alteration or commercial use, including those for text and data mining, AI training, and similar technologies. © 2026 Nordan T et al. JAMA Cardiology.

^✉

Corresponding Author: Tetsushi Nakao, MD, PhD, Heart and Vascular Institute, Mass General Brigham, 77 Avenue Louis Pasteur, Boston, MA 02115 (tnakao1@bwh.harvard.edu).

Author Contributions: Dr Nakao had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Nordan, Bellomo, Billaud, Libby, Natarajan, Nakao.

Acquisition, analysis, or interpretation of data: Bellomo, Uddin, Xue, Cho, Paruchuri, Billaud, Natarajan, Nakao.

Drafting of the manuscript: Nordan, Natarajan, Nakao.

Critical review of the manuscript for important intellectual content: All authors.

Statistical analysis: Nordan, Nakao.

Obtained funding: Libby, Natarajan, Nakao.

Administrative, technical, or material support: Bellomo, Cho, Libby, Nakao.

Supervision: Bellomo, Cho, Billaud, Libby, Natarajan, Nakao.

Conflict of Interest Disclosures: Dr Bellomo reported a grant from the National Heart, Lung, and Blood Institute (NHLBI) during the conduct of the study. Dr Paruchuri reported research grants paid to her institution from Allelica, Amgen, AstraZeneca, Boston Scientific, Genentech/Roche, Ionis, NewAmsterdam Pharma, and Novartis, personal fees from NewAmsterdam Pharma, and speaking fees from PeerView Institute for Medical Education Inc outside the submitted work. Dr Libby reported grants from the National Heart, Lung, and Blood Institute during the conduct of the study; and grants from Genentech, Novartis, and Novo Nordisk, scientific advisory board participation for Abcentra, Amgen, Caristo Diagnostics, Elucid Bioimaging, Kowa Pharmaceuticals, Novartis, Olatec Therapeutics, PlaqueTec, Polygon Therapeutics, Soley Therapeutics, TenSixteen Bio, and XBiotech Inc, financial interest in Soley Therapeutics, TenSixteen Bio, and XBiotech Inc, personal fees from Abcentra Inc, Analysis Group, DrugFarm, GlaxoSmithKline, Monte Rosa Therapeutics, Ventyx, and XBiotech Inc, serving on the board of directors for Abcentra Inc, and involvement in clinical trials for Abcentra, Amgen, Baim Institute, Beren Therapeutics, DrugFarm, Editas, Eli Lilly and Co, Esperion Therapeutics, Genentech, GlaxoSmithKline, Incyte, Kowa Pharmaceuticals, Monte Rosa Therapeutics, Novartis, Novo Nordisk, Sanofi-Regeneron, and Ventyx outside the submitted work. Dr Natarajan reported grants from Allelica, Amgen, Apple, Boston Scientific, Cleerly, Genentech/Roche, Ionis, Novartis, and Silence Therapeutics, personal fees from AIRNA, Allelica, Amgen, Apple, AstraZeneca, Bain Capital, Blackstone Life Sciences, Bristol Myers Squibb, Broadview Ventures, Creative Education Concepts, CRISPR Therapeutics, Eli Lilly and Co, Esperion Therapeutics, Foresite Capital, Foresite Labs, Genentech/Roche, GV, HeartFlow, Incyte, Magnet Biomedicine, Merck, Novartis, Novo Nordisk, TenSixteen Bio, Tourmaline Bio, and Ursa Medicines, equity in Bolt, Candela, Mercury, MyOme, Parameter Health, Preciseli, and TenSixteen Bio, royalties from Recora, and spousal employment at Vertex Pharmaceuticals outside the submitted work. Dr Nakao reported grants from NHLBI during the conduct of the study; and speaker fees from Kowa Co Ltd outside the submitted work. No other disclosures were reported.

Funding/Support: This work was supported by grants from NHLBI (Dr Nordan: T32HL007604; Dr Bellomo: F32HL174327; Dr Cho: K99HL177340; Dr Libby: R01HL170000, R01HL163099, R01HL151627, R01HL157073, R01HL166538; Dr Natarajan: R01HL168894; Dr Nakao: R00HL165024), the National Institute of Aging (Dr Libby: R01AG063839), and the RRM Charitable Fund (Dr Libby).

Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Data Sharing Statement: See the Supplement.

Additional Information: The UK Biobank was accessed through application 7089. Secondary use of the UK Biobank data was approved by the Massachusetts General Hospital institutional review board (2021P002228). The Mass General Brigham Biobank was accessed under protocol number 2018P001236.

^✉

Corresponding author.

PMCID: PMC13628381 PMID: 42814449

Abstract

This cohort study evaluates the association between loss of chromosome Y and the incidence of aortic aneurysm based on anatomic location.

Abdominal aortic aneurysm (AAA) accounts for nearly 170 000 deaths globally each year. Followed by cigarette smoking and older age, male sex is the cardinal AAA risk factor. However, the etiology of this sex disparity remains unclear, and no effective therapy yet exists to inhibit aneurysmal growth.

Hematologic loss of chromosome Y (LOY), or Y-chromosome loss in a subset of blood cells, is the most prevalent somatic genomic alteration observed in older men. LOY has emerged as a powerful predictor of cardiovascular mortality in this population and has been posited to explain the dichotomous sex distribution of several diseases, including aortic aneurysm. Although the pathophysiologies of aortic aneurysm vary significantly by anatomic location, no prior studies, to our knowledge, have examined the associations of LOY with AAA and thoracic aortic aneurysm (TAA) separately.

Using data from the UK Biobank (UKB) and Mass General Brigham Biobank (MGBB), we evaluated the association between LOY and the incidence of aortic aneurysm based on anatomic location.

Methods

The study protocol to analyze UKB and MGBB data was approved by the Mass General Brigham Institutional Review Board. All participants provided written informed consent. All data analyses were conducted between January 2025 and August 2026.

In this cohort study, we included UKB and MGBB participants who had genotyping array data and covariate information. LOY was previously detected from microarray intensity (UK Biobank Lung Exome Variant Evaluation [BiLEVE] and UK Biobank Axiom arrays in UKB; Illumina Global Screening Array in MGBB) using the MoChA software implementation and trichotomized by cell fraction (CF) using a previously defined cutoff with a modification for further granularity (low-CF LOY, 0% < CF < 9%; mid-CF LOY, 9% ≤ CF ≤ 17%; and high-CF LOY, CF > 17%). AAA and TAA were defined by International Classification of Diseases, Ninth Revision (ICD-9) and ICD-10 and procedure codes in both cohorts and further confirmed by radiology reports in the MGBB cohort.

In the UKB cohort, we modeled time to incident AAA or TAA using competing-risks regression with death as a competing risk, adjusting for age, smoking status, type 2 diabetes, hyperlipidemia, hypertension, and the first 10 genetic principal components at baseline. Participants were censored at last follow-up or 15 years. Sensitivity analyses used logistic regression including incident and prevalent cases and examined LOY as a continuous variable using competing-risks regression, with adjustment for identical covariates. Complete case analysis was used for multivariable modeling. MGBB validation used logistic regression given limited follow-up with identical covariates.

Analyses used R version 4.4.3 (R Foundation) and Stata version 17 (StataCorp LLC) statistical software. Two-tailed P < .05 was considered statistically significant.

Results

In the UKB cohort, among 221 486 men (mean [SD] age, 56.7 [8.2] years) without known aortic aneurysms who were genotyped, there were 187 295 men (84.6%) without LOY, 26 901 (11.8%) with low-CF LOY, 4887 (2.2%) with mid-CF LOY, and 2403 (1.1%) with high-CF LOY. Increasing LOY burden was associated with older age and higher rates of ever smoking, hypertension, diabetes, and hypercholesterolemia (Table).

Table. Baseline Characteristics of Men in the UK Biobank Cohort.

Characteristic	LOY status				P value for trend
Characteristic	None (n = 187 295)	Low, CF 0% to <9% (n = 26 901)	Mid, CF 9%-17% (n = 4887)	High, CF >17% (n = 2403)	P value for trend
Age, mean (SD), y	55.7 (8.2)	62.0 (5.6)	63.9 (4.3)	64.7 (4.0)	<.001
BMI, mean (SD)	27.9 (4.3)	27.6 (4.0)	27.6 (3.8)	27.5 (3.9)	<.001
Smoking, No. (%)
Never	96 191 (51.4)	10 842 (40.3)	1554 (31.8)	621 (25.8)	<.001
Prior	69 495 (37.1)	11 774 (43.8)	2322 (47.5)	1143 (47.6)
Current	21 609 (11.5)	4285 (15.9)	1011 (20.7)	639 (26.6)
Diabetes, No. (%)	12 768 (6.9)	2024 (7.5)	391 (8.0)	196 (8.2)	<.001
Hypertension, No. (%)	60 607 (32.4)	10 448 (38.8)	2025 (41.4)	1011 (42.1)	<.001
Hyperlipidemia, No. (%)	33 642 (18.0)	6579 (24.5)	1323 (27.1)	684 (28.5)	<.001
Antihypertensive agent, No. (%)	47 791 (25.5)	9270 (34.5)	1879 (38.4)	934 (38.9)	<.001
Lipid-lowering therapy, No. (%)	45 639 (24.4)	9180 (34.1)	1861 (38.1)	960 (40.0)	<.001
WBC count, mean (SD), /µL	6800 (2100)	7200 (1800)	7500 (1900)	7600 (2000)	<.001
RBC count, mean (SD), ×10⁶/µL	4.8 (0.4)	4.7 (0.4)	4.7 (0.4)	4.6 (0.4)	<.001
Platelet count, mean (SD), ×10³/µL	238 (56)	239 (55)	243 (58)	249 (61)	<.001
Cholesterol, mg/dL
Total	212.36 (42.47)	208.49 (42.47)	204.63 (42.47)	204.63 (42.47)	<.001
LDL-C	135.14 (34.75)	131.27 (34.75)	127.41 (34.75)	127.41 (34.75)	<.001
HDL-C	50.19 (11.58)	50.19 (11.58)	50.19 (11.58)	50.19 (11.58)	<.001
CF of LOY, median (IQR), %	NA	3.7 (1.9-5.6)	11.6 (10.1-13.7)	23.3 (19.5-29.4)	<.001

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Abbreviations: BMI, body mass index (calculated as weight in kilograms divided by height in meters squared); CF, cell fraction; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LOY, loss of chromosome Y; NA, not applicable; RBC, red blood cell; WBC, white blood cell.

SI conversion factors: To convert WBC count to ×10⁹ per liter, multiply by 0.001; RBC count to ×10¹² per liter, multiply by 1; platelet count to ×10⁹ per liter, multiply by 1; and total cholesterol, LDL-C, and HDL-C to millimoles per liter, multiply by 0.0259.

During a median (IQR) follow-up of 13.5 (12.8-14.2) years, 931 men (0.4%) developed AAA. The unadjusted incident rate increased as the LOY CF increased (Figure, A). For multivariable models, proportional hazards were confirmed using time-interaction terms. After adjustment, AAA risk increased dose dependently (low-CF LOY: subhazard ratio [sHR], 1.12 [95% CI, 0.96-1.34]; mid-CF LOY: sHR, 1.40 [95% CI, 1.07-1.84]; high-CF LOY: sHR, 1.73 [95% CI, 1.27-2.35]). In contrast, 221 men (0.1%) developed TAA with no significant unadjusted trend (Figure, B) or adjusted association (low-CF LOY: sHR, 0.82 [95% CI, 0.49-1.37]; mid-CF LOY: sHR, 1.08 [95% CI, 0.40-2.92]; high-CF LOY: sHR, 0.56 [95% CI, 0.08-4.10]). Examining LOY as a continuous predictor demonstrated increased risk of AAA development as LOY increased (sHR, 1.02 [95% CI, 1.01-1.04] per 1% CF increase); a significant association between TAA and LOY was not observed (sHR, 0.98 [95% CI, 0.92-1.03] per 1% CF increase). Sensitivity analyses including prevalent cases confirmed the AAA association (low-CF LOY: adjusted odds ratio [aOR], 1.09 [95% CI, 0.93-1.29]; mid-CF LOY: aOR, 1.46 [95% CI, 1.12-1.91]; high-CF LOY: aOR, 1.74 [95% CI, 1.29-2.36]) but no association with TAA.

Two-panel Kaplan–Meier plots of aneurysm incidence versus follow-up time by LOY group. Panel A at left titled Abdominal aortic aneurysm. Vertical axis labeled Cumulative incidence of A A A, percent, with tick marks at zero, one, two, and three. Horizontal axis labeled Follow-up time, y, ranging from zero to fifteen with labeled ticks at zero, three, six, nine, twelve, and fifteen. Four stepwise curves: magenta labeled L O Y high, greater than seventeen percent; blue labeled L O Y mid, nine percent to seventeen percent; orange labeled L O Y low, zero percent to nine percent; dark gray labeled No L O Y. A boxed legend in the upper left lists these four groups with matching line colors. By year fifteen, the magenta curve is near two point two percent, the blue curve near one point five percent, the orange curve near zero point eight percent, and the dark gray curve near zero point three percent. Below panel A, a No. at risk table lists counts at the same time points: L O Y high 2403, 2363, 2264, 2120, 1952, 619; L O Y mid 4887, 4827, 4674, 4446, 4163, 1263; L O Y low 26901, 26622, 25970, 25058, 23851, 7605; No L O Y 187295, 186122, 183398, 179624, 174660, 58641. Panel B at right titled Thoracic aortic aneurysm. Vertical axis labeled Cumulative incidence of T A A, percent, from zero to one point zero with ticks every zero point two. Horizontal axis labeled Follow-up time, y, from zero to fifteen with the same labeled ticks. Four stepwise curves with the same color mapping; the blue curve rises earliest and reaches about zero point two percent by year fifteen, orange and dark gray are near zero point one percent, and magenta remains near zero until a late rise to about zero point zero six to zero point zero seven percent. Below panel B, No. at risk counts: L O Y high 2403, 2368, 2275, 2137, 1979, 630; L O Y mid 4887, 4830, 4687, 4472, 4199, 1280; L O Y low 26901, 26642, 26029, 25140, 23957, 7635; No L O Y 187295, 186155, 183511, 179809, 174890, 58739. — A, Incidence of AAA, defined by *International Classification of Diseases, 10th Revision* (*ICD-10*) codes I71.3 and I71.4, *ICD-9* codes 4413 and 4414, or Office of Population Censuses and Surveys Classification of Interventions and Procedures version 4 (OPCS-4) codes L18.3, L18.4, L18.5, L19.3, L19.4, L19.5, L27.1, L27.2, L28.1, and L28.2. B, Incidence of TAA, defined by *ICD-10* codes I71.1 and I71.2, *ICD-9* codes 4411 and 4412, or OPCS-4 codes L18.1, L18.2, L19.1, L19.2, L27.3, and L28.3. Data are stratified by LOY status.

Among 14 569 men in the MGBB cohort (mean [SD] age, 54.9 [16.8] years), 1758 men (12.1%) had LOY, 536 (3.7%) had AAA, and 399 (2.7%) had TAA. LOY was associated with AAA, with increasing estimates by CF (low-CF LOY: aOR, 1.09 [95% CI, 0.81-1.46]; mid-CF LOY: aOR, 1.26 [95% CI, 0.82-1.92]; high-CF LOY: aOR, 1.38 [95% CI, 1.02-1.87]), but not with TAA.

Discussion

In 2 independent cohorts, LOY was associated with AAA but not TAA in a burden-dependent manner, identifying LOY as a novel, common somatic risk factor for AAA in older men. Despite a known association with age and smoking, LOY was associated with AAA independent of these traditional drivers, suggesting a distinct contribution.

Prior studies on LOY in aortic aneurysm are sparse. One small case-control study found a higher proportion of LOY in peripheral T lymphocytes among individuals with AAA, and a landmark study showed an association between LOY and global aortopathy but lacked granularity to distinguish thoracic from abdominal disease. Our findings are consistent with these observations while overcoming their limited phenotyping and small sample sizes, and they could point toward integrated screening and personalized follow-up of LOY burden and AAA development in older men.

Limitations include the observational study design, which precludes causal inference, and the small number of TAA cases, which yielded wide confidence intervals and limited statistical power to exclude an association at the highest LOY burden.

Although the biological mechanisms remain to be elucidated, we identify LOY as a novel and common risk factor for AAA in older men.

Supplement.

Data Sharing Statement

jamacardiol-e263981-s001.pdf^{(14.9KB, pdf)}

References

1.Golledge J, Thanigaimani S, Powell JT, Tsao PS. Pathogenesis and management of abdominal aortic aneurysm. Eur Heart J. 2023;44(29):2682-2697. doi: 10.1093/eurheartj/ehad386 [DOI] [PMC free article] [PubMed] [Google Scholar]
2.Kent KC, Zwolak RM, Egorova NN, et al. Analysis of risk factors for abdominal aortic aneurysm in a cohort of more than 3 million individuals. J Vasc Surg. 2010;52(3):539-548. doi: 10.1016/j.jvs.2010.05.090 [DOI] [PubMed] [Google Scholar]
3.Thompson DJ, Genovese G, Halvardson J, et al. ; International Lung Cancer Consortium (INTEGRAL-ILCCO); Breast Cancer Association Consortium; Consortium of Investigators of Modifiers of BRCA1/2; Endometrial Cancer Association Consortium; Ovarian Cancer Association Consortium; Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) Consortium; Kidney Cancer GWAS Meta-Analysis Project; eQTLGen Consortium; Biobank-Based Integrative Omics Study (BIOS) Consortium; 23andMe Research Team . Genetic predisposition to mosaic Y chromosome loss in blood. Nature. 2019;575(7784):652-657. doi: 10.1038/s41586-019-1765-3 [DOI] [PMC free article] [PubMed] [Google Scholar]
4.Sano S, Horitani K, Ogawa H, et al. Hematopoietic loss of Y chromosome leads to cardiac fibrosis and heart failure mortality. Science. 2022;377(6603):292-297. doi: 10.1126/science.abn3100 [DOI] [PMC free article] [PubMed] [Google Scholar]
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6.Koyama S, Wang Y, Paruchuri K, et al. Genetics and context for precision health in Greater Boston. Nat Commun. 2025;16(1):11661. doi: 10.1038/s41467-025-66598-8 [DOI] [PMC free article] [PubMed] [Google Scholar]
7.Zekavat SM, Lin SH, Bick AG, et al. ; Biobank Japan Project; FinnGen Consortium . Hematopoietic mosaic chromosomal alterations increase the risk for diverse types of infection. Nat Med. 2021;27(6):1012-1024. doi: 10.1038/s41591-021-01371-0 [DOI] [PMC free article] [PubMed] [Google Scholar]
8.Loh PR, Genovese G, McCarroll SA. Monogenic and polygenic inheritance become instruments for clonal selection. Nature. 2020;584(7819):136-141. doi: 10.1038/s41586-020-2430-6 [DOI] [PMC free article] [PubMed] [Google Scholar]
9.Weyrich M, Cremer S, Gerster M, et al. Loss of Y chromosome and cardiovascular events in chronic kidney disease. Circulation. 2024;150(10):746-757. doi: 10.1161/CIRCULATIONAHA.124.069139 [DOI] [PMC free article] [PubMed] [Google Scholar]
10.Tang D, Han Y, Lun Y, et al. Y chromosome loss is associated with age-related male patients with abdominal aortic aneurysms. Clin Interv Aging. 2019;14:1227-1241. doi: 10.2147/CIA.S202188 [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplement.

Data Sharing Statement

jamacardiol-e263981-s001.pdf^{(14.9KB, pdf)}

[hld260013r1] 1.Golledge J, Thanigaimani S, Powell JT, Tsao PS. Pathogenesis and management of abdominal aortic aneurysm. Eur Heart J. 2023;44(29):2682-2697. doi: 10.1093/eurheartj/ehad386 [DOI] [PMC free article] [PubMed] [Google Scholar]

[hld260013r2] 2.Kent KC, Zwolak RM, Egorova NN, et al. Analysis of risk factors for abdominal aortic aneurysm in a cohort of more than 3 million individuals. J Vasc Surg. 2010;52(3):539-548. doi: 10.1016/j.jvs.2010.05.090 [DOI] [PubMed] [Google Scholar]

[hld260013r3] 3.Thompson DJ, Genovese G, Halvardson J, et al. ; International Lung Cancer Consortium (INTEGRAL-ILCCO); Breast Cancer Association Consortium; Consortium of Investigators of Modifiers of BRCA1/2; Endometrial Cancer Association Consortium; Ovarian Cancer Association Consortium; Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) Consortium; Kidney Cancer GWAS Meta-Analysis Project; eQTLGen Consortium; Biobank-Based Integrative Omics Study (BIOS) Consortium; 23andMe Research Team . Genetic predisposition to mosaic Y chromosome loss in blood. Nature. 2019;575(7784):652-657. doi: 10.1038/s41586-019-1765-3 [DOI] [PMC free article] [PubMed] [Google Scholar]

[hld260013r4] 4.Sano S, Horitani K, Ogawa H, et al. Hematopoietic loss of Y chromosome leads to cardiac fibrosis and heart failure mortality. Science. 2022;377(6603):292-297. doi: 10.1126/science.abn3100 [DOI] [PMC free article] [PubMed] [Google Scholar]

[hld260013r5] 5.Bycroft C, Freeman C, Petkova D, et al. The UK Biobank resource with deep phenotyping and genomic data. Nature. 2018;562(7726):203-209. doi: 10.1038/s41586-018-0579-z [DOI] [PMC free article] [PubMed] [Google Scholar]

[hld260013r6] 6.Koyama S, Wang Y, Paruchuri K, et al. Genetics and context for precision health in Greater Boston. Nat Commun. 2025;16(1):11661. doi: 10.1038/s41467-025-66598-8 [DOI] [PMC free article] [PubMed] [Google Scholar]

[hld260013r7] 7.Zekavat SM, Lin SH, Bick AG, et al. ; Biobank Japan Project; FinnGen Consortium . Hematopoietic mosaic chromosomal alterations increase the risk for diverse types of infection. Nat Med. 2021;27(6):1012-1024. doi: 10.1038/s41591-021-01371-0 [DOI] [PMC free article] [PubMed] [Google Scholar]

[hld260013r8] 8.Loh PR, Genovese G, McCarroll SA. Monogenic and polygenic inheritance become instruments for clonal selection. Nature. 2020;584(7819):136-141. doi: 10.1038/s41586-020-2430-6 [DOI] [PMC free article] [PubMed] [Google Scholar]

[hld260013r9] 9.Weyrich M, Cremer S, Gerster M, et al. Loss of Y chromosome and cardiovascular events in chronic kidney disease. Circulation. 2024;150(10):746-757. doi: 10.1161/CIRCULATIONAHA.124.069139 [DOI] [PMC free article] [PubMed] [Google Scholar]

[hld260013r10] 10.Tang D, Han Y, Lun Y, et al. Y chromosome loss is associated with age-related male patients with abdominal aortic aneurysms. Clin Interv Aging. 2019;14:1227-1241. doi: 10.2147/CIA.S202188 [DOI] [PMC free article] [PubMed] [Google Scholar]

PERMALINK

Loss of Chromosome Y and Risk of Abdominal Aortic Aneurysm

Taylor Nordan, MD

Tiffany R Bellomo, MD

Md Mesba Uddin, PhD

Liying Xue, MS

So Mi Jemma Cho, PhD

Kaavya Paruchuri, MD

Marie Billaud, PhD

Peter Libby, MD

Pradeep Natarajan, MD, MMSc

Tetsushi Nakao, MD, PhD

Abstract

Methods

Results

Table. Baseline Characteristics of Men in the UK Biobank Cohort.

Figure. Kaplan-Meier Curves for the Survival Analysis of the Incidence of Abdominal Aortic Aneurysm (AAA) and Thoracic Aortic Aneurysm (TAA) by Hematologic Loss of Chromosome Y (LOY) Status at Baseline in 221 486 Men in the UK Biobank.

Discussion

References

Associated Data

Supplementary Materials

ACTIONS

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PERMALINK

Loss of Chromosome Y and Risk of Abdominal Aortic Aneurysm

Taylor Nordan, MD

Tiffany R Bellomo, MD

Md Mesba Uddin, PhD

Liying Xue, MS

So Mi Jemma Cho, PhD

Kaavya Paruchuri, MD

Marie Billaud, PhD

Peter Libby, MD

Pradeep Natarajan, MD, MMSc

Tetsushi Nakao, MD, PhD

Abstract

Methods

Results

Table. Baseline Characteristics of Men in the UK Biobank Cohort.

Figure. Kaplan-Meier Curves for the Survival Analysis of the Incidence of Abdominal Aortic Aneurysm (AAA) and Thoracic Aortic Aneurysm (TAA) by Hematologic Loss of Chromosome Y (LOY) Status at Baseline in 221 486 Men in the UK Biobank.

Discussion

References

Associated Data

Supplementary Materials

ACTIONS

PERMALINK

RESOURCES

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