Evidence mapPaperPMID 42387180Full record

ArticleGeroScience2026

Longitudinal lipidomic markers of cardiac aging and risk of coronary heart disease in American Indians: the Strong Heart Family Study.

Mingjing Chen, Yixi Sun, Guanhong Miao, Xiaoxiao Wen, Alexander C Razavi, Camilo Fernandez, Mary J Roman, Richard B Devereux, Richard R Fabsitz, Ying Zhang and 6 more

Abstract read
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In one paragraph

Article in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Mingjing ChenDepartment of Neurology, Johns Hopkins University, Baltimore, MD, USA.
Yixi SunDivision of Epidemiology and Biostatistics, School of Public Health, University of Illinois Chicago, Chicago, IL, USA.
Guanhong MiaoHealth Informatics Institute, University of South Florida, 3650 Spectrum Blvd, Tampa, FL, 33612, USA.
Xiaoxiao WenHealth Informatics Institute, University of South Florida, 3650 Spectrum Blvd, Tampa, FL, 33612, USA.
Alexander C RazaviEmory Center for Heart Disease Prevention, Emory University School of Medicine, Atlanta, GA, USA.
Camilo FernandezTulane University Health Sciences Center, New Orleans, LA, USA.
Mary J RomanDivision of Cardiology, Weill Cornell Medical College, New York City, NY, USA.
Richard B DevereuxDivision of Cardiology, Weill Cornell Medical College, New York City, NY, USA.
Richard R FabsitzMissouri Breaks Industries Research Inc, Eagle Butte, SD, USA.
Ying ZhangDepartment of Biostatistics and Epidemiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Jason G UmansMedStar Health Research Institute, Hyattsville, MD, USA.
Shelley A ColeTexas Biomedical Research Institute, San Antonio, TX, USA.
Lydia A BazzanoTulane University Health Sciences Center, New Orleans, LA, USA.
Oliver FiehnWest Coast Metabolomics Center, University of California-Davis, Davis, CA, USA.
Tanika N KellyDivision of Epidemiology and Biostatistics, School of Public Health, University of Illinois Chicago, Chicago, IL, USA.
Jinying ZhaoHealth Informatics Institute, University of South Florida, 3650 Spectrum Blvd, Tampa, FL, 33612, USA. jinyingz@usf.edu.ORCID http://orcid.org/0000-0003-3243-2660

Funding

National Institute of Health R01DK107532
6 · The paper itself

Abstract

Age-related decline in left ventricular (LV) diastolic function is a hallmark of cardiac aging and an early precursor to cardiovascular disease. While dyslipidemia is a known driver of coronary heart disease (CHD), the molecular pathways linking lipid metabolism to cardiac aging and subsequent CHD risk remain poorly understood. Furthermore, longitudinal lipidomic profiling of cardiac aging in large human populations has not been systematically conducted. Using an untargeted LC-MS, we repeatedly measured 1542 fasting plasma lipid species in 1801 American Indians across two clinical exams in the Strong Heart Family Study (SHFS) (mean age at baseline: 40.0 years; mean interval: 5.5 years apart). We examined longitudinal associations between individual lipid species and measures of cardiac aging (E/A ratio, isovolumic relaxation time, and deceleration time) using generalized estimation equation (GEE), adjusted for demographic, lifestyle, and clinical factors. Significant associations were then replicated in the Bogalusa Heart Study (BHS) (mean age at baseline: 48.1 years). Frailty Cox proportional hazards models were used to examine whether cardiac aging-related lipids predicted incident CHD over a 20-year follow-up. We found that multiple lipid species, primarily glycerophospholipids, glycerolipids, and sphingomyelins, were associated with measures of cardiac aging, with the majority showing inverse associations. Some of these associations were confirmed in a biracial cohort of African American and White participants. Additionally, baseline levels of specific glycerophospholipids and fatty acids associated with diastolic function (E/A ratio and deceleration time) were linked to a reduced risk of CHD (HR range: 0.21-0.86). Conversely, other E/A-associated glycerophospholipids were linked to increased CHD risk (HR range: 1.24-1.34). In summary, we identified distinct lipidomic signatures associated with trajectories of subclinical cardiac aging, several of which also predict later-life CHD risk. These findings highlight molecular correlates of cardiac aging from midlife into older adulthood and suggest that lipidomic pathways may serve as early biomarkers for future: Keywords are required, The following are suggested: "Cardiac aging, Risk, Lipidomic markers". Please check if correct. CHD.

Indexed as

Cardiac agingCoronary heart disease riskLipidomic markers

Identifiers

PMID42387180

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.