Evidence map›Paper›PMID 40435179›Full record

ArticlePloS one2025

Long-term glycemic variability and the risk of cardiovascular diseases in type 2 diabetic patients: Effect of hypothetical interventions using parametric g-formula in a population-based historical cohort study.

Khadije Maajani, Ensieh Nasli-Esfahani, Noushin Fahimfar, Ali Sheidaei, Mohammad Ali Mansournia, Kamran Yazdani

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

Who cites it

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Observational
4 · The record

Corrections and comments

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

6 authors.

Khadije MaajaniDepartment of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Ensieh Nasli-EsfahaniDiabetes Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Noushin FahimfarDepartment of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Ali SheidaeiDepartment of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0002-0480-5768
Mohammad Ali MansourniaDepartment of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Kamran YazdaniDepartment of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0001-6666-1272

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHarmful effects of long-term HbA1c and fasting plasma glucose (FPG) variability on cardiovascular diseases (CVD) have not been causally examined. We employed a parametric g-formula to estimate the causal effect of HbA1C and fasting plasma glucose (FPG) variability on CVD.

methodsThis retrospective cohort study was conducted on 2078 patients with type 2 diabetes who were free of CVD and aged >18 years at the entrance to the clinic (2017-2022), with at least three HbA1c and FPG measurements. Variability was calculated using standard deviation (SD), and coefficient of variation (CV). We used the parametric g-formula to estimate the 5-year risk, risk ratio, and risk difference of CVD under different deciles of HbA1c-SD/CV, FPG-SD/CV, HbA1C levels (≤5%, 5 to ≤7%, and >7), and joint exposure to different deciles of HbA1c-SD and HbA1c values, adjusted for time-varying confounders that are affected by prior exposure.

resultsThe observed and simulated 5-year risk of CVD under no intervention were 11.6% (95% CI: 10.3, 13.1) and 11.03% (95% CI: 10.2, 12.6) for HbA1C-SD model. The estimated 5-year risk of CVD was increased from the 8.01% (95% CI: 7.5, 10.1%) in the first decile to 15.2% (95% CI: 14.1, 17.7%) in the tenth decile of HbA1c-SD. The results for FPG-SD were similar. Within the stable level of HbA1c (5 to ≤7%) the risk ratio increased from 1.37 (95% CI: 1.19, 1.48) in the first decile to 2.76 (95% CI: 2.06, 3.09) in the tenth decile of HbA1c-SD. Under a joint intervention of HbA1c <5% and the first decile of HbA1c-SD, CVD risk decreased by 6.4% (95%CI: 4.9, 7.3%) compared to the natural course.

conclusionsEven within a stable HbA1c level, long-term glycemic variability may be a strong predictor of CVD.

Indexed as

Blood GlucoseCardiovascular DiseasesDiabetes Mellitus, Type 2AdultAgedCohort StudiesFastingFemaleGlycated HemoglobinHumansMaleMiddle AgedRetrospective StudiesRisk FactorsBlood GlucoseGlycated Hemoglobinhemoglobin A1c protein, human

Identifiers

PMID40435179
PMCPMC12118876

What Socratic holds

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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.