Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 Mar 30;19(1):41.
doi: 10.1186/s12933-020-01017-4.

Change in Glucose Intolerance Status and Risk of Incident Cardiovascular Disease: Tehran Lipid and Glucose Study

Affiliations
Free PMC article

Change in Glucose Intolerance Status and Risk of Incident Cardiovascular Disease: Tehran Lipid and Glucose Study

Maryam Kabootari et al. Cardiovasc Diabetol. .
Free PMC article

Abstract

Background: To assess the impact of changes in different glucose tolerance states on risk of incident cardiovascular disease (CVD)/coronary heart disease (CHD).

Methods: A total of 4094 Iranians (43.9% men) aged ≥ 30 years, without diabetes and CVD at enrolment were included. The following categories were defined both at baseline visit and 3 years later (second visit): normal fasting glucose (NFG), normal glucose tolerance (NGT), NFG and NGT (NFG/NGT), impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and IFG and/or IGT (IFG/IGT). Changes in the categories, i.e. regression to normoglycemia, remaining in previous status and progression to diabetes were assessed. We used Cox's proportional hazard models adjusted for traditional risk factors and their changes, to estimate the hazard ratio (HR) with 95% confidence interval (CI) of different changing categories for incident CVD/CHD.

Results: During a median follow-up of 12.42 years, 428 subjects (men = 265) experienced CVD. Considering persistent NFG/NGT as reference, participants who shifted from NFG/NGT to IFG/IGT showed a lower hazard of CVD in the fully adjusted model, HR 0.72 [95% CI 0.52-0.996, P = 0.048]. Moreover, subjects who shifted from IFG, IGT and IFG/IGT to diabetes had an increased risk of CVD/CHD. The risk however, was only statistically significant for those with IFG/IGT, 1.61 [(1.03-2.51), P = 0.04] for CVD and 1.75 [(1.10-2.78), P = 0.02] for CHD; considering IFG/IGT at both visits as reference. Furthermore, those who regressed from IFG/IGT to normoglycemia were at the same risk as those remained in IFG/IGT state, 1.12 [(0.79-1.60), P = 0.52] for CVD and 1.04 [(0.70-1.53), P = 0.85] for CHD. Among a subgroup of population with insulin data (n = 803) those with insulin resistance (IR) that converted to diabetes showed a higher risk for CVD, 3.68 [(1.49-9.06), P = 0.01] and CHD, 2.76 [(1.00-7.60), P = 0.05] events in the fully adjusted model.

Conclusions: Among participants with IFG, IGT or IFG/IGT at baseline, only those who developed diabetes had a higher risk of developing CVD/CHD. Persistent IFG/IGT was not associated with higher risk, compared with those reverted to normoglycemia. Moreover, subjects who converted from NFG/NGT to incident IFG/IGT showed a signal for lower risk of CVD/CHD.

Keywords: Cardiovascular disease; Impaired fasting glucose; Impaired glucose tolerance.

Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Timeline of the study design. Subjects without diabetes and cardiovascular disease at first visit (1999–2002) or (2002–2005) were followed 3 years later for the following changes: (1) Normal fasting glucose (NFG) to NFG or impaired fasting glucose (IFG), (2) Normal glucose tolerance (NGT) to NGT or impaired glucose tolerance (IGT), (3) NFG and NGT (NFG/NGT) to NFG/NGT or IFG/IGT, (4) IFG to NFG, IFG or diabetes, (5) IGT to NGT, IGT or diabetes and 6) IFG and/or IGT (IFG/IGT) to NFG/NGT, IFG/IGT or diabetes. Regarding the limited number of those with normoglycemia at baseline who directly converted to diabetes [NFG to diabetes (n = 60), NGT to diabetes (n = 52), NFG/NGT to diabetes (n = 24)], these groups were excluded
Fig. 2
Fig. 2
HRs (95% CI) of CVD and CHD for subjects with incident IFG, IGT and IFG/IGT. HR, hazard ratios; CI, confidence interval; CVD, cardiovascular disease; CHD, coronary heart disease; NFG, normal fasting glucose; IFG, impaired fasting glucose; NGT, normal glucose tolerance; IGT, impaired glucose tolerance. NFG/NGT was defined as those with both NFG and NGT states. IFG/IGT was defined as those with IFG and/or IGT. Model 1: Age, sex. Model 2: Model 1 + systolic blood pressure, diastolic blood pressure, total cholesterol, high density lipoprotein-cholesterol, waist circumference, eGFR, physical activity, smoking, education and use of anti-hypertensive drugs. Model 3: Model 2 + change of waist circumference, total cholesterol and high density lipoprotein-cholesterol. a Hazard of CVD in subjects with incident IFG compared to those with NFG in both visits; b hazard of CVD in subjects with incident IGT compared to those with NGT in both visits; c hazard of CVD in subjects with incident IFG/IGT compared to those with NFG/NGT in both visits; d hazard of CHD in subjects with incident IFG compared to those with NFG in both visits; e hazard of CHD in subjects with incident IGT compared to those with NGT in both visits; f hazard of CHD in subjects with incident IFG/IGT compared to those with NFG/NGT in both visits
Fig. 3
Fig. 3
HRs (95% CI) of CVD and CHD for subjects with glucose intolerance at the first visit with their changing status at first follow-up. HR, hazard ratios; CI, confidence interval; CVD, cardiovascular disease; CHD, coronary heart disease; NFG normal fasting glucose; IFG, impaired fasting glucose; NGT, normal glucose tolerance; IGT, impaired glucose tolerance. NFG/NGT was defined as those with both NFG and NGT states. IFG/IGT was defined as those with IFG and/or IGT. Model 1: Age, sex. Model 2: Model 1 systolic blood pressure, diastolic blood pressure, total cholesterol, high density lipoprotein-cholesterol, waist circumference, eGFR physical activity, smoking, education and use of anti-hypertensive drug. Model 3: Model 2 + change of waist circumference, total cholesterol and high density lipoprotein-cholesterol. a Hazard of CVD in subjects with IFG at the first examination; b hazard of CVD in subjects with IGT at the first examination; c hazard of CVD in subjects with IFG/IGT at the first examination; d hazard of CHD in subjects with IFG at the first examination; e hazard of CHD in subjects with IGT at the first examination; f hazard of CHD in subjects with IFG/IGT at the first examination

Similar articles

See all similar articles

References

    1. Tabák AG, Herder C, Rathmann W, Brunner EJ, Kivimäki M. Prediabetes: a high-risk state for diabetes development. Lancet. 2012;379(9833):2279–2290. doi: 10.1016/S0140-6736(12)60283-9. - DOI - PMC - PubMed
    1. Geva M, Shlomai G, Berkovich A, Maor E, Leibowitz A, Tenenbaum A, Grossman E. The association between fasting plasma glucose and glycated hemoglobin in the prediabetes range and future development of hypertension. Cardiovasc Diabetol. 2019;18(1):53. doi: 10.1186/s12933-019-0859-4. - DOI - PMC - PubMed
    1. Sánchez E, Betriu À, López-Cano C, Hernández M, Fernández E, Purroy F, Bermúdez-López M, Farràs-Sallés C, Barril S, Pamplona R. Characteristics of atheromatosis in the prediabetes stage: a cross-sectional investigation of the ILERVAS project. Cardiovasc Diabetol. 2019;18(1):1–12. doi: 10.1186/s12933-019-0962-6. - DOI - PMC - PubMed
    1. Huang Y, Cai X, Mai W, Li M, Hu Y. Association between prediabetes and risk of cardiovascular disease and all cause mortality: systematic review and meta-analysis. BMJ. 2016;355:i5953. doi: 10.1136/bmj.i5953. - DOI - PMC - PubMed
    1. Esteghamati A, Gouya MM, Abbasi M, Delavari A, Alikhani S, Alaedini F, Safaie A, Forouzanfar M, Gregg EW. Prevalence of diabetes and impaired fasting glucose in the adult population of Iran: National Survey of Risk Factors for Non-Communicable Diseases of Iran. Diabetes Care. 2008;31(1):96–98. doi: 10.2337/dc07-0959. - DOI - PubMed

LinkOut - more resources

Feedback