Nondiabetic glucometabolic status and progression of aortic stiffness

The whitehall II study

Carmel M. McEniery, Ian B. Wilkinson, Nanna B. Johansen, Daniel R. Witte, Archana Singh-Manoux, Mika Kivimaki, A. Tabák, Eric J. Brunner, Martin J. Shipley

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

OBJECTIVE Aortic stiffness is an important predictor of futuremorbidity andmortality. Diabetes is associated with increased aortic stiffness, but the importance of nondiabetic glucometabolic status for accelerated aortic stiffening is unclear. We tested the hypothesis that adverse glucometabolic status is associated with accelerated aortic stiffening in individuals without diabetes, independently of known risk factors for arterial stiffening. RESEARCH DESIGN AND METHODS Glucometabolic status and other cardiovascular risk factors were assessed at baseline in 2008-09, and carotid femoral pulse wave velocity (cfPWV) at baseline and follow-up in 2012-13, in 4, 386 participants without diabetes of theWhitehall II Study. RESULTS The mean age of the cohort at cfPWV baseline was 60 years, and 74% were male. cfPWV increased from (mean ± SE) 8.30± 0.03 to 8.98± 0.04 m/s during 4 years of follow-up. At baseline, cfPWV was associated with fasting and 2-h postload glucose, HbA1c, and HOMA-insulin resistance (HOMA-IR). HbA1c and HOMA-IR were associated with progression of cfPWV after adjusting for physiological confounders and cardiovascular risk factors. A 1 SD higher HbA1c and HOMA-IR were associated with greater increases in cfPWV (0.11 m/s per 5 years [95% CI 0.04, 0.18], P = 0.003 and 0.09 m/s per 5 years [0.01, 0.17], P = 0.03, respectively). Additional adjustment for BMI weakened the association with HOMA-IR but not with HbA1c. CONCLUSIONS HbA1c is independently associated with accelerated progression of aortic stiffness in individuals without diabetes. These findings suggest that long-term glucometabolic status, even in individuals without diabetes, could be an important target for preventative strategies against vascular aging.

Original languageEnglish
Pages (from-to)599-606
Number of pages8
JournalDiabetes Care
Volume40
Issue number4
DOIs
Publication statusPublished - Apr 1 2017

Fingerprint

Pulse Wave Analysis
Vascular Stiffness
Thigh
Insulin Resistance
Blood Vessels
Fasting
Glucose

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Advanced and Specialised Nursing

Cite this

McEniery, C. M., Wilkinson, I. B., Johansen, N. B., Witte, D. R., Singh-Manoux, A., Kivimaki, M., ... Shipley, M. J. (2017). Nondiabetic glucometabolic status and progression of aortic stiffness: The whitehall II study. Diabetes Care, 40(4), 599-606. https://doi.org/10.2337/dc16-1773

Nondiabetic glucometabolic status and progression of aortic stiffness : The whitehall II study. / McEniery, Carmel M.; Wilkinson, Ian B.; Johansen, Nanna B.; Witte, Daniel R.; Singh-Manoux, Archana; Kivimaki, Mika; Tabák, A.; Brunner, Eric J.; Shipley, Martin J.

In: Diabetes Care, Vol. 40, No. 4, 01.04.2017, p. 599-606.

Research output: Contribution to journalArticle

McEniery, CM, Wilkinson, IB, Johansen, NB, Witte, DR, Singh-Manoux, A, Kivimaki, M, Tabák, A, Brunner, EJ & Shipley, MJ 2017, 'Nondiabetic glucometabolic status and progression of aortic stiffness: The whitehall II study', Diabetes Care, vol. 40, no. 4, pp. 599-606. https://doi.org/10.2337/dc16-1773
McEniery CM, Wilkinson IB, Johansen NB, Witte DR, Singh-Manoux A, Kivimaki M et al. Nondiabetic glucometabolic status and progression of aortic stiffness: The whitehall II study. Diabetes Care. 2017 Apr 1;40(4):599-606. https://doi.org/10.2337/dc16-1773
McEniery, Carmel M. ; Wilkinson, Ian B. ; Johansen, Nanna B. ; Witte, Daniel R. ; Singh-Manoux, Archana ; Kivimaki, Mika ; Tabák, A. ; Brunner, Eric J. ; Shipley, Martin J. / Nondiabetic glucometabolic status and progression of aortic stiffness : The whitehall II study. In: Diabetes Care. 2017 ; Vol. 40, No. 4. pp. 599-606.
@article{2252992464a24dc5b1bdf918d5f894f2,
title = "Nondiabetic glucometabolic status and progression of aortic stiffness: The whitehall II study",
abstract = "OBJECTIVE Aortic stiffness is an important predictor of futuremorbidity andmortality. Diabetes is associated with increased aortic stiffness, but the importance of nondiabetic glucometabolic status for accelerated aortic stiffening is unclear. We tested the hypothesis that adverse glucometabolic status is associated with accelerated aortic stiffening in individuals without diabetes, independently of known risk factors for arterial stiffening. RESEARCH DESIGN AND METHODS Glucometabolic status and other cardiovascular risk factors were assessed at baseline in 2008-09, and carotid femoral pulse wave velocity (cfPWV) at baseline and follow-up in 2012-13, in 4, 386 participants without diabetes of theWhitehall II Study. RESULTS The mean age of the cohort at cfPWV baseline was 60 years, and 74{\%} were male. cfPWV increased from (mean ± SE) 8.30± 0.03 to 8.98± 0.04 m/s during 4 years of follow-up. At baseline, cfPWV was associated with fasting and 2-h postload glucose, HbA1c, and HOMA-insulin resistance (HOMA-IR). HbA1c and HOMA-IR were associated with progression of cfPWV after adjusting for physiological confounders and cardiovascular risk factors. A 1 SD higher HbA1c and HOMA-IR were associated with greater increases in cfPWV (0.11 m/s per 5 years [95{\%} CI 0.04, 0.18], P = 0.003 and 0.09 m/s per 5 years [0.01, 0.17], P = 0.03, respectively). Additional adjustment for BMI weakened the association with HOMA-IR but not with HbA1c. CONCLUSIONS HbA1c is independently associated with accelerated progression of aortic stiffness in individuals without diabetes. These findings suggest that long-term glucometabolic status, even in individuals without diabetes, could be an important target for preventative strategies against vascular aging.",
author = "McEniery, {Carmel M.} and Wilkinson, {Ian B.} and Johansen, {Nanna B.} and Witte, {Daniel R.} and Archana Singh-Manoux and Mika Kivimaki and A. Tab{\'a}k and Brunner, {Eric J.} and Shipley, {Martin J.}",
year = "2017",
month = "4",
day = "1",
doi = "10.2337/dc16-1773",
language = "English",
volume = "40",
pages = "599--606",
journal = "Diabetes Care",
issn = "1935-5548",
publisher = "American Diabetes Association Inc.",
number = "4",

}

TY - JOUR

T1 - Nondiabetic glucometabolic status and progression of aortic stiffness

T2 - The whitehall II study

AU - McEniery, Carmel M.

AU - Wilkinson, Ian B.

AU - Johansen, Nanna B.

AU - Witte, Daniel R.

AU - Singh-Manoux, Archana

AU - Kivimaki, Mika

AU - Tabák, A.

AU - Brunner, Eric J.

AU - Shipley, Martin J.

PY - 2017/4/1

Y1 - 2017/4/1

N2 - OBJECTIVE Aortic stiffness is an important predictor of futuremorbidity andmortality. Diabetes is associated with increased aortic stiffness, but the importance of nondiabetic glucometabolic status for accelerated aortic stiffening is unclear. We tested the hypothesis that adverse glucometabolic status is associated with accelerated aortic stiffening in individuals without diabetes, independently of known risk factors for arterial stiffening. RESEARCH DESIGN AND METHODS Glucometabolic status and other cardiovascular risk factors were assessed at baseline in 2008-09, and carotid femoral pulse wave velocity (cfPWV) at baseline and follow-up in 2012-13, in 4, 386 participants without diabetes of theWhitehall II Study. RESULTS The mean age of the cohort at cfPWV baseline was 60 years, and 74% were male. cfPWV increased from (mean ± SE) 8.30± 0.03 to 8.98± 0.04 m/s during 4 years of follow-up. At baseline, cfPWV was associated with fasting and 2-h postload glucose, HbA1c, and HOMA-insulin resistance (HOMA-IR). HbA1c and HOMA-IR were associated with progression of cfPWV after adjusting for physiological confounders and cardiovascular risk factors. A 1 SD higher HbA1c and HOMA-IR were associated with greater increases in cfPWV (0.11 m/s per 5 years [95% CI 0.04, 0.18], P = 0.003 and 0.09 m/s per 5 years [0.01, 0.17], P = 0.03, respectively). Additional adjustment for BMI weakened the association with HOMA-IR but not with HbA1c. CONCLUSIONS HbA1c is independently associated with accelerated progression of aortic stiffness in individuals without diabetes. These findings suggest that long-term glucometabolic status, even in individuals without diabetes, could be an important target for preventative strategies against vascular aging.

AB - OBJECTIVE Aortic stiffness is an important predictor of futuremorbidity andmortality. Diabetes is associated with increased aortic stiffness, but the importance of nondiabetic glucometabolic status for accelerated aortic stiffening is unclear. We tested the hypothesis that adverse glucometabolic status is associated with accelerated aortic stiffening in individuals without diabetes, independently of known risk factors for arterial stiffening. RESEARCH DESIGN AND METHODS Glucometabolic status and other cardiovascular risk factors were assessed at baseline in 2008-09, and carotid femoral pulse wave velocity (cfPWV) at baseline and follow-up in 2012-13, in 4, 386 participants without diabetes of theWhitehall II Study. RESULTS The mean age of the cohort at cfPWV baseline was 60 years, and 74% were male. cfPWV increased from (mean ± SE) 8.30± 0.03 to 8.98± 0.04 m/s during 4 years of follow-up. At baseline, cfPWV was associated with fasting and 2-h postload glucose, HbA1c, and HOMA-insulin resistance (HOMA-IR). HbA1c and HOMA-IR were associated with progression of cfPWV after adjusting for physiological confounders and cardiovascular risk factors. A 1 SD higher HbA1c and HOMA-IR were associated with greater increases in cfPWV (0.11 m/s per 5 years [95% CI 0.04, 0.18], P = 0.003 and 0.09 m/s per 5 years [0.01, 0.17], P = 0.03, respectively). Additional adjustment for BMI weakened the association with HOMA-IR but not with HbA1c. CONCLUSIONS HbA1c is independently associated with accelerated progression of aortic stiffness in individuals without diabetes. These findings suggest that long-term glucometabolic status, even in individuals without diabetes, could be an important target for preventative strategies against vascular aging.

UR - http://www.scopus.com/inward/record.url?scp=85019573908&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85019573908&partnerID=8YFLogxK

U2 - 10.2337/dc16-1773

DO - 10.2337/dc16-1773

M3 - Article

VL - 40

SP - 599

EP - 606

JO - Diabetes Care

JF - Diabetes Care

SN - 1935-5548

IS - 4

ER -