Decline in ankle-brachial index is stronger in poorly than in well controlled diabetes: Results from the Heinz Nixdorf Recall cohort study.


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
05 2019
Historique:
received: 26 11 2018
revised: 19 02 2019
accepted: 20 02 2019
pubmed: 15 3 2019
medline: 4 6 2020
entrez: 15 3 2019
Statut: ppublish

Résumé

The ankle-brachial index (ABI) is a marker of atherosclerosis and a diagnostic criterion for peripheral arterial disease (PAD). We studied the association between HbA1c and ABI in subjects with and without diabetes. In the Heinz Nixdorf Recall Study, a population-based cohort study in Germany (N = 4,814, age 45-75 years), ABI was measured at baseline, at 5- and 10-year follow-up. Subjects with ABI <0.9, ABI >1.4 or self-reported PAD at baseline were excluded from analyses. In 3199 participants, we assessed associations between HbA1c and incident PAD (ABI < 0.9) and change in ABI, respectively, using logistic and linear regression models. Subjects without diabetes, with HbA1c < 5.7% were used as reference group. Compared to the reference group, 10-year decline in ABI was -0.066 (95% confidence interval: -0.117; -0.016) and -0.021 (-0.063; 0.021) in subjects with poorly (≥7.0% HbA1c) and well (<7.0% HbA1c) controlled previously known diabetes; -0.010 (-0.054; 0.034) in those with newly detected diabetes diagnosed by HbA1c ≥ 6.5%, and -0.005 (-0.023; 0.013) in those without diabetes, with HbA1c 5.7-6.4%. For poorly controlled diabetes, odds ratios for low ABI (<0.9) were 3.5 (1.6-7.9), and 3.1 (1.3-7.0) after 5- and 10-year follow-up, respectively. The incidence of Mönckeberg disease (ABI > 1.4) was low (6/288 (2.4%) over 5 years). Decline in ABI was stronger in poorly than well-controlled diabetes. Subjects with newly detected diabetes diagnosed by the new HbA1c criterion (≥6.5%) did not show an increased decline in ABI over 10 years.

Sections du résumé

BACKGROUND AND AIMS
The ankle-brachial index (ABI) is a marker of atherosclerosis and a diagnostic criterion for peripheral arterial disease (PAD). We studied the association between HbA1c and ABI in subjects with and without diabetes.
METHODS
In the Heinz Nixdorf Recall Study, a population-based cohort study in Germany (N = 4,814, age 45-75 years), ABI was measured at baseline, at 5- and 10-year follow-up. Subjects with ABI <0.9, ABI >1.4 or self-reported PAD at baseline were excluded from analyses. In 3199 participants, we assessed associations between HbA1c and incident PAD (ABI < 0.9) and change in ABI, respectively, using logistic and linear regression models. Subjects without diabetes, with HbA1c < 5.7% were used as reference group.
RESULTS
Compared to the reference group, 10-year decline in ABI was -0.066 (95% confidence interval: -0.117; -0.016) and -0.021 (-0.063; 0.021) in subjects with poorly (≥7.0% HbA1c) and well (<7.0% HbA1c) controlled previously known diabetes; -0.010 (-0.054; 0.034) in those with newly detected diabetes diagnosed by HbA1c ≥ 6.5%, and -0.005 (-0.023; 0.013) in those without diabetes, with HbA1c 5.7-6.4%. For poorly controlled diabetes, odds ratios for low ABI (<0.9) were 3.5 (1.6-7.9), and 3.1 (1.3-7.0) after 5- and 10-year follow-up, respectively. The incidence of Mönckeberg disease (ABI > 1.4) was low (6/288 (2.4%) over 5 years).
CONCLUSIONS
Decline in ABI was stronger in poorly than well-controlled diabetes. Subjects with newly detected diabetes diagnosed by the new HbA1c criterion (≥6.5%) did not show an increased decline in ABI over 10 years.

Identifiants

pubmed: 30870706
pii: S0021-9150(19)30107-8
doi: 10.1016/j.atherosclerosis.2019.02.021
pii:
doi:

Substances chimiques

Glycated Hemoglobin A 0
hemoglobin A1c protein, human 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

37-43

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Bernd Kowall (B)

Center of Clinical Epidemiology, Institute for Medical Informatics, Biometry and Epidemiology, Medical Faculty, University Duisburg-Essen, Essen, Germany. Electronic address: bernd.kowall@uk-essen.de.

Raimund Erbel (R)

Institute for Medical Informatics, Biometry and Epidemiology, University Clinic Essen, University Duisburg-Essen, Essen, Germany.

Susanne Moebus (S)

Center for Urban Epidemiology, Institute for Medical Informatics, Biometry and Epidemiology, University Clinic Essen, Essen, Germany.

Nils Lehmann (N)

Institute for Medical Informatics, Biometry and Epidemiology, University Clinic Essen, University Duisburg-Essen, Essen, Germany.

Knut Kröger (K)

Clinic of Vascular Medicine, Helios Klinikum Krefeld, Krefeld, Germany.

Andreas Stang (A)

Center of Clinical Epidemiology, Institute for Medical Informatics, Biometry and Epidemiology, Medical Faculty, University Duisburg-Essen, Essen, Germany; School of Public Health, Department of Epidemiology Boston University, 715 Albany Street, Talbot Building, Boston, MA, 02118, USA.

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