Electrocardiographic markers in patients with type 2 diabetes and the role of diabetes duration

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Dokumenter

  • Fulltext

    Forlagets udgivne version, 1,5 MB, PDF-dokument

Background
The association between type 2 diabetes and electrocardiographic (ECG) markers are incompletely explored and the dependence on diabetes duration is largely unknown. We aimed to investigate the electrocardiographic (ECG) changes associated with type 2 diabetes over time.

Methods
In this cross-sectional study, we matched people with type 2 diabetes 1:1 on sex, age, and body mass index with people without diabetes from the general population. We regressed ECG markers with the presence of diabetes and the duration of clinical diabetes, respectively, adjusted for sex, age, body mass index, smoking, heart rate, diabetes medication, renal function, hypertension, and myocardial infarction.

Results
We matched 988 people with type 2 diabetes (332, 34% females) with as many controls. Heart rate was 8 bpm higher (p < 0.001) in people with vs. without type 2 diabetes, but the difference declined with increasing diabetes duration. For most depolarization markers, the difference between people with and without type 2 diabetes increased progressively with diabetes duration. On average, R-wave amplitude was 6 mm lower in lead V5 (p < 0.001), P-wave duration was 5 ms shorter (p < 0.001) and QRS duration was 3 ms (p = 0.03). Among repolarization markers, T-wave amplitude (measured in V5) was lower in patients with type 2 diabetes (1 mm lower, p < 0.001) and the QRS-T angle was 10 degrees wider (p = 0.002). We observed no association between diabetes duration and repolarization markers.

Conclusions
Type 2 diabetes was independently associated with electrocardiographic depolarization and repolarization changes. Differences in depolarization markers, but not repolarization markers, increased with increasing diabetes duration.
OriginalsprogEngelsk
TidsskriftJournal of Electrocardiology
Vol/bind84
Sider (fra-til)129-136
Antal sider8
ISSN0022-0736
DOI
StatusUdgivet - 2024

Bibliografisk note

Funding Information:
JLI is supported by a grant from the Danish Cardiovascular Academy (PD2Y-2,023,004-DCA). The Danish Cardiovascular Academy is funded by the Novo Nordisk Foundation and the Danish Heart Foundation, grant number NNF20SA0067242. CE is partly funded by the Laboratory Medicine Endowment Fund of Boston Children's Hospital. JKK is partly funded by the Danish Independent Research Fund.

Publisher Copyright:
© 2024 The Authors

ID: 391210053