Format

Send to

Choose Destination
See comment in PubMed Commons below
Scand J Clin Lab Invest. 2008;68(7):654-9. doi: 10.1080/00365510802018330.

A combined abnormality in heart rate variation and QT corrected interval is a strong predictor of cardiovascular death in type 1 diabetes.

Author information

  • 1Department of Endocrinology, Copenhagen University Hospital, Denmark.

Abstract

OBJECTIVE:

Long-term diabetes is associated with excess morbidity and mortality, and cardiovascular autonomic neuropathy and QTc interval abnormalities are both predictive of early cardiovascular death in diabetes. We aimed to investigate the effect of these risk factors in a large cohort of type 1 diabetic patients followed prospectively for 10 years.

MATERIAL AND METHODS:

Three-hundred-and-ninety-one type 1 diabetic mellitus patients (240 M and 151 F, age 41.8 years +/- 9.9 (mean +/-SD), duration of DM 27.3 years +/- 8.2) were followed in an outpatient setting.

RESULTS:

Patients with decreased heart rate variability had an excess overall mortality that diminished after adjusting for conventional cardiovascular risk factors; hazard ratio 2.5 (0.9-6.8; p = 0.071) compared to patients with normal heart rate variability. Likewise, prolonged QTc interval was associated with premature death with an adjusted hazard ratio of 2.3 (1.3-4.0; p = 0.005). In a combined analysis, patients with abnormal values for heart rate variability and QTc had a poorer prognosis compared to patients with normal test values for both parameters (adjusted hazard ratio 6.7 (1.8-25; p = 0.005)). Of the 34 patients with both test values abnormal, 15 died and 14 of these from cardiovascular causes.

CONCLUSIONS:

We conclude that combined abnormality in heart rate variability and QTc is a strong predictor of mortality in type 1 diabetes independently of conventional risk factors. These results have implications for future screening and treatment programmes for cardiovascular disease in type 1 diabetes.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Write to the Help Desk