Generalised anxiety disorder is an independent predictor of cardiovascular mortality in type 2 diabetes: The Fremantle Diabetes Study Phase II (#215)
Depression
is associated with mortality in type 2 diabetes (T2DM). There is also a robust
association between generalised anxiety disorder (GAD) and cardiovascular disease
(CVD) events in outpatients with coronary heart disease, but few studies have
evaluated the role of GAD in T2DM. We therefore examined whether GAD is
independently associated with increased risk of subsequent CVD mortality in
T2DM.
The longitudinal Fremantle Diabetes Study Phase II includes 1551 participants with T2DM recruited between 2008 and 2011. Of these, 141 (9.1%) had died by end-June 2013, 6 from unknown causes. Of the remaining 135 deaths, 39 (28.9%) were from CVD. Of the 1545 participants with known causes of death, 1425 (92.5%) completed the validated GAD Scale questionnaire at study entry and were followed to death/census at end-June 2013, a mean±SD of 3.7±1.0 years.
At baseline, the 1425 participants were 66±11 years old, 53% were male, their median [inter-quartile range] diabetes duration was 9 [3-16] years, and 68 (4.8%) had GAD. In those who died from CVD vs other causes vs survivors, 14.3% vs 2.4% vs 4.7% had GAD at baseline (trend P=0.033), whilst 23.5% vs 12.2% vs 12.0% (trend P=0.14) had depression defined by the PHQ-9. In Kaplan-Meier analysis, GAD significantly predicted CVD death (log rank test, P=0.004). The Table displays the Cox proportional hazards model of independent predictors of CVD mortality, excluding GAD, with age as the time-line. Marital status, educational attainment, body mass index, heart rate, systolic blood pressure, diabetes duration, loge(NT-proBNP) did not enter the model. After adjusting for this model, participants with GAD at baseline were threefold more likely to have died from CVD (3.26 (1.17-9.08), P=0.024).
In community-based T2DM, the presence of GAD but not depression at baseline independently predicted increased CVD mortality during nearly 4 years’ follow-up. Mechanisms underlying this association warrant further study.
The longitudinal Fremantle Diabetes Study Phase II includes 1551 participants with T2DM recruited between 2008 and 2011. Of these, 141 (9.1%) had died by end-June 2013, 6 from unknown causes. Of the remaining 135 deaths, 39 (28.9%) were from CVD. Of the 1545 participants with known causes of death, 1425 (92.5%) completed the validated GAD Scale questionnaire at study entry and were followed to death/census at end-June 2013, a mean±SD of 3.7±1.0 years.
At baseline, the 1425 participants were 66±11 years old, 53% were male, their median [inter-quartile range] diabetes duration was 9 [3-16] years, and 68 (4.8%) had GAD. In those who died from CVD vs other causes vs survivors, 14.3% vs 2.4% vs 4.7% had GAD at baseline (trend P=0.033), whilst 23.5% vs 12.2% vs 12.0% (trend P=0.14) had depression defined by the PHQ-9. In Kaplan-Meier analysis, GAD significantly predicted CVD death (log rank test, P=0.004). The Table displays the Cox proportional hazards model of independent predictors of CVD mortality, excluding GAD, with age as the time-line. Marital status, educational attainment, body mass index, heart rate, systolic blood pressure, diabetes duration, loge(NT-proBNP) did not enter the model. After adjusting for this model, participants with GAD at baseline were threefold more likely to have died from CVD (3.26 (1.17-9.08), P=0.024).
In community-based T2DM, the presence of GAD but not depression at baseline independently predicted increased CVD mortality during nearly 4 years’ follow-up. Mechanisms underlying this association warrant further study.
HR (95% CI) |
P-value |
|
Male |
2.44 (1.12-5.33) |
0.025 |
Aboriginal |
73.8 (20.7-262.4) |
<0.001 |
Current smoker |
3.41 (1.37-8.53) |
0.009 |
On insulin |
3.89 (1.80-8.41) |
0.001 |
On lipid-modifying treatment |
0.30 (0.15-0.61) |
0.001 |
eGFR ≥90 ml/min/1.73m2 |
2.88 (1.03-8.10) |
0.045 |
CCI: 0 |
1.00 |
|
1-2 |
2.68 (1.13-6.36) |
0.025 |
≥3 |
6.07 (2.50-14.75) |
<0.001 |