Table 4.
Impact of Endothelial Function on Incident (Pre‐)Diabetes Mellitus After 5‐Year Follow‐Up
| Measurements of Endothelial Function | No. | Model 1a | Model 2b | Model 3c | |||
|---|---|---|---|---|---|---|---|
| Relative Risk (95% CI) | P Value | Relative Risk (95% CI) | P Value | Relative Risk (95% CI) | P Value | ||
| Estimates (per 1‐SD decline of endothelial function marker) for incident pre–diabetes mellitus | |||||||
| Reactive hyperemia index | 6125 | 1.15 (1.09–1.21) | <0.0001 | 1.08 (1.02–1.15) | 0.010 | 1.08 (1.02–1.15) | 0.012 |
| Baseline pulse amplitude | 6125 | 1.15 (1.10–1.21) | <0.0001 | 1.12 (1.05–1.18) | 0.00023 | 1.12 (1.06–1.19) | 0.00019 |
| Flow‐mediated dilation | 6849 | 1.08 (1.02–1.14) | 0.00015 | 1.08 (1.02–1.14) | 0.014 | 1.08 (1.02–1.14) | 0.012 |
| Baseline brachial artery diameter | 7271 | 1.18 (1.10–1.26) | <0.0001 | 1.14 (1.06–1.23) | 0.00080 | 1.14 (1.06–1.23) | 0.00080 |
| Estimates (per 1‐SD decline of endothelial function marker) for incident diabetes mellitus | |||||||
| Reactive hyperemia index | 8536 | 1.42 (1.25–1.60) | <0.0001 | 1.16 (1.01–1.34) | 0.040 | 1.16 (1.01–1.34) | 0.041 |
| Baseline pulse amplitude | 8536 | 1.33 (1.20–1.46) | <0.0001 | 1.17 (1.02–1.33) | 0.023 | 1.17 (1.02–1.33) | 0.022 |
| Flow‐mediated dilation | 9633 | 1.19 (1.04–1.37) | 0.014 | 1.01 (0.86–1.18) | 0.94 | 1.01 (0.86–1.19) | 0.92 |
| Baseline brachial artery diameter | 10 371 | 1.20 (1.02–1.41) | 0.027 | 0.96 (0.79–1.16) | 0.65 | 0.95 (0.79–1.16) | 0.63 |
Relative risks and 95% CIs are derived from a Poisson regression model with robust variance estimation, modeling for incident (pre–)diabetes mellitus (dependent variable) per 1‐SD decline in endothelial function (independent variable). Flow‐mediated dilation and reactive hyperemia index were modeled as inverse term (multiplied by −1), to provide estimates reflecting increased risk.
Model 1 was adjusted for sex, age, and socioeconomic status.
Model 2 was additionally adjusted for arterial hypertension, waist/height ratio, pack‐years of smoking, non–high‐density lipoprotein/high‐density lipoprotein ratio, physical activity, family history of myocardial infarction or stroke, cardiovascular disease (comprising congestive heart failure, coronary artery disease, myocardial infarction, stroke, atrial fibrillation, and peripheral artery disease), and medication use (antithrombotic agents, antihypertensives, diuretics, β blockers, calcium channel blocker, agents acting on the renin‐angiotensin‐aldosterone system, and lipid‐modifying agents).
Model 3 was additionally adjusted for C‐reactive protein.