Table 3.

Association of Baseline Endothelial Function on HbA_1c Levels After 5‐Year Follow‐Up

Measurements of Endothelial Function	No.	Model 1a		Model 2b		Model 3c
		β Estimate per SD (95% CI)	P Value	β Estimate per SD (95% CI)	P Value	β Estimate per SD (95% CI)	P Value
Reactive hyperemia index	8435	−0.028 (−0.039 to −0.017)	<0.0001	−0.020 (−0.034 to −0.007)	0.0025	−0.020 (−0.033 to −0.007)	0.0029
Baseline pulse amplitude	8435	0.027 (0.016 to 0.038)	<0.0001	0.015 (0.001 to 0.029)	0.035	0.015 (0.001 to 0.029)	0.033
Flow‐mediated dilation	9522	−0.016 (−0.026 to −0.006)	0.0016	−0.003 (−0.015 to 0.008)	0.62	−0.003 (−0.015 to 0.009)	0.59
Baseline brachial artery diameter	10 261	0.032 (0.019 to 0.046)	<0.0001	0.015 (−0.001 to 0.030)	0.068	0.015 (−0.001 to 0.030)	0.066

β Estimates and 95% CIs are derived from a linear regression model, modeling for HbA_1c levels (dependent variable) per 1‐SD increase in endothelial function (independent variable). Patients with intake of drugs affecting blood glucose at baseline and follow‐up were excluded from analyses. HbA_1c indicates hemoglobin A_1c.

^aModel 1 was adjusted for baseline HbA_1c, sex, age, and socioeconomic status.

^bModel 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).

^cModel 3 was additionally adjusted for C‐reactive protein.