Patients with chronic obstructive pulmonary disease (COPD) are at an increased cardiovascular risk; however, the underlying mechanisms for this relationship are ill defined. Altered glucose metabolism may increase cardiovascular risk via impaired endothelial function.
We conducted a longitudinal pilot study to assess the interrelationship between systemic vascular function, glucose metabolism, and lung function in patients with COPD. Eighteen non-smoking patients with stable moderate-to-severe COPD [67 % male; median (first to third quartiles) Forced Expiratory Volume in 1 second (FEV1) % predicted: 38 % (28–55 %); body mass index: 26 kg/m2 (24–28 kg/m2)] free from cardiovascular risk factors were evaluated. Systemic vascular function was assessed by means of flow-mediated dilation technique of the brachial artery. Laboratory measurements included fasting blood glucose levels, circulating concentrations of insulin, C-reactive protein, and fibrinogen. Homeostatic model assessment of insulin resistance (HOMA-IR) was determined. Measurements were performed at baseline and were repeated after 12 months.
Flow-mediated dilation significantly decreased from 13.5 % (11–15 %) at baseline to 9.8 % (6–12 %; p = 0.002) at the follow-up visit, whereas both fasting blood glucose concentrations and HOMA-IR increased from 94 mg/dl (86–103 mg/dl) to 102 mg/dl (94–111 mg/dl; p = 0.027) and from 1.2 (0.8–2.1) to 1.7 (1.2–3.0; p = 0.023), respectively. There was a significant relationship between changes in endothelial function and changes in fasting serum glucose (r = − 0.483, p = 0.009), HOMA-IR (r = − 0.441, p = 0.019), and FEV1 (r = 0.336, p = 0.05).
Altered glucose metabolism may be associated with progression of endothelial dysfunction in patients with COPD.