Ischemic heart disease and peripheral vascular diseases are prevalent in COPD and it is estimated that any 10% decrease in forced expiratory volume in 1second (FEV1) is associated with 30% increased cardiovascular risk of death. Endothelial dysfunction may be one of the mechanistic pathways that link between COPD and cardiovascular mortality. Our aim was to study the vascular reactivity of patients with stable COPD and to try to correlate endothelial dysfunction, vascular reactivity and functional capacity of these patients that eventually may lead to cardiovascular mortality.

METHODS: This was a prospective study. Twenty-three consecutive ambulatory COPD patients were enrolled. All were smoking men, aged 64.4±8.4years. Twenty-two healthy volunteers aged 44.7±11.7years, BMI of 25.2±4.2, height of 172±8cm served as the control group. Vascular studies included endothelial function and ankle brachial index.

RESULTS: Baseline diameter of the brachial artery was larger in COPD patients compared with controls. The absolute change in diameter post hyperemia was significantly less in patients (0.004±0.02cm vs. 0.05±0.02cm, p<0.001) and COPD patients responded to hyperemia by constriction instead of dilatation (FMD% was -0.6±6.3% in patients vs. 15.6±7.6% in controls, p<0.001). There was no difference in ABI in patients and controls (0.95±0.26 vs. 1.06±0.16, p=0.07).

DISCUSSION: We found that patients with COPD have dilated arteries, have impaired ability to respond to high shear stress that triggers nitric oxide dependent flow mediated dilatation, and have also impaired ability to function - represented by the poor 6minute walk test.