Background: COPD patients may be prone to cerebral small vessel disease resulting in perivascular white matter lesions and consequent cognitive decline. The pathophysiological background of these observations is not completely understood. It is hypothesized that COPD may involve systemic vascular dysfunction extending to the brain. The present study aimed to assess whether acetazolamide-induced cerebral vasoreactivity and cerebrovascular reserve capacity are impaired in patients with COPD. Methods: A total of 17 patients with COPD and 20 healthy control subjects underwent transcranial Doppler monitoring before and after IV administration of 15 mg/kgBW acetazolamide for 20 min. Cerebrovascular reactivity (CVR) was defined as a percent increase in blood flow velocity in the middle cerebral artery (MBFV) after acetazolamide. Cerebrovascular reserve capacity (CVRC) was defined as the maximal percent change in MBFV during the entire registration. Results: Administration of acetazolamide resulted in a slight decrease in pH and a mild increase in PaCO2 (both p < 0.001) in COPD patients. Absolute MBFV values were consequently higher, and pulsatility indices were lower in control subjects compared to those measured in patients with COPD. The CVR at different time points after acetazolamide and CVRC did not show any difference between COPD patients and control subjects. Conclusions: In the present study, in normocapnic mild and normocapnic moderate COPD patients, cerebrovascular reactivity is not impaired, indicating that in mild stages, cerebral arteriolar function is preserved. Further studies, using patient selection based on different severity stages of the disease, may show whether alteration of the cerebral arteriolar function is responsible for the white matter lesions and cognitive decline observed in severe COPD patients.
Szabó-Szűcs et al. (Mon,) studied this question.