AECOPD suggesting that the exacerbation altered FMD
even in those of advanced age. Our patients were not free
from cardiovascular risk factors, which may have lowered
their FMD. However, because the FMD improved following resolution of AECOPD we feel that the exacerbation
worsened any pre-existing vascular dysfunction that was
present.
All of our patients were treated with corticosteroids which
may have affected FMD and NMD. The effect of acute administration of glucocorticoids on vascular function is not
entirely understood and conflicting evidence exists. One
study reported that corticosteroids alter vascular function
while a second reported that the acute administration of corticosteroids has no effect (39, 40). Although all of our patients
were treated acutely with corticosteroids none of them were
on chronic therapy prior to AECOPD hospitalization.
Another limitation was the loss of patient follow-up for repeat FMD and NMD. This was largely due to the severity of
the underlying disease of patients hospitalized for AECOPD.
A larger study with a greater rate of follow-up will be needed
to definitely characterize the changes in FMD and NMD that
occur during exacerbation and following resolution of patients hospitalized with AECOPD.
In conclusion, this study demonstrates that both the endothelium and vascular smooth muscle contribute to vascular dysfunction COPD. The acute and chronic systemic vascular effects of COPD were shown by impairment in both
FMD and NMD during an acute exacerbation, which improved but remain below normal at resolution. Further research is needed on a larger scale to elaborate the mechanisms
of vascular impairment during AECOPD and to explore potential treatments.
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