COPD: Journal of Chronic Obstructive Pulmonary Disease, 8:60–65, 2011
ISSN: 1541-2555 print / 1541-2563 online
Copyright C ; Informa Healthcare USA, Inc.
DOI: 10.3109/15412555.2011.558541
ORIGINAL RESEARCH
Hospitalized Acute Exacerbation of COPD Impairs Flow and
Nitroglycerin-Mediated Peripheral Vascular Dilation
Nathaniel Marchetti,1 David E. Ciccolella,1 Michael R. Jacobs,1 Aaron Crookshank,1 John P. Gaughan,2
Mohammed A. Kashem,3 Alfred A. Bove,3 and Gerard J. Criner1
1Department of Physiology, Temple University School of Medicine, Philadelphia, Pennsylvania, United States 2Division of
Cardiology; Temple University School of Medicine, Philadelphia, Pennsylvania, United States 3Division of Pulmonary and Critical
Care Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania, United States
Vascular function, as measured by flow mediated dilation
(FMD) and nitroglycerin mediated dilation (NMD), is impaired
in COPD. Increases in systemic inflammatory mediators during
acute exacerbations of COPD (AECOPD) may further impair
vascular function and may account for the increased
prevalence of cardiovascular disease in COPD patients.
Similarly it may account for the increased morbidity and
mortality in COPD patients hospitalized with acute
exacerbations. We hypothesized that FMD and NMD would be
impaired during AECOPD requiring hospitalization and that
vascular function would improve upon AECOPD resolution. We
used FMD and NMD to evaluate vascular function in 19 patients
hospitalized with AECOPD. FMD and NMD were repeated
approximately three months later in 8 of these patients. In
these eight patients significant improvements were observed
in FMD (2.6 ± 1.5% vs 5.1 ± 2.4%, p = 0.04) and NMD (5.0 ±
2.6% vs 13.3 ± 4.5, p = 0.02) after resolution of their
exacerbation. We conclude that endothelial and vascular
smooth muscle function is markedly impaired during AECOPD
requiring hospitalization and improves following resolution.
The systemic vascular impairment that occurs during AECOPD
may partially explain the observed increased in cardiac
morbidity and mortality that occur in this population.
Keywords: Chronic Obstructive Pulmonary Disease, acute
exacerbation of COPD, Vascular Dysfunction
INTRODUCTION
Cardiac morbidity and mortality occurs at rates 2–3-fold
higher in stable COPD patients as compared to age matched
non-COPD patients (1–3). Additionally, cardiovascular dis-
eases are a common cause of death in patients hospitalized
for severe acute exacerbations of COPD (AECOPD) (4–6).
Cardiovascular disease and COPD are both associated with
elevated markers of systemic inflammation, but the mecha-
nisms behind the relationship of COPD and heightened sys-
temic inflammation are not well understood (7). It is possible
that the inflammatory mediators produced in the lung during
AECOPD simply “spillover” into the systemic circulation, or
that the cause of pulmonary inflammation (usually tobacco
smoke) simultaneously produces systemic inflammation. Al-
ternatively COPD may incite biological processes in the lung
that kindle systemic inflammation via oxidative stress and tis-
sue hypoxia (8).
Study partially funded by Pennsylvania Department of Health PA-DOH 02-70-2
Correspondence to: Nathaniel Marchetti, DO, Department of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia,
Pennsylvania, United States. Phone: (215) 707-3336, Fax: (215) 707-6867. email: marchent@tuhs.temple.edu
