COPD: Journal of Chronic Obstructive Pulmonary Disease, 8:57–59, 2011
ISSN: 1541-2555 print / 1541-2563 online
Copyright C ; 2011 Informa Healthcare USA, Inc.
DOI: 10.3109/15412555.2011.559376
EDITORIAL
Lung Function and Aortic Calcification–Hardening the Evidence or
Inflaming the Need for Further Research?
Charlotte E. Bolton1 and John R. Cockcroft2
Nottingham Respiratory Biomedical Research Unit, University of Nottingham, Clinical Sciences Building, City Hospital, Hucknall
Road. Nottingham. NG5 1PB, United Kingdom,1 Wales Heart Research Institute, Cardiff University, Heath Park, Cardiff. CF14 4XN
United Kingdom2
Keywords: aortic calcification, arterialstiffness, COPD, lung
function
Large elastic arteries such as the aorta not only provide
a conduit for blood flow but also fulfill a dynamic role in
buffering the large intermittent pressure changes due to ventricular ejection in order to minimise end organ and mi-crovascular damage and allow a more constant blood flow
through smaller vessels. However, this buffering capacity is
lost during the ageing process and in disease states associated
with premature vascular ageing.
It has been known for some time that impaired lung function (1) and lung function decline (2) are risk factors that predict cardiovascular (CV) death and morbidity over and above
the traditional risk factors. Furthermore, chronic respiratory
disease states, such as chronic obstructive pulmonary disease
(COPD) are also associated with greater CV risk (3) as well
as with other traditional risk factors such as diabetes mellitus (4), insulin resistance (5) and a systemic inflammatory
state (6). Despite this, lung function is not routinely assessed
in CV clinics, nor are CV measurements made in respiratory
clinics.
Aortic stiffness, as assessed by carotid femoral PWV (CF-
PWV) has established itself as a non invasive predictor of CV
disease in both the general population and in at-risk groups
such as hypertension and renal failure (7,8). This has focused
intense research interest into the possible pathophysiological
mechanisms responsible for large artery stiffening (9). The
recognition that conventional risk factors such as diabetes
and hypercholesterolaemia play little part in determining CF-
PWV (10), suggests that other, as yet, poorly understood
pathophysiological mechanisms may be more involved. Fur-
thermore, recent evidence suggests the fascinating possibility
that regional aortic PWV may be influenced by differential
pathophysiological processes. Recently, impaired lung func-
tion was an independent variable of CF-PWV in 800 men in
the Caerphilly Prospective study (11). In parallel, increased
aortic stiffness has been reported in patients with chronic res-
piratory disease such as COPD (12,13) and COPD related to
alpha 1 antitrypsin deficiency (14), thus supporting the in-
clusion of assessment of arterial stiffness in the modern man-
agement of patients with chronic respiratory disease.
For “COPD-2010-0057 — Pulmonary Function is Associated with Distal Aortic Calcium, not Proximal Aortic Distensibility. MESA Lung Study”
Correspondence to: Dr. Charlotte E. Bolton, Nottingham Respiratory Biomedical Research Unit, University of Nottingham, Clinical Sciences
Building, City Hospital, Hucknall Road. Nottingham. NG5 1PB, UK, Phone: 0115 8231677, Fax: 0115 8231946, email: charlotte.bolton@
nottingham.ac.uk. John R. Cockcroft, Wales Heart Research Institute, Cardiff University, Heath Park, Cardiff CF14 4XN, United Kingdom.
e-mail: cockcroftjr@cf.ac.uk.
