worsens and that pulmonary capillary blood volume
remains within normal limits when heart failure is mild
and increases when heart failure becomes severe.
The pulmonary capillary blood volume expansion has
been interpreted as a compensatory mechanism aimed
at preserving DLCO in patients with heart failure.
However, the correlation between lung mechanics
and DLCO impairment in heart failure is not completely
appreciated. We postulated that because the thoracic
volume is relatively unexpandable, a competition for
the intrathoracic space between lungs and heart may
exist when cardiomegaly is part of the heart failure syn-
The current study was therefore undertaken to
assess changes in lung volume and mechanics and in
alveolar-capillary membrane diffusing capacity that are
associated with cardiac enlargement.
We offered to enroll in the study all patients who were eval-
uated for heart failure at our Heart Failure Unit between Sep-
tember 1, 1998, and December 31, 1998, who were in stable
clinical condition, who fulfilled the study inclusion criteria,
and who provided informed consent to the study. We enrolled
80 patients but were able to obtain reliable measurements in
72 patients (17 women and 55 men, 62 ± 10 years). Twenty
patients were smokers, 15 had quit smoking for ≥5 years, and
the others had never smoked. The cause of heart failure was
In heart failure, impairment of lung mechanics, usu-
ally a restrictive lung disease,
and of lung diffusion
capacity for carbon monoxide (DLCO)
is often seen.
Both influence exercise capacity, probably the most reli-
able indicator of the disease severity. Indeed, during
exercise, vital capacity and tidal volume are lower, and
the greater the severity of heart failure
of lung mechanics is associated with improvement of
Similarly, DLCO correlates with
and its improvement may correlate
with the increase of exercise capacity.
DLCO may be partitioned into its 2 subcomponents:
(1) the molecular diffusion of carbon monoxide across
the alveolar-capillary membrane (DM) and (2) the chem-
ical reaction of carbon monoxide with the pulmonary
capillary blood available for gas exchange. It has
recently been shown that DM reduces as heart failure
From Centro Cardiologico, Fondazione Monzino, IRCCS, Istituto di Cardiologia
dell’ Università degli Studi, Centro di Studio per le Ricerche Cardiovascolari, CNR.
Supported by research grants from Istituto di Cardiologia, Centro Cardiologico,
IRCCS, Università di Milano and Centro di Studio per le Ricerche Cardiovascolari
Submitted April 10, 2000; accepted July 14, 2000.
Reprint requests: Dr PierGiuseppe Agostoni, Istituto di Cardiologia, Centro Cardio-
logico, Università di Milano, Via Parea 4, 20138 Milan, Italy.
Copyright © 2000 by Mosby, Inc.
1097-6744/2000/$12.00 + 0 4/90/110282
Cardiomegaly as a possible cause of lung
dysfunction in patients with heart failure
PierGiuseppe Agostoni, MD, PhD, Gaia Cattadori, MD, Marco Guazzi, MD, PhD, Pietro Palermo, MD, Maurizio
Bussotti, MD, and Giancarlo Marenzi, MD Milan, Italy
Our hypothesis is that an enlarged heart may compete for space with the lungs, causing a restrictive pat-
tern that is often seen in patients with chronic heart failure.
Eighty patients with stable congestive heart failure in New York Heart Association classes II and III partici-
pated in the study. We measured cardiothoracic index (chest radiography), FEV
, vital capacity, alveolar volume, lung diffu-
sion capacity for carbon monoxide (DLCO), and its 2 subcomponents alveolar-capillary membrane diffusion (DM), and pul-
monary capillary blood volume.
Reliable measurements were obtained in 72 of 80 participants enrolled. Cardiothoracic index averaged 57% ±
, vital capacity, alveolar volume, DLCO, and DM were inversely related to the cardiothoracic index (r = –0.514,
–0.557, –0.522, –0.475, and –0.480, respectively). However, the relations of DLCO and DM with the cardiothoracic
index were lost when DLCO and DM were adjusted for alveolar volume. A significant correlation (P < .01) was found
between alveolar volume and vital capacity, FEV
, and DLCO (r = 0.799, 0.705, and 0.614, respectively). At multivariate
analysis, cardiothoracic index, FEV
, and pulmonary capillary blood volume were independent predictors of DLCO,
whereas alveolar volume, FEV
, and left ventricular ejection fraction were independent predictors of DM.
Cardiac enlargement in chronic heart failure appears to be involved in causing restrictive lung pattern
and a reduced alveolar volume that disturbs carbon monoxide diffusion. (Am Heart J 2000;140:e24.)