Today, heart failure incidence has increased,
and the lifetime risk of developing heart failure
reaches up to 20%. Despite the increasing variety
of treatments for heart failure, it is still a disease
with high mortality.[
17] Heart failure mortality
determinants are metabolic test (pVO2), 6-MWT,
kidney function tests, N-terminal pro–B-type
natriuretic peptide (NT-pro BNP) value, and right
ventricular functions. In the latest studies conducted,
it is thought that the results of respiratory function
tests and diffusion tests may also be determinants of
heart failure mortality.
The most important reason for both outpatient
clinic admissions and hospitalizations of heart
failure patients is dyspnea due to pulmonary edema.
To evaluate the patients in terms of pulmonary
edema, thoracic ultrasonography, B-line count, and
pleural effusion were also added to examinations, such as physical examination findings and chest
radiography.
In chronic heart failure, alveolar-capillary
membrane changes due to hemodynamic stress
caused by increased capillary pressure and changes
on the alveolocapillary membrane are irreversible
and result in remodeling. Neurohumoral activation
due to physical stress caused by increased pulmonary
capillary pressure and a decrease in cardiac output
stimulates mesenchymal cells and fibrocytes in the
interstitium and causes myofibroblasts to proliferate
and differentiate. With myofibroblast proliferation,
the amount of elastin and collagen begins to increase
in the interstitial tissue of the alveolar-capillary
membrane, that is, in the extracellular matrix. There
is an increase in type 4 collagen and alveolar-capillary
membrane thickness. Alveolar-capillary membrane
thickening positively reduces pulmonary edema
formation; therefore, it protects against increased
fluid permeability. However, it causes a decrease in
gas diffusion and the formation of restrictive lung
syndrome due to increased stiffness, contributing to
the development of pulmonary hypertension and a
decrease in exercise tolerance. Due to alveolar-capillary
membrane thickening, there is a decrease in diffusing
capacity in patients with heart failure and a decrease
in FVC (restrictive pattern), even if FEV1/FVC is
normal. It is thought that the current situation may be
the predictor of mortality.[12-16]
In the study conducted by Van Iterson et al.,[18]
patients with low DLCO results were found to have
lower pVO2 values in the metabolic test result. As
a result of the study, it was observed that there was
a decrease in the diffusing capacity of patients with
moderate and severe heart failure, and the result of
DLCO could be a predictor of mortality, similar to
pVO2, in heart failure patients. In our study, DLCO
was found to be lower in the group with >15 B-lines,
and >15 B-lines may be a determinant of mortality,
similar to DLCO and pVO2.
Puri et al.[19] administered 10 mL/kg/min 0.9%
saline to 10 patients with heart failure, and when the
diffusion test results were performed 1 h after the
infusion, it was found that the results of alveolarcapillary
membrane conductance, FEV1, and peak
expiratory flow rates (PEFR) decreased. A saline
infusion was given to the patients in the healthy control
group, and no change was detected in the respiratory
function test and diffusion test performed 1 h later. Similar results were obtained in our study, and it was
observed that the results of DLCO, FVC, and FEV1
were lower in those with >15 B-lines (extravascular
fluid retention in the lung). It was observed that the
results of DLCO, FVC, and FEV1 might be lower as
a result of the increase in alveolar-capillary membrane
thickness due to hemodynamic stress caused by
excessive extravascular fluid retention.
When another study of Puri et al.[20] was examined,
alveolar-capillary membrane diffusive capasity,
DLCO, and alveolar volume decreased in the group
with heart failure compared to healthy individuals.
Although healthy individuals were not included in
our study, it is thought that patients with >15 B-lines
may have had increased alveolar-capillary membrane
thickness, and as a result, DLCO was found to be
lower due to decreased permeability.
Morosin et al.[21] found that pVO2, FEV1, and FVC
were lower in the group with DLCO <80% compared
to those with DLCO >80% in patients with stable
heart failure. Similarly, in our study, FVC and FEV1
were low together with DLCO in the group with
>15 B-lines.
Melenovsky et al.[22] included 186 heart failure
patients and 21 healthy control group patients in their
study. Pulmonary radiographs of heart failure patients
were interpreted and grouped as the wet lung group
with a congestion score index >0.5 (n=74) and the dry
lung group with a congestion index score <0.5 (n=112).
Right catheterization, respiratory function tests,
diffusion tests, and echocardiography were applied to
the wet and dry lung groups. When all findings were
compared between the two groups, FVC and DLCO
were lower in the heart failure group with wet lungs.
When the two groups were compared in terms of
FEV1/FVC, it was found that there was no significant
difference. Furthermore, in the heart failure group
with wet lungs, pulmonary artery compliance was
lower, pulmonary vascular resistance and pulmonary
stub pressures were higher, right ventricular functions
were lower, DLCO results were lower, and a restrictive
pattern was observed in the pulmonary function test.
In their median follow-up of 333 (interquartile range
80-875) days, it was shown that mortality increased
in the wet lung group. In our study, in the group with
>15 B-lines, right ventricular functions were found
to be lower, DLCO was lower, pulmonary vascular
resistance was higher, and a restrictive pattern was
observed due to the pulmonary function test. It was observed that there is a significant correlation between
the results of our study and the results of the study
conducted by Melenovsky et al.[22]
In the study conducted by Coiro et al.,[23] it was
determined that the patient group with >30 B-lines
had higher mortality, and hospitalization was more
frequent as a result of thoracic ultrasonography
performed before discharge in heart failure patients.
In our study, follow-up could not be performed with
mortality and rehospitalization, but in the group
with >15 B-lines, DLCO was lower, right ventricular
functions were higher, the rate of patients with
E/e΄ >15% was higher, VCI diameter was more dilated,
and pulmonary vascular resistance pressure was higher.
These findings are accepted as an indicator of a poor
prognosis.
In the CHAMPION study, a device that
can measure pulmonary artery pressure with
CardioMEMS was evaluated by implanting. In the
device follow-up, it was observed that the mean
pulmonary artery and pulmonary stub pressure
increased during the process from dry lung to
pulmonary edema, and if the pulmonary edema
picture increased more in the follow-up of DLCO
followed by FVC, FEV1/FVC decreased.[24] In our
study, DLCO and FVC were low in patients with
>15 B-lines (pulmonary edema), but FEV1/FVC
decreased.
In the study conducted by Platz et al.,[25] thoracic
ultrasonography was examined by an eight-region
scanning method before discharge in heart failure
patients. It was observed that patients with >3 B-lines
had higher mortality and rehospitalization rates. In
our study, mortality was not calculated, but in the
group with >15 B-lines, the right ventricular function
was found to be more suppressed, DLCO was lower,
and pulmonary vascular resistance was higher, which
could be a predictor of mortality.
In the study by Agostoni et al.,[16] heart failure
patients were subjected to metabolic testing and
grouped as <12, 12-16, and 16-20 according to
the pVO2 results. In the group with pVO2 <12,
DLCO, alveolar volume, capillary volume, and
alveolar-capillary membrane diffusive capasity were
lower than in the other groups. Similarly, in our
study, the 6-MWT, performed to evaluate functional
capacity, and the DLCO were lower in the group
with >15 B-lines.
There are some limitations to this study.
Short- and long-term follow-up of the patients after
discharge from the hospital in terms of mortality and
rehospitalization frequency would have been beneficial
to the study. Identifying the effect of a B-line number
>15 on mortality and hospitalization frequency
could support the study results. Although it was not
included in our study’s method, a higher number of
patients who underwent right heart catheterization
and had measured right atrial pressure/left atrial
pressure, pulmonary arterial pressure, and pulmonary
vascular resistance values could contribute to the
study. Checking the number of B-lines by thoracic
ultrasonography during diffusion tests and before
discharge could provide the accuracy of the study
results and a better determination of the congestion
status of the patients.
In conclusion, a B-line number >15 alone may be
predictive in terms of decreased diffusion capacity,
decreased right ventricular function, increased
pulmonary vascular resistance, and restrictive pattern in
respiratory function. There are poor prognosis indicators,
such as a 6-MWT and right ventricular function for
heart failure. In the group with a B-line number >15,
decreased DLCO as a result of decreased six-min
walking capacity, more pressure on right ventricular
functions, and lower follow-up DLCO suggests that it
may be an indicator of poor prognosis in heart failure.
Ethics Committee Approval: The study protocol was
approved by the Ege University Faculty of Medicine Ethics
Committee (date: January-December 2018, no: 18-2.1/31).
The study was conducted in accordance with the principles of
the Declaration of Helsinki.
Patient Consent for Publication: A written informed
consent was obtained from each patient.
Data Sharing Statement: The data that support the
findings of this study are available from the corresponding
author upon reasonable request.
Author Contributions: All authors contributed equally
to the article.
Conflict of Interest: The authors declared no conflicts
of interest with respect to the authorship and/or publication
of this article.
Funding: The authors received no financial support for
the research and/or authorship of this article.