An Echocardiographic and Doppler Study |
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ABSTRACT |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Abnormal left ventricular (LV) diastolic function has frequently been reported in patients with chronic obstructive pulmonary disease (COPD). In the present work, diastolic function was studied by a combined analysis of pulmonary venous and mitral blood flow velocities in 34 patients with COPD clinically stable and without history of heart disease, and 20 control subjects. We confirmed the increased contribution of the atrial contraction to the LV filling in COPD patients in comparison with control subjects; furthermore, a decreased left atrial (LA) filling during the ventricular systole was observed. Changes in LV filling were not the consequence of a systolic dysfunction, because LV systolic function was normal. Doppler indices indicated that LA pressure was below 15 cm H2O in all the patients with COPD and control subjects. Several factors can be put forward to explain these changes; the first one is tachycardia. In addition to hypoxemia and medications, echocardiography suggested that a decreased LV preload participated in increased heart rate. Analysis of Doppler transmitral and pulmonary venous flows demonstrated the role of the ventricular interdependence because a correlation existed between LA and LV filling pattern and right ventricle pressure and diameter.
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In chronic obstructive pulmonary disease (COPD), left ventricular (LV) systolic functional disorders are rare, unless there is an associated history of heart disease. In a recent study, Dario-Vizza and colleagues assessed the frequency of systolic dysfunction to be less than 5% (1). However, abnormal diastolic function appears to be more frequent. The first studies that reported diastolic dysfunction were based on interventional catheterization (2, 3). They were confirmed by experimental research in animals (4, 5) and in humans using Doppler ultrasound (6, 7). According to these more recent studies, the frequency of abnormalities in LV relaxation has been suggested to be approximately 90% in patients with COPD.
Over the last few years, Doppler studies of diastolic function have been completed by the combined analysis of mitral and pulmonary venous flow, and the evaluation of filling pressure is now accessible (8). In the present work, LV systolic function and LV diastolic function, derived from the transmitral flow, were studied in a population of patients with severe COPD in comparison to a control population. Furthermore, the study was completed by an exploration of the pulmonary venous flows, which reflect left atrial (LA) filling and permit an estimation of LA pressure. The combination of all these parameters allowed a better analysis of the diastolic function and a better understanding of the mechanisms of the filling disorders.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Patients
Patients with COPD were included in the study. All were clinically stable. Patients with systemic hypertension, history of congenital, rheumatic, or ischemic heart disease, chronic atrial fibrillation, complete right or left bundle branch block, or cardiac failure were excluded. The diagnosis of COPD was based on clinical history, physical findings, chest radiography, pulmonary function tests, and arterial blood gases. Pulmonary function was studied with a spirometer (ILmeter 1304; Masterlab Jaeger, Würzberg, Germany). Forced expiratory volume in one second (FEV1.0) and vital capacity (VC) were measured in all the subjects within a week before the Doppler echocardiographic study. The results were expressed as a percentage of the predicted values.
Doppler Echocardiographic Parameters
The Doppler echocardiographic examinations were performed using a commercially available Doppler echocardiograph (Diasonics Vingmed CFM 750 A; GE Ultrasound, Courtaboeuf, France) and a transducer array of 2.5 MHz. Images were obtained from the parasternal views (long axis and short axis) and from an apical four-chamber view. The subjects were placed in a left lateral decubitus position for the parasternal views and in a supine position for the apical four-chamber view. Subjects stay at rest for 10 min before the ultrasonographic examination. Recordings were obtained at a paper speed of 100 mm/s with simultaneous tracing of the electrocardiogram.
Cardiac diameters. LA diameter, left ventricle end-systolic and end-diastolic diameters (LVESD, LVEDD), left ventricle end-systolic and
end-diastolic interventricular septal thickness (LVESSEP, LVEDSEP), left ventricle end-systolic and end-diastolic posterior wall thickness (LVESPW, LVEDPW), and right ventricle end-systolic and end-diastolic diameters (RVESD, RVEDD) were measured by M-mode echocardiography from the left parasternal short- and long-axis views.
Left ventricular mass (LVM) was calculated with the application of
Devereux's formula (9): LVM = 1.04 × [(LVEDD + LVEDSEP + LVEDPW)3 
LVEDD3] 13.6.
LV systolic function. Standard indexes of global LV systolic performance were ejection fraction (EF) and LV percent fractional shortening (%FS). %FS was taken as the ratio (LVEDD LVESD/
LVEDD), EF was determined using the Teicholz formula. Heart rate
(HR) was recorded by echocardiogram and rate was averaged over 60 s.
Systolic pulmonary arterial pressure. Systolic pulmonary artery pressure (Ppa) was derived from tricuspid or pulmonary regurgitation. Tricuspid regurgitant flow was identified in continuous Doppler mode from the apical four-chamber view. The Bernoulli equation, as simplified by Hatle and Angelsen, was used to calculate the systolic transtricuspid gradient that equals 4V2 (in which V is the maximal regurgitant velocity in m/s). Right atrial (RA) pressure was arbitrarily fixed to a value of 10 mm Hg and the systolic Ppa was obtained as suggested by Currie and coworkers by the equation (10): Systolic Ppa = gradient RV/RA + 10.
When no tricuspid regurgitant flow could be identified, pulmonary regurgitant flow was searched. Continuous-wave Doppler was used to record early and late maximal velocity of the regurgitant flow. Early and late diastolic gradients were estimated using the simplified Bernoulli equation and systolic Ppa was calculated as follows (11):
Systolic Ppa = (3 × early diastolic gradient)
(2 × late diastolic gradient) + 10
LV diastolic function. Recordings were all performed at the end of a normal expiration to eliminate the effects of respiration on the studied parameters. Measurements were averaged from, at least, three consecutive beats.
Transmitral flow. Pulsed Doppler transmitral flows were obtained from the apical four-chamber view, positioning the sample volume at the mitral valve leaflet tips. Doppler velocity curves were recorded at 100 mm/s. Peak velocity and velocity time integral (VTI) of the initial flow (E wave), representing the early filling phase, and of the late flow (A wave), representing the atrial contraction, were measured (Figure 1). The peak velocities ratio (E/A), the total VTI (total LV filling; i.e., E wave VTI + A wave VTI), and the ratio of the A wave VTI to the total VTI (relative contribution of atrial contraction to the total LV filling) were calculated. The following variables were also measured: duration of the transmitral A wave, pressure half time (PHT), and isovolumetric relaxation time (IVRT). PHT was the half time of the deceleration of the early diastolic transmitral flow, which reflected the rapidity of the pressure gradient drop from LA to LV. IVRT was the interval from the aortic closure signal to the mitral valve opening signal.
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Pulmonary venous flow. Pulmonary venous flow velocities were obtained in pulsed Doppler from the apical four-chamber view, positioning the sample volume 0.5 to 1 cm into the upper right pulmonary vein. Three distinct components were determined: forward systolic flow (S wave), divided into early systolic flow related to the atrial relaxation and late systolic flow related to the increase of the pulmonary vein pressure after RV contraction and also due to the movement of the mitral annulus during the LV contraction; forward diastolic flow (D wave), related to the decrease of LA pressure after the mitral wave opening; and the atrial reversal flow (pulmonary reversal A wave) during the atrial contraction (Figure 2). Peak velocities and VTI were measured for the three components as well as the duration of the pulmonary reversal A wave. The systolic fraction of pulmonary venous forward flow was the ratio of the systolic VTI to the sum of the systolic and diastolic VTI.
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LA pressure. Estimations of LA pressure were obtained from the comparison of mitral and pulmonary venous flow velocities (12, 13). Duration of the pulmonary A reversal flow exceeding the duration of the mitral A flow indicates an increase in LA pressure, exceeding 15 mm Hg (13). A decreased systolic filling fraction of pulmonary venous forward flow below 0.4 is also considered as a sign of elevated LA pressure (13).
Controls
Twenty control subjects were studied. They were healthy volunteers. The same procedures for the ultrasonic examinations were applied.
Intraobserver and Interobserver Variabilities
Examinations were recorded on videotape and analyzed by two independent investigators. Variability was assessed in all patients and control subjects by two independent observers (AB, PA) and by one observer (AB) on two different occasions. The mean percentages of intraobserver and interobserver variabilities were, respectively, 5.8% and 6.9% for transmitral E peak flow velocity; 3.0% and 3.6% for transmitral A peak flow velocity; 0.9% and 1.3% for E/A ratio; 5.5% and 7.7% for IVRT; 5.1% and 6.0% for mitral A-wave duration; 9.5% and 11.2% for pulmonary venous S peak flow velocity; 10.3% and 11.8% for pulmonary venous D peak flow velocity; 3.6% and 4.3% for systolic fraction of pulmonary venous forward flow; 2.8% and 3.7% for the S/D ratio; 16.0% and 18.7% for pulmonary venous reversal A peak flow velocity; and 8.9% and 10.1% for pulmonary venous A wave duration.
Statistical Analysis
Continuous variables were expressed as mean ± 1 standard deviation. Statistical tests were run on Sigma Stat software. Analysis of differences among patients and control subjects was made using unpaired Student's t test. In the event of cohorts of variables not having a normal distribution, comparisons were done with Mann-Whitney U test. The chi-square test was used to determine correlation between qualitative parameters; Yates' correction was used where small numbers were involved. This test was used to compare the incidence of inversed E/A ratio in patients with COPD and control subjects.
To investigate the relationship between right and left cavities in the COPD group, Pearson correlation tests were used between RV dimensions and pressure (RVEDD, RVESD, RVEDD LVEDD, systolic Ppa) and LV and LA filling parameters (transmitral and pulmonary venous flow velocities and VTI, PHT, IVRT). In the event of cohorts of variables without a normal distribution, comparisons were done with a Spearman test. Differences between groups were considered significant at p < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Patients
Fifty-two patients were initially screened. Of these 52 patients, 18 presented with an echographic image of poor quality which did not allow satisfactory measurements of LV and LA filling parameters. As LV diastolic function was the goal of our study, those patients were excluded. Their characteristics (mean age 60 ± 17 yr, FEV1.0: 0.97 ± 0.45 L/s; VC 2.20 ± 0.9 L; FEV1.0/VC 45 ± 15%; PaO2 59 ± 11 mm Hg; PaCO2 48 ± 9 mm Hg) did not differ from those of the patients studied (Table 1). Satisfactory echocardiograms could be performed in 34 patients, who were included in the study. Their lung function tests and arterial blood gas values are listed in Table 1. Mean FEV1.0 was 0.96 ± 0.39 L/s and mean FEV1.0/VC ratio was 43%, demonstrating a high degree of bronchial obstruction in our patients.
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Control subjects were healthy volunteers without respiratory or cardiac history. Their lung function tests were normal. Control subjects and patients were well matched for sex, age, and height (Table 2). Patients with COPD exhibited a significantly lower body weight.
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Echocardiographic Variables
Comparison between patients with COPD and control subjects. LV systolic function. HR was significantly increased in patients with COPD when compared with the control subjects (Table 2). Standard indices of global LV systolic function were not different in the two groups (Table 4).
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LEFT CAVITIESRight and left cavities. Right ventricular dimensions including RVEDD, RVESD, and the RVEDD/LVEDD ratio were markedly and significantly enlarged (Figure 2) in the COPD group (Table 3). A tricuspid regurgitant flow was identified in 70% of the COPD patients and 75% of the control subjects; a pulmonary regurgitant flow was identified in another 12% of the COPD patients and 15% of the control group. systolic Ppa measurements were satisfactorily obtained in 82% of the patients with COPD and 90% of the control subjects. Systolic Ppa was significantly higher in COPD patients compared with the control subjects (Table 3). LV diameters were comparable in COPD patients and control subjects (Table 4).
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LV and LA filling. LV and LA filling profiles differ significantly in patients with COPD when compared with the control subjects (Tables 5 and 6). E/A ratio was significantly lower in patients with COPD (p < 0.02). The transmitral flow pattern exhibited a dominant A wave with inverse E/A ratio (E/A < 1) in 26 patients with COPD (76%) and in only seven control subjects (35%) (p = 0.003, chi-square test). As tachycardia may have modified LV filling indices, adjustment for HR was made on time parameters, IVRT and PHT. IVRT adjusted for individual HR appeared significantly longer in COPD patients (p < 0.001). PHT adjusted for HR tended to show a difference but without reaching significance (p = 0.07).
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LA pressure. The duration of the pulmonary A venous reversal flow exceeded the duration of the mitral A-wave flow in one COPD patient and one control subject. Systolic filling fraction of pulmonary venous forward flow was greater than 0.4 in all patients and control subjects (Table 6).
Correlation between RV indices and LV and LA filling in
patients with COPD. There was no significant correlation between right ventricle diameters and transmitral peak velocities
and VTI. However, systolic Ppa positively correlated with
IVRT (r = 0.4, p < 0.05). The peak flow velocity and VTI of
the pulmonary forward systolic flow inversely correlated with
RVEDD (respectively, r = 0.65, p = 0.0001 and r = 0.64,
p = 0.0003), with RVESD (respectively, r = 0.6, p = 0.0002 and r = 0.56, p < 0.005), with RVEDD/LVEDD ratio (respectively, r = 0.6, p = 0.0003, and r = 0.65, p = 0.0003), and
with systolic Ppa (r = 0.4, p < 0.05, and r = 0.4, p < 0.05).
The systolic fraction of pulmonary venous forward flow inversely correlated with RVEDD (r = 0.39, p < 0.05), with RVESD (r = 0.43, p = 0.02), and with RVEDD-LVEDD ratio (r = 0.47, p < 0.02).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The present investigation is the first one, to our knowledge, that performed a complete and totally noninvasive hemodynamic study in patients with COPD, including LV and LA filling. We obtained satisfactory results in 65% of 52 unselected patients with COPD, which underlines the limits of ultrasonography in those patients. In the 34 patients studied, pulmonary venous flow seemed more difficult to analyze with a greater intra- and intervariability, when compared with the transmitral flow. However, variabilities remained low, approximately 10% for the pulmonary D and S peak flow velocity, and below 5% for the systolic filling fraction of pulmonary venous forward flow or the S/D ratio.
Our study on the transmitral Doppler flow pattern confirmed that changes occurred in LV filling profile in patients with COPD in comparison to a control group. We demonstrated in the COPD group a significantly decreased E/A ratio. The contribution of the atrial contraction to LV filling was significantly increased (44% versus 38%; Table 5). This underscores the importance of maintaining the sinus rhythm in these patients. Age is one of the most cited factors that usually modify the LV filling profile (14). In young subjects, LV elastic recoil is vigorous and myocardial relaxation is swift, so most of the LV filling is completed during early diastole (E wave) with only a small contribution of filling during the atrial contraction (A wave).
With age, early filling decreases and the contribution of the atrial contraction increases. Inverse E/A ratio is normally observed in subjects older than 60 yr of age. However, in the present study, the control subjects and patients with COPD were paired for age and this factor may not have interfered. When compared, our two populations significantly differed for mean weight, suggesting that patients with COPD suffer from malnutrition. However, this factor is not known to influence LV filling and therefore does not provide an explanation for the discrepancies observed.
Many factors can be put forward to explain the change in
the LV filling profile, some of them well evidenced by Doppler echography. The first and most important factor is the significantly increased HR in the COPD group. Tachycardia
shortened the diastolic filling period and atrial contraction
may have occurred before the early filling was completed; the
transmitral A peak velocity will be higher than it would be
if the HR were slower. This tachycardia may be due to multiple causes including hypoxemia or medications. Our patients
all presented with a marked hypoxemia and COPD patients are known to show a more pronounced reaction to low blood
oxygen content (15). Medications given to the COPD patients
included 
2-agonist, theophylline, or atropine, all potentially
responsible for tachycardia. But, apart from these, ultrasonographic examinations showed a decreased LV filling volume in
the COPD group, as demonstrated by the significant decline
in the total transmitral VTI (i.e., E wave VTI + A wave VTI)
(Table 5). This decreased LV preload in stable patients with
COPD has rarely been reported in the literature, and may
have contributed to the acceleration of the HR. Reduced LV
preload could be due to reduced venous return flow or to hypovolemia.
Obstruction of the bronchi, severe in our COPD patients (Table 1), may have increased intrinsic positive end-expiratory pressure and limited the venous return blood flow (16). A recent study also showed that patients with obstructive pulmonary disease tended to be systemically vasodilated (17), depending on the severity of hypoxemia. Experimental research in healthy subjects submitted to long periods of altitude- induced hypoxia has shown a marked decrease in LV preload, owing to a reduction in their plasma volume (18). The mechanism might be the inhibition of sodium reabsorption in the renal tubules secondary to hypoxemia. Although the present study well demonstrated the decreased LV preload, it failed to explore the different mechanisms responsible. With reduced venous return flow, absolute or relative hypovolemia will have to be checked in a population of stable patients with COPD.
However, after adjustment of the filling data to individual HR differences persisted, indicating that others factors may have influenced the results. Doppler echocardiography clearly showed phenomena of ventricular interdependence. Physiologically, RV and LV are two distinct chambers that are anatomically and functionally bound in some ways: both share the interventricular septum and both are enclosed in the pericardium. As a consequence, alterations in RV size and function will influence LV performance. Ventricular interaction is a marked phenomenon in patients with COPD. In the present study, we demonstrated in COPD patients, both a RV systolic overload, evidenced by a significantly increased systolic Ppa, and a RV dilatation evidenced by a significantly increased RVEDD/LVEDD ratio. Elevation of systolic Ppa led to an increased RV pressure and to a decreased gradient pressure from RV to LV, with modifications of the septum kinetics.
Elevation of systolic Ppa also induces a dilation of the right heart chambers, which shifts the interventricular septum (6, 19, 20) and decreases LV filling (Figure 3). The result is a restriction in early LV filling and a prolonged isovolumetric relaxation time (21). In the present study, we not only observed changes in transmitral flow profile (inverse E/A), but also found that IVRT in the COPD group was positively correlated to systolic Ppa. IVRT adjusted for HR was significantly prolonged in the COPD group compared with the control group. These observations demonstrated the participation of the ventricular interdependence in the modifications of LV filling profile.
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Changes in the LV filling rate do not seem to be the consequence of a LV systolic dysfunction, because the parameters of LV systolic function were similar in both groups. This result is in agreement with previous findings in patients with COPD (22). Moreover, there was no evidence of LV hypertrophy in our COPD group, which might have explained LV filling abnormality. An increase in LV mass has been inconsistently described in patients with COPD (3, 25) and related to concomitant diseases such as hypertension (26). The absence of LV hypertrophy in our patients was probably due to the exclusion of patients with hypertension or cardiac failure. Hypoxia is an additional possible cause for the alteration of LV relaxation in these patients, but hypercapnia may antagonize this effect (27).
Moreover, our study of pulmonary venous flow showed an alteration of LA filling in patients with COPD. The S/D ratio and the systolic fraction of the pulmonary venous forward flow were significantly lower in the COPD group compared with the control subjects. This alteration in LA filling could have been related to an increased LA pressure.
However, pulmonary flow parameters (i.e., systolic fraction of pulmonary venous forward flow and duration of the pulmonary A reversal wave) do not support this hypothesis. LA pressure in the COPD group always remained below 15 mm Hg. This is in accordance with previous studies using catheterization, which have found normal mean wedge pressure in almost all patients with COPD. In the present study, we demonstrated a relationship between RV dimensions and the LA filling profile: The systolic fraction of pulmonary venous forward flow, which represents LA filling during the ventricular systole (28), inversely correlated with RVEDD, RVESD, and RVEDD/ LVEDD ratio, meaning that, the more the RV was dilated and overloaded, the less the LA filled during the ventricular systole. One explanation could be a reduced forward movement of the mitral annulus during the ventricular systole, induced by the shift of the interventricular septum. These elements also contributed to the ventricular interdependence, previously demonstrated in the Doppler analysis of transmitral flow.
In conclusion, our study confirms that changes occur in LA and LV filling in stable COPD patients. Contribution of LV filling during the atrial contraction becomes greater, which underlines the importance of maintaining a sinus rhythm in these patients, and LA filling decreases during the ventricular systole. However, these abnormal LA and LV filling profiles do not result in a major elevation of filling pressure at rest. These changes are the result of several factors, including increased HR. Tachycardia is secondary to hypoxemia or medications, but also to a decreased LV preload, as suggested by the decrease in the transmitral VTI. When adjusted to individual HR, differences still persist in LV filling parameters between patients with COPD and control subjects, so that other factors must be considered. The present Doppler echocardiographic study well demonstrates the phenomenon of ventricular interdependence, as modifications in LV and LA filling correlate to RV pressure and diameter. Others parameters such as relaxation disorders due to hypoxia may be involved, but are not presently explored.
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Footnotes |
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Correspondence and requests for reprints should be addressed to Alain Boussuges, M.D., Service de Réanimation Médicale et Hyperbarie, Hôpital Salvator, 249 Boulevard de Sainte-Marguerite, 13274 Marseille Cedex 9, France. E-mail: jsainty{at}mail.ap-hm.fr
(Received in original form August 17, 1999 and in revised form January 31, 2000).
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References |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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 G.-C. Funk, I. Lang, P. Schenk, A. Valipour, S. Hartl, and O. C. Burghuber Left Ventricular Diastolic Dysfunction in Patients With COPD in the Presence and Absence of Elevated Pulmonary Arterial Pressure Chest, June 1, 2008; 133(6): 1354 - 1359. [Abstract] [Full Text] [PDF]
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 H. Watz, B. Waschki, C. Boehme, M. Claussen, T. Meyer, and H. Magnussen Extrapulmonary Effects of Chronic Obstructive Pulmonary Disease on Physical Activity: A Cross-sectional Study Am. J. Respir. Crit. Care Med., April 1, 2008; 177(7): 743 - 751. [Abstract] [Full Text] [PDF]
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F. H. Rutten, M.-J. M. Cramer, J.-W. J. Lammers, D. E. Grobbee, and A. W. Hoes Heart failure and chronic obstructive pulmonary disease: An ignored combination? Eur J Heart Fail, November 1, 2006; 8(7): 706 - 711. [Abstract] [Full Text] [PDF]
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 K.-O. Larsen, I. Sjaastad, A. Svindland, K. A. Krobert, O. H. Skjonsberg, and G. Christensen Alveolar hypoxia induces left ventricular diastolic dysfunction and reduces phosphorylation of phospholamban in mice Am J Physiol Heart Circ Physiol, August 1, 2006; 291(2): H507 - H516. [Abstract] [Full Text] [PDF]
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C. Tji-Joong Gan, J.-W. Lankhaar, J. T. Marcus, N. Westerhof, K. M. Marques, J. G. F. Bronzwaer, A. Boonstra, P. E. Postmus, and A. Vonk-Noordegraaf Impaired left ventricular filling due to right-to-left ventricular interaction in patients with pulmonary arterial hypertension Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1528 - H1533. [Abstract] [Full Text] [PDF]
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 F. H Rutten, K. G M Moons, M.-J. M Cramer, D. E Grobbee, N. P A Zuithoff, J.-W. J Lammers, and A. W Hoes Recognising heart failure in elderly patients with stable chronic obstructive pulmonary disease in primary care: cross sectional diagnostic study BMJ, December 10, 2005; 331(7529): 1379. [Abstract] [Full Text] [PDF]
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A. Vonk-Noordegraaf, J. T. Marcus, S. Holverda, B. Roseboom, and P. E. Postmus Early Changes of Cardiac Structure and Function in COPD Patients With Mild Hypoxemia Chest, June 1, 2005; 127(6): 1898 - 1903. [Abstract] [Full Text] [PDF]
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 R. J. van den Hout, H. J. Lamb, J. G. van den Aardweg, R. Schot, P. Steendijk, E. E. van der Wall, J. J. Bax, and A. de Roos Real-Time MR Imaging of Aortic Flow: Influence of Breathing on Left Ventricular Stroke Volume in Chronic Obstructive Pulmonary Disease Radiology, November 1, 2003; 229(2): 513 - 519. [Abstract] [Full Text] [PDF]
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M. J. TOBIN Chronic Obstructive Pulmonary Disease, Pollution, Pulmonary Vascular Disease, Transplantation, Pleural Disease, and Lung Cancer in AJRCCM 2000 Am. J. Respir. Crit. Care Med., November 15, 2001; 164(10): 1789 - 1804. [Full Text] [PDF]
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