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(Chest. 2001;119:1755-1760.)
© 2001 American College of Chest Physicians

Angiotensin-Converting Enzyme Inhibitor Therapy Improves Respiratory Muscle Strength in Patients With Heart Failure*

Catherine Coirault, MD, PhD; Albert Hagège, MD, PhD; Denis Chemla, MD, PhD; Marie-Dominique Fratacci, MD, PhD; Claude Guérot, MD and Yves Lecarpentier, MD, PhD

* From the U 451 INSERM (Dr. Coirault), Laboratoire d’Optique Appliquée-ENSTA-Ecole Polytechnique, Palaiseau; Service de Cardiologie (Dr. Hagège and Guérot), Hôpital Boucicaut, Paris; Service d’Explorations Fonctionnelles (Drs. Chemla and Lecarpentier), Centre Hospitalier et Universitaire de Bicêtre, Assistance Publique-Hôpitaux de Paris, Le Kremlin-Bicêtre; and IRIS (Dr. Fratacci), Courbevoie, France.

Correspondence to: Catherine Coirault, MD, PhD, INSERM 451-LOA-Ensta-Ecole Polytechnique, Batterie de l’Yvette, 91761 Palaiseau Cedex, France; e-mail: coirault{at}enstay.ensta.fr


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: Respiratory muscle strength has been shown to be reduced in patients with chronic heart failure. The purpose of this prospective study was to determine whether long-term therapy with the angiotensin-converting enzyme (ACE) inhibitor perindopril improves respiratory muscle strength in patients with chronic heart failure.

Patients and methods: Eighteen patients with stable chronic heart failure were administered perindopril, 4 mg/d, in addition to their standard therapy for a period of 6 months. Fourteen patients completed the study. Maximum inspiratory pressure (PImax) and maximum expiratory pressure (PEmax) expressed in percentage of predicted values, left ventricular ejection fraction (LVEF) determined by means of two-dimensional echocardiography, and pulmonary volumes were obtained before and after therapy.

Measurements and results: As compared to baseline, there was a significant increase in both PImax and PEmax after therapy (57 ± 27% predicted vs 78 ± 36% predicted and 62 ± 20% predicted vs 73 ± 15% predicted, respectively; each p < 0.05). LVEF increased (34 ± 5% vs 41 ± 10%; p < 0.05); functional class improved by >= 1 New York Heart Association (NYHA) class in five patients. There were no changes in pulmonary volumes. No correlation was found between changes in PImax and PEmax and changes in either LVEF or NYHA functional class.

Conclusions: In patients with chronic heart failure, long-term therapy with the ACE inhibitor perindopril improved respiratory muscle strength, as indicated by significant increases in PImax and PEmax.

Key Words: angiotensin • heart failure • respiratory muscles


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Respiratory muscle weakness and pulmonary abnormalities are likely to be responsible for some of the limiting symptoms in patients with chronic heart failure. Numerous studies1 2 3 4 5 6 7 have reported decreased maximum respiratory mouth pressures in chronic heart failure patients. The reduction in muscle strength may contribute to dyspnea by increasing the ratio of the pressure developed at the mouth during tidal ventilation to the maximum inspiratory pressure (PImax).4 Efforts to prevent or to reverse the development of respiratory muscle weakness in patients with symptomatic left ventricular dysfunction are therefore warranted. Selective respiratory muscle training8 and nasal continuous positive airway pressure9 have been shown to improve respiratory muscle function in chronic heart failure patients. In addition, aerobic training10 and cardiac transplantation11 help reduce the excessive ventilatory response to exercise in these patients.

Angiotensin-converting enzyme (ACE) inhibitors prolong life12 and may significantly improve both symptoms and exercise tolerance in patients with heart failure.13 14 15 Improvements in exercise capacity are associated with a gradual reversal of chronic structural alterations in peripheral skeletal muscle.15 16 In animal models of chronic cardiac disease, the ACE inhibitor perindopril tends to prevent the reduction in intrinsic diaphragm performance.17 18 19 The possibility that ACE inhibitor therapy improves respiratory muscle function has not been studied in patients with chronic heart failure.

The aim of this prospective study was to investigate the effects of long-term ACE inhibitor therapy on respiratory muscle strength in patients with chronic heart failure. Accordingly, maximum respiratory mouth pressures, lung volumes, left ventricular ejection fraction (LVEF), and symptoms of heart failure were determined before and after long-term therapy with perindopril. The relations between the respiratory findings and the degree of cardiac improvement after therapy were also analyzed.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patient Population
Patients < 75 years of age meeting the following criteria were included in our 6-month prospective study: a history of chronic heart failure as defined by symptoms of left ventricular dysfunction, left ventricular dilation, and resting LVEF <= 40%. Patients were excluded if they had had the following: (1) a myocardial infarction within 3 months, (2) recent congestive heart decompensation (within 10 days), (3) prior treatment with ACE inhibitors, or (4) an episode of respiratory tract infection within 1 month. Other exclusion criteria included primary pulmonary or neuromuscular diseases, aortic stenosis, chronic renal failure, women of child-bearing age, and contraindications to ACE inhibitor therapy. The study was approved by the Comité Consultatif de Protection des Personnes dans la Recherche Biomédicale de l’hôpital de Bicêtre. Written informed consent was obtained from all subjects prior to enrollment.

Study Design
Clinical assessment, LVEF, and respiratory data were registered at baseline (premedication measurements) and at the end of the study period. Perindopril was administered at an initial dose of 2 mg po once daily. After 15 days, the dose was increased to 4 mg/d unless symptoms of hypotension or other side effects developed. Medication was kept constant throughout the study period in all patients who completed the study. During the study period, patients did not receive any forms of cardiac or pulmonary rehabilitation. Follow-up visits occurred at 15 days, 3 months, and 6 months after the beginning of ACE therapy.

Respiratory Muscle Strength and Pulmonary Function
Respiratory muscle strength was assessed by measuring maximum static respiratory pressures. PImax at residual volume (RV) and maximum expiratory pressure (PEmax) at total lung capacity (TLC) were used as indexes of inspiratory and expiratory muscle strength, respectively. All measurements were performed by the same experienced technician. Patients breathed through a mouth piece attached to a three-way valve connected to a spirometer. Mouth pressures were measured with a pressure transducer (Respiratory Pressures Module type; Medical Graphics; St. Paul, MN) [pressure range of ± 300 cm H2O]. Measurements were made with patients in the seated position, and efforts were sustained for 2 to 3 s. Cheek compression was maintained to minimize facial muscle contribution to pressure measurements during the PEmax maneuver.20 A small leak via a 22-gauge needle was incorporated during the PImax and PEmax maneuvers to help keep the glottis open, thereby preventing the subject from generating additional negative pressure with facial or pharyngeal muscles. Each effort was displayed on a digital monitor, and the patients were vigorously coaxed by the examiner to better their efforts using visual feedback. After instruction in the techniques for performing each maneuver, PImax and PEmax were recorded in triplicate or until a stable value was achieved.20 Results were expressed in absolute values and as percentage of predicted values based on normal values for age, sex, and body surface area.21

FVC, FEV1, TLC, RV, and tidal volume (VT) were determined by plethysmography (D Body Plethysmograph; MedGraphics system 1085; Medical Graphics). FEV1, FVC, and TLC were expressed both in absolute values and as percentage of normal predicted values. The ratio of physiologic dead space to VT (VD/VT) was calculated from the Bohr equation: VD/VT = (PaCO2 - PeCO2)/PaCO2 x VT, where PeCO2 is the mixed expired carbon dioxide partial pressure. All the respiratory function measurements were performed on the same day, allowing sufficient rest between each maneuver.

Cardiac Function and Symptom Assessment
Symptoms of chronic heart failure were assessed according to the New York Heart Association (NYHA) functional class. In class I, chronic heart failure does not limit physical activity; in class II and III, chronic heart failure results in slight (class II) or marked (class III) limitation of physical activity; in class IV, chronic heart failure results in inability to carry any physical activity without discomfort. Two-dimensional echocardiographic studies were performed according to the recommendations of the American Society of Echocardiography.22 We used a Sonos 2500 device equipped with a 2.5 to 3.5-MHz probe (Hewlett Packard; Andover, MA). Left ventricular end-diastolic volume (EDV) and end-systolic volume were obtained from the apical four-chamber and two-chamber views by a modified Simpson’s rule, from which LVEF was automatically calculated as the difference between EDV and end-systolic volume normalized to EDV.

Statistical Analysis
Data were analyzed on an intention-to-treat basis. The analysis set was defined as all patients having at least one evaluation of the main criteria (ie, PImax and PEmax during treatment). Comparisons of values at the end of the study with baseline values were made using two-tailed paired t tests. Relationships among variables were examined by least-squares linear regression analysis. Correlations between changes (from baseline) in PImax and PEmax on the one hand and changes in NYHA functional class, LVEF, and spirometry on the other hand were also studied. Data are expressed as mean values ± SD unless otherwise indicated. A value of p < 0.05 was considered significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Patient Population
Eighteen patients with stable chronic heart failure were included in the study (17 men and 1 woman). Baseline clinical characteristics of the study population are given in Table 1 . The cause of heart failure was coronary artery disease (n = 7) or dilated cardiomyopathy (n = 11), while three patients presented with concomitant significant mitral insufficiency. At entry to the study, four patients were in NYHA functional class I, six patients were in class II, and eight patients were in class III. Patients were treated with diuretics (n = 11), digitalis (n = 4), vasodilators (n = 7), ß-blockers (n = 4), and antiarrhythmic drugs (n = 5). Nine patients had a history of smoking, and six patients were current smokers (41 ± 25 pack-years). Four patients were withdrawn from the study for the following reasons: death (n = 1), drug-related adverse events (cough, n = 1; arterial hypotension, n = 1), and unavailable for follow-up (n = 1). The analysis was performed on the 14 patients who completed the study.


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  		Table 1.. Clinical Characteristics of the Included Population*

 
Pulmonary Function Data
Pulmonary function data are summarized in Table 2 . At baseline, chronic heart failure patients showed a slight reduction in predicted FVC and FEV1 values, with no change in the FEV1/FVC ratio. VD/VT was slightly increased. There were no significant changes in lung volumes over the course of the study (Table 2) .


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  		Table 2.. Respiratory Data at Baseline and After 6 Months of Therapy With Perindopril in Patients With Chronic Heart Failure*

 
Maximum Inspiratory and Expiratory Pressures
The influence of ACE inhibitor therapy on PImax and PEmax is depicted in Fig 1 . At baseline, PImax and PEmax were approximately 57 to 62% of predicted normal values, respectively (Fig 1) . Over the study period, there was a significant increase in both PImax (62 ± 33 cm H2O at baseline vs 83 ± 42 cm H2O at the end of the study period [representing, respectively, 57 ± 27% and 78 ± 34% of predicted values; p < 0.05]) and PEmax (84 ± 28 cm H2O at baseline vs 98 ± 20 cm H2O [representing, respectively, 62 ± 20% and 73 ± 15% of predicted values; p < 0.05]). No significant correlation was found between changes in maximum mouth pressures and spirometric data.



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  		Figure 1.. Individual (open circle) and mean ± SE (closed circle) values of PImax and PEmax expressed as percentage of predicted values. PImax was measured at RV (left panel) and PEmax was measured at TLC (right panel). Two subjects did not satisfactorily perform one of the PImax measurements, so that only 12 pairs of PImax data points appear in the graph. There was a significant improvement in both PImax and PEmax over the study period.

 
Symptom Assessment and Left Ventricular Function
Functional class improved by one or more NYHA class in 5 of 14 patients. There was no significant correlation between changes in NYHA functional class and changes in respiratory parameters. Individual echocardiographic LVEF before and after perindopril therapy are shown in Figure 2 . LVEF increased significantly (34 ± 5% vs 41 ± 10%; p < 0.05). There was no correlation between changes in LVEF and changes in respiratory muscle pressures.



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  		Figure 2.. Individual (open circle) and mean ± SE (closed circle) values of LVEF (in percent) as determined by echocardiography. There was a significant increase in LVEF over the study period (p < 0.05 vs baseline).

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
We examined the effects of long-term therapy with the ACE inhibitor perindopril on respiratory muscle function in chronic heart failure patients. Our results suggest that perindopril improved maximum inspiratory and expiratory muscle strength in patients with stable chronic heart failure. Changes in respiratory pressures did not correlate with changes in LVEF, pulmonary volumes, or NYHA functional class.

The present study provides the first evidence that respiratory muscle weakness in chronic heart failure patients is at least partially reversible with ACE inhibitor therapy. As compared to baseline, chronic heart failure patients demonstrated a 21% absolute improvement in PImax after long-term therapy with perindopril while PEmax improved by about 10% (Fig 1) . Numerous studies1 2 3 4 5 6 have reported a reduction in maximum respiratory mouth pressure in patients with chronic heart failure comparable to those seen in our patients. In these studies, as in ours, maximum respiratory mouth pressures were used as an estimate of respiratory muscle strength. Although dependent on maximal patient effort, maximum static mouth pressures have been shown to be highly reproducible over time.21 In a study7 involving patients with chronic heart failure, when esophageal pressure was recorded during maximal sniff, the reduction obtained in diaphragm strength was more moderate than that obtained from static mouth pressure maneuvers. This suggests that maximum static mouth pressure may overestimate the reduction in diaphragm strength in chronic heart failure patients. However, it is generally considered that one can gain reliable information by monitoring changes in maximum respiratory mouth pressure over time in the individual patients.21 Lung volume is a major determinant of the length and curvature of the respiratory muscles, and may therefore influence maximum mouth pressure. An increase in PImax may result from a change in RV, but no such change was observed in our patients over the study period (Table 2) . Furthermore, there was no correlation between the changes in respiratory pressures and those in lung volumes. Therefore, changes in lung volumes cannot account for improvement in respiratory pressures in perindopril-treated chronic heart failure patients. Taken together, these findings strongly suggest that increases in PImax and PEmax after long-term perindopril therapy reflected an improvement in respiratory muscle strength in chronic heart failure patients. This result is consistent with the improved intrinsic diaphragm performance reported after perindopril therapy, both in a genetically polymyopathic model17 18 and in a rabbit model of chronic cardiac overload.19

The increase in PEmax was lower than the increase in PImax. Importantly, abdominal muscles are known to contribute substantially to PEmax while PImax is essentially dependent on diaphragm muscle.21 Structural and functional differences between diaphragm and other skeletal muscles during chronic heart failure2 3 19 may help explain the different effects of ACE therapy on inspiratory and expiratory pressures.

In chronic heart failure patients, previous studies13 15 have demonstrated beneficial effects of ACE inhibitors on exercise capacity. Long-term therapy with ACE inhibitors improves peripheral skeletal muscle flow, femoral oxygen extraction, and peak oxygen consumption (O2) during exercise in chronic heart failure patients.13 15 A highly significant correlation has been reported between peak exercise femoral blood flow and peak O2.13 15 In addition, inspiratory muscle strength is a determinant of peak O2 in chronic heart failure.23 Improved PImax after selective respiratory muscle training in chronic heart failure patients is associated with a significant increase in peak O2.8 It is thus possible that the increased PImax observed in our study may help explain the increased peak O2 after ACE inhibitor therapy. However, since peak O2 was not determined in our study, further studies are needed to clarify this point.

In the present study, changes in respiratory mouth pressure did not correlate with changes in LVEF. These findings are consistent with previous studies showing that exercise intolerance correlates poorly with LVEF,14 24 although respiratory muscle weakness has been found to be more pronounced in more severe chronic heart failure patients according to the NYHA classes.5 25 Increases in muscle mass26 and in fiber area,16 and partial reversal of mitochondrial27 and metabolic abnormalities16 have been reported after ACE inhibitor therapy. In experimental animal models of cardiac failure, improved diaphragm muscle performance after ACE therapy has been attributed mainly to a beneficial effect on crossbridge number.18 19 28 Enhanced muscle performance after long-term ACE inhibitor therapy likely reflected intrinsic changes in the biochemical and structural characteristics of skeletal muscle. Such mechanisms may help improve respiratory muscle strength, thereby improving PImax and PEmax.

Our study has several limitations. It was an uncontrolled study. ACE inhibitor therapy is so far the only treatment that prolongs life in chronic heart failure. Therefore, for ethical reasons, a comparison group of chronic heart failure patients treated with placebo was not included. The population studied was composed predominantly of men, with only one woman in the group. It would be interesting to perform additional analyses on different subsets of patients with chronic heart failure with regard to the heart function, lung volume, or NYHA-class variables. However, the sample size of chronic heart failure patients was too small for such valuable multivariate analysis to be performed. Improvement in respiratory muscle performance after ACE inhibitor therapy requires confirmation in larger trials. It was not within the scope of our study to test the cardiopulmonary exercise responses after long-term administration of ACE inhibitor. Further studies are needed to determine whether improved respiratory muscle strength after ACE inhibitor therapy correlates with the improvement in exercise endurance in stable congestive heart failure. In our study, four patients were receiving digoxin at inclusion. Diaphragmatic strength improves significantly after acute digoxin administration in patients with COPD.29 However, there are a number of arguments against the potential confounding effects of digoxin on our data. Our patients did not suffer from COPD. Two of these patients withdrew from the study, so that only two patients treated with digoxin were taken into account in the full analysis set. In addition, one of the two remaining treated patients had been receiving digoxin for at least 3 years, the other being treated for 1 month. Thus, baseline measurements were performed in patients already treated with digoxin for at least several weeks. The effects of long-term digoxin administration on respiratory pressures in patients with chronic heart failure have yet to be established. Taking these limitations into account, the present study indicates that long-term therapy with the ACE inhibitor perindopril partially reverses respiratory muscle weakness, as assessed by a significant improvement in maximum respiratory pressures.


   Footnotes
 
Abbreviations: ACE = angiotensin-converting enzyme; EDV = end-diastolic volume; LVEF = left ventricular ejection fraction; NYHA = New York Heart Association; PEmax = maximum expiratory pressure; PImax = maximum inspiratory pressure; RV = residual volume; TLC = total lung capacity; VD/VT = ratio of physiologic dead space to tidal volume; O2 = oxygen consumption; VT = tidal volume

This work was supported in part by Servier Laboratories, IRIS, Courbevoie, France.

Received for publication June 8, 2000. Accepted for publication December 12, 2000.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. De Troyer, A, Estenne, M, Yernault, JC (1980) Disturbance of respiratory muscle function in patients with mitral valve disease. Am J Med 69,867-873[CrossRef][ISI][Medline]
  2. Hammond, MD, Bauer, KA, Sharp, JT, et al (1990) Respiratory muscle strength in congestive heart failure. Chest 98,1091-1094[Abstract/Free Full Text]
  3. McParland, C, Resch, EF, Krishnan, B, et al (1995) Inspiratory muscle weakness in chronic heart failure: role of nutrition and electrolyte status and systemic myopathy. Am J Respir Crit Care Med 151,1101-1107[Abstract]
  4. Mancini, DM, Henson, D, La Manca, J, et al (1992) Respiratory muscle function and dyspnea in patients with chronic congestive heart failure. Circulation 86,909-918[Abstract/Free Full Text]
  5. Ambrosino, N, Opasich, C, Crotti, P, et al (1994) Breathing pattern, ventilatory drive and respiratory muscle strength in patients with chronic heart failure. Eur Respir J 7,17-22[Abstract]
  6. Evans, SA, Watson, L, Hawkins, M, et al (1995) Respiratory muscle strength in chronic heart failure. Thorax 50,625-628[Abstract/Free Full Text]
  7. Hughes, PD, Polkey, MI, Harris, ML, et al (1999) Diaphragm strength in chronic heart failure. Am J Respir Crit Care Med 160,529-534[Abstract/Free Full Text]
  8. Mancini, DM, Henson, D, La Manca, J, et al (1995) Benefit of selective respiratory muscle training on exercise capacity in patients with chronic congestive heart failure. Circulation 91,320-329[Abstract/Free Full Text]
  9. Granton, JT, Naughton, MT, Benard, DC, et al (1996) CPAP improves inspiratory muscle strength in patients with heart failure and central sleep apnea. Am J Respir Crit Care Med 153,277-282[Abstract]
  10. Sullivan, M, Higginbotham, M, Cobb, F (1989) Exercise training in patients with chronic heart failure delays ventilatory anaerobic threshold and improves submaximal exercise performance. Circulation 79,324-329[Abstract/Free Full Text]
  11. Marzo, KP, Wilson, JR, Mancini, DM (1992) Effects of cardiac transplantation on ventilatory response to exercise. Am J Cardiol 69,547-553[CrossRef][ISI][Medline]
  12. . The SOLVD Investigators. (1991) Effects of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 325,293-302[Abstract]
  13. Mancini, DM, Davis, L, Wexler, JP, et al (1987) Dependence of enhanced maximal exercise performance on increased peak skeletal muscle perfusion during long-term captopril therapy in heart failure. J Am Coll Cardiol 10,845-850[Abstract]
  14. Massie, BM (1988) Exercise tolerance in congestive heart failure: role of cardiac function, peripheral blood flow and muscle metabolism and effect of treatment. Am J Med 84(suppl 3A),75-82
  15. Drexler, H, Banhart, U, Meinertz, T, et al (1989) Contrasting peripheral short-term and long-term effects of converting enzyme inhibition in patients with congestive heart failure: a double-blind, placebo-controlled trial. Circulation 79,491-502[Abstract/Free Full Text]
  16. Shaufelberger, M, Andersson, G, Erickson, BO, et al (1996) Skeletal muscle changes in patients with chronic heart failure before and after treatment with enalapril. Eur Heart J 17,1678-1685[Abstract/Free Full Text]
  17. Chemla, D, Scalbert, E, Desché, P, et al (1992) Effects of perindopril on myocardial inotropy, lutropy and economy, and on diaphragmatic contractility in the cardiomyopathic Syrian hamster. J Pharmacol Exp Ther 262,516-525[Abstract/Free Full Text]
  18. Lecarpentier, Y, Coirault, C, Lerebours, G, et al (1997) Effects of angiotensin converting enzyme inhibition on crossbridge properties of diaphragm in cardiomyopathic hamsters of the dilated Bio 53–58 strain. Am J Respir Crit Care Med 155,630-636[Abstract]
  19. Coirault, C, Langeron, O, Lambert, F, et al (1999) Impaired skeletal muscle performance in the early stage of cardiac pressure overload in rabbits: beneficial effects of angiotensin converting enzyme inhibition. J Pharmacol Exp Ther 291,70-75[Abstract/Free Full Text]
  20. Rubinstein, I, Slutsky, AS, Rebuck, AS, et al (1988) Assessment of maximal expiratory pressure in healthy adults. J Appl Physiol 64,2215-2219[Abstract/Free Full Text]
  21. Bruschi, C, Cerveri, I, Zoia, MC, et al (1992) Reference values of maximal respiratory mouth pressures: a population-based study. Am Rev Respir Dis 146,790-793[ISI][Medline]
  22. . ACC/AHA (1997) Guidelines for the clinical application of echography: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Clinical Application of Echography) Circulation 95,1686-1744[Free Full Text]
  23. Chua, TP, Anker, SD, Harrington, D, et al (1995) Inspiratory muscle strength is a determinant of oxygen consumption in chronic heart failure. Br Heart J 74,381-385[Abstract/Free Full Text]
  24. Franciosa, JA, Park, M, Levine, TB (1981) Lack of correlation between exercise capacity and indexes of resting left ventricular performance in heart failure. Am J Cardiol 47,33-39[CrossRef][ISI][Medline]
  25. Nishimura, Y, Maeda, H, Tanaka, K, et al (1994) Respiratory muscle strength and hemodynamics in chronic heart failure. Chest 105,355-359[Abstract/Free Full Text]
  26. Jondeau, G, Dib, JC, Dubourg, O, et al (1996) Relation of functional improvement in congestive heart failure after quinapril therapy to peripheral limitation. Am J Cardiol 79,635-638[CrossRef]
  27. Drexler, H, Riede, U, Münzel, T, et al (1992) Alterations of skeletal muscle in chronic heart failure. Circulation 85,1751-1759[Abstract/Free Full Text]
  28. Lecarpentier Y, Péry N, Coirault C, et al. Intrinsic alterations of diaphragm muscle in experimental cardiomyopathy. Am Heart J 1993; 126:3, 770–776
  29. Aubier, M, Murciano, D, Viires, N, et al (1987) Effects of digoxin on diaphragmatic strength generation in patients with chronic obstructive pulmonary disease during acute respiratory failure Am Rev Respir Dis 135,544-548[ISI][Medline]



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